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2020-05-27T18:33:46Z

M Jahan: Created blank page

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2020-05-27T18:14:55Z

M Jahan: Created page with "Ahmad Muneeb, MBBS[mailto:ahmadmuneeb92@live.com]"

[[User:Ahmadmuneeb|Ahmad Muneeb, MBBS]][mailto:ahmadmuneeb92@live.com]

Restless legs syndrome

2020-05-06T05:23:48Z

M Jahan: Reverted edits by M Jahan (talk) to last revision by Jesus Hernandez

__NOTOC__
{{Infobox_Disease |
Name = Restless legs syndrome |
Image = RLS-Schlafmuster.jpg |
Caption = Sleep pattern of a Restless Legs Syndrome patient (red) vs. a healthy sleep pattern (blue). |
}}
{{Restless legs syndrome}}

'''For patient information click [[{{PAGENAME}} (patient information)|here]]'''

{{CMG}}; {{AE}} {{CZ}} {{JH}}

{{SK}} Wittmaack-Ekbom's syndrome; RLS
==[[Restless legs syndrome overview|Overview]]==

==[[Restless legs syndrome historical perspective|Historical Perspective]]==

==[[Restless legs syndrome classification|Classification]]==

==[[Restless legs syndrome pathophysiology|Pathophysiology]]==

==[[Restless legs syndrome causes|Causes]]==

==[[Restless legs syndrome differential diagnosis|Differentiating Restless legs syndrome from other Diseases]]==

==[[Restless legs syndrome epidemiology and demographics|Epidemiology and Demographics]]==

==[[Restless legs syndrome risk factors|Risk Factors]]==

==[[Restless legs syndrome screening|Screening]]==

==[[Restless legs syndrome natural history, complications and prognosis|Natural History, Complications and Prognosis]]==

==Diagnosis==
[[Restless legs syndrome diagnostic criteria|Diagnostic Criteria]] | [[Restless legs syndrome history and symptoms|History and Symptoms]] | [[Restless legs syndrome physical examination|Physical Examination]] | [[Restless legs syndrome laboratory findings|Laboratory Findings]] | [[Restless legs syndrome electrocardiogram|Electrocardiogram]] | [[Restless legs syndrome other diagnostic studies|Other Diagnostic Studies]]

==Treatment==
[[Restless legs syndrome medical therapy|Medical Therapy]] | [[Restless legs syndrome surgery | Surgery]] | [[Restless legs syndrome primary prevention|Primary Prevention]] | [[Restless legs syndrome secondary prevention|Secondary Prevention]] | [[Restless legs syndrome cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Restless legs syndrome future or investigational therapies|Future or Investigational Therapies]]

==Case Studies==
[[Restless legs syndrome case study one|Case #1]]

==Related Chapters==
*[[Actigraphy]]
*[[Parasomnia]]
*[[Disease mongering]]

{{Diseases of the nervous system|state=collapsed}}

[[Category:Sleep disorders]]
[[Category:Syndromes]]
[[Category:Neurology]]
[[Category:Primary care]]

[[ca:Síndrome de les cames neguitoses]]
[[de:Restless-Legs-Syndrom]]
[[es:Síndrome de las piernas inquietas]]
[[fr:Syndrome des jambes sans repos]]
[[ms:Sindrom kaki resah]]
[[ja:むずむず脚症候群]]
[[pl:Zespół niespokojnych nóg]]
[[pt:Síndrome das pernas inquietas]]
[[fi:Levottomat jalat]]
[[sv:Rastlösa ben]]

{{WH}}
{{WS}}

Fibromuscular dysplasia physical examination

2020-05-06T05:21:11Z

M Jahan: Reverted edits by M Jahan (talk) to last revision by Mehrian.jafari

__NOTOC__
{{Fibromuscular dysplasia}}

{{CMG}}; {{AE}}{{M.B}}

==Overview==
Patients with FMD usually appear normal. In physical examination of patients with FMD mild to moderate [[hypertension]] may be detected. In the auscultation of [[neck]] among patients with involvement of [[Common carotid artery|carotid artery]] or auscultation of [[epigastric]] or flank of [[Renovascular disease|renovascular]] FMD bruits may be heard. Eventullay due to nonspecific sypmtoms and sings of FMD, the diagnosis of this disease needs highly clinical suspicion of healthcare provider.

==Physical Examination==

*Physical examination of patients with fibromuscular dysplasia is usually normal. However the most common presentation of [[renal artery]] FMD is [[renovascular hypertension]], but in the physical examination of patients enrolled in the US registry for fibromuscular dysplasia mean blood pressure was 130/75 mm Hg.<ref>{{Cite journal
| author = [[Jeffrey W. Olin]], [[James Froehlich]], [[Xiaokui Gu]], [[J. Michael Bacharach]], [[Kim Eagle]], [[Bruce H. Gray]], [[Michael R. Jaff]], [[Esther S. H. Kim]], [[Pam Mace]], [[Alan H. Matsumoto]], [[Robert D. McBane]], [[Eva Kline-Rogers]], [[Christopher J. White]] & [[Heather L. Gornik]]
| title = The United States Registry for Fibromuscular Dysplasia: results in the first 447 patients
| journal = [[Circulation]]
| volume = 125
| issue = 25
| pages = 3182–3190
| year = 2012
| month = June
| doi = 10.1161/CIRCULATIONAHA.112.091223
| pmid = 22615343
}}</ref>

*The presence of [[carotid bruits]] on physical examination has low [[sensitivity]] however its [[specificity]] for identifying extracranial FMD is highly suggestive.
*The presence of an epigastric or [[Flanks|flank]] bruit on physical examination, such as [[carotid bruits]] is low, however, its presence strongly suggestive of [[Kidney|renal]] or [[Mesentery|mesenteric]] FMD.
*Focal neurological deficits, [[cranial nerve]] involvement, [[pupil]] abnormality or [[ptosis]] (findings consistent with [[Horner syndrome]]) may be detected in FMD.
===Appearance of the Patient===
*Patients with FMD usually appear normal.
===Vital Signs===
*High blood pressure may be seen among patients with renovascular FMD.
===Skin===
*Skin examination of patients with FMD is normal.

===HEENT===
*HEENT examination of patients with FMD is normal.
===Neck===
*[[Carotid bruits]] may be auscultated unilaterally or bilaterally using the bell of the stethoscope.
===Abdomen===
*In abdominal examination of patients with FMD, epigastric or flank bruits may be heard.

===Extremities===
*While FMD involving the lower extremities most commonly involves the external [[iliac]] arteries, extremities examination of patients with FMD is usually normal, however, a bruit caused by [[iliac]] FMD may be heard in the lower abdomen from the [[umbilicus]] to the [[Inguinal region|inguinal]] region.
*FMD involving the upper extremities most commonly involves the [[Brachial artery|brachial]] arteries, in some cases, there may be discrepant blood pressures in the arms. Arm [[claudication]] or a [[bruit]] heard over the antecubital fossa is uncommon but may occur.<ref>{{Cite journal
| author = [[Jeffrey W. Olin]], [[Heather L. Gornik]], [[J. Michael Bacharach]], [[Jose Biller]], [[Lawrence J. Fine]], [[Bruce H. Gray]], [[William A. Gray]], [[Rishi Gupta]], [[Naomi M. Hamburg]], [[Barry T. Katzen]], [[Robert A. Lookstein]], [[Alan B. Lumsden]], [[Jane W. Newburger]], [[Tatjana Rundek]], [[C. John Sperati]] & [[James C. Stanley]]
| title = Fibromuscular dysplasia: state of the science and critical unanswered questions: a scientific statement from the American Heart Association
| journal = [[Circulation]]
| volume = 129
| issue = 9
| pages = 1048–1078
| year = 2014
| month = March
| doi = 10.1161/01.cir.0000442577.96802.8c
| pmid = 24548843
}}</ref>

==References==
{{Reflist|2}}

{{WH}}
{{WS}}
[[Category: (name of the system)]]

Spinal stenosis

2020-05-06T05:20:30Z

M Jahan: Reverted edits by M Jahan (talk) to last revision by Christopher Popma

__NOTOC__
{{Spinal stenosis}}
For patient information click [[Spinal stenosis (patient information)|here]]

{{CMG}}; '''Associate Editor-In-Chief:''' {{CZ}}
==[[Spinal stenosis overview|Overview]]==

==[[Spinal stenosis classification|Classification]]==

==[[Spinal stenosis pathophysiology|Pathophysiology]]==

==[[Spinal stenosis causes|Causes]]==

==[[Spinal stenosis differential diagnosis|Differentiating Spinal stenosis from other Diseases]]==

==[[Spinal stenosis epidemiology and demographics|Epidemiology and Demographics]]==

==[[Spinal stenosis risk factors|Risk Factors]]==

==[[Spinal stenosis natural history, complications and prognosis|Natural History, Complications and Prognosis]]==

==Diagnosis==
[[Spinal stenosis history and symptoms|History and Symptoms]] | [[Spinal stenosis physical examination|Physical Examination]] | [[Spinal stenosis x ray|X Ray]] | [[Spinal stenosis CT|CT]] | [[Spinal stenosis MRI|MRI]] | [[Spinal stenosis other diagnostic studies|Other Diagnostic Studies]]

==Treatment==
[[Spinal stenosis medical therapy|Medical Therapy]] | [[Spinal stenosis surgery|Surgery]] | [[Spinal stenosis cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Spinal stenosis future or investigational therapies|Future or Investigational Therapies]]

==Case Studies==
:[[Spinal stenosis case study one|Case #1]]

{{Diseases of the musculoskeletal system and connective tissue}}

[[Category:Skeletal disorders]]
[[Category:Rheumatology]]
[[Category:Orthopedics]]

[[nl:Wervelkanaalstenose]]

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

Cavernous sinus thrombosis

2020-05-06T05:19:50Z

M Jahan: Reverted edits by M Jahan (talk) to last revision by Charmaine Patel

__NOTOC__
{{Cavernous sinus thrombosis}}
{{CMG}}

{{SK}} CST, thrombosis of the cavernous intracranial sinus, cavernous sinus syndrome, parasellar lesions, carotid-cavernous fistulas, C-C fistulas,

==[[Cavernous sinus thrombosis overview|Overview]]==

==[[Cavernous sinus thrombosis historical perspective|Historical Perspective]]==

==[[Cavernous sinus thrombosis pathophysiology|Pathophysiology]]==

==[[Cavernous sinus thrombosis causes|Causes]]==

==[[Cavernous sinus thrombosis differential diagnosis|Differentiating Cavernous sinus thrombosis from other Diseases]]==

==[[Cavernous sinus thrombosis epidemiology and demographics|Epidemiology and Demographics]]==

==[[Cavernous sinus thrombosis risk factors|Risk Factors]]==

==[[Cavernous sinus thrombosis natural history, complications and prognosis|Natural History, Complications and Prognosis]]==

==Diagnosis==

[[Cavernous sinus thrombosis history and symptoms|History and Symptoms ]] | [[ Cavernous sinus thrombosis physical examination|Physical Examination]] | [[Cavernous sinus thrombosis laboratory findings|Laboratory Findings]] | [[Cavernous sinus thrombosis CT|CT]] | [[Cavernous sinus thrombosis MRI|MRI]] | [[Cavernous sinus thrombosis other imaging findings|Other Imaging Findings]] | [[Cavernous sinus thrombosis other diagnostic studies|Other Diagnostic Studies]]

==Treatment==
[[Cavernous sinus thrombosis medical therapy|Medical Therapy]] | [[Cavernous sinus thrombosis surgery |Surgery]] | [[Cavernous sinus thrombosis primary prevention|Primary Prevention]] | [[Cavernous sinus thrombosis secondary prevention|Secondary Prevention]] | [[Cavernous sinus thrombosis cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Cavernous sinus thrombosis future or investigational therapies|Future or Investigational Therapies]]

==Case Studies==
[[Cavernous sinus thrombosis case study one|Case #1]]

== Acknowledgements ==
The content on this page was first contributed by: [[C. Michael Gibson]] M.S., M.D.

{{WikiDoc Help Menu}}
{{WS}}

[[Category:Disease]]
[[Category:Neurology]]
[[Category:Hematology]]

Spina bifida causes

2020-05-06T05:14:28Z

M Jahan:

__NOTOC__
{{Spina bifida}}

{{CMG}}; {{AE}} {{sali}}{{MMJ}}
==Overview==
There is no well-known cause of spina bifida. It may result from a variety of occupational, environmental, genetic, and viral [[Spina bifida risk factors|risk factors]], such as a family history of neural tube defects and folate deficiency.

==Causes==
There is no well-known cause of spina bifida. It may result from a variety of occupational, environmental, genetic, and viral [[Spina bifida risk factors|risk factors]], such as a family history of neural tube defects and folate deficiency.

==References==
{{Reflist|2}}

{{WH}}
{{WS}}
[[Category: (name of the system)]]

Spina bifida causes

2020-05-06T05:13:02Z

M Jahan:

__NOTOC__
{{Spina bifida}}

{{CMG}}; {{AE}} {{sali}}
==Overview==
There is no well known cause of spina bifida. It may result from a variety of occupational, environmental, genetic, and viral [[Spina bifida risk factors|risk factors]], such as a family history of neural tube defects and folate deficiency.

==Causes==
There is no well known cause of spina bifida. It may result from a variety of occupational, environmental, genetic, and viral [[Spina bifida risk factors|risk factors]], such as a family history of neural tube defects and folate deficiency.

==References==
{{Reflist|2}}

{{WH}}
{{WS}}
[[Category: (name of the system)]]

Transverse myelitis

2020-05-06T05:06:59Z

M Jahan:

__NOTOC__
{{Transverse myelitis}}
'''For patient information, click [[Transverse myelitis (patient information)|here]]'''

{{CMG}}; {{AE}}{{sali}}, {{MMJ}}

{{SK}}

==[[Transverse myelitis overview|Overview]]==

==[[Transverse myelitis historical perspective|Historical Perspective]]==

==[[Transverse myelitis classification|Classification]]==

==[[Transverse myelitis pathophysiology|Pathophysiology]]==

==[[Transverse myelitis causes|Causes]]==

==[[Transverse myelitis differential diagnosis|Differentiating Transverse myelitis from other Diseases]]==

==[[Transverse myelitis epidemiology and demographics|Epidemiology and Demographics]]==

==[[Transverse myelitis risk factors|Risk Factors]]==

==[[Transverse myelitis screening|Screening]]==

==[[Transverse myelitis natural history, complications and prognosis|Natural History, Complications and Prognosis]]==

==Diagnosis==
[[Transverse myelitis diagnostic study of choice|Diagnostic study of choice]] | [[Transverse myelitis history and symptoms|History and Symptoms]] | [[Transverse myelitis physical examination|Physical Examination]] | [[Transverse myelitis laboratory findings|Laboratory Findings]] | [[Transverse myelitis electrocardiogram|Electrocardiogram]] | [[Transverse myelitis x ray|X-Ray Findings]] | [[Transverse myelitis echocardiography and ultrasound|Echocardiography and Ultrasound]] | [[Transverse myelitis CT scan|CT-Scan Findings]] | [[Transverse myelitis MRI|MRI Findings]] | [[Transverse myelitis other imaging findings|Other Imaging Findings]] | [[Transverse myelitis other diagnostic studies|Other Diagnostic Studies]]

==Treatment==
[[Transverse myelitis medical therapy|Medical Therapy]] | [[Transverse myelitis interventions|Interventions]] | [[Transverse myelitis surgery|Surgery]] | [[Transverse myelitis primary prevention|Primary Prevention]] | [[Transverse myelitis secondary prevention|Secondary Prevention]] | [[Transverse myelitis cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Transverse myelitis future or investigational therapies|Future or Investigational Therapies]]

==Case Studies==
[[Transverse myelitis case study one|Case #1]]

[[Category: (name of the system)]]

Central pontine myelinolysis medical therapy

2020-05-06T05:06:26Z

M Jahan:

__NOTOC__
{{Central pontine myelinolysi}}
{{CMG}}; {{AE}} {{sali}}, {{MMJ}}

==Overview==
Treatment of patients with central pontine myelinolysis is mainly supportive because once the [[Osmotic demyelination syndrome|osmotic demyelination]] has begun, there is no cure or specific treatment. Alcoholic patients should receive vitamin supplementation including [[vitamin B6]], [[Vitamin B9|B9]], and [[Vitamin B12|B12]] and evaluation of their nutritional status.

==Medical Therapy==
Treatment of patients with central pontine myelinolysis is mainly supportive because once the [[Osmotic demyelination syndrome|osmotic demyelination]] has begun, there is no cure or specific treatment.<ref name="pmid24569125">{{cite journal| author=Spasovski G, Vanholder R, Allolio B, Annane D, Ball S, Bichet D et al.| title=Clinical practice guideline on diagnosis and treatment of hyponatraemia. | journal=Eur J Endocrinol | year= 2014 | volume= 170 | issue= 3 | pages= G1-47 | pmid=24569125 | doi=10.1530/EJE-13-1020 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24569125 }}</ref><ref name="pmid11803185">{{cite journal| author=Lampl C, Yazdi K| title=Central pontine myelinolysis. | journal=Eur Neurol | year= 2002 | volume= 47 | issue= 1 | pages= 3-10 | pmid=11803185 | doi=10.1159/000047939 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11803185 }}</ref>

Alcoholic patients should receive vitamin supplementation including [[vitamin B6]], [[Vitamin B9|B9]] and [[Vitamin B12|B12]] and evaluation of their nutritional status.<ref name="pmid7466381">{{cite journal| author=Kleinschmidt-DeMasters BK, Norenberg MD| title=Rapid correction of hyponatremia causes demyelination: relation to central pontine myelinolysis. | journal=Science | year= 1981 | volume= 211 | issue= 4486 | pages= 1068-70 | pmid=7466381 | doi=10.1126/science.7466381 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7466381 }}</ref>

==References==
{{Reflist|2}}

{{WH}}
{{WS}}
[[Category: (name of the system)]]

Central pontine myelinolysis causes

2020-05-06T05:04:02Z

M Jahan:

__NOTOC__
{{Central pontine myelinolysis}}

{{CMG}}; {{AE}} {{sali}}, {{MMJ}}
==Overview==
The most common cause of central pontine myelinolysis is rapid correction(>48-hours duration) of [[hyponatremia]] in patients with the history of prolonged [[hyponatremia]]. Other causes of central pontine myelinolysis may include: Lengthened orthotopic [[liver transplantation]], [[hypophosphatemia]] secondary to [[refeeding syndrome]], deficiencies in neuronal/glial cell energy supply and utilization which produce [[glial cell]] [[apoptosis]] and thus the clinical syndrome of central pontine myelinolysis and prolonged [[ischemia]].

==Causes==
===Common Causes===
The most common cause of central pontine myelinolysis is rapid correction(>48-hours duration) of [[hyponatremia]] in patients with the history of prolonged [[hyponatremia]].<ref name="pmid29295827">{{cite journal| author=Seliger S, Kestenbaum B| title=Commentary on Treatment of Severe Hyponatremia. | journal=Clin J Am Soc Nephrol | year= 2018 | volume= 13 | issue= 4 | pages= 650-651 | pmid=29295827 | doi=10.2215/CJN.13381217 | pmc=5969468 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29295827 }} </ref><ref name="pmid15300900">{{cite journal| author=Yu J, Zheng SS, Liang TB, Shen Y, Wang WL, Ke QH| title=Possible causes of central pontine myelinolysis after liver transplantation. | journal=World J Gastroenterol | year= 2004 | volume= 10 | issue= 17 | pages= 2540-3 | pmid=15300900 | doi=10.3748/wjg.v10.i17.2540 | pmc=4572157 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15300900 }} </ref>

Other causes of central pontine myelinolysis may include:<ref name="pmid20182780">{{cite journal| author=Norenberg MD| title=Central pontine myelinolysis: historical and mechanistic considerations. | journal=Metab Brain Dis | year= 2010 | volume= 25 | issue= 1 | pages= 97-106 | pmid=20182780 | doi=10.1007/s11011-010-9175-0 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20182780 }} </ref><ref name="pmid26557081">{{cite journal| author=Yamashita C, Shigeto H, Maeda N, Torii T, Ohyagi Y, Kira J| title=A Case of Central Pontine Myelinolysis Caused by Hypophosphatemia Secondary to Refeeding Syndrome. | journal=Case Rep Neurol | year= 2015 | volume= 7 | issue= 3 | pages= 196-203 | pmid=26557081 | doi=10.1159/000440711 | pmc=4637517 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26557081 }} </ref><ref name="pmid11430268">{{cite journal| author=Ashrafian H, Davey P| title=A review of the causes of central pontine myelinosis: yet another apoptotic illness? | journal=Eur J Neurol | year= 2001 | volume= 8 | issue= 2 | pages= 103-9 | pmid=11430268 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11430268 }} </ref><ref name="pmid8324964">{{cite journal| author=Giannetti AV, Pittella JE| title=Ischemic and hemorrhagic necrosis of the pons with anatomical location similar to that of central pontine myelinolysis in a chronic alcoholic patient. | journal=Clin Neuropathol | year= 1993 | volume= 12 | issue= 3 | pages= 156-9 | pmid=8324964 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8324964 }} </ref>

*Lengthened orthotopic [[liver transplantation]]
*[[Hypophosphatemia]] secondary to [[refeeding syndrome]]
*Deficiencies in [[neuronal]]/[[Glial cells|glial cell]] energy supply and utilization which produce [[glial cell]] [[apoptosis]] and thus the clinical syndrome of central pontine myelinolysis
*Prolonged [[ischemia]]

==References==
{{Reflist|2}}

{{WH}}
{{WS}}
[[Category: (name of the system)]]

Creutzfeldt-Jakob disease causes

2020-05-06T05:02:53Z

M Jahan:

__NOTOC__
{{‪Creutzfeldt-Jakob disease‬}}
{{CMG}} {{AE}} {{sali}}, {{MMJ}}
==Overview==
Creutzfeldt-Jakob disease is caused by the presence of a [[prion]] [[protein]], an abnormal isoform of a [[cellular]] [[glycoprotein]]. [[Prion]]s are transmissible particles that are devoid of [[nucleic acid]] and seem to be composed exclusively of a modified protein (PrPSc). The normal, [[cellular]] PrP ([[PrPC]]) is converted into [[PrPSc]] through a posttranslational process during which it acquires a high beta-sheet content.

==Causes==
*Creutzfeldt-Jakob disease is caused by the presence of a [[prion]] [[protein]], an abnormal isoform of a [[cellular]] [[glycoprotein]].<ref name="www.cdc.gov">{{Cite web | last = | first = | title = http://www.cdc.gov/ncidod/dvrd/cjd/qa_cjd_infection_control.htm#what | url = http://www.cdc.gov/ncidod/dvrd/cjd/qa_cjd_infection_control.htm#what | publisher = | date = | accessdate = 14 February 2014 }}</ref>
*[[Prion]]s are transmissible particles that are devoid of [[nucleic acid]] and seem to be composed exclusively of a modified protein ([[PrPSc]]). The normal, cellular PrP ([[PrPC]]) is converted into [[PrPSc]] through a posttranslational process during which it acquires a high beta-sheet content.<ref name="pmid9811807">{{cite journal| author=Prusiner SB| title=Prions. | journal=Proc Natl Acad Sci U S A | year= 1998 | volume= 95 | issue= 23 | pages= 13363-83 | pmid=9811807 | doi= | pmc=33918 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9811807 }} </ref>

==References==
{{Reflist|2}}
{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

[[Category:Neurology]]
[[Category:Disease]]
[[Category:Transmissible spongiform encephalopathies]]
[[Category:Needs causes]]
[[Category:Needs overview]]

Central pontine myelinolysis pathophysiology

2020-05-06T05:02:45Z

M Jahan:

__NOTOC__
{{Central pontine myelinolysis}}
{{CMG}}; {{AE}} {{sali}}, {{MMJ}}

==Overview==
It is understood that central pontine myelinolysis is caused by the rapid correction of [[hyponatremia]]. The [[CNS]] is particularly susceptible to reductions in [[plasma osmolarity]], specially during [[hyponatremia]] which is the most commonly encountered [[electrolyte disturbance]]. When a decrease in the plasma [[osmolarity]] happens, neural cells first swell but then they are able to regain their original volume through the release of inorganic and organic osmolytes and exit of osmotically obligated water. Subsequent exposure to hypertonic stress(e.g., correction of [[hyponatremia]] with hypertonic I.V. solutions)resulting from a rapid correction of [[hyponatremia]] causes the [[ions]] to quickly re-enter the intracellular space and compels the water to follow. If the serum [[sodium]] levels rise too rapidly, the increased extracellular tonicity will continue to drive water out of the brain's cells because the brain cells do not have enough time to bring extracellular sodium into the cell, so the water goes out very fast. This can lead to cellular dysfunction and central pontine myelinolysis and finally death.

==Pathophysiology==
===Pathogenesis===

*It is understood that central pontine myelinolysis is caused by rapid correction of [[hyponatremia]].<ref name="pmid24682140">{{cite journal| author=Mascarenhas JV, Jude EB| title=Central pontine myelinolysis: electrolytes and beyond. | journal=BMJ Case Rep | year= 2014 | volume= 2014 | issue= | pages= | pmid=24682140 | doi=10.1136/bcr-2013-203516 | pmc=3975522 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24682140 }} </ref><ref name="pmid23760391" />
*The [[CNS]] is particularly susceptible to reductions in [[plasma osmolarity]], specially during [[hyponatremia]] which is the most commonly encountered [[electrolyte disturbance]].
*When a decrease in the plasma [[osmolarity]] happens, neural cells first swell but then they are able to regain their original volume through the:<ref name="pmid23760391">{{cite journal| author=Khosya S, Meena H| title=Central pontine myelinolysis. | journal=Indian J Med Res | year= 2013 | volume= 137 | issue= 5 | pages= 993-4 | pmid=23760391 | doi= | pmc=3734697 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23760391 }} </ref><ref name="pmid18256030">Burg MB, Ferraris JD (2008) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=18256030 Intracellular organic osmolytes: function and regulation.] ''J Biol Chem'' 283 (12):7309-13. [http://dx.doi.org/10.1074/jbc.R700042200 DOI:10.1074/jbc.R700042200] PMID: [https://pubmed.gov/18256030 18256030]</ref>
*#Release of inorganic and organic osmolytes
*#Exit of osmotically obligated water
*A subsequent exposure to hypertonic stress(e.g., correction of [[hyponatremia]] with hypertonic I.V. solution's)resulting from a rapid correction of [[hyponatremia]] causes the [[ions]] to quickly re-enter the intracellular space and compels the water to follow.<ref name="pmid30357070">{{cite journal| author=Sheikh AB, Afzal RM, Sagheer S, Bukhari MM, Javed A, Nasrullah A et al. z| title=The Dilemma of Inadvertent Pontine Demyelinosis: A Review of Literature. | journal=Cureus | year= 2018 | volume= 10 | issue= 8 | pages= e3174 | pmid=30357070 | doi=10.7759/cureus.3174 | pmc=6197531 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30357070 }} </ref><ref name="pmid23760391" /><ref name="pmid24682140" />
*If the serum sodium levels rise too rapidly, the increased [[Extracellular|extracellular tonicity]] will continue to drive water out of the brain neurons because the brain cells do not have enough time to bring [[Extracellular|extracellular sudiom]] into the cell, so the water goes out very fast instead.<ref name="pmid23760391">{{cite journal| author=Khosya S, Meena H| title=Central pontine myelinolysis. | journal=Indian J Med Res | year= 2013 | volume= 137 | issue= 5 | pages= 993-4 | pmid=23760391 | doi= | pmc=3734697 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23760391 }} </ref><ref name="pmid24682140" />
*This can lead to cellular dysfunction and central pontine myelinolysis and finally death.<ref name="pmid23760391">{{cite journal| author=Khosya S, Meena H| title=Central pontine myelinolysis. | journal=Indian J Med Res | year= 2013 | volume= 137 | issue= 5 | pages= 993-4 | pmid=23760391 | doi= | pmc=3734697 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23760391 }} </ref><ref name="pmid24682140" />

==Genetics==

There is no association between central pontine myelinolysis and genetic factors.

==Gross Pathology==

* On gross pathology of patients with central pontine myelinolysis a red, central, triangular region of softening may be seen with preservation of the surrounding [[parenchyma]] on opened sagittally [[pons]] and [[Medulla oblongata|medulla]] from the ventral aspect.<ref name="pmid29177819">{{cite journal| author=Haynes HR, Gallagher PJ, Cordaro A, Likeman M, Love S| title=A case of chronic asymptomatic central pontine myelinolysis with histological evidence of remyelination. | journal=Forensic Sci Med Pathol | year= 2018 | volume= 14 | issue= 1 | pages= 106-108 | pmid=29177819 | doi=10.1007/s12024-017-9933-y | pmc=5830465 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29177819 }} </ref>
*Central and symetrical [[demyelination]] in the base of the [[pons]] in cross section samples<ref name="pmid24887055">{{cite journal| author=Robinson CA, Adiele RC, Tham M, Lucchinetti CF, Popescu BF| title=Early and widespread injury of astrocytes in the absence of demyelination in acute haemorrhagic leukoencephalitis. | journal=Acta Neuropathol Commun | year= 2014 | volume= 2 | issue= | pages= 52 | pmid=24887055 | doi=10.1186/2051-5960-2-52 | pmc=4035095 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24887055 }} </ref>

 

==Microscopic Pathology==
On microscopic histopathological analysis, the following features are characteristic findings of central pontine myelinolysis:<ref name="pmid17071802">{{cite journal| author=Love S| title=Demyelinating diseases. | journal=J Clin Pathol | year= 2006 | volume= 59 | issue= 11 | pages= 1151-9 | pmid=17071802 | doi=10.1136/jcp.2005.031195 | pmc=1860500 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17071802 }} </ref><ref name="pmid24887055">{{cite journal| author=Robinson CA, Adiele RC, Tham M, Lucchinetti CF, Popescu BF| title=Early and widespread injury of astrocytes in the absence of demyelination in acute haemorrhagic leukoencephalitis. | journal=Acta Neuropathol Commun | year= 2014 | volume= 2 | issue= | pages= 52 | pmid=24887055 | doi=10.1186/2051-5960-2-52 | pmc=4035095 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24887055 }} </ref>
*

* Loss of myelinated fibers at the base of the pons that is usually central and symmetrical but also can be neither

*The lesions are sharply demarcated and contain sheets of lipid‐laden [[Macrophage|macrophages]] and large numbers of reactive [[Astrocyte|astrocytes]].
*Infiltration by [[Lymphocyte|lymphocytes]] is sparse or absent.
*Axons and neurons are mostly well preserved.
*Symmetrically spared “islands” of [[myelinated]] [[white matter]]

 

==References==
{{Reflist|2}}

{{WH}}
{{WS}}
[[Category: (name of the system)]]

Creutzfeldt-Jakob disease pathophysiology

2020-05-06T05:02:05Z

M Jahan:

__NOTOC__
{{‪Creutzfeldt-Jakob disease‬}}
{{CMG}} {{AE}} {{sali}}, {{MMJ}}
==Overview==
The majority of cases of Creutzfeldt-Jakob disease are thought to occur sporadically from [[prions]] by an unknown route of transmission. Reports on transmission by [[human growth hormone]] products, [[grafting]], [[Electrode|surgical electrode implantation]], and consumption of infected products have been described. Once transmitted, the CJD [[prion]] promotes refolding of the native proteins into the diseased state. The number of misfolded [[protein]] molecules increases exponentially, and the process leads to a large quantity of insoluble [[prions]] in the affected cells, resulting in [[cell death]]. On gross histopathological analysis, the brain tissue appears "spongy" with areas of perforation within the brain tissue. On microscopic histopathological analysis, spongiform changes, neuronal loss, [[astrocyte]] proliferation, and deposition of [[prion]] proteins in the brain are characteristic findings.

==Pathophysiology==

===Transmission===
* The majority of cases of Creutzfeldt-Jakob disease are thought to occur sporadically from prions by an unknown route of transmission.
* The defective protein associated with Creutzfeldt-Jakob disease can be inherited (familial form) or transmitted ([[Iatrogenesis|iatrogenic]] form) through the following:
** [[Human growth hormone]] (hGH) products
** [[Corneal grafting]]
** Dural grafts or [[electrode]] implants<ref>{{cite web|title =Questions and Answers: Creutzfeldt-Jakob Disease Infection-Control Practices|work =Infection Control Practices/CJD (Creutzfeldt-Jakob Disease, Classic)|publisher =Centers for Disease Control and Prevention|date =[[January 4]][[2007]]|url = http://www.cdc.gov/ncidod/dvrd/cjd/qa_cjd_infection_control.htm#sterilization|accessdate = 2007-06-09}}</ref><ref>{{cite web|title =WHO Infection Control Guidelines for Transmissible Spongiform Encephalopathies|Publisher =World Health Organization: Communicable Disease Surveillance and Control|date =[[26 March]] [[1999]]|url =http://www.who.int/csr/resources/publications/bse/WHO_CDS_CSR_APH_2000_3/en/|accessdate = 2007-06-09}}</ref><ref>{{cite journal |author=McDonnell G, Burke P. | title=The challenge of prion decontamination | journal=Clin Infect Dis | year=2003 | volume=36 | pages=1152–4 }}</ref>
** Use of [[Human growth hormone|HGH]] drawn from the [[pituitary gland]]s of [[cadaver]]s<ref name="titleHGH Linked to Brain Eater">{{cite web |url=http://www.wired.com/news/medtech/0,1286,62998,00.html |title=HGH Linked to Brain Eater |accessdate=2007-12-02 |format= |work=}}</ref>
** Consumption of infected animals
** Cannibalism
*The incubation period of prions is unknonw, but it is speculated that the disease may develop many years (up to 30-50 years) after initial exposure. However, these reports remain controversial.<ref>{{cite web|url=http://www.nature.com/nature/journal/v407/n6800/full/407025a0.html|title=Diamond, J.M. (2000)"Archaeology: Talk of cannibalism" ''Nature'' 407, 25-26}}</ref>
=== Pathogenesis ===
* The CJD prion promotes refolding of the native [[proteins]] into the diseased state.
* The number of misfolded [[protein]] molecules increases exponentially, and the process leads to a large quantity of insoluble [[prions]] in the affected cells.
* This mass of misfolded [[protein]]s disrupts cell function and causes cell death.
* Once the prion is transmitted, the defective proteins invade the brain and are produced in a self-sustaining [[feedback loop]], causing exponential spread of the prion.
[[cadaver|<nowiki/>]]
===Mutations===
* [[Mutations]] in the gene responsible for the production of prion protein can cause misfolding of the alpha helical regions into beta pleated sheets.
* This change in the conformation disables the ability of the protein to undergo digestion.
* Individuals may also acquire CJD genetically through the [[mutation]] occurring [[PRNP|''PRNP'']] gene.

== Pathology ==

===Gross Pathology===
* On gross histopathological analysis, the brain tissue appears "spongy" with areas of perforation within the brain tissue.

=== Microscopic Pathology ===
* CJD is associated with the build-up of abnormal [[prion]] [[proteins]].

* The following microscopic findings may be present in CJD:
** Presence of florid plaques, defined as round, packed deposits of abnormal prion protein (in variant CJD)
** Spongiform changes
** Neuronal loss
** [[Astrocyte]] proliferation
** Deposition of prion protein throughout the brain<ref name="Sellars-2002">{{Cite journal | last1 = Sellars | first1 = RJ. | last2 = Collie | first2 = DA. | last3 = Will | first3 = RJ. | title = Progress in understanding Creutzfeldt-Jakob disease. | journal = AJNR Am J Neuroradiol | volume = 23 | issue = 7 | pages = 1070-2 | month = Aug | year = 2002 | doi = | PMID = 12169459 }}</ref>

[[Image:Spongiform changes in CJD.jpg|left|220px|Spongiform changes in brain in CJD]]
 

==References==
{{Reflist|2}}

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[[Category:Neurology]]
[[Category:Disease]]
[[Category:Transmissible spongiform encephalopathies]]
[[Category:Needs overview]]

Central pontine myelinolysis historical perspective

2020-05-06T05:01:52Z

M Jahan:

__NOTOC__
{{Central pontine myelinolysis}}

{{CMG}}; {{AE}}{{sali}}, {{MMJ}}

==Overview==
Central pontine myelinolysis was first discovered by '''Raymond Delacy Adams''', an an American [[neurologist]], in 1959. '''Raymond Delacy Adams''' and colleagues observed a rapidly evolving [[quadriplegia]] and [[pseudobulbar palsy]] in a young alcoholic man whose postmortem examination showed a large, symmetrical, essentially [[Demyelination|demyelinative]] lesion occupying the greater part of the base of the [[pons]] In 1950.

==Historical Perspective==

===Discovery===

* Central pontine myelinolysis was first discovered by '''Raymond Delacy Adams''', an an American [[neurologist]], in 1959.<ref name="pmid20445423">{{cite journal| author=Fisher CM| title=Dr. Raymond Delacy Adams (1911-2008): an appreciation. | journal=Neurologist | year= 2010 | volume= 16 | issue= 3 | pages= 141-2 | pmid=20445423 | doi=10.1097/NRL.0b013e3181c9280a | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=20445423 }} </ref><ref name="pmid13616772" /><ref name="pmid27610136" /><ref name="pmid16687066" />

*'''Raymond Delacy Adams''' and colleagues observed a rapidly evolving [[quadriplegia]] and [[pseudobulbar palsy]] in a young alcoholic man whose postmortem examination showed a large, symmetrical, essentially [[Demyelination|demyelinative]] lesion occupying the greater part of the base of the [[pons]] In 1950.<ref name="pmid13616772">{{cite journal| author=ADAMS RD, VICTOR M, MANCALL EL| title=Central pontine myelinolysis: a hitherto undescribed disease occurring in alcoholic and malnourished patients. | journal=AMA Arch Neurol Psychiatry | year= 1959 | volume= 81 | issue= 2 | pages= 154-72 | pmid=13616772 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13616772 }} </ref><ref name="pmid27610136">{{cite journal| author=Mohammed AS, Boddu P, Yazdani DF| title=Clinical Evolution of Central Pontine Myelinolysis in a Patient with Alcohol Withdrawal: A Blurred Clinical Horizon. | journal=Case Rep Med | year= 2016 | volume= 2016 | issue= | pages= 6065259 | pmid=27610136 | doi=10.1155/2016/6065259 | pmc=5004014 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27610136 }} </ref><ref name="pmid16687066">{{cite journal| author=Kumar S, Fowler M, Gonzalez-Toledo E, Jaffe SL| title=Central pontine myelinolysis, an update. | journal=Neurol Res | year= 2006 | volume= 28 | issue= 3 | pages= 360-6 | pmid=16687066 | doi=10.1179/016164106X110346 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16687066 }} </ref>

==References==
{{Reflist|2}}

{{WH}}
{{WS}}

Creutzfeldt-Jakob disease classification

2020-05-06T05:00:53Z

M Jahan:

{{Creutzfeldt-Jakob disease}}

{{CMG}}; {{AE}}{{sali}}, {{MMJ}}
==Overview==

Creutzfeldt-Jakob disease may be classified into four groups: '''Sporadic CJD,''' '''familial CJD''' and '''iatrogenic CJ'''. '''Sporadic CJD''' is the most common type and is [[idiopathic]]. '''Familial CJD''' is caused by inheritance of abnormal prions and is exceptionally rare. '''Iatrogenic CJ''' is very rare and the principal sources of outbreaks are: contaminated [[growth hormone]] derived from human cadavers with undiagnosed CJD infections, contaminated [[dura mater]] grafts, [[Neurosurgery|neurosurgical]] instrument contamination, [[Corneal graft|corneal grafts]], [[Gonadotrophic|gonadotrophic hormone]] and [[Blood transfusion|transfusion of blood]] products.
==Classification==

Creutzfeldt-Jakob disease may be classified into four groups:<ref name="pmid22411235">{{cite journal| author=Sikorska B, Knight R, Ironside JW, Liberski PP| title=Creutzfeldt-Jakob disease. | journal=Adv Exp Med Biol | year= 2012 | volume= 724 | issue= | pages= 76-90 | pmid=22411235 | doi=10.1007/978-1-4614-0653-2_6 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22411235 }} </ref>
* '''Sporadic CJD'''<ref name="pmid19863257">{{cite journal| author=Sharma S, Mukherjee M, Kedage V, Muttigi MS, Rao A, Rao S| title=Sporadic Creutzfeldt-Jakob disease--a review. | journal=Int J Neurosci | year= 2009 | volume= 119 | issue= 11 | pages= 1981-94 | pmid=19863257 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19863257 }} </ref>
** Most common, [[idiopathic]]
** Average age of onset is approximately 65 years

* '''Familial CJD'''<ref name="pmid27929804">{{cite journal| author=Clift K, Guthrie K, Klee EW, Boczek N, Cousin M, Blackburn P et al.| title=Familial Creutzfeldt-Jakob Disease: Case report and role of genetic counseling in post mortem testing. | journal=Prion | year= 2016 | volume= 10 | issue= 6 | pages= 502-506 | pmid=27929804 | doi=10.1080/19336896.2016.1254858 | pmc=5161295 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27929804 }} </ref>
**Inheritance of abnormal prion
**Exceptionally rare

* '''Iatrogenic CJ'''<ref name="pmid22607808">{{cite journal| author=Brown P, Brandel JP, Sato T, Nakamura Y, MacKenzie J, Will RG et al.| title=Iatrogenic Creutzfeldt-Jakob disease, final assessment. | journal=Emerg Infect Dis | year= 2012 | volume= 18 | issue= 6 | pages= 901-7 | pmid=22607808 | doi=10.3201/eid1806.120116 | pmc=3358170 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22607808 }} </ref>
**Very rare: only occasional cases with exceptionally long incubation periods are still appearing.
**The principal sources of these outbreaks are:<ref name="pmid22607808">{{cite journal| author=Brown P, Brandel JP, Sato T, Nakamura Y, MacKenzie J, Will RG et al.| title=Iatrogenic Creutzfeldt-Jakob disease, final assessment. | journal=Emerg Infect Dis | year= 2012 | volume= 18 | issue= 6 | pages= 901-7 | pmid=22607808 | doi=10.3201/eid1806.120116 | pmc=3358170 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22607808 }} </ref><ref name="www.cdc.gov">{{Cite web | last = | first = | title = http://www.cdc.gov/ncidod/dvrd/cjd/qa_cjd_infection_control.htm | url = http://www.cdc.gov/ncidod/dvrd/cjd/qa_cjd_infection_control.htm | publisher = | date = | accessdate = 14 February 2014 }}</ref>
***Contaminated [[growth hormone]] derived from human cadavers with undiagnosed CJD infections
***Contaminated [[dura mater]] grafts
***[[Neurosurgery|Neurosurgical]] instrument contamination
***[[Corneal graft|Corneal grafts]]
***[[Gonadotrophic|Gonadotrophic hormone]]
***[[Blood transfusion|Transfusion of blood]] products

Sporadic CJD (sCJD) may be classified based on molecular and phenotypic features into the following subtypes:<ref name="Parchi-1999">{{Cite journal | last1 = Parchi | first1 = P. | last2 = Giese | first2 = A. | last3 = Capellari | first3 = S. | last4 = Brown | first4 = P. | last5 = Schulz-Schaeffer | first5 = W. | last6 = Windl | first6 = O. | last7 = Zerr | first7 = I. | last8 = Budka | first8 = H. | last9 = Kopp | first9 = N. | title = Classification of sporadic Creutzfeldt-Jakob disease based on molecular and phenotypic analysis of 300 subjects. | journal = Ann Neurol | volume = 46 | issue = 2 | pages = 224-33 | month = Aug | year = 1999 | doi = | PMID = 10443888 }}</ref>
{| class="wikitable"
|-
! align="center" style="background:#4479BA; color: #FFFFFF;" + |'''Previous Classification'''
! align="center" style="background:#4479BA; color: #FFFFFF;" + |'''sCJD Variants'''
! align="center" style="background:#4479BA; color: #FFFFFF;" + |'''Clinical Features'''
! align="center" style="background:#4479BA; color: #FFFFFF;" + |'''Neuropathological Features'''
|-
|Myoclonic, Heidenhan variants ||MM1 or MV1 ||Rapidly progressive [[dementia]] [[Myoclonus]] Altered vision Unilateral signs in beginning Typical [[EEG]] findings ||[[Occipital lobe|Occipital cortex]] involvement Confluent vacuoles Perivacuolar PrP staining
|-
|Ataxic variant ||VV2 ||[[Ataxia]] in early stage [[Dementia]] in later stages Typical EEG findings absent ||Brain-stem nuclei and subcortical areas are affected Perinuclear PrP staining Plaque like focal Prp deposits
|-
|Kuru-plaques variant ||MV2 ||[[Ataxia]] [[Dementia]] Typical EEG findings absent Longer duration (>2 yrs) compared to other variants ||Amyloid-kuru plaques in [[cerebellum]] Plaque like focal PrP deposits
|-
|Thalamic variant ||MM2 (thalamic) ||[[Insomnia]] Hyperactivity [[Ataxia]] [[Cognitive impairment]] Typical EEG findings absent ||[[Thalamus|Thalamic]] and [[inferior olive]] atrpohy Spongiosis could be absent Lower amount of PrP staining
|-
| ||MM2 (cortical) ||Dementia Typical EEG findings are absent||Large confluent vacuoles Perivacuolar PrP staining All layers of cortex are affected
|-
| ||VV1 ||Dementia Typical EEG finding are absent||Diffuse cortical involvement along with [[straitum]] [[Cerebellum]] is spared No large confluent vacuoles are present Lower amount of PrP staining
|-
|}
Abbreviations: PrP=Prion protein 
MM, VV and MV are genotypes of PrP 
MM1: MM genotype type 1 (M:Methionine;V:Valine), MV1:MV genotype type 1, VV2:VV genotype type 2, MV2:MV genotype type 2 
Type 1 and type 2 are based on the molecular mass of PrP, type 1: 19 kd, type 2: 21kd


==Distinction Between Classic and Variant Creutzfeldt-Jakob disease==
The following table demonstrates distinguishing features for classic and variant Creutzfeldt-Jakob disease:

{| style="border:#c9c9c9 1px solid; margin: 1em 1em 1em 0; border-collapse: collapse;" cellspacing="0" cellpadding="4" {{table}}
! align="center" style="background:#4479BA; color: #FFFFFF;" + |'''Characteristic'''
! align="center" style="background:#4479BA; color: #FFFFFF;" + |'''Classic CJD'''
! align="center" style="background:#4479BA; color: #FFFFFF;" + |'''Variant CJD'''
|-
| Median age at death||68 years||28 years
|-
| Median duration of symptoms||4 to 5 months||13 to 14 months
|-
| Common clinical manifestations||Dementia, early neurologic signs||Psychiatric symptoms, painful dyesthesiasis, delayed neurological signs
|-
| Periodic sharp waves on EEG||Present||Absent
|-
| "Pulvinar sign" on MRI||Not reported||Usually present
|-
| "Florid plaques" on neuropathology||Rare / absent||Abundant
|-
| Immunohistochemical analysis of brain tissue||Variable accumulation||Marked accumulation of protease-resistance prion protein
|-
| Agent in lymphoid tissue||Not detected||Detected
|-
| Glycoform ratioo on immunoblot analysis of protease-resistance prion protein||Not reported||Marked accumulation of protease-resistance prion protein
|}
Adapted from Belay E. Schonberger L. Variant Creutzfeldt-Jakob disease and bovine spongiform encephalopathy. Clin Lab Med. 2002;22:849-62.<ref name="pmid12489284">{{cite journal| author=Belay ED, Schonberger LB| title=Variant Creutzfeldt-Jakob disease and bovine spongiform encephalopathy. | journal=Clin Lab Med | year= 2002 | volume= 22 | issue= 4 | pages= 849-62, v-vi | pmid=12489284 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12489284 }} </ref>

==References==
{{Reflist|2}}
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[[Category:Neurology]]
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Central pontine myelinolysis overview

2020-05-06T04:57:27Z

M Jahan:

__NOTOC__
{{Central pontine myelinolysis}}
{{CMG}}; {{AE}}{{sali}}{{MMJ}}

 

== Overview ==
The most common cause of central pontine myelinolysis is a rapid correction(>48-hours duration) of [[hyponatremia]] in patients with the history of prolonged [[hyponatremia]]. Other causes of central pontine myelinolysis may include: Lengthened orthotopic [[liver transplantation]], [[hypophosphatemia]] secondary to [[refeeding syndrome]], deficiencies in neuronal/glial cell energy supply and utilization which produce [[glial cell]] [[apoptosis]] and thus the clinical syndrome of central pontine myelinolysis and prolonged [[ischemia]]. The most potent risk factor in the development of central pontine myelinolysis is [[hyponatremia]]. Other risk factors include: Liver dysfunction and [[liver diseases]], [[hypocholesterolemia]], [[alcoholism]], [[malnutrition]], systemic medical disease and [[hemodialysis]]. Brain MRI is the gold standard test for the diagnosis of central pontine myelinolysis. The following findings on performing Brain MRI are confirmatory for central pontine myelinolysis: T2 hyperintensity in the central [[pontine]] region in the axial plane and hyperintense lesion in the midpons in the midsagittal T2-weighted [[MRI]]. Treatment of patients with central pontine myelinolysis is mainly supportive because once the [[Osmotic demyelination syndrome|osmotic demyelination]] has begun, there is no cure or specific treatment. Alcoholic patients should receive vitamin supplementation including [[vitamin B6]], [[Vitamin B9|B9]] and [[Vitamin B12|B12]] and evaluation of their nutritional status.

==Historical Perspective==
Central pontine myelinolysis was first discovered by '''Raymond Delacy Adams''', an an American [[neurologist]], in 1959. '''Raymond Delacy Adams''' and colleagues observed a rapidly evolving [[quadriplegia]] and [[pseudobulbar palsy]] in a young alcoholic man whose postmortem examination showed a large, symmetrical, essentially [[Demyelination|demyelinative]] lesion occupying the greater part of the base of the [[pons]] In 1950.

==Pathophysiology==
It is understood that central pontine myelinolysis is caused by the rapid correction of [[hyponatremia]]. The [[CNS]] is particularly susceptible to reductions in [[plasma osmolarity]], specially during [[hyponatremia]] which is the most commonly encountered [[electrolyte disturbance]]. When a decrease in the plasma [[osmolarity]] happens, neural cells first swell but then they are able to regain their original volume through the release of inorganic and organic osmolytes and exit of osmotically obligated water. Subsequent exposure to hypertonic stress(e.g., correction of [[hyponatremia]] with hypertonic I.V. solutions)resulting from a rapid correction of [[hyponatremia]] causes the [[ions]] to quickly re-enter the intracellular space and compels the water to follow. If the serum sodium levels rise too rapidly, the increased extracellular tonicity will continue to drive water out of the brain's cells because the brain cells do not have enough time to bring extracellular sodium into the cell, so the water goes out very fast. This can lead to cellular dysfunction and central pontine myelinolysis and finally death.

==Causes==
The most common cause of central pontine myelinolysis is rapid correction(>48-hours duration) of [[hyponatremia]] in patients with the history of prolonged [[hyponatremia]]. Other causes of central pontine myelinolysis may include: Lengthened orthotopic [[liver transplantation]], [[hypophosphatemia]] secondary to [[refeeding syndrome]], deficiencies in neuronal/glial cell energy supply and utilization which produce [[glial cell]] [[apoptosis]] and thus the clinical syndrome of central pontine myelinolysis and prolonged [[ischemia]].

==Differentiating central pontine myelinolysis from Other Diseases==
On the basis central pontine myelinolysis must be differentiated diseases that cause acute [[confusion]], [[lethargy]], [[speech difficulties]] and bilateral [[weakness]] or [[quadriplegia]] such as: [[Posterior leucoencephalopathy syndrome|Posterior leukoencephalopathy syndrome]], [[Encephalitis|infective encephalitis]], [[Brain stem infarction|ischemic Brain stem infarction]], [[thalamus]] [[infarction]] due [[thrombosis]] of the [[basilar artery]], diffuse [[hypoxic encephalopathy]], [[metastasis to the brain]] and [[brain tumors]] such as [[glioma]].

==Epidemiology and Demographics==
The prevalence of central pontine myelinolysis is approximately 250–500 per 100,000 in the general population. Among hospitalized patients in the [[Intensive care unit|ICU]] the incidence of central pontine myelinolysis is approximately 2500 per 100,000 patients. Among patients undergoing [[liver transplantation]] the incidence of central pontine myelinolysis is approximately 10,000 per 100,000 patients. The case-[[mortality rate]] of central pontine myelinolysis is approximately 12%. Patients of all age groups may develop central pontine myelinolysis but the incidence of central pontine myelinolysis increases with age. There is no racial predilection to central pontine myelinolysis. Central pontine myelinolysis affects men and women equally. There is no regional predilection to central pontine myelinolysis.

==Risk Factors==
The most potent risk factor in the development of central pontine myelinolysis is [[hyponatremia]]. Other risk factors include: Liver dysfunction and [[liver diseases]], [[hypocholesterolemia]], [[alcoholism]], [[malnutrition]], systemic medical disease and [[hemodialysis]].

==Natural History, Complications, and Prognosis==

The symptoms of central pontine myelinolysis typically develop immediately after injury to the neurons of the [[brain stem]]. Patients, with Central Pontine Myelinolysis, may develop permanent neurological damages. Common complications of central pontine myelinolysis include: [[Locked-In syndrome|Locked-in syndrome]], [[quadriparesis]], [[ataxia]], acute [[Psychosis]], [[pseudobulbar palsy]], [[parkinson's disease]] symptoms, [[dystonia]], [[pneumonia]], [[coma]] and death. The mortality of patients with central pontine myelinolysis is approximately 8% in the acute setting. Approximately 65% of patients with central pontine myelinolysis may achieve a good or moderate outcome (no functional deficit or independence despite minor deficits). Depending on the time of the diagnosis, the prognosis may vary and the disease may be potentially reversible when therapeutic interventions are initiated rapidly.
==Diagnosis==
===Diagnostic Study of Choice===
Brain MRI is the gold standard test for the diagnosis of central pontine myelinolysis. The following findings on performing Brain MRI are confirmatory for central pontine myelinolysis: T2 hyperintensity in the central [[pontine]] region in the axial plane and hyperintense lesion in the midpons in the midsagittal T2-weighted [[MRI]].

===History and Symptoms===
Patients with central pontine myelinolysis may have a positive history of: [[Malnutrition]], [[Alcohol abuse|alcohol use disorder]], [[chronic liver disease]], [[hyperemesis gravidarum]], [[hypophosphatemia]] secondary to [[refeeding syndrome]] and prolonged [[Ischemia|ischemia.]] These patients with central pontine myelinolysis most commonly have a history of rapid [[sodium]] correction, greater than 0.5-1.0 mEq/L per hour. The most susceptible patients are those with: Chronic [[hyponatremia]] (>48 hours), severe [[hyponatremia]] (Na <120 mEq/L) and both chronic [[hyponatremia]] and severe [[hyponatremia]]. Common symptoms of central pontine myelinolysis include: Spastic [[quadriparesis]], [[dysarthria]], [[pseudobulbar palsy]] and [[altered mental status]]. In some patients, parkinsonian features, behavioral manifestations, and [[neuropsychological]] symptoms can also be present: [[Personality changes]], [[labile affect]], [[disinhibition]], poor judgment, [[Delusional disorder|paranoid delusions]], [[emotional lability]], [[delirium]], [[hallucinations]] and [[catatonia]].

===Laboratory Findings===
Laboratory finding consistent with the diagnosis of central pontine myelinolysis is hypoosmotic [[hyponatremia]] and the rapid correction of [[hyponatremia]] is the cause of central pontine myelinolysis.

===CT scan===
Brain CT scan may be helpful in the diagnosis of central pontine myelinolysis. Findings on CT scan suggestive of central pontine myelinolysis include: A symmetric, centrally located region of low attenuation within the [[pons]] and symmetric low-attenuation foci within the lateral [[thalami]].

===MRI===
Brain and [[spinal cord]] MRIs may be helpful in the diagnosis of Central pontine myelinolysis. Findings on MRI diagnostic of Central pontine myelinolysis include: Symmetric signal intensity abnormality in the central pons at T2-weighted and FLAIR imaging which may progress to classic hyperintense “trident-shaped” central pontine abnormality, with sparing of the ventrolateral pons and corticospinal tracts, decreased T1 signal intensity, fluid attenuated inversion recovery (FLAIR) hyperintense lesion in the [[pons]] and intramedullary central T2 hyperintensity at axial T2W of [[spinal cord]] and sagittal T2W of thoracic [[spinal cord]].

==Treatment==
===Medical Therapy===
Treatment of patients with central pontine myelinolysis is mainly supportive because once the [[Osmotic demyelination syndrome|osmotic demyelination]] has begun, there is no cure or specific treatment. Alcoholic patients should receive vitamin supplementation including [[vitamin B6]], [[Vitamin B9|B9]] and [[Vitamin B12|B12]] and evaluation of their nutritional status.

===Primary Prevention===
To minimize the risk of central pontine myelinolysis developing from its most common cause, overly rapid reversal of hyponatremia, the hyponatremia should be corrected slowly. The primary goals of treating hypernatremia are estimating the magnitude of water deficit, determining the proper rate of correction, addressing the concurrent electrolyte or volume deficits and calculating the fluid deficit regimen using the estimated water deficit and desired rate of correction. Correcting sodium level is vital in order to prevent any permanent brain damage.

==References==
{{reflist|2}}

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[[Category: (name of the system)]]

Creutzfeldt-Jakob disease

2020-05-06T04:56:50Z

M Jahan:

__NOTOC__
{{Creutzfeldt-Jakob disease}}

{{CMG}}; {{AE}}{{sali}}, {{MMJ}}
==[[Creutzfeldt-Jakob disease overview|Overview]]==

==[[Creutzfeldt-Jakob disease historical perspective|Historical Perspective]]==

==[[Creutzfeldt-Jakob disease classification|Classification]]==

==[[Creutzfeldt-Jakob disease pathophysiology|Pathophysiology]]==

==[[Creutzfeldt-Jakob disease causes|Causes]]==

==[[Creutzfeldt-Jakob disease differential diagnosis|Differentiating Creutzfeldt-Jakob disease from other Diseases]]==

==[[Creutzfeldt-Jakob disease epidemiology and demographics|Epidemiology and Demographics]]==

==[[Creutzfeldt-Jakob disease risk factors|Risk Factors]]==

==[[Creutzfeldt-Jakob disease screening|Screening]]==

==[[Creutzfeldt-Jakob disease natural history, complications and prognosis|Natural History, Complications and Prognosis]]==

==Diagnosis==
[[Creutzfeldt-Jakob disease diagnostic study of choice|Diagnostic study of choice]] | [[Creutzfeldt-Jakob disease history and symptoms|History and Symptoms]] | [[Creutzfeldt-Jakob disease physical examination|Physical Examination]] | [[Creutzfeldt-Jakob disease laboratory findings|Laboratory Findings]] | [[Creutzfeldt-Jakob disease electrocardiogram|Electrocardiogram]] | [[Creutzfeldt-Jakob disease x ray|X-Ray Findings]] | [[Creutzfeldt-Jakob disease echocardiography and ultrasound|Echocardiography and Ultrasound]] | [[Creutzfeldt-Jakob disease CT scan|CT-Scan Findings]] | [[Creutzfeldt-Jakob disease MRI|MRI Findings]] | [[Creutzfeldt-Jakob disease other imaging findings|Other Imaging Findings]] | [[Creutzfeldt-Jakob disease other diagnostic studies|Other Diagnostic Studies]]

==Treatment==
[[Creutzfeldt-Jakob disease medical therapy|Medical Therapy]] | [[Creutzfeldt-Jakob disease interventions|Interventions]] | [[Creutzfeldt-Jakob disease surgery|Surgery]] | [[Creutzfeldt-Jakob disease primary prevention|Primary Prevention]] | [[Creutzfeldt-Jakob disease secondary prevention|Secondary Prevention]] | [[Creutzfeldt-Jakob disease cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Creutzfeldt-Jakob disease future or investigational therapies|Future or Investigational Therapies]]

==Case Studies==
[[Creutzfeldt-Jakob disease case study one|Case #1]]

[[Category: (name of the system)]]

Optic neuritis

2020-05-06T04:53:26Z

M Jahan:

{{SI}}
{{CMG}} {{AE}} {{sali}}, {{MMJ}}
==Historical Perspective==

===Discovery===
*Optic neuritis was first discovered by von Graefe and Nettleship, in late nineteenth century when [[ophthalmoscopy]] became part of the [[ophthalmic]] examination.<ref name="pmid11756864">{{cite journal |vauthors=Volpe NJ |title=Optic neuritis: historical aspects |journal=J Neuroophthalmol |volume=21 |issue=4 |pages=302–9 |date=December 2001 |pmid=11756864 |doi= |url=}}</ref>
*The association between [[systemic sclerosis]] and optic neuritis was made by the early 1900's but there was much controversy and misunderstanding about its differential diagnosis, [[pathogenesis]], and possible treatment.<ref name="pmid11756864">{{cite journal |vauthors=Volpe NJ |title=Optic neuritis: historical aspects |journal=J Neuroophthalmol |volume=21 |issue=4 |pages=302–9 |date=December 2001 |pmid=11756864 |doi= |url=}}</ref>
*Optic neuritis was first distinguished from [[infectious]],[[hereditary]], [[Toxic optic neuropathy|toxic]], [[Nutritional optic neuropathy|nutritional]], and [[Ischemic optic neuropathy|ischemic optic neuropathie]]<nowiki/>s during the twentieth century.<ref name="pmid11756864">{{cite journal |vauthors=Volpe NJ |title=Optic neuritis: historical aspects |journal=J Neuroophthalmol |volume=21 |issue=4 |pages=302–9 |date=December 2001 |pmid=11756864 |doi= |url=}}</ref>
*During late twentieth century, the development of [[Magnetic resonance imaging|MRI]] and the results from recent clinical trials, discovered the relationship between optic neuritis and [[multiple sclerosis]].<ref name="pmid11756864">{{cite journal |vauthors=Volpe NJ |title=Optic neuritis: historical aspects |journal=J Neuroophthalmol |volume=21 |issue=4 |pages=302–9 |date=December 2001 |pmid=11756864 |doi= |url=}}</ref>
==Classification==
Optic neuritis may be classified into atypical or typical subtypes based on its clinical features.<ref name="pmid3414716">{{cite journal |vauthors=Kliethermes MA |title=Working parents in two-pharmacist marriages |journal=Am J Hosp Pharm |volume=45 |issue=7 |pages=1500 |date=July 1988 |pmid=3414716 |doi= |url=}}</ref>
*Atypical optic neuritis entails clinical manifestations that deviate from classic pattern of optic neuritis features.<ref name="pmid26467052">{{cite journal |vauthors=Gaier ED, Boudreault K, Rizzo JF, Falardeau J, Cestari DM |title=Atypical Optic Neuritis |journal=Curr Neurol Neurosci Rep |volume=15 |issue=12 |pages=76 |date=December 2015 |pmid=26467052 |doi=10.1007/s11910-015-0598-1 |url=}}</ref>
*Atypical features to consider include:<ref name="pmid26467052">{{cite journal |vauthors=Gaier ED, Boudreault K, Rizzo JF, Falardeau J, Cestari DM |title=Atypical Optic Neuritis |journal=Curr Neurol Neurosci Rep |volume=15 |issue=12 |pages=76 |date=December 2015 |pmid=26467052 |doi=10.1007/s11910-015-0598-1 |url=}}</ref>
**Lack of [[pain]]
**Simultaneous or near-simultaneous onset
**Lack of response to or relapse upon tapering from [[corticosteroids]]
**Optic neuritis due nerve head or peripapillary [[hemorrhages]]

*

==Pathophysiology==

===Pathogenesis===
*The exact [[pathogenesis]] of optic neuritis is not completely understood.<ref name="pmid22888383">{{cite journal |vauthors=Hoorbakht H, Bagherkashi F |title=Optic neuritis, its differential diagnosis and management |journal=Open Ophthalmol J |volume=6 |issue= |pages=65–72 |date=2012 |pmid=22888383 |pmc=3414716 |doi=10.2174/1874364101206010065 |url=}}</ref><ref name="pmid24331795">{{cite journal |vauthors=Toosy AT, Mason DF, Miller DH |title=Optic neuritis |journal=Lancet Neurol |volume=13 |issue=1 |pages=83–99 |date=January 2014 |pmid=24331795 |doi=10.1016/S1474-4422(13)70259-X |url=}}</ref>

* But It is likely due to some [[inflammatory]] process which leads to delayed type IV [[hypersensitivity]] reaction induced by released [[Cytokines|cytokine]]<nowiki/>s and other inflammatory mediators from activated peripheral [[T-cells]] which can cross the [[blood brain barrier]] and cause destruction of [[myelin]], neural [[cell death]] and [[Axonal|axonal degeneration]].<ref name="pmid22888383">{{cite journal |vauthors=Hoorbakht H, Bagherkashi F |title=Optic neuritis, its differential diagnosis and management |journal=Open Ophthalmol J |volume=6 |issue= |pages=65–72 |date=2012 |pmid=22888383 |pmc=3414716 |doi=10.2174/1874364101206010065 |url=}}</ref><ref name="pmid24331795">{{cite journal |vauthors=Toosy AT, Mason DF, Miller DH |title=Optic neuritis |journal=Lancet Neurol |volume=13 |issue=1 |pages=83–99 |date=January 2014 |pmid=24331795 |doi=10.1016/S1474-4422(13)70259-X |url=}}</ref>
* In addition to involvement of the [[myelin sheath]] ([[white matter]]), latest technologies such as [[optical coherence tomography]] (OCT) suggest involvement of [[axons]] ([[Gray matter|gray matte]]<nowiki/>r) in this process.<ref name="pmid22888383">{{cite journal |vauthors=Hoorbakht H, Bagherkashi F |title=Optic neuritis, its differential diagnosis and management |journal=Open Ophthalmol J |volume=6 |issue= |pages=65–72 |date=2012 |pmid=22888383 |pmc=3414716 |doi=10.2174/1874364101206010065 |url=}}</ref><ref name="pmid24331795">{{cite journal |vauthors=Toosy AT, Mason DF, Miller DH |title=Optic neuritis |journal=Lancet Neurol |volume=13 |issue=1 |pages=83–99 |date=January 2014 |pmid=24331795 |doi=10.1016/S1474-4422(13)70259-X |url=}}</ref>
*

* Findings suggestive of optic neuritis in microscopic histopathological analysis include:<ref name="pmid3700386">{{cite journal |vauthors=Taniguchi S, Kawano T, Kakunaga T, Baba T |title=Differences in expression of a variant actin between low and high metastatic B16 melanoma |journal=J. Biol. Chem. |volume=261 |issue=13 |pages=6100–6 |date=May 1986 |pmid=3700386 |doi= |url=}}</ref>
** Reduced [[axon]] counts
** [[Optic atrophy]]
** [[Inflammation]]
** [[Demyelination]]
** Axonal loss
** [[Intracellular]] [[Neurofilament|neurofilaments]]

==Causes==
* The exact cause of optic neuritis is unknown.<ref name="pmid3178158">{{cite journal |vauthors=Marechal F, Berthiot G, Deltour G |title=Serum levels of CA-50, CA-19.9, CA-125, CA-15.3, enolase and carcino-embryonic antigen in non neoplastic diseases of the lung |journal=Anticancer Res. |volume=8 |issue=4 |pages=677–80 |date=1988 |pmid=3178158 |doi= |url=}}</ref><ref name="pmid5398737">{{cite journal |vauthors=Bourdial J |title=[Otorhinolaryngologic action in asthmatics] |language=French |journal=Maroc Med |volume=49 |issue=523 |pages=209–17 |date=April 1969 |pmid=5398737 |doi= |url=}}</ref><ref name="pmid16554529">{{cite journal |vauthors=Balcer LJ |title=Clinical practice. Optic neuritis |journal=N. Engl. J. Med. |volume=354 |issue=12 |pages=1273–80 |date=March 2006 |pmid=16554529 |doi=10.1056/NEJMcp053247 |url=}}</ref>
* But It is likely due invasion of the [[immune system]] to the [[myelin]], resulting in [[inflammation]] and damage to the [[myelin]].
The following [[autoimmune]] are associated with optic neuritis:<ref name="pmid3178158">{{cite journal |vauthors=Marechal F, Berthiot G, Deltour G |title=Serum levels of CA-50, CA-19.9, CA-125, CA-15.3, enolase and carcino-embryonic antigen in non neoplastic diseases of the lung |journal=Anticancer Res. |volume=8 |issue=4 |pages=677–80 |date=1988 |pmid=3178158 |doi= |url=}}</ref><ref name="pmid5398737">{{cite journal |vauthors=Bourdial J |title=[Otorhinolaryngologic action in asthmatics] |language=French |journal=Maroc Med |volume=49 |issue=523 |pages=209–17 |date=April 1969 |pmid=5398737 |doi= |url=}}</ref><ref name="pmid16554529">{{cite journal |vauthors=Balcer LJ |title=Clinical practice. Optic neuritis |journal=N. Engl. J. Med. |volume=354 |issue=12 |pages=1273–80 |date=March 2006 |pmid=16554529 |doi=10.1056/NEJMcp053247 |url=}}</ref>
* '''Multiple sclerosis:'''
** [[Multiple sclerosis]] is the first main cause of optic neuritis.<ref name="pmid5398737">{{cite journal |vauthors=Bourdial J |title=[Otorhinolaryngologic action in asthmatics] |language=French |journal=Maroc Med |volume=49 |issue=523 |pages=209–17 |date=April 1969 |pmid=5398737 |doi= |url=}}</ref>
** 50% of patients with multiple sclerosis finally develop optic neuritis.<ref name="pmid16554529">{{cite journal |vauthors=Balcer LJ |title=Clinical practice. Optic neuritis |journal=N. Engl. J. Med. |volume=354 |issue=12 |pages=1273–80 |date=March 2006 |pmid=16554529 |doi=10.1056/NEJMcp053247 |url=}}</ref>
* '''Neuromyelitis optica'''
** In [[Neuromyelitis optica]], inflammation recurs in the [[optic nerve]] and [[spinal cord]].

* '''Infections:'''
** [[Lyme disease]]
** [[Cat-scratch disease]]
** [[Syphilis]]
** [[Measles]]
** [[Mumps]]
** [[Herpes simplex]]

==Differentiating Optic Neuritis from other Diseases==
Optic neuritis must be differentiated from other diseases that cause sudden [[eye pain]] and [[vision loss]] such as:<ref name="pmid3414716">{{cite journal |vauthors=Kliethermes MA |title=Working parents in two-pharmacist marriages |journal=Am J Hosp Pharm |volume=45 |issue=7 |pages=1500 |date=July 1988 |pmid=3414716 |doi= |url=}}</ref>
# Leber’s Hereditary Optic Neuropathy (LHON)<ref name="pmid3414716" /> which results from point [[mutations]] in [[mitochondrial DNA]] and subsequent mitochondrial dysfunction, causing bilateral central vision loss.<ref name="pmid4492634">{{cite journal |vauthors=Fujimori H |title=[Pulmonary tuberculosis--keypoints in nursing of pregnant and puerperal patients] |language=Japanese |journal=Josanpu Zasshi |volume=27 |issue=12 |pages=40–3 |date=December 1973 |pmid=4492634 |doi= |url=}}</ref>
# [[Anterior ischemic optic neuropathy|Nonarteritic Anterior Ischemic Optic Neuropathy]] (AION)<ref name="pmid3414716">{{cite journal |vauthors=Kliethermes MA |title=Working parents in two-pharmacist marriages |journal=Am J Hosp Pharm |volume=45 |issue=7 |pages=1500 |date=July 1988 |pmid=3414716 |doi= |url=}}</ref>
#* It is the most common form of ischemic [[optic neuropathy]] and the second most common optic neuropathy.
#* It is more common in patients over the age of 50 years with [[Vasculopathies|vasculopathic]] risk factors such as:
#** [[Diabetes mellitus]]
#** [[Hypertension]]
#** [[Obstructive sleep apnea]]

==Epidemiology and Demographics==

=== Incidence ===
* The [[incidence]] of optic neuritis is approximately 5 to 6.4 per 100 000 individuals in US.<ref name="pmid3178158">{{cite journal |vauthors=Marechal F, Berthiot G, Deltour G |title=Serum levels of CA-50, CA-19.9, CA-125, CA-15.3, enolase and carcino-embryonic antigen in non neoplastic diseases of the lung |journal=Anticancer Res. |volume=8 |issue=4 |pages=677–80 |date=1988 |pmid=3178158 |doi= |url=}}</ref><ref name="pmid7854520">{{cite journal |vauthors=Rodriguez M, Siva A, Cross SA, O'Brien PC, Kurland LT |title=Optic neuritis: a population-based study in Olmsted County, Minnesota |journal=Neurology |volume=45 |issue=2 |pages=244–50 |date=February 1995 |pmid=7854520 |doi= |url=}}</ref><ref name="pmid5057861">{{cite journal |vauthors=Percy AK, Nobrega FT, Kurland LT |title=Optic neuritis and multiple sclerosis. An epidemiologic study |journal=Arch. Ophthalmol. |volume=87 |issue=2 |pages=135–9 |date=February 1972 |pmid=5057861 |doi= |url=}}</ref>

=== Age ===
* Optic neuritis commonly affects patients between the ages of 15 and 49.<ref name="pmid3105615">{{cite journal |vauthors=Self SG, Grossman EA |title=Linear rank tests for interval-censored data with application to PCB levels in adipose tissue of transformer repair workers |journal=Biometrics |volume=42 |issue=3 |pages=521–30 |date=September 1986 |pmid=3105615 |doi= |url=}}</ref>

=== Race ===
* Optic neuritis usually affects individuals of the Caucasians race eight times more frequently than Blacks and Asians.<ref name="pmid3178158">{{cite journal |vauthors=Marechal F, Berthiot G, Deltour G |title=Serum levels of CA-50, CA-19.9, CA-125, CA-15.3, enolase and carcino-embryonic antigen in non neoplastic diseases of the lung |journal=Anticancer Res. |volume=8 |issue=4 |pages=677–80 |date=1988 |pmid=3178158 |doi= |url=}}</ref><ref name="pmid17967837" /><ref name="pmid2124032" /><ref name="pmid9482360" />
* Black populations individuals are less likely to develop optic neuritis.<ref name="pmid3178158">{{cite journal |vauthors=Marechal F, Berthiot G, Deltour G |title=Serum levels of CA-50, CA-19.9, CA-125, CA-15.3, enolase and carcino-embryonic antigen in non neoplastic diseases of the lung |journal=Anticancer Res. |volume=8 |issue=4 |pages=677–80 |date=1988 |pmid=3178158 |doi= |url=}}</ref><ref name="pmid17967837">{{cite journal |vauthors=Bhigjee AI, Moodley K, Ramkissoon K |title=Multiple sclerosis in KwaZulu Natal, South Africa: an epidemiological and clinical study |journal=Mult. Scler. |volume=13 |issue=9 |pages=1095–9 |date=November 2007 |pmid=17967837 |doi=10.1177/1352458507079274 |url=}}</ref><ref name="pmid2124032">{{cite journal |vauthors=Mbonda E, Larnaout A, Maertens A, Appel B, Lowenthal A, Mbede J, Evrard P |title=Multiple sclerosis in a black Cameroonian woman |journal=Acta Neurol Belg |volume=90 |issue=4 |pages=218–22 |date=1990 |pmid=2124032 |doi= |url=}}</ref><ref name="pmid9482360">{{cite journal |vauthors=Phillips PH, Newman NJ, Lynn MJ |title=Optic neuritis in African Americans |journal=Arch. Neurol. |volume=55 |issue=2 |pages=186–92 |date=February 1998 |pmid=9482360 |doi= |url=}}</ref>

=== Gender ===
* Women are more commonly affected by optic neuritis than men.<ref name="pmid3414716">{{cite journal |vauthors=Kliethermes MA |title=Working parents in two-pharmacist marriages |journal=Am J Hosp Pharm |volume=45 |issue=7 |pages=1500 |date=July 1988 |pmid=3414716 |doi= |url=}}</ref>

=== Region ===
* The [[incidence]] of optic neuritis is highest in populations located at higher latitudes such as:<ref name="pmid3178158">{{cite journal |vauthors=Marechal F, Berthiot G, Deltour G |title=Serum levels of CA-50, CA-19.9, CA-125, CA-15.3, enolase and carcino-embryonic antigen in non neoplastic diseases of the lung |journal=Anticancer Res. |volume=8 |issue=4 |pages=677–80 |date=1988 |pmid=3178158 |doi= |url=}}</ref><ref name="pmid19878630">{{cite journal |vauthors=Shams PN, Plant GT |title=Optic neuritis: a review |journal=Int MS J |volume=16 |issue=3 |pages=82–9 |date=September 2009 |pmid=19878630 |doi= |url=}}</ref><ref name="pmid4015470">{{cite journal |vauthors=Kurtzke JF |title=Optic neuritis or multiple sclerosis |journal=Arch. Neurol. |volume=42 |issue=7 |pages=704–10 |date=July 1985 |pmid=4015470 |doi= |url=}}</ref>
** Northern United States
** Northern and Western Europe
** New Zealand and Southern Australia

==Risk Factors==
===Common Risk Factors===
* Common risk factors in the development of optic neuritis include:
*# Age
*#* Optic neuritis most often affects adults between the ages of 15 and 49.<ref name="pmid3105615" />
*# Sex
*#* Women are much more likely to develop optic neuritis than men are.<ref name="pmid3414716" />
*# Race
*#* Optic neuritis usually affects individuals of the Caucasians race eight times more frequently than Blacks and Asians.<ref name="pmid3178158" /><ref name="pmid17967837" /><ref name="pmid2124032" /><ref name="pmid9482360" />
*#* Black populations individuals are less likely to develop optic neuritis.<ref name="pmid3178158" /><ref name="pmid17967837" /><ref name="pmid2124032" /><ref name="pmid9482360" />
*# [[Genetic mutation]]<ref name="pmid20301353">{{cite journal |vauthors=Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJH, Stephens K, Amemiya A, Yu-Wai-Man P, Chinnery PF |title= |journal= |volume= |issue= |pages= |date= |pmid=20301353 |doi= |url=}}</ref>
*# [[Multiple sclerosis]]<ref name="pmid12789593">{{cite journal |vauthors=Chan JW |title=Optic neuritis in multiple sclerosis |journal=Ocul. Immunol. Inflamm. |volume=10 |issue=3 |pages=161–86 |date=September 2002 |pmid=12789593 |doi= |url=}}</ref>
*# [[Trauma]]<ref name="pmid4457437">{{cite journal |vauthors=Haslbeck M |title=[Insulin secretion after glucose loading. Studies on insulin secretion in healthy and diabetic subjects after administration of glucose] |language=German |journal=Fortschr. Med. |volume=92 |issue=32 |pages=1317–8 |date=November 1974 |pmid=4457437 |doi= |url=}}</ref>
*# [[Nutritional deficiencies]]<ref name="pmid25345287">{{cite journal |vauthors=Sawicka-Pierko A, Obuchowska I, Mariak Z |title=Nutritional optic neuropathy |journal=Klin Oczna |volume=116 |issue=2 |pages=104–10 |date=2014 |pmid=25345287 |doi= |url=}}</ref>
*# Compression of the [[optic nerve]]<ref name="pmid5546777">{{cite journal |vauthors=Primicerio B |title=[Competitions for the position of sanitary personnel in hospitals] |language=Italian |journal=Policlinico Prat |volume=78 |issue=2 |pages=72–7 |date=January 1971 |pmid=5546777 |doi= |url=}}</ref>
*# Arteritic [[optic neuropathy]]<ref name="pmid2701125">{{cite journal |vauthors=Dyras M, Stós B, Zemowski W |title=[Possibilities of combined maxillary-orthopaedic and prosthetic treatment of malocclusion in adult patients] |language=Polish |journal=Protet Stomatol |volume=39 |issue=3 |pages=134–9 |date=1989 |pmid=2701125 |doi= |url=}}</ref>
*# [[Diabetes]]<ref name="pmid6354403">{{cite journal |vauthors=Warren SA, Warren KG |title=Optic neuritis, diabetes mellitus and multiple sclerosis: a three-way association |journal=Can. J. Ophthalmol. |volume=18 |issue=5 |pages=228–32 |date=August 1983 |pmid=6354403 |doi= |url=}}</ref>
*# [[Glaucoma]]<ref name="pmid3939751">{{cite journal |vauthors=Holmberg D, Lundkvist I, Forni L, Ivars F, Coutinho A |title=Absence of immunoglobulin heavy chain expression results in altered kappa/lambda light chain ratios |journal=J. Mol. Cell. Immunol. |volume=2 |issue=1 |pages=51–6 |date=1985 |pmid=3939751 |doi= |url=}}</ref>
* Common risk factors in the recurrence of optic neuritis include:<ref name="pmid4177903">{{cite journal |vauthors=Dabholkar AS, Tewari HB |title=The functional significance of the presence of acid phosphatase at the nucleic-acid synthesizing sites in the nuclei of the neurons of the cephalothoracic ganglionic masses of palaemnius |journal=Acta Neurol. Scand. |volume=44 |issue=5 |pages=533–41 |date=1968 |pmid=4177903 |doi= |url=}}</ref><ref name="pmid12789593">{{cite journal |vauthors=Chan JW |title=Optic neuritis in multiple sclerosis |journal=Ocul. Immunol. Inflamm. |volume=10 |issue=3 |pages=161–86 |date=September 2002 |pmid=12789593 |doi= |url=}}</ref>
*# Underlying diseases such as:
*#* [[Neuromyelitis optica]]
*#* [[Multiple sclerosis]]
*# Unilateral optic neuritis
*# Early initiation of [[glucocorticoid]]

==Natural History, Complications and Prognosis==

=== Natural History ===
* The symptoms of optic neuritis usually develop in the second decade of life, and start with symptoms such as pain on movement of the eyes, followed by a worsening of [[vision]].<ref name="pmid4581115">{{cite journal |vauthors=Wilson BJ |title=12,13-Epoxytrichothecenes: potential toxic contaminants of foods |journal=Nutr. Rev. |volume=31 |issue=6 |pages=169–72 |date=June 1973 |pmid=4581115 |doi= |url=}}</ref>
* Common symptoms of optic neuritis include:<ref name="pmid4581115">{{cite journal |vauthors=Wilson BJ |title=12,13-Epoxytrichothecenes: potential toxic contaminants of foods |journal=Nutr. Rev. |volume=31 |issue=6 |pages=169–72 |date=June 1973 |pmid=4581115 |doi= |url=}}</ref><ref name="pmid1734247">{{cite journal |vauthors=Beck RW, Cleary PA, Anderson MM, Keltner JL, Shults WT, Kaufman DI, Buckley EG, Corbett JJ, Kupersmith MJ, Miller NR |title=A randomized, controlled trial of corticosteroids in the treatment of acute optic neuritis. The Optic Neuritis Study Group |journal=N. Engl. J. Med. |volume=326 |issue=9 |pages=581–8 |date=February 1992 |pmid=1734247 |doi=10.1056/NEJM199202273260901 |url=}}</ref>
*# Pain on movement of the eyes which is sever and so disturbing
*# Seeing things darkly, unclearly, and with [[Contrast|poor contrast]]
*# Dirty and pale Colors
*# [[Visual field loss]]
*# Disturbed [[color vision]]
*# Flashing lights
* After a sub acute onset, the patient’s [[visual acuity]] continues to deteriorate for a few more days; in the untreated course of the disease, it generally reaches its nadir in one to two weeks and then improves again.<ref name="pmid4581115">{{cite journal |vauthors=Wilson BJ |title=12,13-Epoxytrichothecenes: potential toxic contaminants of foods |journal=Nutr. Rev. |volume=31 |issue=6 |pages=169–72 |date=June 1973 |pmid=4581115 |doi= |url=}}</ref>

=== Complications ===
* Common complications of optic neuritis include:<ref name="pmid3178158">{{cite journal |vauthors=Marechal F, Berthiot G, Deltour G |title=Serum levels of CA-50, CA-19.9, CA-125, CA-15.3, enolase and carcino-embryonic antigen in non neoplastic diseases of the lung |journal=Anticancer Res. |volume=8 |issue=4 |pages=677–80 |date=1988 |pmid=3178158 |doi= |url=}}</ref><ref name="pmid80680">{{cite journal |vauthors= |title=Henry Edmund Seiler |journal=Lancet |volume=2 |issue=8092 Pt 1 |pages=747 |date=September 1978 |pmid=80680 |doi= |url=}}</ref>
**Side effects of [[corticosteroids]] use
**Permanent [[optic nerve]] damage
**Decreased [[visual acuity]]
***In some cases of optic neuritis, partial loss of color discrimination might persist.

=== Prognosis ===
* The long-term visual prognosis of idiopathic optic neuritis is generally good.<ref name="pmid3116540">{{cite journal |vauthors=Sagalovich VIa, Solov'eva IP, Kunichan AD, Nemsadze MN |title=[Effectiveness of single and fractional administration of isoniazid in the treatment of dogs infected with isoniazid-resistant strains of Mycobacterium tuberculosis] |language=Russian |journal=Probl Tuberk |volume= |issue=7 |pages=49–53 |date=1987 |pmid=3116540 |doi= |url=}}</ref>
* More than 90% of the patients recover a visual acuity of 20/40 or better by 6 months.<ref name="pmid3116540">{{cite journal |vauthors=Sagalovich VIa, Solov'eva IP, Kunichan AD, Nemsadze MN |title=[Effectiveness of single and fractional administration of isoniazid in the treatment of dogs infected with isoniazid-resistant strains of Mycobacterium tuberculosis] |language=Russian |journal=Probl Tuberk |volume= |issue=7 |pages=49–53 |date=1987 |pmid=3116540 |doi= |url=}}</ref>
* Findings associated with poor visual outcome at 6 months include:<ref name="pmid15477504">{{cite journal |vauthors=Achiron A, Kishner I, Sarova-Pinhas I, Raz H, Faibel M, Stern Y, Lavie M, Gurevich M, Dolev M, Magalashvili D, Barak Y |title=Intravenous immunoglobulin treatment following the first demyelinating event suggestive of multiple sclerosis: a randomized, double-blind, placebo-controlled trial |journal=Arch. Neurol. |volume=61 |issue=10 |pages=1515–20 |date=October 2004 |pmid=15477504 |doi=10.1001/archneur.61.10.1515 |url=}}</ref><ref name="pmid3116540">{{cite journal |vauthors=Sagalovich VIa, Solov'eva IP, Kunichan AD, Nemsadze MN |title=[Effectiveness of single and fractional administration of isoniazid in the treatment of dogs infected with isoniazid-resistant strains of Mycobacterium tuberculosis] |language=Russian |journal=Probl Tuberk |volume= |issue=7 |pages=49–53 |date=1987 |pmid=3116540 |doi= |url=}}</ref>
** A cut-off level of vision ≤ 20/50
** Contrast sensitivity of <1.0 log units
** A [[visual field]] mean deviation of ≤ – 15 dB after 1 month in the Optic Neuritis Treatment Trial.
* Despite the relatively good visual outcome, most patients show a degree of long-lasting damage to the [[optic nerve]], such as:<ref name="pmid3116540">{{cite journal |vauthors=Sagalovich VIa, Solov'eva IP, Kunichan AD, Nemsadze MN |title=[Effectiveness of single and fractional administration of isoniazid in the treatment of dogs infected with isoniazid-resistant strains of Mycobacterium tuberculosis] |language=Russian |journal=Probl Tuberk |volume= |issue=7 |pages=49–53 |date=1987 |pmid=3116540 |doi= |url=}}</ref>
** A pale [[optic disc]]
** Loss of retinal nerve fibers
** Prolonged latency in the [[Visual evoked potential|visual evoked response]]
** Thinning of the [[optic nerve]] on MR

==Diagnosis==

=== Diagnosis studies ===
The diagnosis of typical optic neuritis is usually made clinically.<ref name="pmid3414716">{{cite journal |vauthors=Kliethermes MA |title=Working parents in two-pharmacist marriages |journal=Am J Hosp Pharm |volume=45 |issue=7 |pages=1500 |date=July 1988 |pmid=3414716 |doi= |url=}}</ref>

The classic triad for diagnosis of optic neuritis consist of:<ref name="pmid3414716">{{cite journal |vauthors=Kliethermes MA |title=Working parents in two-pharmacist marriages |journal=Am J Hosp Pharm |volume=45 |issue=7 |pages=1500 |date=July 1988 |pmid=3414716 |doi= |url=}}</ref><ref name="pmid19878630">{{cite journal |vauthors=Shams PN, Plant GT |title=Optic neuritis: a review |journal=Int MS J |volume=16 |issue=3 |pages=82–9 |date=September 2009 |pmid=19878630 |doi= |url=}}</ref><ref name="pmid3379920">{{cite journal |vauthors=Wells H |title=A discussion of the KDI Quik Test Drug Screen |journal=J Anal Toxicol |volume=12 |issue=2 |pages=111 |date=1988 |pmid=3379920 |doi= |url=}}</ref>
#[[Visual loss]]
#Periocular pain
#[[Dyschromatopsia]]
[[MRI]] is the diagnosis study of choice for visualising the [[optic nerve]].

The following result of MRI is confirmatory of optic neuritis:
* Swollen retrobulbar intra-orbital segment of the optic nerve with a high T2 signal. High T2 signal persists and may be permanent;
* Atrophied nerve in chronic cases

Other diagnosis studies which may help to diagnosis of optic neuritis include:<ref name="pmid4347010">{{cite journal |vauthors=Ishikawa Y |title=[Electronmicroscopic observations on cultured rabbit lens cells infected with herpes virus] |language=Japanese |journal=Nippon Ganka Gakkai Zasshi |volume=76 |issue=10 |pages=1213–24 |date=October 1972 |pmid=4347010 |doi= |url=}}</ref><ref name="pmid28531809">{{cite journal |vauthors=Pihl-Jensen G, Schmidt MF, Frederiksen JL |title=Multifocal visual evoked potentials in optic neuritis and multiple sclerosis: A review |journal=Clin Neurophysiol |volume=128 |issue=7 |pages=1234–1245 |date=July 2017 |pmid=28531809 |doi=10.1016/j.clinph.2017.03.047 |url=}}</ref><ref name="pmid3005938">{{cite journal |vauthors=Rao NA, Calandra AJ, Sevanian A, Bowe B, Delmage JM, Marak GE |title=Modulation of lens-induced uveitis by superoxide dismutase |journal=Ophthalmic Res. |volume=18 |issue=1 |pages=41–6 |date=1986 |pmid=3005938 |doi=10.1159/000265413 |url=}}</ref>
* [[Functional MRI]]
* [[Multifocal visual evoked potential]]
* [[Optical coherence tomography]] (OCT)

===Symptoms===
* The symptoms of optic neuritis usually develop in the second decade of life, and start with symptoms such as pain on movement of the eyes, followed by a worsening of [[vision]].<ref name="pmid4581115">{{cite journal |vauthors=Wilson BJ |title=12,13-Epoxytrichothecenes: potential toxic contaminants of foods |journal=Nutr. Rev. |volume=31 |issue=6 |pages=169–72 |date=June 1973 |pmid=4581115 |doi= |url=}}</ref>
* Common symptoms of optic neuritis include:<ref name="pmid4581115">{{cite journal |vauthors=Wilson BJ |title=12,13-Epoxytrichothecenes: potential toxic contaminants of foods |journal=Nutr. Rev. |volume=31 |issue=6 |pages=169–72 |date=June 1973 |pmid=4581115 |doi= |url=}}</ref><ref name="pmid1734247">{{cite journal |vauthors=Beck RW, Cleary PA, Anderson MM, Keltner JL, Shults WT, Kaufman DI, Buckley EG, Corbett JJ, Kupersmith MJ, Miller NR |title=A randomized, controlled trial of corticosteroids in the treatment of acute optic neuritis. The Optic Neuritis Study Group |journal=N. Engl. J. Med. |volume=326 |issue=9 |pages=581–8 |date=February 1992 |pmid=1734247 |doi=10.1056/NEJM199202273260901 |url=}}</ref><ref name="pmid26396053">{{cite journal |vauthors=Wilhelm H, Schabet M |title=The Diagnosis and Treatment of Optic Neuritis |journal=Dtsch Arztebl Int |volume=112 |issue=37 |pages=616–25; quiz 626 |date=September 2015 |pmid=26396053 |pmc=4581115 |doi=10.3238/arztebl.2015.0616 |url=}}</ref>
*# Pain on movement of the eyes which is sever and so disturbing
*# Seeing things darkly, unclearly, and with [[Contrast|poor contrast]]
*# Dirty and pale Colors
*# [[Visual field loss]]
*# Disturbed [[color vision]]
*# Flashing lights
* After a sub acute onset, the patient’s [[visual acuity]] continues to deteriorate for a few more days; in the untreated course of the disease, it generally reaches its nadir in one to two weeks and then improves again.<ref name="pmid4581115">{{cite journal |vauthors=Wilson BJ |title=12,13-Epoxytrichothecenes: potential toxic contaminants of foods |journal=Nutr. Rev. |volume=31 |issue=6 |pages=169–72 |date=June 1973 |pmid=4581115 |doi= |url=}}</ref>

===Physical Examination===
Physical examination of patients with optic neuritis is usually remarkable for:<ref name="pmid3414716">{{cite journal |vauthors=Kliethermes MA |title=Working parents in two-pharmacist marriages |journal=Am J Hosp Pharm |volume=45 |issue=7 |pages=1500 |date=July 1988 |pmid=3414716 |doi= |url=}}</ref><ref name="pmid19878630">{{cite journal |vauthors=Shams PN, Plant GT |title=Optic neuritis: a review |journal=Int MS J |volume=16 |issue=3 |pages=82–9 |date=September 2009 |pmid=19878630 |doi= |url=}}</ref><ref name="pmid16554529">{{cite journal |vauthors=Balcer LJ |title=Clinical practice. Optic neuritis |journal=N. Engl. J. Med. |volume=354 |issue=12 |pages=1273–80 |date=March 2006 |pmid=16554529 |doi=10.1056/NEJMcp053247 |url=}}</ref>
* Ophthalmic examination findings:
** [[Papillitis]] with swollen [[optic disc]]
** Normal [[optic disc]] appearance (2/3 of cases) in retrobulbar neuritis type of optic neuritis
** Perineuritis, which involves the [[optic nerve]] sheath while the optic disc may or may not be swollen
** Neuroretinitis with [[Optic disc|optic disc oedema]] and macular star exudates
* Unilateral loss of [[visual acuity]]
* Reduced contrast sensitivity
* Ipsilateral relative afferent pupillary defect
* [[Visual field]] defect
* [[Color blindness|Dyschromatopsia]]

===Laboratory Findings===
* There are no specific diagnostic laboratory findings associated with optic neuritis.
* If [[multiple sclerosis]] is suspected, extensive laboratory testing is recommended in the neurologic guidelines.<ref name="pmid4581115">{{cite journal |vauthors=Wilson BJ |title=12,13-Epoxytrichothecenes: potential toxic contaminants of foods |journal=Nutr. Rev. |volume=31 |issue=6 |pages=169–72 |date=June 1973 |pmid=4581115 |doi= |url=}}</ref><ref name="pmid5398757">{{cite journal |vauthors=Mialaret J |title=[Apropos of M. Lagrot's article entitled "Dispute" in vagotomy on selection, chemical tests and associated antrectomy] |language=French |journal=Mem Acad Chir (Paris) |volume=95 |issue=6 |pages=194–6 |date=1969 |pmid=5398757 |doi= |url=}}</ref>
* Other recommended laboratory tests for all patients with optic neuritis include:<ref name="pmid4581115">{{cite journal |vauthors=Wilson BJ |title=12,13-Epoxytrichothecenes: potential toxic contaminants of foods |journal=Nutr. Rev. |volume=31 |issue=6 |pages=169–72 |date=June 1973 |pmid=4581115 |doi= |url=}}</ref><ref name="pmid1857074">{{cite journal |vauthors=Kanareĭkin KF |title=[Soviet neuropathology in the Great Patriotic War 1941-1945] |language=Russian |journal=Klin Med (Mosk) |volume=69 |issue=5 |pages=4–6 |date=May 1991 |pmid=1857074 |doi= |url=}}</ref>
** [[C-reactive protein]]
** [[Complete blood count]]
** Serum chemistry
** [[Blood sugar]]
** [[Vitamin B12|Vitamin B12]]
** [[Rheumatoid factor]]
** [[Antinuclear antibodies]]
** [[Antiphospholipid antibodies|Anti-phospholipid antibodies]]
** [[Anti-dsDNA antibody|Anti-ds-DNA antibodies]]
** [[Lupus anticoagulant]]
** Serum [[angiotensin-converting enzyme]] test
** ''[[Borrelia burgdorferi|Borrelia]]'' serology
** [[Urinalysis]]

===Imaging Findings===
Among all imaging studies, [[MRI]] is the diagnosis study of choice for visualising the [[optic nerve]].

The following result of [[Magnetic resonance imaging|MRI]] is confirmatory of optic neuritis:
* Swollen retrobulbar intra-orbital segment of the optic nerve with a high T2 signal. High T2 signal persists and may be permanent;
* Atrophied nerve in chronic cases

Other diagnosis studies which may help to diagnosis of optic neuritis include:<ref name="pmid4347010" /><ref name="pmid28531809" /><ref name="pmid3005938" />
* [[Functional MRI]]
* [[Multifocal visual evoked potential]]
* [[Optical coherence tomography]] (OCT)

===Other Diagnostic Studies===
There are no widely used other diagnosis studies for diagnosis of optic neuritis.

==Treatment==
===Medical Therapy===
Optic neuritis requires prompt treatment.

The mainstay of treatment for optic neuritis is [[corticosteroid]] therapy and is recommended among all patients who develop optic neuritis.<ref name="pmid4581115">{{cite journal |vauthors=Wilson BJ |title=12,13-Epoxytrichothecenes: potential toxic contaminants of foods |journal=Nutr. Rev. |volume=31 |issue=6 |pages=169–72 |date=June 1973 |pmid=4581115 |doi= |url=}}</ref>

Some [[pharmacologic]] medical therapies for optic neuritis include:<ref name="pmid4581115">{{cite journal |vauthors=Wilson BJ |title=12,13-Epoxytrichothecenes: potential toxic contaminants of foods |journal=Nutr. Rev. |volume=31 |issue=6 |pages=169–72 |date=June 1973 |pmid=4581115 |doi= |url=}}</ref>
# [[Prednisone|Oral prednisone]] treatment at a dose of 1 mg/kg body weight /day for 14 days
# intravenous [[methylprednisolon]]<nowiki/>e treatment at 500–1000 mg/day for 3_5 days followed by oral prednisolone (1 mg/kg BW) for 11 days

===Surgery===
*In the case of [[optic canal]] compression in patients with severe optic neuritis, [[surgery]] is used to decompress the orbital compartment by exposure of the intracanalicular part of the [[optic nerve]].<ref name="pmid3721018">{{cite journal |vauthors=Cieciura L, Krakowski G |title=Ultrastructural studies on the mitochondria of the pinealocyte under conditions of persistent lighting--L24 |journal=Folia Histochem. Cytobiol. |volume=24 |issue=1 |pages=33–7 |date=1986 |pmid=3721018 |doi= |url=}}</ref>
*Modern craniomaxillofacial surgery requires detailed consideration of the diagnosis and treatment of traumatic visual pathway damage with the ultimate goal of preserving [[visual acuity]].<ref name="pmid3721018">{{cite journal |vauthors=Cieciura L, Krakowski G |title=Ultrastructural studies on the mitochondria of the pinealocyte under conditions of persistent lighting--L24 |journal=Folia Histochem. Cytobiol. |volume=24 |issue=1 |pages=33–7 |date=1986 |pmid=3721018 |doi= |url=}}</ref>

===Prevention===
There are no established measures for the primary prevention of optic neuritis.

==References==
{{reflist|2}}

{{Eye pathology}}
[[Category:Neurology]]
[[Category:Ophthalmology]]
[[Category:Needs Content]]
[[Category:Rheumatology]]

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}

Central pontine myelinolysis

2020-05-06T04:52:52Z

M Jahan:

__NOTOC__
[[Image: Pontine myelinolysis.jpg|thumb|Right|PX:400|Loss of myelinated fibers at the basilar part of the pons in the brainstem (Luxol-Fast blue stain)

Source: Wikipedia: Jensflorian

<nowiki>https://en.wikipedia.org/wiki/Central_pontine_myelinolysis#Pathophysiology</nowiki>]]
{{Central pontine myelinolysis}}
'''For patient information, click [[Central pontine myelinolysis(patient information)|here]]'''

{{CMG}}; {{AE}} {{sali}}, {{MMJ}}

{{SK}}

==[[Central pontine myelinolysis overview|Overview]]==

==[[Central pontine myelinolysis historical perspective|Historical Perspective]]==

==[[Central pontine myelinolysis classification|Classification]]==

==[[Central pontine myelinolysis pathophysiology|Pathophysiology]]==

==[[Central pontine myelinolysis causes|Causes]]==

==[[Central pontine myelinolysis differential diagnosis|Differentiating Central pontine myelinolysis from other Diseases]]==

==[[Central pontine myelinolysis epidemiology and demographics|Epidemiology and Demographics]]==

==[[Central pontine myelinolysis risk factors|Risk Factors]]==

==[[Central pontine myelinolysis screening|Screening]]==

==[[Central pontine myelinolysis natural history, complications and prognosis|Natural History, Complications and Prognosis]]==

==Diagnosis==
[[Central pontine myelinolysis diagnostic study of choice|Diagnostic study of choice]] | [[Central pontine myelinolysis history and symptoms|History and Symptoms]] | [[Central pontine myelinolysis physical examination|Physical Examination]] | [[Central pontine myelinolysis laboratory findings|Laboratory Findings]] | [[Central pontine myelinolysis electrocardiogram|Electrocardiogram]] | [[Central pontine myelinolysis x ray|X-Ray Findings]] | [[Central pontine myelinolysis echocardiography and ultrasound|Echocardiography and Ultrasound]] | [[Central pontine myelinolysis CT scan|CT-Scan Findings]] | [[Central pontine myelinolysis MRI|MRI Findings]] | [[Central pontine myelinolysis other imaging findings|Other Imaging Findings]] | [[Central pontine myelinolysis other diagnostic studies|Other Diagnostic Studies]]

==Treatment==
[[Central pontine myelinolysis medical therapy|Medical Therapy]] | [[Central pontine myelinolysis interventions|Interventions]] | [[Central pontine myelinolysis surgery|Surgery]] | [[Central pontine myelinolysis primary prevention|Primary Prevention]] | [[Central pontine myelinolysis secondary prevention|Secondary Prevention]] | [[Central pontine myelinolysis cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Central pontine myelinolysis future or investigational therapies|Future or Investigational Therapies]]

==Case Studies==
[[Central pontine myelinolysis case study one|Case #1]]

[[Category: (name of the system)]]

Friedreich's ataxia causes

2020-05-06T04:42:55Z

M Jahan:

Spina bifida medical therapy

2020-05-06T04:42:18Z

M Jahan:

__NOTOC__
{{Spina bifida}}
{{CMG}}; {{AE}}{{sali}}, {{MMJ}}

==Overview==
Spina bifida requires prompt treatment. The mainstay of treatment for spina bifida is [[surgery]].

==Medical Therapy==
* Spina bifida requires prompt treatment.
* The mainstay of treatment for spina bifida is [[surgery]].

==References==
{{Reflist|2}}

{{WH}}
{{WS}}
[[Category: (name of the system)]]

Friedreich's ataxia

2020-05-06T04:40:56Z

M Jahan:

__NOTOC__
{{Friedreich's ataxia}}

{{CMG}}, {{AE}} {{sali}}, [[User:M Jahan|Mohamadmostafa Jahansouz M.D]]

==[[Friedreich's ataxia overview|Overview]]==

==[[Friedreich's ataxia historical perspective|Historical Perspective]]==

==[[Friedreich's ataxia classification|Classification]]==

==[[Friedreich's ataxia pathophysiology|Pathophysiology]]==

==[[Friedreich's ataxia causes|Causes]]==

==[[Friedreich's ataxia differential diagnosis|Differentiating Any Disease from other Diseases]]==

==[[Friedreich's ataxia epidemiology and demographics|Epidemiology and Demographics]]==

==[[Friedreich's ataxia risk factors|Risk Factors]]==

==[[Friedreich's ataxia screening|Screening]]==

==[[Friedreich's ataxia natural history, complications and prognosis|Natural History, Complications and Prognosis]]==

==Diagnosis==
[[Friedreich's ataxia history and symptoms|History and Symptoms]] | [[Friedreich's ataxia physical examination|Physical Examination]] | [[Friedreich's ataxia laboratory findings|Laboratory Findings]] | [[Friedreich's ataxia electrocardiogram|Electrocardiogram]] | [[Friedreich's ataxia chest x ray|Chest X Ray]] | [[Friedreich's ataxia CT|CT]] | [[Friedreich's ataxia MRI|MRI]] | [[Friedreich's ataxia echocardiography or ultrasound|Echocardiography or Ultrasound]] | [[Friedreich's ataxia other imaging findings|Other Imaging Findings]] | [[Friedreich's ataxia other diagnostic studies|Other Diagnostic Studies]]

==Treatment==
[[Friedreich's ataxia medical therapy|Medical Therapy]] | [[Friedreich's ataxia surgery|Surgery]] | [[Friedreich's ataxia primary prevention|Primary Prevention]] | [[Friedreich's ataxia secondary prevention|Secondary Prevention]] | [[Friedreich's ataxia cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Friedreich's ataxia future or investigational therapies|Future or Investigational Therapies]]

==Case Studies==
[[Category:Projects]]
[[Category:Help]]
[[Friedreich's ataxia here case study one|Case #1]]

{{Infobox_Disease |
Name = {{PAGENAME}} |
Image = |
Caption = |
DiseasesDB = 4980 |
ICD10 = {{ICD10|G|11|1|g|10}} |
ICD9 = {{ICD9|334.0}} |
ICDO = |
OMIM = 229300 |
MedlinePlus = |
MeshID = D005621 |
}}
{{SI}}

[[Category:Neurological disorders]]
[[Category:Genetic disorders]]
[[Category:Mitochondrial diseases]]
[[es:Ataxia de Friedreich]]
[[fr:Ataxie de Friedreich]]
[[pl:Choroba Friedreicha]]

Spina bifida pathophysiology

2020-05-06T04:39:34Z

M Jahan:

__NOTOC__
{{Spina bifida}}

{{CMG}}; {{AE}} {{sali}}, {{MMJ}}
==Overview==
Spina bifida is a congenital malformation in which the spinal column is split (bifid) as a result of failed closure of the embryonic neural tube, during the fourth week post-fertilization. In normal infants, the [[neural tube]] closes by the end of the 4 week of conception, but in patients with spina bifida, some parts of the [[neural tube]] fails to develop or close that causes defects in the [[spinal cord]] and in the [[Vertebra|vertebral]] bones. Spina bifida also may be classified according to the tyoe of the vertebrate defect into 2 subtypes: [[Spina bifida occulta]]: In this type of spina bifida, the defect of [[vertebrate]] is covered by [[skin]] ("Occulta" means "hidden"). The [[spinal cord]] does not stick out through the skin, although the skin over the lower spine may have a patch of hair, a [[birthmark]], or a dimple above the groove between the [[buttocks]]. Spina ifida aperta: In this type of spina bifida , the defect is widely open and is sub classified into 2 types: Meningocele and Myelomeningocele. Spina bifida may be caused by the increase of [[cerebrospinal fluid]] (CSF) volume in the [[central nervous system]] during the first weeks of [[embryogenesis]]. [[Venous insufficiency]] is the main cause of the increase of [[cerebrospinal fluid]] and it may be caused by any disease that reduces space for venous volume. The development of spina bifida may be the result of multiple genetically defect in the genes important in the metabolism of: [[Folic Acid|Folic acid]], [[glucose]], [[Retinoid|retinoids]], [[apoptosis]], [[genes]] that regulate [[transcription]] in early [[embryogenesis]], [[methionine]] Cycle genes, [[methylation]] genes, [[glucose]] Homeostasis genes, cell Recognition and Migration genes, [[DNA]] Repair genes and transcription Factors genes. Conditions associated with spina bifida include: [[Hydrocephalus]], [[Budd-Chiari syndrome|chiari II Malformation]], [[paralysis]], urination and deification incontinences, atex Allergy, learning Disabilities, [[sexual problems]], emotional problems, [[obesity]] and vision problems.

==Pathophysiology==
* Spina bifida is a congenital malformation in which the spinal column is split (bifid) as a result of failed closure of the embryonic neural tube, during the fourth week post-fertilization.<ref name="pmid5327787">{{cite journal |vauthors=Kenworthy ME |title=Introducing the American Orthopsychiatric Association's president for 1966-67: Norman V. Lourie |journal=Am J Orthopsychiatry |volume=36 |issue=4 |pages=587–9 |date=July 1966 |pmid=5327787 |doi= |url=}}</ref>
* In normal infants, the [[neural tube]] closes by the end of the 4 week of conception, but in patients with spina bifida, some parts of the [[neural tube]] fails to develop or close that causes defects in the [[spinal cord]] and in the [[Vertebra|vertebral]] bones.
* Spina bifida also may be classified according to the tyoe of the vertebrate defect into 2 subtypes:
** [[Spina bifida occulta]]: In this type of spina bifida, the defect of [[vertebrate]] is covered by [[skin]] ("Occulta" means "hidden"). The [[spinal cord]] does not stick out through the skin, although the skin over the lower spine may have a patch of hair, a [[birthmark]], or a dimple above the groove between the [[buttocks]].<ref name="pmid5327787">{{cite journal |vauthors=Kenworthy ME |title=Introducing the American Orthopsychiatric Association's president for 1966-67: Norman V. Lourie |journal=Am J Orthopsychiatry |volume=36 |issue=4 |pages=587–9 |date=July 1966 |pmid=5327787 |doi= |url=}}</ref>
** Spina ifida aperta: In this type of spina bifida , the defect is widely open and is sub classified into 2 types: Meningocele and Myelomeningocele.<ref name="pmid5327787">{{cite journal |vauthors=Kenworthy ME |title=Introducing the American Orthopsychiatric Association's president for 1966-67: Norman V. Lourie |journal=Am J Orthopsychiatry |volume=36 |issue=4 |pages=587–9 |date=July 1966 |pmid=5327787 |doi= |url=}}</ref>
===Pathogenesis===
*Spina bifida may be caused by the increase of [[cerebrospinal fluid]] (CSF) volume in the [[central nervous system]] during the first weeks of [[embryogenesis]].<ref name="pmid18405364">{{cite journal |vauthors=Williams H |title=A unifying hypothesis for hydrocephalus, Chiari malformation, syringomyelia, anencephaly and spina bifida |journal=Cerebrospinal Fluid Res |volume=5 |issue= |pages=7 |date=April 2008 |pmid=18405364 |pmc=2365936 |doi=10.1186/1743-8454-5-7 |url=}}</ref>
*[[Venous insufficiency]] is the main cause of the increase of [[cerebrospinal fluid]] and it may be caused by any disease that reduces space for venous volume.<ref name="pmid18405364">{{cite journal |vauthors=Williams H |title=A unifying hypothesis for hydrocephalus, Chiari malformation, syringomyelia, anencephaly and spina bifida |journal=Cerebrospinal Fluid Res |volume=5 |issue= |pages=7 |date=April 2008 |pmid=18405364 |pmc=2365936 |doi=10.1186/1743-8454-5-7 |url=}}</ref>

==Genetics==
The development of spina bifida may be the result of multiple genetically defect in the genes important in the metabolism of:<ref>{{cite journal |vauthors=Schmoldt A, Benthe HF, Haberland G, Holder AA, Wootton JC, Baron AJ, Chambers GK, Fincham JR, Alekseeva IG, Lapina GP, Tulovskaia ZD, Izmaĭlova VN |title=Digitoxin metabolism by rat liver microsomes |journal=Biochem. Pharmacol. |volume=24 |issue=17 |pages=1639–41 |date=September 1975 |pmid=10 |pmc=5922622 |doi= |url=}}</ref>

*[[Folic Acid|Folic acid]]
*[[Glucose]]
*[[Retinoid|Retinoids]]
Other genes which may be contributed in the development of the spina bifida include:
*[[Genes]] important in [[apoptosis]]
*[[Genes]] that regulate [[transcription]] in early [[embryogenesis]]
*[[Methionine]] Cycle genes
*[[Methylation]] genes
*[[Glucose]] Homeostasis genes
*Cell Recognition and Migration genes
*[[DNA]] Repair genes
*Transcription Factors genes such as:<ref name="pmid3053142">{{cite journal |vauthors=Nordman H, Keskinen H, Alanko K |title=[The changing spectrum of occupational diseases of the lung] |language=Finnish |journal=Duodecim |volume=104 |issue=6 |pages=473–9 |date=1988 |pmid=3053142 |doi= |url=}}</ref>
*#''[[HOXA1|HOX]]''s
*#''[[PAX1|PAX]]''s
*#''[[MSX1|MSX]]2''
*#''T'' [[brachyury]]
*#''[[TFAP2A|TFAP2a]]''
*#''[[ZIC1|ZICs]]''
*#''[[BRCA1]]''
*#''[[CITED2]]''
*#''[[TP53]]''
*#''SLUG''

== Associated Conditions ==
Conditions associated with spina bifida include:<ref name="pmid21193992">{{cite journal |vauthors=Jenkinson MD, Campbell S, Hayhurst C, Clark S, Kandasamy J, Lee MK, Flynn A, Murphy P, Mallucci CL |title=Cognitive and functional outcome in spina bifida-Chiari II malformation |journal=Childs Nerv Syst |volume=27 |issue=6 |pages=967–74 |date=June 2011 |pmid=21193992 |doi=10.1007/s00381-010-1368-7 |url=}}</ref><ref name="pmid1799681">{{cite journal |vauthors=Behe MJ, Beasty AM |title=Co-polymer tracts in eukaryotic, prokaryotic, and organellar DNA |journal=DNA Seq. |volume=1 |issue=5 |pages=291–302 |date=1991 |pmid=1799681 |doi= |url=}}</ref><ref name="pmid4316301">{{cite journal |vauthors=Temin HM, Mizutani S |title=RNA-dependent DNA polymerase in virions of Rous sarcoma virus |journal=Nature |volume=226 |issue=5252 |pages=1211–3 |date=June 1970 |pmid=4316301 |doi= |url=}}</ref><ref name="pmid28991086">{{cite journal |vauthors=Brochard C, Peyronnet B, Dariel A, Ménard H, Manunta A, Ropert A, Neunlist M, Bouguen G, Siproudhis L |title=Bowel Dysfunction Related to Spina Bifida: Keep It Simple |journal=Dis. Colon Rectum |volume=60 |issue=11 |pages=1209–1214 |date=November 2017 |pmid=28991086 |doi=10.1097/DCR.0000000000000892 |url=}}</ref><ref name="pmid10231329">{{cite journal |vauthors=Bernardini R, Novembre E, Lombardi E, Mezzetti P, Cianferoni A, Danti DA, Mercurella A, Vierucci A |title=Risk factors for latex allergy in patients with spina bifida and latex sensitization |journal=Clin. Exp. Allergy |volume=29 |issue=5 |pages=681–6 |date=May 1999 |pmid=10231329 |doi= |url=}}</ref><ref name="pmid1955048">{{cite journal |vauthors=Gaston H |title=Ophthalmic complications of spina bifida and hydrocephalus |journal=Eye (Lond) |volume=5 ( Pt 3) |issue= |pages=279–90 |date=1991 |pmid=1955048 |doi=10.1038/eye.1991.44 |url=}}</ref>
* [[Hydrocephalus]]
* [[Budd-Chiari syndrome|Chiari II Malformation]]
* [[Paralysis]]
* Urination and deification incontinences
* Latex Allergy
* Learning Disabilities
* [[Sexual problems]]
* Emotional problems
* [[Obesity]]
* Vision problems

==References==
{{Reflist|2}}

{{WH}}
{{WS}}
[[Category: (name of the system)]]

Friedreich's ataxia pathophysiology

2020-05-06T04:38:52Z

M Jahan:

__NOTOC__
{{Friedreich's ataxia}}
{{CMG}} ; {{AE}}{{sali}}, [[User:M Jahan|Mohamadmostafa Jahansouz M.D]]

==Overview==
It is understood that Friedreich’s ataxia is the result of a [[homozygous]] [[guanine]]-[[adenine]]-[[adenine]] (GAA) [[Trinucleotide repeat expansion disorders|trinucleotide repeat expansion]] on chromosome 9q13 that causes a transcriptional defect of the [[frataxin]] gene. [[Frataxin]] is a small mitochondrial protein and deficiency of [[frataxin]] is responsible for all clinical and morphological manifestations of Friedreich’s ataxia. The severity of the disease is directly related to the length of the [[Trinucleotide repeat expansion disorders|trinucleotide repeat expansion]] and long expansions lead to early onset, severe clinical illness, and death in young adult life. Patients with short [[Trinucleotide repeat expansion disorders|trinucleotide repeat expansion]] have a later onset and a more benign course and even some of them are not diagnosed during life. Friedreich’s ataxia is transmitted in [[Autosomal recessive disorder|autosomal recessive]] pattern. Because the [[frataxin]] protein has multiple functions in the normal state, the exact role of frataxin deficiency in the pathogenesis of Friedreich's ataxia is still unclear. Conditions associated with friedreich’s ataxia include: [[Hypertrophic cardiomyopathy]], [[diabetes mellitus]], [[scoliosis]], distal wasting, [[optic atrophy]], [[sensorineural deafness]], [[sleep apnea]] and [[pes cavus]] in 55% to 75% of cases. On gross [[pathology]] involvement of spinal cord, [[cerebellum]], and heart are characteristic findings of Friedreich's ataxia. '''Spinal cord''' lesions include: Decreased transverse diameter of the [[spinal cord]] at all levels, thin and gray dorsal spinal roots, smallness and gray discoloration of the [[dorsal column]], thin and gray [[gracile]] and [[Cuneate fasciculus|cuneate fasciculi]] and [[fiber]] loss in the anterolateral fields corresponding to [[Spinocerebellar tract|spinocerebellar]] and [[Corticospinal tract|corticospinal tracts]]. '''Cerebellum''' lesions include [[atrophy]] of the [[Dentate nucleus|dentate nuclei]] and its efferent fibers. '''Heart''' findings include: Increased heart weight, increased thickness of left and right ventricular walls and [[interventricular septum]], dilatation of the [[ventricles]] and "marble”-like discoloration of the [[myocardium]]. On microscopic histopathological analysis, involvement of [[spinal cord]], [[cerebellum]], [[heart]] and [[pancreas]] are characteristic findings of Friedreich's ataxia. Friedreich’s ataxia mostly affects the [[dorsal root ganglia]] (DRG) of the spinal cord. It affects the entire DGR but is most prominent in subcapsular regions. Cell stains in samples of DGN reveal: An overall reduction in the size of [[ganglion cells]], the absence of very large [[Neuron|neurons]] and large [[Myelinated|myelinated fibers]], clusters of nuclei representing “residual nodules” that indicate an invasion-like entry of [[Satellite cells|satellite]] cells into the [[cytoplasm]] of neurons, progressive destruction of neuronal cytoplasm in cytoskeletal stains, such as for class-III-β-tubulin, greatly thickened [[satellite cells]], residual nodules remain strongly reactive with anti-S100α in the satellite cells and increased [[ferritin]] immunoreactivity in satellite cells. Friedreich’s ataxia mostly affects the [[dentate nucleus]] of [[cerebellum]]. Cell stains in samples of [[cerebellum]] reveal: The absence of very large [[Neuron|neurons]], severe loss of [[γ-aminobutyric acid]] (GABA)-containing terminals in the immunostaining with an antibody to [[glutamic acid decarboxylase]] (GAD), grumose degeneration in the immunostaining with anti-GAD, punctate reaction product in areas known to be rich in [[Mitochondrion|mitochondria]], namely, neuronal cytoplasm and synaptic terminals and [[Frataxin]]-deficient [[mitochondria]]. Cell stains in samples of heart reveal: Collections of tiny reactive inclusions in a small percentage of [[Cardiomyocyte|cardiomyocytes]] that are arranged in parallel with [[myofibrils]] in the iron stains, electron-dense inclusions in [[Mitochondrion|mitochondria]] and [[myocardial]] fiber necrosis and an inflammatory reaction in the severe cases of [[cardiomyopathy]]. Cell stains in samples of [[pancreas]] reveal: Lose of the sharp demarcation of the [[synaptophysin]]-positive [[Islets of Langerhans|islets]] of [[pancreas]] and the “fade” appearance of the β-cells into the surrounding exocrine [[pancreas]].

==Pathophysiology==
===Pathogenesis and genetics===
*It is understood that Friedreich’s ataxia is the result of a [[homozygous]] [[guanine]]-[[adenine]]-[[adenine]] (GAA) [[Trinucleotide repeat expansion disorders|trinucleotide repeat expansion]] on chromosome 9q13 that causes a [[Transcriptional regulation|transcriptional]] defect of the [[frataxin]] gene.<ref name="pmid11269509">{{cite journal |vauthors=Bit-Avragim N, Perrot A, Schöls L, Hardt C, Kreuz FR, Zühlke C, Bubel S, Laccone F, Vogel HP, Dietz R, Osterziel KJ |title=The GAA repeat expansion in intron 1 of the frataxin gene is related to the severity of cardiac manifestation in patients with Friedreich's ataxia |journal=J. Mol. Med. |volume=78 |issue=11 |pages=626–32 |date=2001 |pmid=11269509 |doi= |url=}}</ref>
*[[Frataxin]] is a small mitochondrial protein and deficiency of [[frataxin]] is responsible for all clinical and morphological manifestations of Friedreich’s ataxia.<ref name="pmid21315377">{{cite journal |vauthors=Koeppen AH |title=Friedreich's ataxia: pathology, pathogenesis, and molecular genetics |journal=J. Neurol. Sci. |volume=303 |issue=1-2 |pages=1–12 |date=April 2011 |pmid=21315377 |pmc=3062632 |doi=10.1016/j.jns.2011.01.010 |url=}}</ref>
*The severity of the disease is directly related to the length of the [[Trinucleotide repeat expansion disorders|trinucleotide repeat expansion]] and long expansions lead to early onset, severe clinical illness, and death in young adult life.<ref name="pmid22993450">{{cite journal |vauthors=Martino D, Stamelou M, Bhatia KP |title=The differential diagnosis of Huntington's disease-like syndromes: 'red flags' for the clinician |journal=J. Neurol. Neurosurg. Psychiatry |volume=84 |issue=6 |pages=650–6 |date=June 2013 |pmid=22993450 |pmc=3646286 |doi=10.1136/jnnp-2012-302532 |url=}}</ref>
*Patients with short [[Trinucleotide repeat expansion disorders|trinucleotide repeat expansion]] have a later onset and a more benign course and even some of them are not diagnosed during life.<ref name="pmid23334592">{{cite journal |vauthors=Koeppen AH, Mazurkiewicz JE |title=Friedreich ataxia: neuropathology revised |journal=J. Neuropathol. Exp. Neurol. |volume=72 |issue=2 |pages=78–90 |date=February 2013 |pmid=23334592 |pmc=3817014 |doi=10.1097/NEN.0b013e31827e5762 |url=}}</ref>
*Friedreich’s ataxia is transmitted in [[Autosomal recessive disorder|autosomal recessive]] pattern.<ref name="pmid21691434">{{cite journal |vauthors=Payne RM |title=The Heart in Friedreich's Ataxia: Basic Findings and Clinical Implications |journal=Prog. Pediatr. Cardiol. |volume=31 |issue=2 |pages=103–109 |date=May 2011 |pmid=21691434 |pmc=3117664 |doi=10.1016/j.ppedcard.2011.02.007 |url=}}</ref>
*Because the frataxin protein has multiple functions in the normal state, the exact role of [[frataxin]] deficiency in the pathogenesis of Friedreich's ataxia is still unclear.<ref name="pmid21315377">{{cite journal |vauthors=Koeppen AH |title=Friedreich's ataxia: pathology, pathogenesis, and molecular genetics |journal=J. Neurol. Sci. |volume=303 |issue=1-2 |pages=1–12 |date=April 2011 |pmid=21315377 |pmc=3062632 |doi=10.1016/j.jns.2011.01.010 |url=}}</ref> These functions include:<ref name="pmid16677095">{{cite journal |vauthors=Napoli E, Taroni F, Cortopassi GA |title=Frataxin, iron-sulfur clusters, heme, ROS, and aging |journal=Antioxid. Redox Signal. |volume=8 |issue=3-4 |pages=506–16 |date=2006 |pmid=16677095 |pmc=1805116 |doi=10.1089/ars.2006.8.506 |url=}}</ref><ref name="pmid15176725">{{cite journal |vauthors=Isaya G, O'Neill HA, Gakh O, Park S, Mantcheva R, Mooney SM |title=Functional studies of frataxin |journal=Acta Paediatr Suppl |volume=93 |issue=445 |pages=68–71; discussion 72–3 |date=May 2004 |pmid=15176725 |doi= |url=}}</ref><ref name="pmid18393441">{{cite journal |vauthors=Schagerlöf U, Elmlund H, Gakh O, Nordlund G, Hebert H, Lindahl M, Isaya G, Al-Karadaghi S |title=Structural basis of the iron storage function of frataxin from single-particle reconstruction of the iron-loaded oligomer |journal=Biochemistry |volume=47 |issue=17 |pages=4948–54 |date=April 2008 |pmid=18393441 |pmc=3932613 |doi=10.1021/bi800052m |url=}}</ref><ref name="pmid21315377">{{cite journal |vauthors=Koeppen AH |title=Friedreich's ataxia: pathology, pathogenesis, and molecular genetics |journal=J. Neurol. Sci. |volume=303 |issue=1-2 |pages=1–12 |date=April 2011 |pmid=21315377 |pmc=3062632 |doi=10.1016/j.jns.2011.01.010 |url=}}</ref>
**Biogenesis of [[Iron-sulfur cluster|iron-sulfur clusters]]
**[[Iron]] [[Chaperone|chaperoning]]
**Iron storage
**Control of iron-mediated oxidative tissue damage

==Associated Conditions==
Conditions associated with friedreich’s ataxia include:
*Hypertrophic cardiomyopathy<ref name="pmid23859344">{{cite journal |vauthors=Weidemann F, Störk S, Liu D, Hu K, Herrmann S, Ertl G, Niemann M |title=Cardiomyopathy of Friedreich ataxia |journal=J. Neurochem. |volume=126 Suppl 1 |issue= |pages=88–93 |date=August 2013 |pmid=23859344 |doi=10.1111/jnc.12217 |url=}}</ref>
*[[Diabetes mellitus]]<ref name="pmid5602235">{{cite journal |vauthors=Gudowski G, Grossmann P, Robbe K |title=[The prednisolone provocation test in chronic pyelonephritis in children] |language=German |journal=Kinderarztl Prax |volume=35 |issue=10 |pages=441–5 |date=October 1967 |pmid=5602235 |doi= |url=}}</ref>
*[[Scoliosis]]<ref name="pmid18388721">{{cite journal |vauthors=Milbrandt TA, Kunes JR, Karol LA |title=Friedreich's ataxia and scoliosis: the experience at two institutions |journal=J Pediatr Orthop |volume=28 |issue=2 |pages=234–8 |date=March 2008 |pmid=18388721 |doi=10.1097/BPO.0b013e318164fa79 |url=}}</ref>
*Distal wasting<ref name="pmid6106966">{{cite journal |vauthors=Hofstetter JR, Chevaux F, Fontolliet C |title=[Alcoholic hepatitis] |language=German |journal=Schweiz Med Wochenschr |volume=110 |issue=38 |pages=1370–5 |date=September 1980 |pmid=6106966 |doi= |url=}}</ref>
*[[Optic atrophy]]<ref name="pmid6106966">{{cite journal |vauthors=Hofstetter JR, Chevaux F, Fontolliet C |title=[Alcoholic hepatitis] |language=German |journal=Schweiz Med Wochenschr |volume=110 |issue=38 |pages=1370–5 |date=September 1980 |pmid=6106966 |doi= |url=}}</ref>
*[[Sensorineural deafness]]<ref name="pmid6106966">{{cite journal |vauthors=Hofstetter JR, Chevaux F, Fontolliet C |title=[Alcoholic hepatitis] |language=German |journal=Schweiz Med Wochenschr |volume=110 |issue=38 |pages=1370–5 |date=September 1980 |pmid=6106966 |doi= |url=}}</ref>
*[[Sleep apnea]]<ref name="pmid17049722">{{cite journal |vauthors=Reddy PL, Grewal RP |title=Friedreich's ataxia: a clinical and genetic analysis |journal=Clin Neurol Neurosurg |volume=109 |issue=2 |pages=200–2 |date=February 2007 |pmid=17049722 |doi=10.1016/j.clineuro.2006.09.003 |url=}}</ref>
*[[Pes cavus]] in 55% to 75% of cases<ref name="pmid20301458">{{cite journal |vauthors=Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJH, Stephens K, Amemiya A, Bidichandani SI, Delatycki MB |title= |journal= |volume= |issue= |pages= |date= |pmid=20301458 |doi= |url=}}</ref>

==Gross Pathology==
On gross pathology involvement of spinal cord, [[cerebellum]], and heart are characteristic findings of Friedreich's ataxia.

'''Spinal cord''' lesions include:<ref name="pmid21315377">{{cite journal |vauthors=Koeppen AH |title=Friedreich's ataxia: pathology, pathogenesis, and molecular genetics |journal=J. Neurol. Sci. |volume=303 |issue=1-2 |pages=1–12 |date=April 2011 |pmid=21315377 |pmc=3062632 |doi=10.1016/j.jns.2011.01.010 |url=}}</ref><ref name="pmid3817014">{{cite journal |vauthors=Nath P, Getzenberg R, Beebe D, Pallansch L, Zelenka P |title=c-myc mRNA is elevated as differentiating lens cells withdraw from the cell cycle |journal=Exp. Cell Res. |volume=169 |issue=1 |pages=215–22 |date=March 1987 |pmid=3817014 |doi= |url=}}</ref>
*Decreased transverse diameter of the [[spinal cord]] at all levels
**The thinning is especially evident in the thoracic region
*Thin and gray dorsal spinal roots
*Smallness and gray discoloration of the [[dorsal column]]
*Thin and gray [[gracile]] and [[Cuneate fasciculus|cuneate fasciculi]]
*Fiber loss in the anterolateral fields corresponding to [[Spinocerebellar tract|spinocerebellar]] and [[Corticospinal tract|corticospinal tracts]]
'''Cerebellum''' lesions include:
*Atrophy of the [[Dentate nucleus|dentate nuclei]] and its efferent fibers<ref name="pmid4215469">{{cite journal |vauthors=Mian N, Pover WF |title=Loss of cellular material from suspensions of isolated epithelial cells of guinea pig small intestine |journal=Biomedicine |volume=20 |issue=3 |pages=186–91 |date=May 1974 |pmid=4215469 |doi= |url=}}</ref>
'''Heart''' findings include:
*Increased heart weight<ref name="pmid2474513">{{cite journal |vauthors=Howdle PD, Hanson DG, Trejdosiewicz LK, Ciclitira PJ, Smart CJ, Walker WA |title=Responses of antigen-specific long-term murine T cell lines to wheat gliadin fractions |journal=Int. Arch. Allergy Appl. Immunol. |volume=89 |issue=2-3 |pages=269–74 |date=1989 |pmid=2474513 |doi= |url=}}</ref>
*Increased thickness of left and right ventricular walls and [[interventricular septum]]<ref name="pmid6354072">{{cite journal |vauthors=Churkina LN, Vasiurenko ZP, Smirnov VV, Kiprianova EA, Garagulia AD |title=[Effect of antibiotic AL-87 on the fatty acid composition of microorganisms in different taxonomic groups] |language=Russian |journal=Antibiotiki |volume=28 |issue=7 |pages=489–94 |date=July 1983 |pmid=6354072 |doi= |url=}}</ref>
*Dilatation of the [[ventricles]]<ref name="pmid6354072">{{cite journal |vauthors=Churkina LN, Vasiurenko ZP, Smirnov VV, Kiprianova EA, Garagulia AD |title=[Effect of antibiotic AL-87 on the fatty acid composition of microorganisms in different taxonomic groups] |language=Russian |journal=Antibiotiki |volume=28 |issue=7 |pages=489–94 |date=July 1983 |pmid=6354072 |doi= |url=}}</ref>
*“Marble”-like discoloration of the [[myocardium]]<ref name="pmid21315377">{{cite journal |vauthors=Koeppen AH |title=Friedreich's ataxia: pathology, pathogenesis, and molecular genetics |journal=J. Neurol. Sci. |volume=303 |issue=1-2 |pages=1–12 |date=April 2011 |pmid=21315377 |pmc=3062632 |doi=10.1016/j.jns.2011.01.010 |url=}}</ref>

==Microscopic Pathology==
On microscopic histopathological analysis, involvement of [[spinal cord]], [[cerebellum]], [[heart]] and [[pancreas]] are characteristic findings of Friedreich's ataxia.

'''<big>Spinal cord</big>'''
*Friedreich’s ataxia mostly affects the [[dorsal root ganglia]] (DRG) of the spinal cord. It affects the entire DGR but is most prominent in subcapsular regions.<ref name="pmid19727777">{{cite journal |vauthors=Koeppen AH, Morral JA, Davis AN, Qian J, Petrocine SV, Knutson MD, Gibson WM, Cusack MJ, Li D |title=The dorsal root ganglion in Friedreich's ataxia |journal=Acta Neuropathol. |volume=118 |issue=6 |pages=763–76 |date=December 2009 |pmid=19727777 |doi=10.1007/s00401-009-0589-x |url=}}</ref>
*Cell stains in samples of DGN reveal:<ref name="pmid21315377">{{cite journal |vauthors=Koeppen AH |title=Friedreich's ataxia: pathology, pathogenesis, and molecular genetics |journal=J. Neurol. Sci. |volume=303 |issue=1-2 |pages=1–12 |date=April 2011 |pmid=21315377 |pmc=3062632 |doi=10.1016/j.jns.2011.01.010 |url=}}</ref><ref name="pmid3817014">{{cite journal |vauthors=Nath P, Getzenberg R, Beebe D, Pallansch L, Zelenka P |title=c-myc mRNA is elevated as differentiating lens cells withdraw from the cell cycle |journal=Exp. Cell Res. |volume=169 |issue=1 |pages=215–22 |date=March 1987 |pmid=3817014 |doi= |url=}}</ref><ref name="pmid4294979">{{cite journal |vauthors=Kono R |title=[Suspected human hepatitis virus] |language=Japanese |journal=Saishin Igaku |volume=22 |issue=6 |pages=1334–7 |date=June 1967 |pmid=4294979 |doi= |url=}}</ref><ref name="pmid4855486">{{cite journal |vauthors=Wykle RL, Schremmer JM |title=A lysophospholipase D pathway in the metabolism of ether-linked lipids in brain microsomes |journal=J. Biol. Chem. |volume=249 |issue=6 |pages=1742–6 |date=March 1974 |pmid=4855486 |doi= |url=}}</ref>
**An overall reduction in the size of [[ganglion cells]]
**The absence of very large [[Neuron|neurons]] and large [[Myelinated|myelinated fibers]]
**Clusters of nuclei representing “residual nodules” that indicate an invasion-like entry of [[Satellite cells|satellite]] cells into the [[cytoplasm]] of neurons.
**Progressive destruction of neuronal cytoplasm in [[cytoskeletal]] stains, such as for class-III-β-tubulin
**Greatly thickened [[satellite cells]]
**Residual nodules remain strongly reactive with anti-S100α in the satellite cells
**Increased [[ferritin]] immunoreactivity in satellite cells
'''<big>Cerebellum</big>'''
*Friedreich’s ataxia mostly affects the [[dentate nucleus]] of [[cerebellum]]<ref name="pmid17443334">{{cite journal |vauthors=Koeppen AH, Michael SC, Knutson MD, Haile DJ, Qian J, Levi S, Santambrogio P, Garrick MD, Lamarche JB |title=The dentate nucleus in Friedreich's ataxia: the role of iron-responsive proteins |journal=Acta Neuropathol. |volume=114 |issue=2 |pages=163–73 |date=August 2007 |pmid=17443334 |doi=10.1007/s00401-007-0220-y |url=}}</ref>
*Cell stains in samples of [[cerebellum]] reveal:
**The absence of very large [[Neuron|neurons]]<ref name="pmid21315377">{{cite journal |vauthors=Koeppen AH |title=Friedreich's ataxia: pathology, pathogenesis, and molecular genetics |journal=J. Neurol. Sci. |volume=303 |issue=1-2 |pages=1–12 |date=April 2011 |pmid=21315377 |pmc=3062632 |doi=10.1016/j.jns.2011.01.010 |url=}}</ref>
**Severe loss of [[γ-aminobutyric acid]] ([[GABA]])-containing terminals in the immunostaining with an antibody to [[glutamic acid decarboxylase]] (GAD)<ref name="pmid21638087">{{cite journal |vauthors=Koeppen AH, Davis AN, Morral JA |title=The cerebellar component of Friedreich's ataxia |journal=Acta Neuropathol. |volume=122 |issue=3 |pages=323–30 |date=September 2011 |pmid=21638087 |pmc=4890974 |doi=10.1007/s00401-011-0844-9 |url=}}</ref>
**Grumose degeneration in the immunostaining with anti-GAD<ref name="pmid21315377">{{cite journal |vauthors=Koeppen AH |title=Friedreich's ataxia: pathology, pathogenesis, and molecular genetics |journal=J. Neurol. Sci. |volume=303 |issue=1-2 |pages=1–12 |date=April 2011 |pmid=21315377 |pmc=3062632 |doi=10.1016/j.jns.2011.01.010 |url=}}</ref>
**Punctate reaction product in areas known to be rich in [[Mitochondrion|mitochondria]], namely, neuronal cytoplasm and synaptic terminals<ref name="pmid21315377">{{cite journal |vauthors=Koeppen AH |title=Friedreich's ataxia: pathology, pathogenesis, and molecular genetics |journal=J. Neurol. Sci. |volume=303 |issue=1-2 |pages=1–12 |date=April 2011 |pmid=21315377 |pmc=3062632 |doi=10.1016/j.jns.2011.01.010 |url=}}</ref>
**[[Frataxin]]-deficient [[mitochondria]]<ref name="pmid5383992">{{cite journal |vauthors=Broghammer H |title=Therapeutic effect of gelatin plasma substitutes in experimental shock |journal=Bibl Haematol |volume=33 |issue= |pages=223–31 |date=1969 |pmid=5383992 |doi= |url=}}</ref>
'''<big>Heart</big>'''
*Cell stains in samples of heart reveal:<ref name="pmid21315377">{{cite journal |vauthors=Koeppen AH |title=Friedreich's ataxia: pathology, pathogenesis, and molecular genetics |journal=J. Neurol. Sci. |volume=303 |issue=1-2 |pages=1–12 |date=April 2011 |pmid=21315377 |pmc=3062632 |doi=10.1016/j.jns.2011.01.010 |url=}}</ref>
**Collections of tiny reactive inclusions in a small percentage of [[Cardiomyocyte|cardiomyocytes]] that are arranged in parallel with [[myofibrils]] in the iron stains
**Electron-dense inclusions in [[Mitochondrion|mitochondria]]
**[[Myocardial]] fiber necrosis and an inflammatory reaction in the severe cases of [[cardiomyopathy]]
'''<big>Pancreas</big>'''
*Cell stains in samples of [[pancreas]] reveal:<ref name="pmid21315377">{{cite journal |vauthors=Koeppen AH |title=Friedreich's ataxia: pathology, pathogenesis, and molecular genetics |journal=J. Neurol. Sci. |volume=303 |issue=1-2 |pages=1–12 |date=April 2011 |pmid=21315377 |pmc=3062632 |doi=10.1016/j.jns.2011.01.010 |url=}}</ref>
**Lose of the sharp demarcation of the [[synaptophysin]]-positive [[Islets of Langerhans|islets]] of [[pancreas]]
**The “fade” appearance of the β-cells into the surrounding exocrine [[pancreas]]

==References==
{{reflist|2}}

Spina bifida overview

2020-05-06T04:38:16Z

M Jahan:

__NOTOC__
{{Spina bifida}}
{{CMG}}; {{AE}}{{sali}}, {{MMJ}}
==Overview==

==Historical Perspective==
Spina bifida has existed as long as the history of humanity. Evidence of children with characteristic features of spina bifida has been found in the archeological findings and a large number of anthropological figures from early civilizations. Spina bifida was first discovered by Hippocrates, (born c. 460 bce, island of Cos, Greece—died c. 375 bce, Larissa, Thessaly). The first definitive description of spina bifida was made by the Dutch clinician Pieter van Foreest (1522–1597) in the late 1500s. In 1614, Nicolaas Tulp (whose real name was Claes Piereszoon) was the first who coined the term spina bifida. Ligation or amputation of the dural sac was the surgical treatment of spina bifida for centuries. The outcome of this procedure was almost always [[fatal]] because of central [[spinal fluid]] leakage and [[infection]] or the secondary progressive untreated [[hydrocephalus]]. In 1918, Charles H. Frazier started better surgical concepts of repair of spina bifida, with multilayer closures using [[dura]], [[fascia]], muscles, and [[skin]] advocated. In 1967, a study by Sharrard, confirmed that better results were obtained by performing the surgery of spina bifida in the [[perinatal period]]. Now, the surgery of spina bifida in the [[perinatal period]], is the preferred treatment.

==Classification==
Spina bifida may be classified according to the level of the lesion into 3 subtypes: [[Thoracic]], l[[Lumbar|umbar]]<nowiki/>and sacral. It also may be classified according to the tyoe of the vertebrate defect into 2 subtypes: [[Spina bifida occulta]] and spina ifida aperta. Meningocele is a protrusion of the meninges, unaccompanied by neural tissue, through a bony defect in the [[vertebral column]]. Myelomeningocele is the most severe form of spina bifida. It happens when both the meninges and the bottom end of the spinal cord push through the hole in the spine, forming a large fluid-filled sac that bulges out of a patients back.

==Pathophysiology==
Spina bifida is a congenital malformation in which the spinal column is split (bifid) as a result of failed closure of the embryonic neural tube, during the fourth week post-fertilization. In normal infants, the [[neural tube]] closes by the end of the 4 week of conception, but in patients with spina bifida, some parts of the [[neural tube]] fails to develop or close that causes defects in the [[spinal cord]] and in the [[Vertebra|vertebral]] bones. Spina bifida also may be classified according to the tyoe of the vertebrate defect into 2 subtypes: [[Spina bifida occulta]]: In this type of spina bifida, the defect of [[vertebrate]] is covered by [[skin]] ("Occulta" means "hidden"). The [[spinal cord]] does not stick out through the skin, although the skin over the lower spine may have a patch of hair, a [[birthmark]], or a dimple above the groove between the [[buttocks]]. Spina ifida aperta: In this type of spina bifida , the defect is widely open and is sub classified into 2 types: Meningocele and Myelomeningocele. Spina bifida may be caused by the increase of [[cerebrospinal fluid]] (CSF) volume in the [[central nervous system]] during the first weeks of [[embryogenesis]]. [[Venous insufficiency]] is the main cause of the increase of [[cerebrospinal fluid]] and it may be caused by any disease that reduces space for venous volume. The development of spina bifida may be the result of multiple genetically defect in the genes important in the metabolism of: [[Folic Acid|Folic acid]], [[glucose]], [[Retinoid|retinoids]], [[apoptosis]], [[genes]] that regulate [[transcription]] in early [[embryogenesis]], [[methionine]] Cycle genes, [[methylation]] genes, [[glucose]] Homeostasis genes, cell Recognition and Migration genes, [[DNA]] Repair genes and transcription Factors genes. Conditions associated with spina bifida include: [[Hydrocephalus]], [[Budd-Chiari syndrome|chiari II Malformation]], [[paralysis]], urination and deification incontinences, atex Allergy, learning Disabilities, [[sexual problems]], emotional problems, [[obesity]] and vision problems.

==Causes==
There is no well known cause of spina bifida. It may result from a variety of occupational, environmental, genetic, and viral [[Spina bifida risk factors|risk factors]], such as a family history of neural tube defects and folate deficiency.

==Differentiating spina bifida from Other Diseases==
Spina bifida must be differentiated from other diseases that causes [[vertebral column]] defects, spinal deformity and [[neurologic]] abnormalities or [[gait]] abnormalities, such as: Terminal myelocystocele, spine segmental [[dysgenesis]], [[Caudal regression syndrome]] ([[sacral agenesis]]), multiple [[vertebral]] segmentation disorder, [[VACTERL|VACTERL association,]] [[Arnold-Chiari malformation|arnold-chiari malformation]], [[syringomyelia]], [[Scoliosis]], and [[leg length discrepancy]].

==Epidemiology and Demographics==
The incidence of spina bifida is approximately 3.5 per 10,000 live births per year in the U.S. The prevalence of spina bifida is approximately 187 to 890 per 100,000 live births. Before 1960, the case-mortality rate of all forms of spina bifida was 90% to 88%. Now the mortality rate is approximately is 10.1%. The overall [[Ventriculoperitoneal shunt|ventriculoperitoneal]] shunt requirement rate is 33.8%. The [[paraplegia]] rate is 30.7%. The [[neurogenic bladder]] rate is 51.6%. The [[infection]] rate is 6.4% after the surgical procedure. Spina bifida is more commonly observed among preterm newborns. Spina bifida usually affects individuals of the Malays and Chinese and Indians race. Female are more commonly affected by than male. The male\male+female ratio is approximately 42%.

==Risk Factors==
Risk factors in the development of spina bifida may be occupational, environmental, [[genetic]], and [[viral]]. Common maternal nutrition risk factors in the development of spina bifida include: [[Alcohol abuse|Alcohol use]], [[caffeine]] use, low [[Folic Acid|folate]] intake, low dietary quality, elevated glycaemic load or index, low [[methionine]] intake, low serum [[choline]] level, low serum [[vitamin B12]] level, low [[vitamin C]] level, low [[zinc]] intake, [[smoking]], [[hyperthermia]], low [[socio-economic status]], maternal [[infections]] and illnesses, pregestational insulin-dependent [[diabetes]], pregestational [[obesity]], [[Psychosocial|psychosocial stress]] and [[valproic acid]] use. Environmental factors in the development of spina bifida include: Ambient air pollution, disinfectant by-products in drinking water, indoor air pollution, nitrate-related compounds, organic solvents, [[pesticides]] and [[polycyclic aromatic hydrocarbons]].

==Screening==
First time in 1975, it was reported that [[Alpha-fetoprotein|AFP]] levels are often raised in maternal blood in association with [[neural tube defect]] of the fetus and it is an important advance in obstetric practice since it presents the possibility of a screening programme leading to early diagnosis and termination of these abnormal pregnancies. Screening for spina bifida by mother's blood's [[Alpha-fetoprotein|AFP]] [alpha‐fetoprotein] is recommended for all pregnant women with Triple Test. Triple test looks for three specific substances: AFP, hCG, and Estriol. Triple test is performed between the 15th and 20th week of pregnancy preferably in the 16th -18th week. All pregnant women should have triple test dureng pregnancy, but is is more important in pregnants with: Family history of birth defects, age of 35 years or older, [[Diabetes]] and use [[insulin]], viral infection during pregnancy andexposure to high levels of [[Radiation therapy|radiation]]. In patients with high level of [[AFP]], use of ultrasound and amniocentesis may be useful to diagnose open [[neural tube defects]] including spina bifida.

==Natural History, Complications, and Prognosis==

Prognosis of patients with spina bifida is generally poor. Early clinical features of spina bifida include: Weakness or [[paralysis]] in the legs, [[Urinary incontinence]], [[Bowel]] incontinence, [[Sensation]] problems in the [[lower extremity]], Motor problems in the lower extrimity and [[Hydrocephalus]]. If left untreated, 50% of patients with congenital anomalies, especially spina bifida may die soon after birth in the underdeveloped countries. [[Renal failure]] is the commonest cause of death in patients with spina bifida. Common complications of [disease name] include: [[Cardiac]] disease, [[Respiratory disease]], [[Suicidality]] and [[Cancer]].
==Diagnosis==
===Diagnostic Study of Choice===
Ultrasound is the imaging modality of choice for characterisation of the open spina bifida spinal lesions. On two and tree-dimensional ultrasound, spina bifida is characterized by: [[Vertebral anomalies|Vertebral defect]], splayed [[Vertebral|vertebral pedicles]] and disrupted [[vertebrae]]. The [[ultrasound]] must be performed when a positive [[alpha-fetoprotein]] is detected in the triple screening test between the 15th and 20th week of pregnancy to confirm the diagnosis.

===History and Symptoms===
Early symptoms of patients with spina bifida include: Weakness or [[paralysis]] in the legs, [[Urinary incontinence]], [[Bowel]] incontinence, [[Sensation]] problems in the [[lower extremity]], Motor problems in the lower extrimity, [[Headache]], orthopedic abnormalities, difficulties with executive functions, academic skills problems, learning disability and [[Latex allergy|allergy to latex]].

===Physical Examination===
Most patients with spina bifida have normal vital signs. Skin examination of patients with spina bifida is usually remarkable for: Spinal area discoloration or [[birthmarks]], protrusions in the [[lumbar spine]], dimples in the [[lumbar spine]] and patch along the spine. HEENT examination of patients with spina bifida is usually remarkable for: Enlarging head, bulging [[fontanelle]], enlarged [[scalp veins]], [[Cranial bones]] [[suture]] [[diastasis]] and positive [[Macewen's sign|Macewen sign]]. Cardiovascular examination of patients with spina bifida is usually normal but congenital anomalies of the spine have been associated with malformations of the cardiovascular systems. Congenital anomalies of the spine also may be associated with malformations of the genitourinary system. [[Neuromuscular]] examination of patients with spina bifida may be remarkable for: [[Paralysis]], sensation problems, [[Scoliosis]], pressure [[Ulcer|ulcers]], learning disabilities, [[Clonus]], [[Hyperreflexia]] or [[hyporeflexia]], positive (abnormal) [[Plantar reflex|Babinski]] unilaterally, [[Hypertonia|muscle rigidity]], muscle weakness unilaterally or bilaterally, abnormal gait and [[Dysmetria]].

===Laboratory Findings===
There are no specific laboratory findings in the newborn associated with spina bifida. An elevated concentration of Maternal Serum [[Alpha-fetoprotein|Alpha-Fetoprotein]] may be predictive for contemporary detection of spina bifida. Screening for spina bifida by mother's blood's [[Alpha-fetoprotein|AFP]] [alpha‐fetoprotein] is recommended for all pregnant women with Triple Test. Triple test looks for three specific substances: AFP, hCG, and Estriol. Triple test is performed between the 15th and 20th week of pregnancy preferably in the 16th -18th week.

===Electroencephalogram===
Single Infantile [[electroencephalogram]] (EEG) recordings have limited prognostic value for infants born with spina bifida. Serial EEG recordings in combination with other clinical or neurophysiological investigations might ameliorate the contributing predictive value of neonatal EEG.

===X-ray===
Spina bifida occulta is found in up to 10% of people and usually occurs in the low spinal region and in most cases it is asymptomatic. An x-ray may be helpful in the diagnosis of cases of spina bifida who have not been diagnosed before. Findings on an x-ray suggestive of of spina bifida include: Failure of closure of the [[vertebral arch]] and [[scoliosis]].

===Echocardiography and Ultrasound===
Compared with the general population, the prevalence of [[congenital heart disease]] in newborns with [[myelomeningocele]] is increased , however critical disease is uncommon. When the myelomeningocele is prenatally diagnosed, antenatal cardiac screening is complete and normal, and the newborn is clinically well, preoperative [[echocardiography]] is unnecessary. Ultrasound is the imaging modality of choice for characterisation of the open spina bifida spinal lesions. On two and tree-dimensional ultrasound, spina bifida is characterized by: [[Vertebral anomalies|Vertebral defect]], splayed [[Vertebral|vertebral pedicles]] and disrupted [[vertebrae]]. The [[ultrasound]] must be performed when a positive [[alpha-fetoprotein]] is detected in the triple screening test between the 15th and 20th week of pregnancy to confirm the diagnosis.

===CT scan===
CT scan is not widely used for diagnosis of spina bifida but, it may be helpful in the diagnosis of [[hydrocephalus]] and during childhood, a patient with spina bifida will have multiple CT scans of the head.

===MRI===
Spinal and brain MRI may be helpful in the diagnosis of spina bifida. Findings on MRI diagnostic of spina bifida include:[[Herniation]] of a [[CSF]] filled sac through spina bifida, [[CSF]] attenuation lesion in [[conus medullaris]] and other parts of the [[CNS]] and short and thick [[filum terminale]].

==Treatment==
===Medical Therapy===
Spina bifida requires prompt treatment. The mainstay of treatment for spina bifida is [[surgery]].

===Surgery===
The management of open spina bifida is surgery within 48 h of birth. The defect in the spine is closed to minimize the risk of ascending infection that can result in meningitis. Prenatal surgery is the preferred treatment for spina bifida and it usually is done before the 26th week of [[pregnancy]] and it may prevent continuing damage and improve clinical outcome. Intrauterine repair of spina bifida confers multiple advantages to [[infants]], including: Lower rates of [[shunt]] dependency, lower rates of [[hindbrain]] [[herniation]] and better motor and disability functional outcomes. Surgery after birth is done in patients who did not underwent prenatal surgery but the prognosis is worse and there are more possible complications after [[surgery]] in comparison with the prenatal [[surgery]]. The management of open spina bifida is surgery within 48 h of birth. The defect in the spine is closed to minimize the risk of ascending infection that can result in meningitis. Prenatal surgery is the preferred treatment for spina bifida and it usually is done before the 26th week of [[pregnancy]] and it may prevent continuing damage and improve clinical outcome. Intrauterine repair of spina bifida confers multiple advantages to [[infants]], including: Lower rates of [[shunt]] dependency, lower rates of [[hindbrain]] [[herniation]] and better motor and disability functional outcomes. Surgery after birth is done in patients who did not underwent prenatal surgery but the prognosis is worse and there are more possible complications after [[surgery]] in comparison with the prenatal [[surgery]].

===Primary Prevention===
A protective effect of [[folate]] against the development of [[Neural tube defect|neural tube defects]] (NTDs), specifically, spina bifida, is now well recognized, having been established by a lot of clinical research studies over the past half-century. Effective measures for the primary prevention of spina bifida include: Not drinking alcohol, not smoking, not taking drugs, taking [[Folic Acid]] and taking oral daily [[folate]] for all pregnant women. Neural tube closure is completed 28 days (four weeks) from conception, and the preventive effect of folic acid is not effective after that period. So, folate supplementation should start at least 4 weeks before conception and it should continue until at least two months after conception. The recommended intakes of [[folate]] are 4 mg/d for those at high-risk pregnancies(by virtue of a previous NTD pregnancy outcome) and 0.4 mg/d for all others.

==References==
{{reflist|2}}

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Friedreich's ataxia overview

2020-05-06T04:37:25Z

M Jahan:

__NOTOC__
{{Friedreich's ataxia}}
{{CMG}}; {{AE}} {{sali}}, {{MMJ}}
==Historical Perspective==
Friedreich’s ataxia was first discovered by Nikolaus Friedreich, a German [[pathologist]] and [[neurologist]], in 1863. The association between hereditary inheritance and Friedreich’s ataxia was made first time by Nikolaus Friedreich. In 1996, the association between a [[GAA deficiency|GAA]] repeat expansion on [[chromosome 9]] and the development of Friedreich's ataxia was discovered for the first time. Geraint Williams who had Friedreich's ataxia is known for scaling Mount Kilimanjaro in an adaptive [[wheelchair]] known as a Mountain Trike.

==Classification==
There is no established system for the classification of Friedreich's ataxia.

==Pathophysiology==
It is understood that Friedreich’s ataxia is the result of a [[homozygous]] [[guanine]]-[[adenine]]-[[adenine]] (GAA) [[Trinucleotide repeat expansion disorders|trinucleotide repeat expansion]] on chromosome 9q13 that causes a transcriptional defect of the [[frataxin]] gene. [[Frataxin]] is a small mitochondrial protein and deficiency of [[frataxin]] is responsible for all clinical and morphological manifestations of Friedreich’s ataxia. The severity of the disease is directly related to the length of the [[Trinucleotide repeat expansion disorders|trinucleotide repeat expansion]] and long expansions lead to early onset, severe clinical illness, and death in young adult life. Patients with short [[Trinucleotide repeat expansion disorders|trinucleotide repeat expansion]] have a later onset and a more benign course and even some of them are not diagnosed during life. Friedreich’s ataxia is transmitted in [[Autosomal recessive disorder|autosomal recessive]] pattern. Because the frataxin protein has multiple functions in the normal state, the exact role of frataxin deficiency in the pathogenesis of Friedreich's ataxia is still unclear. Conditions associated with friedreich’s ataxia include: [[Hypertrophic cardiomyopathy]], [[diabetes mellitus]], [[scoliosis]], distal wasting, [[optic atrophy]], [[sensorineural deafness]], [[sleep apnea]] and [[pes cavus]] in 55% to 75% of cases. On gross [[pathology]] involvement of [[spinal cord]], [[cerebellum]], and heart are characteristic findings of Friedreich's ataxia. '''Spinal cord''' lesions include: Decreased transverse diameter of the [[spinal cord]] at all levels, thin and gray dorsal spinal roots, smallness and gray discoloration of the [[dorsal column]], thin and gray [[gracile]] and [[Cuneate fasciculus|cuneate fasciculi]] and fiber loss in the anterolateral fields corresponding to [[Spinocerebellar tract|spinocerebellar]] and [[Corticospinal tract|corticospinal tracts]]. '''Cerebellum''' lesions include atrophy of the [[Dentate nucleus|dentate nuclei]] and its efferent fibers. '''Heart''' findings include: Increased heart weight, increased thickness of left and right ventricular walls and [[interventricular septum]], dilatation of the [[ventricles]] and "marble”-like discoloration of the [[myocardium]]. On microscopic histopathological analysis, involvement of [[spinal cord]], [[cerebellum]], [[heart]] and [[pancreas]] are characteristic findings of Friedreich's ataxia. Friedreich’s ataxia mostly affects the [[dorsal root ganglia]] (DRG) of the spinal cord. It affects the entire DGR but is most prominent in subcapsular regions. Cell stains in samples of DGN reveal: An overall reduction in the size of [[ganglion cells]], the absence of very large [[Neuron|neurons]] and large [[Myelinated|myelinated fibers]], clusters of nuclei representing “residual nodules” that indicate an invasion-like entry of [[Satellite cells|satellite]] cells into the [[cytoplasm]] of neurons, progressive destruction of neuronal [[cytoplasm]] in cytoskeletal stains, such as for class-III-β-tubulin, greatly thickened [[satellite cells]], residual nodules remain strongly reactive with anti-S100α in the satellite cells and increased [[ferritin]] immunoreactivity in satellite cells. Friedreich’s ataxia mostly affects the [[dentate nucleus]] of [[cerebellum]]. Cell stains in samples of [[cerebellum]] reveal: The absence of very large [[Neuron|neurons]], severe loss of [[γ-aminobutyric acid]] (GABA)-containing terminals in the immunostaining with an antibody to [[glutamic acid decarboxylase]] (GAD), grumose degeneration in the immunostaining with anti-GAD, punctate reaction product in areas known to be rich in [[Mitochondrion|mitochondria]], namely, neuronal cytoplasm and synaptic terminals and [[Frataxin]]-deficient [[mitochondria]]. Cell stains in samples of heart reveal: Collections of tiny reactive inclusions in a small percentage of [[Cardiomyocyte|cardiomyocytes]] that are arranged in parallel with [[myofibrils]] in the iron stains, electron-dense inclusions in [[Mitochondrion|mitochondria]] and [[myocardial]] fiber necrosis and an inflammatory reaction in the severe cases of [[cardiomyopathy]]. Cell stains in samples of [[pancreas]] reveal: Lose of the sharp demarcation of the [[synaptophysin]]-positive [[Islets of Langerhans|islets]] of [[pancreas]] and the “fade” appearance of the β-cells into the surrounding exocrine [[pancreas]].

==Causes==
It is understood that Friedreich’s ataxia is the result of a [[homozygous]] [[guanine]]-[[adenine]]-[[adenine]] (GAA) [[Trinucleotide repeat expansion disorders|trinucleotide repeat expansion]] on chromosome 9q13 that causes a transcriptional defect of the [[frataxin]] gene. [[Frataxin]] is a small mitochondrial protein and deficiency of [[frataxin]] is responsible for all clinical and morphological manifestations of Friedreich’s ataxia.

==Differentiating Friedreich’s ataxia from Other Diseases==
As Friedreich’s ataxia manifests in a variety of clinical forms and different ages, differentiation must be established in accordance with the manifestations of the disease and onset of the symptoms. The main and most prominent symptom of the Friedreich’s ataxia is [[ataxia]] that worsens over time and it must be differentiated from other diseases that cause progressive [[ataxia]] such as: [[Spinocerebellar ataxia|spinocerebellar ataxias (SCA)]], [[Dentatorubral-pallidoluysian atrophy|dentato-rubro-pallido-luysian atrophy]], [[Episodic ataxia]], [[Spastic ataxia]], [[Abetalipoproteinemia|abetalipoproteinemia,]] [[Refsum's disease|Refsum disease]], hypomyelinating leukoencephalopathy (Hypomyelination, [[basal ganglia]] atrophy, rigidity, [[dystonia]], [[chorea]]), pure cerebellar ataxia, progressive cerebellar [[atrophy]] with epileptic [[encephalopathy]]: Infantile [[seizures]], intellectual deficits, [[microcephaly]], rapid-onset ataxia: [[Cerebellar]] atrophy and CAPOS mutation: ([[Cerebellar ataxia]], [[areflexia]], [[Pes cavus]], [[optic atrophy]], [[sensorineural hearing loss]], and [[Alternating hemiplegia|alternating hemiplegia)]].

==Epidemiology and Demographics==
The incidence of Friedreich’s ataxia is approximately 2-4 per 100,000 individuals worldwide. The prevalence of Friedreich’s ataxia is approximately 2-4 per 100,000 individuals worldwide. Friedreich’s Ataxia commonly affects individuals from early childhood through to early adulthood, starting with poor balance when walking, followed by slurred speech and upper-limb [[ataxia]]. Friedreich’s Ataxia is usually first diagnosed at age 10 to 15 years but onset of disease may be as early as age 2 years and as late as the 8th decade. The GAA triplet repeat expansion that causes Friedreich’s Ataxia usually affects only individuals of the European, North African, Middle Eastern, or Indian origin (Indo-European and Afro-Asiatic speakers). Sub-Saharan Africans, Amerindians, and individuals from China, Japan, and Southeast Asia are less likely to develop Friedreich’s Ataxia. Friedreich’s Ataxia affects men and women equally. Female are more commonly affected by clinical [[fractures]] than male.

==Risk Factors==
Because Friedreich’s Ataxia is a genetic diseases transmitted by [[Autosomal recessive|autosomal recessive pattern]], the most potent risk factor in the development of Friedreich’s Ataxia is strong family history. Other risk factors are unknown. The risk factors for developing associated clinical conditions of Friedreich's ataxia include: GAA1 length and age of diagnosis.

==Screening==
There is insufficient evidence to recommend routine screening for Friedreich’s Ataxia.

==Natural History, Complications, and Prognosis==

The symptoms of Friedreich’s Ataxia usually develop in the second decade of life but the onset of disease may be as early as age 2 years and as late as the 8th decade, and start with progressive [[Ataxia|ataxia.]] Common complications of Friedreich’s Ataxia include: [[Aspiration pneumonia]], [[hypertrophic cardiomyopathy]], [[diabetic coma]], [[embolic stroke]], [[cerebral haemorrhage]], [[trauma]] sequelae and [[Renal failure|renal failure.]] The presence of [[diabetes]] and [[dilated cardiomyopathy]] has a negative impact on survival of patients with Friedreich’s Ataxia. The average age of death of patients with Friedreich’s Ataxia is at 37.5 years. Depending on the extent of the disease progression at the time of diagnosis, the prognosis may vary. The presence of [[hypertrophic cardiomyopathy]] is associated with a particularly poor prognosis among patients with Friedreich’s Ataxia.
==Diagnosis==

=== Diagnosis study of choice ===
Triplet Repeat Primed [[Polymerase chain reaction|PCR]] (TP PCR) is the gold standard test for the diagnosis of Friedreich’s Ataxia. The following finding on performing genetic testing is confirmatory for Friedreich’s Ataxia: GAA [[trinucleotide repeat]] in the first [[intron]] of the [[Frataxin|frataxin gene]] on chromosome 9q13. The TP [[PCR]] must be performed when: The patient presented with symptoms of Friedreich’s Ataxia. History of [[neuromuscular]] disorders in a family because the Friedreich’s Ataxia is an [[Autosomal recessive disorder|autosomal recessive disease]] and some [[heterozygous]] traits may be asymptomatic.

===History and Symptoms===
The hallmark of Friedreich’s Ataxia is progressive [[ataxia]]. The most common symptoms of Friedreich’s Ataxia include: Balance problems and coordination problems. Common symptoms of Friedreich’s Ataxia include: Balance problems, coordination problems (leading to difficulties in writing, as well as in many other daily activities), [[Slurred speech]], hearing problems, vision problems and wallowing problems.

===Physical Examination===
HEENT examination of patients with Friedreich’s ataxia may be remarkable for: [[Nystagmus]], [[dysarthria]], abnormal extra-ocular movements of the eyes, decreased visual acuity and diffuse optic nerve pallor in the [[Ophthalmoscopy|ophthalmoscopic]] exam. Hearing acuity also may be reduced. Most patients with advanced Friedreich's ataxia suffer from a [[Restrictive lung disease|restrictive pulmonary syndrome]] of scoliotic origin. Some of the findings in the lung examination of the patients with Friedeich's ataxia may be due to [[heart failure]].Some of the findings in the lung examination of the patients with Friedeich's ataxia may be due to [[heart failure]]. [[Cardiovascular]] examination of patients with examination of patients with Friedreich’s ataxia may be remarkable for: Harsh [[systolic murmurs]], signs of [[ventricular hypertrophy]], added heart sounds and loud [[Heart sounds#Fourth heart sound S4|S4]]. Back examination of patients with examination of patients with Friedreich’s ataxia may be remarkable for: [[Scoliosis]], [[Kyphosis|hyperkyphosis]] and pelvic obliquity. Neuromuscular examination of patients with Friedreich’s ataxia may be remarkable for: [[Spasticity]], [[Gait ataxia]], [[Dysmetria]] of arms and [[legs]], head titubation, [[atrophy]] and weakness of the distal extremities, absence of [[muscle]] stretch [[reflexes]], loss of joint and vibratory senses, superimposed stocking-and-glove type [[sensory]] [[neuropathy]], [[Dysarthria]], [[Dyspraxia]], [[Foot deformity]] ([[pes cavus]]), [[Hyperreflexia]] / [[hyporeflexia]] / [[areflexia]], positive (abnormal) [[Babinski's Reflex|Babinski]] reflex bilaterally and [[Muscle rigidity]].

===Laboratory Findings===
Some patients with Friedreich's ataxia may have an abnormal laboratory findings such as: Decreased serum [[Ceruloplasmin|ceruloplasmin activity]], elevated [[Transaminases|serum transaminases]] and [[Lactate dehydrogenase|LDH]], elevated [[aldolase]], decrease in serum and [[CSF]] [[albumins]] as well as a significant increase in CSF [[Globulins|B-globulins]], increase in amounts of [[chylomicrons]], low serum [[cholesterol]] and beta-[[lipoproteins]] and absence of [[acanthocytosis]].

===Electrocardiogram===
An [[ECG]] may be helpful in the diagnosis of Friedreich's ataxia. Findings on an [[ECG]] suggestive of Friedreich's ataxia include: [[T-wave]] [[repolarization]] abnormalities especially in the inferior and lateral leads, [[Bundle branch block|Bundle branch blocks]], [[ventricular hypertrophy]], [[right axis deviation]], short [[PR interval]], interatrial block, left [[atrial]] enlargement and right [[atrial]] enlargement.

===X-ray===
An [[x-ray]] may be helpful in the diagnosis of Friedreich's ataxia. Findings on an [[x-ray]] suggestive of Friedreich's ataxia include distorted cardiac silhouette by [[Scoliosis|scoliokyphosis]].

===Echocardiography and Ultrasound===
[[Echocardiography]] may be helpful in the diagnosis of Friedreich's ataxia. Findings on an [[echocardiography]] suggestive of Friedreich's ataxia include: Varying degrees of septal [[hypertrophy]] in approximately 81% of cases, left ventricular free wall [[hypertrophy]] in approximately 61% of cases, slight reduction of left [[ventricular]] internal dimension in approximately 57% of cases and systolic anterior motion of the [[mitral valve]] in approximately 14 % of cases.

===CT scan===
Brain CT scan may be helpful in the diagnosis of Friedreich's ataxia. Findings on CT scan suggestive of Friedreich's ataxia include: Moderate cerebellar atrophy and an increase in the surface area of the [[fourth ventricle]] in two-thirds of the patients, atrophy of the number and width of cerebellar sulci, [[olivopontocerebellar atrophy]] with or without supratentorial [[atrophy]], atrophy of the [[Fourth ventricle]], [[brainstem]] ratio and [[Cerebellopontine angle|cerebellopontine angle cistern]] and increased [[Evans syndrome|Evans]]' index.

===MRI===
Brain MRI may be helpful in the diagnosis of Friedreich's ataxia. Findings on [[MRI]] suggestive of Friedreich's ataxia include: [[Cerebellar hemisphere]] atrophy in approximately 50% of patients, [[atrophy]] of the [[vermis]] in approximately 67% of patients, atrophy of the [[medulla]] and [[supratentorial]] cerebral atrophy in approximately 17% of patients.

===Other Diagnostic Studies===
X-ray fluorescence (HDXRF) may be helpful in the diagnosis of Friedreich's ataxia. Findings on an HDXRF suggestive of Friedreich's ataxia include: Clusters of iron-rich hot-spots with similar mass fractions and significant decrease in zinc concentration in the [[cytoplasm]] of [[fibroblasts]] of patients with friedreich's ataxia.

==Treatment==
===Medical Therapy===
Pharmacologic medical therapy is recommended among patients with Friedreich's ataxia but their affect in decrease the symptoms of Friedreich's ataxia is not significant. Pharmacologic medical therapies for Friedreich's ataxia include [[Physostigmine]], [[Riluzole]] and [[Amantadine]]. The rationale for evaluating [[physostigmine]] in ataxia, including Friedreich's ataxia, is its inhibition of [[acetylcholinesterase]], which prolongs central and peripheral effects of [[acetylcholine]]. The mechanism of action of [[Riluzole]] may be related to the small conductance [[Potassium channels|calcium-activated potassium channels]] that appear to regulate excitability in neurons found within deep cerebellar nuclei. [[Amantadine]] may be helpfull in the treatment of the patients with Freidreich's ataxia.

===Surgery===
Surgery is usually used for patients with either: [[Scoliosis]], progressive [[Equinovarus|equinovarus deformity]], progressive severe [[dysphagia]] with endoscopic [[gastrostomy]] and progressive severe cardiac failure with [[cardiac transplantation]].

===Primary Prevention===
There are no established measures for the primary prevention of Friedreich's ataxia.

===Secondary Prevention===
There are no established measures for the primary prevention of Friedreich's ataxia.

==References==
{{reflist|2}}

{{WikiDoc Help Menu}}
{{WikiDoc Sources}}
[[Category: (name of the system)]]

Spina bifida

2020-05-06T04:37:04Z

M Jahan:

__NOTOC__
{{Spina bifida}}

{{CMG}}; {{AE}} {{sali}}, {{MMJ}}
==[[Spina bifida overview|Overview]]==

==[[Spina bifida historical perspective|Historical Perspective]]==

==[[Spina bifida classification|Classification]]==

==[[Spina bifida pathophysiology|Pathophysiology]]==

==[[Spina bifida causes|Causes]]==

==[[Spina bifida differential diagnosis|Differentiating Spina bifida from other Diseases]]==

==[[Spina bifida epidemiology and demographics|Epidemiology and Demographics]]==

==[[Spina bifida risk factors|Risk Factors]]==

==[[Spina bifida screening|Screening]]==

==[[Spina bifida natural history, complications and prognosis|Natural History, Complications and Prognosis]]==

==Diagnosis==
[[Spina bifida diagnostic study of choice|Diagnostic study of choice]] | [[Spina bifida history and symptoms|History and Symptoms]] | [[Spina bifida physical examination|Physical Examination]] | [[Spina bifida laboratory findings|Laboratory Findings]] | [[Spina bifida electroencephalogram|Electroencephalogram]] | [[Spina bifida x ray|X-Ray Findings]] | [[Spina bifida echocardiography and ultrasound|Echocardiography and Ultrasound]] | [[Spina bifida CT scan|CT-Scan Findings]] | [[Spina bifida MRI|MRI Findings]] | [[Spina bifida other imaging findings|Other Imaging Findings]] | [[Spina bifida other diagnostic studies|Other Diagnostic Studies]]

==Treatment==
[[Spina bifida medical therapy|Medical Therapy]] | [[Spina bifida surgery|Surgery]] | [[Spina bifida primary prevention|Primary Prevention]]

==Case Studies==
[[Spina bifida case study one|Case #1]]

[[Category: (name of the system)]]

Friedreich's ataxia

2020-05-06T04:35:34Z

M Jahan:

__NOTOC__
{{Friedreich's ataxia}}

{{CMG}}, {{AE}} [[User:M Jahan|Mohamadmostafa Jahansouz M.D]], {{sali}}

==[[Friedreich's ataxia overview|Overview]]==

==[[Friedreich's ataxia historical perspective|Historical Perspective]]==

==[[Friedreich's ataxia classification|Classification]]==

==[[Friedreich's ataxia pathophysiology|Pathophysiology]]==

==[[Friedreich's ataxia causes|Causes]]==

==[[Friedreich's ataxia differential diagnosis|Differentiating Any Disease from other Diseases]]==

==[[Friedreich's ataxia epidemiology and demographics|Epidemiology and Demographics]]==

==[[Friedreich's ataxia risk factors|Risk Factors]]==

==[[Friedreich's ataxia screening|Screening]]==

==[[Friedreich's ataxia natural history, complications and prognosis|Natural History, Complications and Prognosis]]==

==Diagnosis==
[[Friedreich's ataxia history and symptoms|History and Symptoms]] | [[Friedreich's ataxia physical examination|Physical Examination]] | [[Friedreich's ataxia laboratory findings|Laboratory Findings]] | [[Friedreich's ataxia electrocardiogram|Electrocardiogram]] | [[Friedreich's ataxia chest x ray|Chest X Ray]] | [[Friedreich's ataxia CT|CT]] | [[Friedreich's ataxia MRI|MRI]] | [[Friedreich's ataxia echocardiography or ultrasound|Echocardiography or Ultrasound]] | [[Friedreich's ataxia other imaging findings|Other Imaging Findings]] | [[Friedreich's ataxia other diagnostic studies|Other Diagnostic Studies]]

==Treatment==
[[Friedreich's ataxia medical therapy|Medical Therapy]] | [[Friedreich's ataxia surgery|Surgery]] | [[Friedreich's ataxia primary prevention|Primary Prevention]] | [[Friedreich's ataxia secondary prevention|Secondary Prevention]] | [[Friedreich's ataxia cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Friedreich's ataxia future or investigational therapies|Future or Investigational Therapies]]

==Case Studies==
[[Category:Projects]]
[[Category:Help]]
[[Friedreich's ataxia here case study one|Case #1]]

{{Infobox_Disease |
Name = {{PAGENAME}} |
Image = |
Caption = |
DiseasesDB = 4980 |
ICD10 = {{ICD10|G|11|1|g|10}} |
ICD9 = {{ICD9|334.0}} |
ICDO = |
OMIM = 229300 |
MedlinePlus = |
MeshID = D005621 |
}}
{{SI}}

[[Category:Neurological disorders]]
[[Category:Genetic disorders]]
[[Category:Mitochondrial diseases]]
[[es:Ataxia de Friedreich]]
[[fr:Ataxie de Friedreich]]
[[pl:Choroba Friedreicha]]

Subependymoma

2020-05-06T04:31:01Z

M Jahan:

__NOTOC__
{{SI}}
{{CMG}}{{AE}}{{sali}}{{MMJ}}{{SR}}
==Historical Perspective==
Subependymoma was first discovered by Ilya Mark Scheinker, a Russian physician, in 1945.<ref name="pmid18397339">{{cite journal| author=Kurian KM, Jones DT, Marsden F, Openshaw SW, Pearson DM, Ichimura K et al.| title=Genome-wide analysis of subependymomas shows underlying chromosomal copy number changes involving chromosomes 6, 7, 8 and 14 in a proportion of cases. | journal=Brain Pathol | year= 2008 | volume= 18 | issue= 4 | pages= 469-73 | pmid=18397339 | doi=10.1111/j.1750-3639.2008.00148.x | pmc=2659379 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18397339 }} </ref>

==Classification==
There is no established system for the [[classification]] of subependymoma.

==Pathophysiology==
===Pathogenesis===
Subependymoma arises from [[subependymal]] [[Glial cell|glial cells]], although it can also arise from [[Astrocyte|astrocytes]] from the [[subependymal]] plate, [[ependymal cells]], and mixed ependymal and astrocytic cells.<ref name="pmid23382616">{{cite journal| author=Saad AF, Bidiwala SB, Layton KF, Snipes GJ, Opatowsky MJ| title=Fourth ventricular subependymoma presenting as worsening headache. | journal=Proc (Bayl Univ Med Cent) | year= 2013 | volume= 26 | issue= 1 | pages= 52-4 | pmid=23382616 | doi= | pmc=PMC3523772 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23382616 }} </ref><ref name="pmid22747714">{{cite journal| author=Jain A, Amin AG, Jain P, Burger P, Jallo GI, Lim M et al.| title=Subependymoma: clinical features and surgical outcomes. | journal=Neurol Res | year= 2012 | volume= 34 | issue= 7 | pages= 677-84 | pmid=22747714 | doi=10.1179/1743132812Y.0000000064 | pmc=4618470 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22747714 }} </ref>

===Gross Pathology===
Subependymoma is most commonly seen in the [[fourth ventricle]], but it can arise anywhere where there is [[ependyma]]. The distribution in the [[ventricular system]] is as follows:<ref name="pathoilogysubepenymoma1">Pathology of subependymoma. Dr Bruno Di Muzio and A.Prof Frank Gaillard et al. Radiopaedia 2016. http://radiopaedia.org/articles/subependymoma. Accessed on January 12, 2016</ref><ref name="pmid22747714" />

*[[Fourth ventricle]]: 50 - 60%
*[[Lateral ventricles]] (usually frontal horns): 30 - 40%
*[[Third ventricle]]: rare
*[[Central canal|Central canal of the spinal cord]]: rare

*On gross pathology, subependymoma is characterized by a small, white to grey, firm, well circumscribed, solid, [[avascular]] mass attached to the ventricular wall by a narrow [[Pedicles|pedicle]].<ref name="pmid23382616" /><ref name="pmid22747714" />

===Microscopic Pathology===
On [[microscopic]] [[Histopathology|histopathological]] [[analysis]], subependymoma is characterized by the following features:<ref name="pathoilogysubepenymoma1" />

* Microcystic spaces and bland appearing [[Cell (biology)|cells]] without appreciable [[atypia|nuclear atypia]] or [[mitoses]].
* The [[Cell nucleus|nuclei]] tend to form clusters.
* No high grade features ([[Mitosis|mitoses]], [[Ki-67 (Biology)|Ki-67]] / [[MIB1|MIBI]] index > 1.5%, [[necrosis]]) are present.
* Loose pseudorosettes are observed.

===Immunohistochemistry===
Subependymoma is characterized by positive [[tumor marker]] [[GFAP]]. Mixed populations of [[Cell (biology)|cells]] may be variably positive for:<ref name="pathoilogysubepenymoma1" /><ref name="pmid28804038">{{cite journal| author=D'Amico RS, Praver M, Zanazzi GJ, Englander ZK, Sims JS, Samanamud JL et al.| title=Subependymomas Are Low-Grade Heterogeneous Glial Neoplasms Defined by Subventricular Zone Lineage Markers. | journal=World Neurosurg | year= 2017 | volume= 107 | issue= | pages= 451-463 | pmid=28804038 | doi=10.1016/j.wneu.2017.08.009 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28804038 }} </ref>

*Olig2
*NHERF1
*[[Sox2]]
*[[CD44]]

==Causes==
The cause of the development of subependymoma has not been identified.

==Differentiating Subependymoma from Other Diseases==
Subependymoma must be differentiated from:<ref name="ddxse1">Intraventricular neoplasms and lesions. Dr Henry Knipe and Dr Vinod G Maller et al. Radiopaedia 2016. http://radiopaedia.org/articles/intraventricular-neoplasms-and-lesions. Accessed on January 12, 2016</ref><ref name="pmid22747714" />

*'''Neoplasms of the ventricular wall and septum pellucidum'''
**[[Ependymoma]]
**[[Adult brain tumors classification|Central neurocytoma]]
**[[Subependymal giant cell astrocytoma]]
*'''Neoplasms of the choroid plexus'''
**[[Choroid plexus]] papilloma and [[carcinoma]]
*'''Others'''
**[[meningioma|Intraventricular meningioma]]
**[[intracerebral metastasis|Intraventricular metastasis]]
**[[Oligodendroglioma]]
**[[Pilocytic astrocytoma]]
**[[Glioblastoma multiforme]]
**[[Medulloblastoma]]
**[[teratoma|Intraventricular teratoma]]

==Epidemiology and Demographics==
===Frequency and Incidence===
*The frequency of [[asymptomatic]] subependymomas was 0.4% in 1,000 serial routine necropsies and 0.7% in [[symptomatic]] subependymomas from 1,000 serial [[Surgery|surgical]] specimens of [[Cranium|intracranial]] [[Neoplasm|neoplasms]].<ref name="pmid2929389">{{cite journal| author=Matsumura A, Ahyai A, Hori A, Schaake T| title=Intracerebral subependymomas. Clinical and neuropathological analyses with special reference to the possible existence of a less benign variant. | journal=Acta Neurochir (Wien) | year= 1989 | volume= 96 | issue= 1-2 | pages= 15-25 | pmid=2929389 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2929389 }} </ref>
* The [[incidence]] of subependymoma was estimated to be 0.7 cases per 100,000 individuals with [[Pathological|pathologically]] proven [[Cranium|intracranial]] [[Neoplasm|neoplasms]].<ref name="pmid22121350">{{cite journal| author=Kurukumbi M, Muley A, Ramidi G, Wynn Z, Trouth AJ| title=A rare case of subependymoma with an atypical presentation: a case report. | journal=Case Rep Neurol | year= 2011 | volume= 3 | issue= 3 | pages= 227-32 | pmid=22121350 | doi=10.1159/000333061 | pmc=3223030 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22121350 }} </ref>
===Age===

*[[Patient|Patients]] of all age groups may develop subependymoma.

*Subependymoma is a rare [[disease]] that tends to affect mi<nowiki/>ddle-aged adults and the elderly population (typically in the 5th to 6th decades).<ref name="epidemiosubepe1">Epidemiology of subependymoma. Dr Bruno Di Muzio and A.Prof Frank Gaillard et al. Radiopaedia 2016. http://radiopaedia.org/articles/subependymoma. Accessed on January 12, 2016</ref>

===Gender===
*Males are more commonly affected with subependymoma than females.
*The male to female ratio is approximately 2.3 to 1.<ref name="epidemiosubepe1" />

==Risk Factors==
The [[Risk factor|risk factors]] in the development of subependymoma are not well defined.

== Natural History, Complications, and Prognosis ==

*If left untreated, [[patients]] with subependymoma may progress to develop [[seizures]] and [[obstructive hydrocephalus]].<ref name="clinicalpresentationsubep1">Clinical presentation of subependymoma. Dr Bruno Di Muzio and A.Prof Frank Gaillard et al. Radiopaedia 2016. http://radiopaedia.org/articles/subependymoma. Accessed on January 12, 2016</ref>
*Subependymoma is a slow-growing [[tumor]] with an indolent course.<ref name="pmid16639322">{{cite journal| author=Ragel BT, Osborn AG, Whang K, Townsend JJ, Jensen RL, Couldwell WT| title=Subependymomas: an analysis of clinical and imaging features. | journal=Neurosurgery | year= 2006 | volume= 58 | issue= 5 | pages= 881-90; discussion 881-90 | pmid=16639322 | doi=10.1227/01.NEU.0000209928.04532.09 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16639322 }} </ref><ref name="pmid28804038">{{cite journal| author=D'Amico RS, Praver M, Zanazzi GJ, Englander ZK, Sims JS, Samanamud JL et al.| title=Subependymomas Are Low-Grade Heterogeneous Glial Neoplasms Defined by Subventricular Zone Lineage Markers. | journal=World Neurosurg | year= 2017 | volume= 107 | issue= | pages= 451-463 | pmid=28804038 | doi=10.1016/j.wneu.2017.08.009 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28804038 }} </ref>

*[[Obstructive hydrocephalus]] is a common complication of subependymoma.<ref name="clinicalpresentationsubep1" />

*The [[prognosis]] of subependymoma is excellent with complete [[excision]] of the [[tumor]].<ref name="pmid23382616" /><ref name="pmid10320142">{{cite journal| author=Prayson RA, Suh JH| title=Subependymomas: clinicopathologic study of 14 tumors, including comparative MIB-1 immunohistochemical analysis with other ependymal neoplasms. | journal=Arch Pathol Lab Med | year= 1999 | volume= 123 | issue= 4 | pages= 306-9 | pmid=10320142 | doi=10.1043/0003-9985(1999)123<0306:S>2.0.CO;2 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10320142 }} </ref>
*Common [[Complication (medicine)|complications]] of subependymoma are [[hydrocephalus]] and focal [[Neurology|neurological]] deficits due to [[Mass effect (medicine)|mass effect]].<ref name="pmid22747714">{{cite journal| author=Jain A, Amin AG, Jain P, Burger P, Jallo GI, Lim M et al.| title=Subependymoma: clinical features and surgical outcomes. | journal=Neurol Res | year= 2012 | volume= 34 | issue= 7 | pages= 677-84 | pmid=22747714 | doi=10.1179/1743132812Y.0000000064 | pmc=4618470 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22747714 }} </ref>

== Diagnosis ==
===Symptoms===
*Typically [[Patient|patients]] of subependymoma are [[asymptomatic]] and small [[Lesion|lesions]] are discovered incidentally.
*[[Symptoms]] of subependymoma include:<ref name="symptsubependymoma1">{{cite journal|last= KE|first= Changshu|title= Subependymoma: a case report and the review of literatures |doi=10.3969/j.issn.1672-6731.2011.01.021|url= http://www.cjcnn.org/index.php/cjcnn/article/view/323}}</ref><ref name="pmid2278665">{{cite journal| author=Park YK, Choi WS, Leem W, Kim YW, Yang MH| title=Symptomatic subependymoma--a case report. | journal=J Korean Med Sci | year= 1990 | volume= 5 | issue= 2 | pages= 111-5 | pmid=2278665 | doi=10.3346/jkms.1990.5.2.111 | pmc=3053733 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2278665 }} </ref><ref name="pmid22747714">{{cite journal| author=Jain A, Amin AG, Jain P, Burger P, Jallo GI, Lim M et al.| title=Subependymoma: clinical features and surgical outcomes. | journal=Neurol Res | year= 2012 | volume= 34 | issue= 7 | pages= 677-84 | pmid=22747714 | doi=10.1179/1743132812Y.0000000064 | pmc=4618470 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22747714 }} </ref>
**'''Symptoms due to elevated intracranial pressure'''
***[[Headache]]
***[[Nausea]]
***[[Vomiting]]
**'''Neurological symptoms'''
***[[Seizures]]
***Sudden loss of awareness
***[[memory loss|Transient loss of memory]]

:*

=== Physical Examination ===

*[[Patient|Patients]] with subependymoma usually appear normal.
*[[Physical examination]] may be remarkable for:<ref name="pmid23607015">{{cite journal| author=Bokhari R, Ghanem A, Alahwal M, Baeesa S| title=Primary isolated lymphoma of the fourth ventricle in an immunocompetent patient. | journal=Case Rep Oncol Med | year= 2013 | volume= 2013 | issue= | pages= 614658 | pmid=23607015 | doi=10.1155/2013/614658 | pmc=3625557 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23607015 }} </ref><ref name="pmid17761056">{{cite journal| author=Hamilton W, Kernick D| title=Clinical features of primary brain tumours: a case-control study using electronic primary care records. | journal=Br J Gen Pract | year= 2007 | volume= 57 | issue= 542 | pages= 695-9 | pmid=17761056 | doi= | pmc=2151783 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17761056 }} </ref><ref name="pmid16547083">{{cite journal| author=Wilne SH, Ferris RC, Nathwani A, Kennedy CR| title=The presenting features of brain tumours: a review of 200 cases. | journal=Arch Dis Child | year= 2006 | volume= 91 | issue= 6 | pages= 502-6 | pmid=16547083 | doi=10.1136/adc.2005.090266 | pmc=2082784 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16547083 }} </ref><ref name="pmid26926614">{{cite journal| author=Perkins A, Liu G| title=Primary Brain Tumors in Adults: Diagnosis and Treatment. | journal=Am Fam Physician | year= 2016 | volume= 93 | issue= 3 | pages= 211-7 | pmid=26926614 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26926614 }} </ref><ref name="pmid22747714">{{cite journal| author=Jain A, Amin AG, Jain P, Burger P, Jallo GI, Lim M et al.| title=Subependymoma: clinical features and surgical outcomes. | journal=Neurol Res | year= 2012 | volume= 34 | issue= 7 | pages= 677-84 | pmid=22747714 | doi=10.1179/1743132812Y.0000000064 | pmc=4618470 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22747714 }} </ref><ref name="pmid25361493">{{cite journal| author=Bi Z, Ren X, Zhang J, Jia W| title=Clinical, radiological, and pathological features in 43 cases of intracranial subependymoma. | journal=J Neurosurg | year= 2015 | volume= 122 | issue= 1 | pages= 49-60 | pmid=25361493 | doi=10.3171/2014.9.JNS14155 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25361493 }} </ref>

:*Abnormal [[pupillary reflex]]
:*[[Visual field]] defects
:*[[Gait]] changes
:*Bilateral [[Babinski sign]]
:*Depressed [[Glasgow coma score|Glasgow coma score (GCS)]]
:*Decreased [[muscle]] strength
:*Decreased [[Deep tendon reflex|deep tendon reflexes]]
:*[[Sensation]] defects
:*[[Hearing (sense)|Hearing]] problems and abnormal [[Rinne test|Rinne]] and [[Weber test|Weber tests]]

=== Laboratory Findings ===
There are no specific laboratory findings associated with subependymoma.

===Electrocardiogram===
There are no [[The electrocardiogram|ECG]] findings associated with subependymoma.

=== X-ray ===
There are no [[X-rays|x-ray]] findings associated with subependymoma.

===Echocardiography or Ultrasound===
There are no [[echocardiography]]/[[ultrasound]] findings associated with sybependymoma.

===CT scan===
[[Head]] [[Computed tomography|CT scan]] is helpful in the [[diagnosis]] of subependymoma. On [[Computed tomography|CT scan]], subependymoma is characterized by:<ref name="radiographicfeaturessubepenedymoma1">Radiographic features of subependymoma. Dr Bruno Di Muzio and A.Prof Frank Gaillard et al. Radiopaedia 2016. http://radiopaedia.org/articles/subependymoma. Accessed on January 12, 2016</ref>

* Iso- and hypodense intraventricular mass
* Positive [[Mass effect (medicine)|mass effect]]
* No enhancement
* If large, it may have [[cystic]] or even [[Calcification|calcific]] components
* No [[vasogenic edema]]

=== MRI ===
[[Brain]] [[MRI]] is helpful in the [[diagnosis]] of subependymoma. On [[MRI]], subependymoma is characterized by:
{| style="border: 0px; font-size: 90%; margin: 3px; width:1000px"
| valign="top" |
|+
! style="background: #4479BA; width: 300px;" |{{fontcolor|#FFF|MRI component}}
! style="background: #4479BA; width: 800px;" |{{fontcolor|#FFF|Findings}}
|-
| style="padding: 5px 5px; background: #DCDCDC; font-weight: bold" align="center" |
T1 weighted image
| style="padding: 5px 5px; background: #F5F5F5;" |
*Iso - hypointense compared to [[white matter]]
*[[Homogeneous]] but may be [[heterogeneous]] in larger [[Lesion|lesions]]
|-
| style="padding: 5px 5px; background: #DCDCDC;font-weight: bold" align="center" |
T2 weighted image
| style="padding: 5px 5px; background: #F5F5F5;" |
*Hyperintense compared to adjacent [[White matter|white]] and [[grey matter]]
*[[Heterogeneous|Heterogeneity]] may be seen in larger [[Lesion|lesions]], with susceptibility related signal drop-out due to [[Calcification|calcifications]]
*No adjacent [[Parenchyma|parenchymal]] [[edema]] (as no [[brain]] [[Invasive (medical)|invasion]] is present)
|-
| style="padding: 5px 5px; background: #DCDCDC;font-weight: bold" align="center" |
T1 weighted image with contrast
| style="padding: 5px 5px; background: #F5F5F5;" |
*Little or no enhancement
|}

=== Other Imaging Findings ===
There are no other [[imaging]] findings associated with subependymoma.

=== Other Diagnostic Studies ===
There are no other [[Diagnosis|diagnostic]] studies associated with subependymoma.

=== Medical Therapy ===
There is no medical therapy available for the treatment of subependymoma.

=== Surgery ===
[[Surgery]] is the mainstay of [[therapy]] for subependymoma. Incidental intraventricular subependymoma can be managed conservatively through MRI surveillance. [[Resection|Surgical resection]] is indicated for:<ref name="pmid22747714" /><ref name="pmid28232153">{{cite journal| author=Nguyen HS, Doan N, Gelsomino M, Shabani S| title=Intracranial Subependymoma: A SEER Analysis 2004-2013. | journal=World Neurosurg | year= 2017 | volume= 101 | issue= | pages= 599-605 | pmid=28232153 | doi=10.1016/j.wneu.2017.02.019 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28232153 }} </ref><ref name="pmid29915887">{{cite journal| author=Varma A, Giraldi D, Mills S, Brodbelt AR, Jenkinson MD| title=Surgical management and long-term outcome of intracranial subependymoma. | journal=Acta Neurochir (Wien) | year= 2018 | volume= 160 | issue= 9 | pages= 1793-1799 | pmid=29915887 | doi=10.1007/s00701-018-3570-4 | pmc=6105212 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29915887 }} </ref>

*[[Symptomatic]] [[Tumor|tumors]]
*[[Tumors]] without a clear [[imaging]] [[diagnosis]]

=== Primary Prevention ===
There are no established measures for the [[Prevention (medical)|secondary prevention]] of subependymoma.

=== Secondary Prevention ===
There are no established measures for the [[Prevention (medical)|primary prevention]] of subependymoma.

==References==
{{Reflist|2}}

[[Category:Pick One of 28 Approved]]

__NOTOC__
==References==
{{reflist|2}}

[[Category:Disease]]
[[Category:Oncology]]
[[Category:Types of cancer]]
[[Category:Rare diseases]]

{{WH}}
{{WS}}
[[Category:Up-To-Date]]
[[Category:Oncology]]
[[Category:Medicine]]
[[Category:Neurology]]
[[Category:Neurosurgery]]

Transverse myelitis risk factors

2020-05-06T04:27:08Z

M Jahan:

__NOTOC__
{{Transverse myelitis}}

{{CMG}}; {{AE}} {{MMJ}}{{sali}}
==Overview==
 

==Risk Factors==
There are no established risk factors for [disease name].

OR

The most potent risk factor in the development of [disease name] is [risk factor 1]. Other risk factors include [risk factor 2], [risk factor 3], and [risk factor 4].

OR

Common risk factors in the development of [disease name] include [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].
===Common Risk Factors===
*Common risk factors in the development of [disease name] may be occupational, environmental, genetic, and viral.
*Common risk factors in the development of [disease name] include:
**[Risk factor 1]
**[Risk factor 2]
**[Risk factor 3]

===Less Common Risk Factors===
*Less common risk factors in the development of [disease name] include:
**[Risk factor 1]
**[Risk factor 2]
**[Risk factor 3]

==References==
{{Reflist|2}}

{{WH}}
{{WS}}
[[Category: (name of the system)]]

Restless legs syndrome pathophysiology

2020-05-06T04:26:58Z

M Jahan:

__NOTOC__
{{Restless legs syndrome}}
{{CMG}}{{AE}}{{MMJ}}{{sali}}
==Overview==

==Pathophysiology==

===Pathogenesis===
*Generally most scientists consider restless legs syndrome(RLS) as a [[Central nervous system|central nervous system (CNS)]]-related disorder, but no specific lesion has been found to be associated with the syndrome.<ref name="pmid19514512" />

* It is thought that RLS is the result of [[central nervous system]] anatomic lesions.<ref name="pmid19514512">{{cite journal| author=Miyamoto M, Miyamoto T, Iwanami M, Suzuki K, Hirata K| title=[Pathophysiology of restless legs syndrome]. | journal=Brain Nerve | year= 2009 | volume= 61 | issue= 5 | pages= 523-32 | pmid=19514512 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19514512 }} </ref>
* Findings in imaging of [[CNS]] witch suggest the relation between the anatomic lesions in [[CNS]] and RLS include:<ref name="pmid19514512">{{cite journal| author=Miyamoto M, Miyamoto T, Iwanami M, Suzuki K, Hirata K| title=[Pathophysiology of restless legs syndrome]. | journal=Brain Nerve | year= 2009 | volume= 61 | issue= 5 | pages= 523-32 | pmid=19514512 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19514512 }} </ref><ref name="pmid27544840">{{cite journal| author=Li X, Allen RP, Earley CJ, Liu H, Cruz TE, Edden RAE et al.| title=Brain iron deficiency in idiopathic restless legs syndrome measured by quantitative magnetic susceptibility at 7 tesla. | journal=Sleep Med | year= 2016 | volume= 22 | issue= | pages= 75-82 | pmid=27544840 | doi=10.1016/j.sleep.2016.05.001 | pmc=4992945 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27544840 }} </ref><ref name="pmid15670702">{{cite journal| author=Etgen T, Draganski B, Ilg C, Schröder M, Geisler P, Hajak G et al.| title=Bilateral thalamic gray matter changes in patients with restless legs syndrome. | journal=Neuroimage | year= 2005 | volume= 24 | issue= 4 | pages= 1242-7 | pmid=15670702 | doi=10.1016/j.neuroimage.2004.10.021 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15670702 }} </ref><ref name="pmid28626420">{{cite journal| author=Guo S, Huang J, Jiang H, Han C, Li J, Xu X et al.| title=Restless Legs Syndrome: From Pathophysiology to Clinical Diagnosis and Management. | journal=Front Aging Neurosci | year= 2017 | volume= 9 | issue= | pages= 171 | pmid=28626420 | doi=10.3389/fnagi.2017.00171 | pmc=5454050 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28626420 }} </ref>
** Presence of morphologic changes in the [[somatosensory cortex]], [[motor cortex]] and thalamic [[Grey matter|gray matter]] in [[Magnetic resonance imaging|MRI]]
** Abnormal bilateral [[cerebellar]] and [[Thalamus|thalamic]] activation during the manifestation of sensory symptoms, with additional [[red nucleus]] and [[reticular formation]] activity during periodic leg movements (PLMS), in functional [[MRI]] study
** Evidences of the role of the [[Limbic system|limbic]] and [[opioid]] systems in [[Single photon emission computed tomography|SPECT]] and [[PET]] studies
** Low [[brain]] [[iron]] concentrations and dysfunction of iron [[metabolism]] and intracellular iron
*** The "iron-dopamine model" explains that [[iron deficiency]] in the brain causes an abnormality in the [[dopaminergic system]] leading to manifestation of RLS.

* RLS symptoms seem to depend on abnormal spinal [[sensorimotor]] integration at the [[spinal cord]] level and abnormal central [[somatosensory]] processing
* In animal models, studies suggest that the All [[dopaminergic system]] and the D3 receptor participates in RLS symptoms

==Genetics==
*[[Genes]] involved in the [[pathogenesis]] of RLS include: RLS 1: 12q and RLS 2: 14q and RLS 3: 9p and RLS 4: 2q and RLS 5: 20p.<ref name="pmid19514512">{{cite journal| author=Miyamoto M, Miyamoto T, Iwanami M, Suzuki K, Hirata K| title=[Pathophysiology of restless legs syndrome]. | journal=Brain Nerve | year= 2009 | volume= 61 | issue= 5 | pages= 523-32 | pmid=19514512 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19514512 }} </ref>
*40% of cases of RLS are familial and are inherited in an [[autosomal dominant]] fashion with [[variable penetrance]].

==Associated Conditions==

Conditions which may be associated with RLS include:<ref name="pmid24747872">{{cite journal| author=Katsi V, Katsimichas T, Kallistratos MS, Tsekoura D, Makris T, Manolis AJ et al.| title=The association of Restless Legs Syndrome with hypertension and cardiovascular disease. | journal=Med Sci Monit | year= 2014 | volume= 20 | issue= | pages= 654-9 | pmid=24747872 | doi=10.12659/MSM.890252 | pmc=3999161 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24747872 }} </ref><ref name="pmid18360657">{{cite journal| author=Cotter PE, O'Keeffe ST| title=Restless leg syndrome: is it a real problem? | journal=Ther Clin Risk Manag | year= 2006 | volume= 2 | issue= 4 | pages= 465-75 | pmid=18360657 | doi= | pmc=1936366 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18360657 }} </ref><ref name="pmid26944272">{{cite journal| author=Trenkwalder C, Allen R, Högl B, Paulus W, Winkelmann J| title=Restless legs syndrome associated with major diseases: A systematic review and new concept. | journal=Neurology | year= 2016 | volume= 86 | issue= 14 | pages= 1336-43 | pmid=26944272 | doi=10.1212/WNL.0000000000002542 | pmc=4826337 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26944272 }} </ref>
*[[Hypertension]]
*[[Cardiovascular disease|Cardiovascular diseases]]
*[[Anxiety]]
*[[Depression]]
*[[Iron deficiency]]
*[[Anemia]]
*[[Kidney diseases]]
*[[Stroke (patient information)|Stroke]]
*[[Parkinson disease]]
*[[Polyneuropathy]]
*[[Multiple sclerosis]]

==Microscopic Pathology==
*The exact [[neuroanatomical]] substrate imbalance which causes restless legs syndrome (RLS) is unknown.<ref name="pmid15197711">{{cite journal| author=Pittock SJ, Parrett T, Adler CH, Parisi JE, Dickson DW, Ahlskog JE| title=Neuropathology of primary restless leg syndrome: absence of specific tau- and alpha-synuclein pathology. | journal=Mov Disord | year= 2004 | volume= 19 | issue= 6 | pages= 695-9 | pmid=15197711 | doi=10.1002/mds.20042 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15197711 }} </ref>
*Chronic [[Ischemia|ischemic]] changes were found in some brain tissue samples of patients whit RLS.<ref name="pmid15197711">{{cite journal| author=Pittock SJ, Parrett T, Adler CH, Parisi JE, Dickson DW, Ahlskog JE| title=Neuropathology of primary restless leg syndrome: absence of specific tau- and alpha-synuclein pathology. | journal=Mov Disord | year= 2004 | volume= 19 | issue= 6 | pages= 695-9 | pmid=15197711 | doi=10.1002/mds.20042 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15197711 }} </ref>

==References==
{{reflist|2}}

[[Category:Sleep disorders]]
[[Category:Syndromes]]
[[Category:Neurology]]
[[Category:Primary care]]

{{WH}}
{{WS}}

Transverse myelitis epidemiology and demographics

2020-05-06T04:26:02Z

M Jahan:

__NOTOC__
{{Transverse myelitis}}

{{CMG}}; {{AE}} {{MMJ}}{{sali}}
==Overview==

==Epidemiology and Demographics==
===Incidence===
*The incidence/prevalence of transverse myelitis is approximately [number range] per 100,000 individuals worldwide.
*In [year], the incidence/prevalence of [disease name] was estimated to be [number range] cases per 100,000 individuals worldwide.

===Prevalence===
*The incidence/prevalence of [disease name] is approximately [number range] per 100,000 individuals worldwide.
*In [year], the incidence/prevalence of [disease name] was estimated to be [number range] cases per 100,000 individuals worldwide.
*The prevalence of [disease/malignancy] is estimated to be [number] cases annually.

===Case-fatality rate/Mortality rate===
*In [year], the incidence of [disease name] is approximately [number range] per 100,000 individuals with a case-fatality rate/mortality rate of [number range]%.
*The case-fatality rate/mortality rate of [disease name] is approximately [number range].

===Age===
*Patients of all age groups may develop [disease name].
*The incidence of [disease name] increases with age; the median age at diagnosis is [#] years.
*[Disease name] commonly affects individuals younger than/older than [number of years] years of age.
*[Chronic disease name] is usually first diagnosed among [age group].
*[Acute disease name] commonly affects [age group].

===Race===
*There is no racial predilection to [disease name].
*[Disease name] usually affects individuals of the [race 1] race. [Race 2] individuals are less likely to develop [disease name].
===Gender===
*[Disease name] affects men and women equally.
*[Gender 1] are more commonly affected by [disease name] than [gender 2]. The [gender 1] to [gender 2] ratio is approximately [number > 1] to 1.

===Region===
*The majority of [disease name] cases are reported in [geographical region].

*[Disease name] is a common/rare disease that tends to affect [patient population 1] and [patient population 2].

===Developed Countries===

===Developing Countries===

==References==
{{Reflist|2}}

{{WH}}
{{WS}}
[[Category: (name of the system)]]

Restless legs syndrome classification

2020-05-06T04:25:53Z

M Jahan:

__NOTOC__
{{Restless legs syndrome}}
{{CMG}}; {{AE}}{{MMJ}}{{sali}}
==Overview==

==Classification==
Restless leg syndrome (RLS), may be classified into two groups:<ref name="pmid18360657">{{cite journal| author=Cotter PE, O'Keeffe ST| title=Restless leg syndrome: is it a real problem? | journal=Ther Clin Risk Manag | year= 2006 | volume= 2 | issue= 4 | pages= 465-75 | pmid=18360657 | doi= | pmc=1936366 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18360657 }} </ref>
*Primary and secondary:
** Primary RLS is [[idiopathic]] and the cause of that is unknown which is familial in up to two thirds of patients. Primary RLS usually begins before approximately 40 to 45 years of age, and can even occur as early as the first year of life. In primary RLS, the onset is often slow.<ref name="pmid23748511">{{cite journal| author=Bogan RK, Cheray JA| title=Restless legs syndrome: a review of diagnosis and management in primary care. | journal=Postgrad Med | year= 2013 | volume= 125 | issue= 3 | pages= 99-111 | pmid=23748511 | doi=10.3810/pgm.2013.05.2636 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23748511 }} </ref>
**Secondary RLS may also be secondary to a number of conditions including:<ref name="pmid23211049">{{cite journal| author=Peeraully T, Tan EK| title=Linking restless legs syndrome with Parkinson's disease: clinical, imaging and genetic evidence. | journal=Transl Neurodegener | year= 2012 | volume= 1 | issue= 1 | pages= 6 | pmid=23211049 | doi=10.1186/2047-9158-1-6 | pmc=3514082 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23211049 }} </ref><ref name="pmid17566122">{{cite journal| author=Allen RP, Earley CJ| title=The role of iron in restless legs syndrome. | journal=Mov Disord | year= 2007 | volume= 22 Suppl 18 | issue= | pages= S440-8 | pmid=17566122 | doi=10.1002/mds.21607 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17566122 }} </ref><ref name="pmid24768121">{{cite journal| author=Srivanitchapoom P, Pandey S, Hallett M| title=Restless legs syndrome and pregnancy: a review. | journal=Parkinsonism Relat Disord | year= 2014 | volume= 20 | issue= 7 | pages= 716-22 | pmid=24768121 | doi=10.1016/j.parkreldis.2014.03.027 | pmc=4058350 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24768121 }} </ref><ref name="pmid25674109">{{cite journal| author=Haider I, Anees M, Shahid SA| title=Restless legs syndrome in end stage renal disease patients on haemodialysis. | journal=Pak J Med Sci | year= 2014 | volume= 30 | issue= 6 | pages= 1209-12 | pmid=25674109 | doi=10.12669/pjms.306.5691 | pmc=4320701 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25674109 }} </ref><ref name="pmid895774">{{cite journal| author=Botez MI, Lambert B| title=Folate deficiency and restless-legs syndrome in pregnancy. | journal=N Engl J Med | year= 1977 | volume= 297 | issue= 12 | pages= 670 | pmid=895774 | doi=10.1056/NEJM197709222971220 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=895774 }} </ref><ref name="pmid3081215">{{cite journal| author=Reynolds G, Blake DR, Pall HS, Williams A| title=Restless leg syndrome and rheumatoid arthritis. | journal=Br Med J (Clin Res Ed) | year= 1986 | volume= 292 | issue= 6521 | pages= 659-60 | pmid=3081215 | doi= | pmc=1339645 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=3081215 }} </ref>
***[[Iron deficiency anemia|Iron deficiency]]
***[[Pregnancy]]
***[[End-stage renal failure]]
***[[varicose vein]]
***Venous reflux
***[[folate deficiency]]
***[[sleep apnea]]
***[[uremia]]
***[[diabetes mellitus|Diabetes]]
***Thyroid problems
***Peripheral neuropathy
***[[Parkinson's disease]]
***Certain [[auto-immune disorders]] such as:
****[[Sjögren's syndrome]],
****[[Celiac Disease]]
****[[rheumatoid arthritis]]
**Secondary RLS is most common in those presenting for the first time in later life.<ref name="pmid18360657">{{cite journal| author=Cotter PE, O'Keeffe ST| title=Restless leg syndrome: is it a real problem? | journal=Ther Clin Risk Manag | year= 2006 | volume= 2 | issue= 4 | pages= 465-75 | pmid=18360657 | doi= | pmc=1936366 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18360657 }} </ref>
==References==
{{reflist|2}}

[[Category:Sleep disorders]]
[[Category:Syndromes]]
[[Category:Neurology]]
[[Category:Primary care]]
[[Category:Needs overview]]

{{WH}}
{{WS}}

Restless legs syndrome historical perspective

2020-05-06T04:24:49Z

M Jahan:

__NOTOC__
{{Restless legs syndrome}}
{{CMG}}; {{AE}}{{MMJ}}{{sali}}

==Overview==

==Historical Perspective==

===Discovery===
*In 1672, Sir Thomas Willis, a British [[anatomist]] and physician was the first to discover the leg discomfort experienced by some of his patients.<ref name="pmid19412460">{{cite journal| author=Byrne R, Sinha S, Chaudhuri KR| title=Restless legs syndrome: diagnosis and review of management options. | journal=Neuropsychiatr Dis Treat | year= 2006 | volume= 2 | issue= 2 | pages= 155-64 | pmid=19412460 | doi= | pmc=2671772 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19412460 }} </ref><ref name="WhoNamedIt">{{WhoNamedIt|synd|2337|Wittmaack-Ekbom syndrome}}</ref>
*In a 1945, Karl-Axel Ekbom a Swedish [[Neurology|neurologist]] described the disease and presented eight cases used for his studies.<ref name="pmid18829374">{{cite journal| author=Teive HA, Munhoz RP, Barbosa ER| title=Professor Karl-Axel Ekbom and restless legs syndrome. | journal=Parkinsonism Relat Disord | year= 2009 | volume= 15 | issue= 4 | pages= 254-7 | pmid=18829374 | doi=10.1016/j.parkreldis.2008.07.011 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18829374 }} </ref>
*In 1995, a large International Restless Legs Syndrome (RLS) Study Group has been formed. As its first task, the group has taken upon itself the role of defining the clinical features of the RLS.<ref name="pmid18829374" />
*In 2002, National Institutes of Health in Bethesda, MA, USA, formulated a revised criteria for the diagnosis of RLS.<ref name="pmid14592341">{{cite journal| author=Allen RP, Picchietti D, Hening WA, Trenkwalder C, Walters AS, Montplaisi J et al.| title=Restless legs syndrome: diagnostic criteria, special considerations, and epidemiology. A report from the restless legs syndrome diagnosis and epidemiology workshop at the National Institutes of Health. | journal=Sleep Med | year= 2003 | volume= 4 | issue= 2 | pages= 101-19 | pmid=14592341 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14592341 }} </ref>

==References==
{{reflist|2}}

[[Category:Sleep disorders]]
[[Category:Syndromes]]
[[Category:Neurology]]
[[Category:Primary care]]
[[Category:Needs content]]

{{WH}}
{{WS}}

Transverse myelitis differential diagnosis

2020-05-06T04:24:36Z

M Jahan:

__NOTOC__
[[Image:Home_logo1.png|right|250px|link=https://www.wikidoc.org/index.php/Transverse_myelitis]]
{{CMG}}; {{AE}}{{TarekNafee}} {{MMJ}}{{sali}}
==Overview==
Transverse myelitis must be differentiated from other diseases that cause [[hypotonia]], [[muscle weakness]], or [[paralysis]] such as: Adult [[botulism]], infant [[botulism]], [[Guillian-Barre syndrome]], [[Eaton lambert syndrome|Eaton Lambert syndrome]], [[myasthenia gravis]], [[electrolyte disturbance]], [[Organophosphate poisoning|organophosphate toxicity]], [[tick paralysis]], [[stroke]][[tetrodotoxin]] poisoning, [[poliomyelitis]], [[Neurosyphilis (patient information)|neurosyphilis,]] [[muscular dystrophy]][[Muscular dystrophy|,]] [[multiple sclerosis]] exacerbation, [[amyotrophic lateral sclerosis]] and [[Myositis|inflammatory myopathy]].

==Differential Diagnosis==
Transverse myelitis must be differentiated from other diseases that may cause [[hypotonia]], [[muscle weakness]], or [[paralysis]]:<ref name="pmid29433111">{{cite journal |vauthors=Kira R |title=[Acute Flaccid Myelitis] |language=Japanese |journal=Brain Nerve |volume=70 |issue=2 |pages=99–112 |date=February 2018 |pmid=29433111 |doi=10.11477/mf.1416200962 |url=}}</ref><ref name="pmid29433111">{{cite journal |vauthors=Kira R |title=[Acute Flaccid Myelitis] |language=Japanese |journal=Brain Nerve |volume=70 |issue=2 |pages=99–112 |date=February 2018 |pmid=29433111 |doi=10.11477/mf.1416200962 |url=}}</ref><ref name="pmid29181601">{{cite journal |vauthors=Hopkins SE |title=Acute Flaccid Myelitis: Etiologic Challenges, Diagnostic and Management Considerations |journal=Curr Treat Options Neurol |volume=19 |issue=12 |pages=48 |date=November 2017 |pmid=29181601 |doi=10.1007/s11940-017-0480-3 |url=}}</ref><ref name="pmid27422805">{{cite journal |vauthors=Messacar K, Schreiner TL, Van Haren K, Yang M, Glaser CA, Tyler KL, Dominguez SR |title=Acute flaccid myelitis: A clinical review of US cases 2012-2015 |journal=Ann. Neurol. |volume=80 |issue=3 |pages=326–38 |date=September 2016 |pmid=27422805 |pmc=5098271 |doi=10.1002/ana.24730 |url=}}</ref><ref name="pmid29028962">{{cite journal |vauthors=Chong PF, Kira R, Mori H, Okumura A, Torisu H, Yasumoto S, Shimizu H, Fujimoto T, Hanaoka N, Kusunoki S, Takahashi T, Oishi K, Tanaka-Taya K |title=Clinical Features of Acute Flaccid Myelitis Temporally Associated With an Enterovirus D68 Outbreak: Results of a Nationwide Survey of Acute Flaccid Paralysis in Japan, August-December 2015 |journal=Clin. Infect. Dis. |volume=66 |issue=5 |pages=653–664 |date=February 2018 |pmid=29028962 |pmc=5850449 |doi=10.1093/cid/cix860 |url=}}</ref><ref name="pmid29482893">{{cite journal |vauthors=Messacar K, Asturias EJ, Hixon AM, Van Leer-Buter C, Niesters HGM, Tyler KL, Abzug MJ, Dominguez SR |title=Enterovirus D68 and acute flaccid myelitis-evaluating the evidence for causality |journal=Lancet Infect Dis |volume=18 |issue=8 |pages=e239–e247 |date=August 2018 |pmid=29482893 |doi=10.1016/S1473-3099(18)30094-X |url=}}</ref><ref name="pmid30200066">{{cite journal |vauthors=Chen IJ, Hu SC, Hung KL, Lo CW |title=Acute flaccid myelitis associated with enterovirus D68 infection: A case report |journal=Medicine (Baltimore) |volume=97 |issue=36 |pages=e11831 |date=September 2018 |pmid=30200066 |pmc=6133480 |doi=10.1097/MD.0000000000011831 |url=}}</ref><ref name="urlBotulism | Botulism | CDC">{{cite web |url=https://www.cdc.gov/botulism/index.html |title=Botulism | Botulism | CDC |format= |work= |accessdate=}}</ref><ref name="pmid3290234">{{cite journal |vauthors=McCroskey LM, Hatheway CL |title=Laboratory findings in four cases of adult botulism suggest colonization of the intestinal tract |journal=J. Clin. Microbiol. |volume=26 |issue=5 |pages=1052–4 |date=May 1988 |pmid=3290234 |pmc=266519 |doi= |url=}}</ref><ref name="pmid16614251">{{cite journal |vauthors=Lindström M, Korkeala H |title=Laboratory diagnostics of botulism |journal=Clin. Microbiol. Rev. |volume=19 |issue=2 |pages=298–314 |date=April 2006 |pmid=16614251 |pmc=1471988 |doi=10.1128/CMR.19.2.298-314.2006 |url=}}</ref><ref name="pmid17224901">{{cite journal |vauthors=Brook I |title=Botulism: the challenge of diagnosis and treatment |journal=Rev Neurol Dis |volume=3 |issue=4 |pages=182–9 |date=2006 |pmid=17224901 |doi= |url=}}</ref><ref name="pmid23642721">{{cite journal |vauthors=Dimachkie MM, Barohn RJ |title=Guillain-Barré syndrome and variants |journal=Neurol Clin |volume=31 |issue=2 |pages=491–510 |date=May 2013 |pmid=23642721 |pmc=3939842 |doi=10.1016/j.ncl.2013.01.005 |url=}}</ref><ref name="pmid23418763">{{cite journal |vauthors=Walling AD, Dickson G |title=Guillain-Barré syndrome |journal=Am Fam Physician |volume=87 |issue=3 |pages=191–7 |date=February 2013 |pmid=23418763 |doi= |url=}}</ref><ref name="pmid21969911">{{cite journal |vauthors=Gilhus NE |title=Lambert-eaton myasthenic syndrome; pathogenesis, diagnosis, and therapy |journal=Autoimmune Dis |volume=2011 |issue= |pages=973808 |date=2011 |pmid=21969911 |pmc=3182560 |doi=10.4061/2011/973808 |url=}}</ref><ref name="pmid14977560">{{cite journal |vauthors=Krishnan C, Kaplin AI, Deshpande DM, Pardo CA, Kerr DA |title=Transverse Myelitis: pathogenesis, diagnosis and treatment |journal=Front. Biosci. |volume=9 |issue= |pages=1483–99 |date=May 2004 |pmid=14977560 |doi= |url=}}</ref><ref name="pmid24305450">{{cite journal |vauthors=Amato AA, Greenberg SA |title=Inflammatory myopathies |journal=Continuum (Minneap Minn) |volume=19 |issue=6 Muscle Disease |pages=1615–33 |date=December 2013 |pmid=24305450 |doi=10.1212/01.CON.0000440662.26427.bd |url=}}</ref><ref name="pmid24365430">{{cite journal |vauthors=Berger JR, Dean D |title=Neurosyphilis |journal=Handb Clin Neurol |volume=121 |issue= |pages=1461–72 |date=2014 |pmid=24365430 |doi=10.1016/B978-0-7020-4088-7.00098-5 |url=}}</ref>
{|
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
! rowspan="2" |Diseases
! colspan="8" |History and Physical
! colspan="2" |Diagnostic tests
! rowspan="2" |Other Findings
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
!Motor Deficit
!Sensory deficit
!Cranial nerve Involvement
!Autonomic dysfunction
!Proximal/Distal/Generalized
!Ascending/Descending/Systemic
!Unilateral (UL)
or Bilateral (BL)

or

No Lateralization (NL)
!Onset
!Lab or Imaging Findings
!Specific test
|-
| style="background: #DCDCDC; padding: 5px; text-align:center;" |Transverse myelitis
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>+</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Proximal > Distal
| style="background: #F5F5F5; padding: 5px; text-align:center" |Systemic
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL or UL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Sudden
| style="background: #F5F5F5; padding: 5px; text-align:center" |MRI & [[Lumbar puncture]]
| style="background: #F5F5F5; padding: 5px; text-align:center" |MRI
| style="background: #F5F5F5; padding: 5px; text-align:center" |History of chronic viral or autoimmune disease (e.g. [[HIV]])
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Botulism|Adult Botulism]]
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>+</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Generalized
| style="background: #F5F5F5; padding: 5px; text-align:center" |Descending
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Sudden
| style="background: #F5F5F5; padding: 5px; text-align:center" |Toxin test
| style="background: #F5F5F5; padding: 5px; text-align:center" |Blood, Wound, or Stool culture
| style="background: #F5F5F5; padding: 5px; text-align:center" |[[Diplopia]], [[Hyporeflexia|Hyporeflexia,]] [[Hypotonia]], possible respiratory paralysis
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |Infant [[Botulism]]
| style="background: #F5F5F5; padding: 5px; text-align:center" |+
| style="background: #F5F5F5; padding: 5px; text-align:center" |-
| style="background: #F5F5F5; padding: 5px; text-align:center" |+
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>+</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Generalized
| style="background: #F5F5F5; padding: 5px; text-align:center" |Descending
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Sudden
| style="background: #F5F5F5; padding: 5px; text-align:center" |Toxin test
| style="background: #F5F5F5; padding: 5px; text-align:center" |Blood, Wound, or Stool culture
| style="background: #F5F5F5; padding: 5px; text-align:center" |[[Flaccid paralysis]] ([[Floppy baby syndrome]]), possible respiratory paralysis
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" | [[Guillian-Barre syndrome]]<ref name="pmid22081202">{{cite journal| author=Talukder RK, Sutradhar SR, Rahman KM, Uddin MJ, Akhter H| title=Guillian-Barre syndrome. | journal=Mymensingh Med J | year= 2011 | volume= 20 | issue= 4 | pages= 748-56 | pmid=22081202 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22081202 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>-</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Generalized
| style="background: #F5F5F5; padding: 5px; text-align:center" |Ascending
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Insidious
| style="background: #F5F5F5; padding: 5px; text-align:center" |CSF: ↑Protein

↓Cells

| style="background: #F5F5F5; padding: 5px; text-align:center" |Clinical & Lumbar Puncture
| style="background: #F5F5F5; padding: 5px; text-align:center" |Progressive [[ascending paralysis]] following infection, possible respiratory paralysis
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" | [[Eaton lambert syndrome|Eaton Lambert syndrome]]<ref name="pmid27412406">{{cite journal| author=Merino-Ramírez MÁ, Bolton CF| title=Review of the Diagnostic Challenges of Lambert-Eaton Syndrome Revealed Through Three Case Reports. | journal=Can J Neurol Sci | year= 2016 | volume= 43 | issue= 5 | pages= 635-47 | pmid=27412406 | doi=10.1017/cjn.2016.268 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27412406 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>+</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Generalized
| style="background: #F5F5F5; padding: 5px; text-align:center" |Systemic
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Intermittent
| style="background: #F5F5F5; padding: 5px; text-align:center" | [[EMG]], repetitive nerve stimulation test (RNS)
| style="background: #F5F5F5; padding: 5px; text-align:center" |[[Voltage gated calcium channel|Voltage gated calcium channe]]<nowiki/>l<nowiki/> (VGCC) antibody
| style="background: #F5F5F5; padding: 5px; text-align:center" |[[Diplopia]], [[ptosis]], improves with movement (as the day progresses)
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Myasthenia gravis]]<ref name="pmid28029925">{{cite journal| author=Gilhus NE| title=Myasthenia Gravis. | journal=N Engl J Med | year= 2016 | volume= 375 | issue= 26 | pages= 2570-2581 | pmid=28029925 | doi=10.1056/NEJMra1602678 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28029925 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>+</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Generalized
| style="background: #F5F5F5; padding: 5px; text-align:center" |Systemic
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Intermittent
| style="background: #F5F5F5; padding: 5px; text-align:center" | [[Electromyography|EMG]], [[Edrophonium|Edrophonium test]]
| style="background: #F5F5F5; padding: 5px; text-align:center" |[[Acetylcholine receptor|Ach receptor]] antibody
| style="background: #F5F5F5; padding: 5px; text-align:center" |[[Diplopia]], [[ptosis]], worsening with movement (as the day progresses)
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Electrolyte disturbance]]<ref name="pmid26813501">{{cite journal| author=Ozono K| title=[Diagnostic criteria for vitamin D-deficient rickets and hypocalcemia-]. | journal=Clin Calcium | year= 2016 | volume= 26 | issue= 2 | pages= 215-22 | pmid=26813501 | doi=CliCa1602215222 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26813501 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>-</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Generalized
| style="background: #F5F5F5; padding: 5px; text-align:center" |Systemic
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Insidious
| style="background: #F5F5F5; padding: 5px; text-align:center" | Electrolyte panel
| style="background: #F5F5F5; padding: 5px; text-align:center" |↓Ca++, ↓Mg++, ↓K+
| style="background: #F5F5F5; padding: 5px; text-align:center" |Possible [[arrhythmia]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Organophosphate poisoning|Organophosphate toxicity]]<ref name="pmid15020723">{{cite journal| author=Kamanyire R, Karalliedde L| title=Organophosphate toxicity and occupational exposure. | journal=Occup Med (Lond) | year= 2004 | volume= 54 | issue= 2 | pages= 69-75 | pmid=15020723 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15020723 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>+</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Generalized
| style="background: #F5F5F5; padding: 5px; text-align:center" |Ascending
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Sudden
| style="background: #F5F5F5; padding: 5px; text-align:center" | Clinical diagnosis: physical exam & history
| style="background: #F5F5F5; padding: 5px; text-align:center" |Clinical suspicion confirmed with RBC AchE activity
| style="background: #F5F5F5; padding: 5px; text-align:center" |History of exposure to i[[Insecticide|nsecticide]] or living in farming environment. with : [[Diarrhea]], [[Urination]], [[Miosis]], [[Bradycardia]], [[Lacrimation]], [[Emesis]], [[Salivation]], [[Sweating]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Tick paralysis]] ([[Dermacentor andersoni|Dermacentor tick]])<ref name="pmid23677663">{{cite journal| author=Pecina CA| title=Tick paralysis. | journal=Semin Neurol | year= 2012 | volume= 32 | issue= 5 | pages= 531-2 | pmid=23677663 | doi=10.1055/s-0033-1334474 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23677663 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>-</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Generalized
| style="background: #F5F5F5; padding: 5px; text-align:center" |Ascending
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Insidious
| style="background: #F5F5F5; padding: 5px; text-align:center" | Clinical diagnosis: physical exam & history
| style="background: #F5F5F5; padding: 5px; text-align:center" |-
| style="background: #F5F5F5; padding: 5px; text-align:center" |History of outdoor activity in Northeastern United States. The tick is often still latched to the patient at presentation (often in head and neck area)
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Tetrodotoxin]] poisoning<ref name="pmid24566728">{{cite journal| author=Bane V, Lehane M, Dikshit M, O'Riordan A, Furey A| title=Tetrodotoxin: chemistry, toxicity, source, distribution and detection. | journal=Toxins (Basel) | year= 2014 | volume= 6 | issue= 2 | pages= 693-755 | pmid=24566728 | doi=10.3390/toxins6020693 | pmc=3942760 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24566728 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>+</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Generalized
| style="background: #F5F5F5; padding: 5px; text-align:center" |Systemic
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Sudden
| style="background: #F5F5F5; padding: 5px; text-align:center" | Clinical diagnosis: physical exam & dietary history
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" | History of consumption of puffer fish species.
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Stroke]]<ref name="pmid8848683">{{cite journal| author=Kuntzer T, Hirt L, Bogousslavsky J| title=[Neuromuscular involvement and cerebrovascular accidents]. | journal=Rev Med Suisse Romande | year= 1996 | volume= 116 | issue= 8 | pages= 605-9 | pmid=8848683 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8848683 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" | +/-
| style="background: #F5F5F5; padding: 5px; text-align:center" | +/-
| style="background: #F5F5F5; padding: 5px; text-align:center" | +/-
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>+/-</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Generalized
| style="background: #F5F5F5; padding: 5px; text-align:center" |Systemic
| style="background: #F5F5F5; padding: 5px; text-align:center" |UL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Sudden
| style="background: #F5F5F5; padding: 5px; text-align:center" | MRI +ve for ischemia or hemorrhage
| style="background: #F5F5F5; padding: 5px; text-align:center" |MRI
| style="background: #F5F5F5; padding: 5px; text-align:center" |Sudden unilateral motor and sensory deficit in a patient with a history of [[Atherosclerosis|atherosclero]]<nowiki/>tic risk factors (diabetes, hypertension, smoking) or [[Atrial fibrillation|atrial fibrillation.]]
|-
| style="background: #DCDCDC; padding: 5px; text-align:center;" | [[Poliomyelitis]]<ref name="pmid19944665">{{cite journal| author=Laffont I, Julia M, Tiffreau V, Yelnik A, Herisson C, Pelissier J| title=Aging and sequelae of poliomyelitis. | journal=Ann Phys Rehabil Med | year= 2010 | volume= 53 | issue= 1 | pages= 24-33 | pmid=19944665 | doi=10.1016/j.rehab.2009.10.002 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19944665 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" |+
| style="background: #F5F5F5; padding: 5px; text-align:center" |+
| style="background: #F5F5F5; padding: 5px; text-align:center" |+
| style="background: #F5F5F5; padding: 5px; text-align:center" |+/-
| style="background: #F5F5F5; padding: 5px; text-align:center" |Proximal > Distal
| style="background: #F5F5F5; padding: 5px; text-align:center" |Systemic
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL or UL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Sudden
| style="background: #F5F5F5; padding: 5px; text-align:center" |
| style="background: #F5F5F5; padding: 5px; text-align:center" |PCR of CSF
| style="background: #F5F5F5; padding: 5px; text-align:center" |Asymmetric paralysis following a flu-like syndrome.
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Neurosyphilis]]<ref name="pmid22482824">{{cite journal| author=Liu LL, Zheng WH, Tong ML, Liu GL, Zhang HL, Fu ZG et al.| title=Ischemic stroke as a primary symptom of neurosyphilis among HIV-negative emergency patients. | journal=J Neurol Sci | year= 2012 | volume= 317 | issue= 1-2 | pages= 35-9 | pmid=22482824 | doi=10.1016/j.jns.2012.03.003 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22482824 }} </ref><ref name="pmid24365430">{{cite journal |vauthors=Berger JR, Dean D |title=Neurosyphilis |journal=Handb Clin Neurol |volume=121 |issue= |pages=1461–72 |year=2014 |pmid=24365430 |doi=10.1016/B978-0-7020-4088-7.00098-5 |url=}}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" | +/-
| style="background: #F5F5F5; padding: 5px; text-align:center" |Generalized
| style="background: #F5F5F5; padding: 5px; text-align:center" |Systemic
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Insidious<nowiki/>
| style="background: #F5F5F5; padding: 5px; text-align:center" |MRI & [[Lumbar puncture]]
| style="background: #F5F5F5; padding: 5px; text-align:center" |CSF [[VDRL]]-specifc
CSF [[FTA-ABS|FTA-Ab]] -sensitive<ref name="pmid22421697">{{cite journal| author=Ho EL, Marra CM| title=Treponemal tests for neurosyphilis--less accurate than what we thought? | journal=Sex Transm Dis | year= 2012 | volume= 39 | issue= 4 | pages= 298-9 | pmid=22421697 | doi=10.1097/OLQ.0b013e31824ee574 | pmc=3746559 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22421697 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" |History of unprotected sex or multiple sexual partners.

History of [[genital ulcer]] ([[chancre]]), diffuse [[Maculopapular rash|maculopapular ras]]<nowiki/>h.
|-
| style="background: #DCDCDC; padding: 5px; text-align:center;" |[[Muscular dystrophy]]<ref name="pmid26457695">{{cite journal| author=Falzarano MS, Scotton C, Passarelli C, Ferlini A| title=Duchenne Muscular Dystrophy: From Diagnosis to Therapy. | journal=Molecules | year= 2015 | volume= 20 | issue= 10 | pages= 18168-84 | pmid=26457695 | doi=10.3390/molecules201018168 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26457695 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>-</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Proximal > Distal
| style="background: #F5F5F5; padding: 5px; text-align:center" |Systemic
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Insidious
| style="background: #F5F5F5; padding: 5px; text-align:center" | Genetic testing
| style="background: #F5F5F5; padding: 5px; text-align:center" |[[Muscle biopsy]]
| style="background: #F5F5F5; padding: 5px; text-align:center" |Progressive proximal lower limb weakness with calf pseudohypertrophy in early childhood. [[Gowers' sign|Gower sign]] positive.
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Multiple sclerosis]] exacerbation<ref name="pmid27432676">{{cite journal| author=Filippi M, Preziosa P, Rocca MA| title=Multiple sclerosis. | journal=Handb Clin Neurol | year= 2016 | volume= 135 | issue= | pages= 399-423 | pmid=27432676 | doi=10.1016/B978-0-444-53485-9.00020-9 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27432676 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>+</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Generalized
| style="background: #F5F5F5; padding: 5px; text-align:center" |Systemic
| style="background: #F5F5F5; padding: 5px; text-align:center" |NL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Sudden
| style="background: #F5F5F5; padding: 5px; text-align:center" |'''[[CSF|↑]]'''[[CSF]] [[IgG]] levels
(monoclonal)
| style="background: #F5F5F5; padding: 5px; text-align:center" |Clinical assessment and [[MRI]] <ref name="pmid8274111">{{cite journal| author=Giang DW, Grow VM, Mooney C, Mushlin AI, Goodman AD, Mattson DH et al.| title=Clinical diagnosis of multiple sclerosis. The impact of magnetic resonance imaging and ancillary testing. Rochester-Toronto Magnetic Resonance Study Group. | journal=Arch Neurol | year= 1994 | volume= 51 | issue= 1 | pages= 61-6 | pmid=8274111 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8274111 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" |[[Blurred vision|Blurry vision]], [[urinary incontinence]], [[fatigue]]
|-
| style="background: #DCDCDC; padding: 5px; text-align:center" |[[Amyotrophic lateral sclerosis]]<ref name="pmid27025851">{{cite journal| author=Riva N, Agosta F, Lunetta C, Filippi M, Quattrini A| title=Recent advances in amyotrophic lateral sclerosis. | journal=J Neurol | year= 2016 | volume= 263 | issue= 6 | pages= 1241-54 | pmid=27025851 | doi=10.1007/s00415-016-8091-6 | pmc=4893385 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27025851 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>-</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Generalized
| style="background: #F5F5F5; padding: 5px; text-align:center" |Systemic
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Insidious
| style="background: #F5F5F5; padding: 5px; text-align:center" | Normal [[Lumbar puncture|LP]] (to rule out DDx)
| style="background: #F5F5F5; padding: 5px; text-align:center" |MRI & [[Lumbar puncture|LP]]
| style="background: #F5F5F5; padding: 5px; text-align:center" |Patient initially presents with [[upper motor neuron]] deficit ([[spasticity]]) followed by [[lower motor neuron]] deficit ([[flaccidity]]).
|-
| style="background: #DCDCDC; padding: 5px; text-align:center;" |[[Myositis|Inflammatory myopathy]]<ref name="pmid26290112">{{cite journal| author=Michelle EH, Mammen AL| title=Myositis Mimics. | journal=Curr Rheumatol Rep | year= 2015 | volume= 17 | issue= 10 | pages= 63 | pmid=26290112 | doi=10.1007/s11926-015-0541-0 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26290112 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>-</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Proximal > Distal
| style="background: #F5F5F5; padding: 5px; text-align:center" |Systemic
| style="background: #F5F5F5; padding: 5px; text-align:center" |UL or BL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Insidious
| style="background: #F5F5F5; padding: 5px; text-align:center" |Elevated [[Creatine kinase|CK]] & [[Aldolase]]
| style="background: #F5F5F5; padding: 5px; text-align:center" |[[Muscle biopsy]]
| style="background: #F5F5F5; padding: 5px; text-align:center" |Progressive proximal muscle weakness in 3rd to 5th decade of life. With or without skin manifestations.
|-
|}

== References ==
{{reflist|2}}
{{WH}}
{{WS}}

Restless legs syndrome overview

2020-05-06T04:23:49Z

M Jahan:

__NOTOC__
{{Restless legs syndrome}}
{{CMG}}{{MMJ}}{{sali}}

==Overview==
Restless legs syndrome is a condition that is characterised by an irresistible urge to move one's legs. It is poorly understood, often misdiagnosed, and believed to be a [[neurological disorder]]. Many people tap their feet or shake their legs resulting from a nervous tic, consumption of stimulants, drug side-effects or other factors; this is usually innocuous, unnoticed, and does not interfere with daily life, quite distinct from Restless Leg Syndrome.

It is sometimes mistakenly called "[[Ekbom syndrome|Ekbom's syndrome]]," but that is an entirely different condition that shares part of the Wittmaack-Ekbom syndrome [[List of eponymous diseases|eponym]]: [[delusional parasitosis]], as both syndromes were described by the same person, Karl-Axel Ekbom. <ref name="WhoNamedIt">{{WhoNamedIt|synd|2337|Wittmaack-Ekbom syndrome}}</ref>

==Historical Perspective==
In a 1945 publication titled 'Restless Legs', Karl-Axel Ekbom described the disease and presented eight cases used for his studies.<ref>Ekbom, K.-A. Restless legs: a clinical study. Acta Med. Scand. (Suppl.) 158: 1-123, 1945.</ref>

Earlier studies were done by Thomas Willis (1622-1675) and by Theodor Wittmaack.<ref name="WhoNamedIt"> </ref> Another early description of the disease and its symptoms were made by George Miller Beard (1839-1883).<ref name="WhoNamedIt"> </ref>

==Pathophysiology==
As with many diseases with diffuse symptoms, there is controversy among physicians, if RLS is a distinct syndrome. The US National Institute of Neurological Diseases and Stroke publishes an information sheet <ref>[http://www.ninds.nih.gov/disorders/restless_legs/detail_restless_legs.htm Restless Legs Syndrome Fact Sheet]</ref> characterizing the syndrome but acknowledging it is a difficult diagnosis. Some physicians doubt that RLS actually exists as a legitimate clinical entity, but believe it to be a kind of "catch-all" category, perhaps related to a general heightened [[sympathetic nervous system]] (SNS) response that could be caused by any number of physical or emotional factors. Other clinicians associate it with lumbosacral spinal subluxations and life stress.

==Epidemiology and Demographics==
Many doctors express the view that the incidence of restless leg syndrome is exaggerated by manufacturers of drugs used to treat it.<ref>{{cite journal |author=Woloshin S, Schwartz L |title=Giving legs to restless legs: a case study of how the media helps make people sick |journal=PLoS Med. |volume=3 |issue=4 |pages=e170 |year=2006 |pmid=16597175 |url=http://dx.doi.org/10.1371/journal.pmed.0030170}}</ref> Other physicians consider it a real entity that has specific diagnostic criteria. <ref>{{cite journal |author=Montplaisir J; Boucher S; Nicolas A; Lesperance P; Gosselin A; Rompré P; Lavigne G |journal=Movement disorders |volume=13 |issue=2 |pages=324-9 |year=1998|pmid=9539348|url=http://www.ncbi.nlm.nih.gov/sites/entrez?db=PubMed&cmd=retrieve&dopt=AbstractPlus&list_uids=9539348}}</ref>

==References==
{{reflist|2}}

[[Category:Sleep disorders]]
[[Category:Syndromes]]
[[Category:Neurology]]
[[Category:Primary care]]

{{WH}}
{{WS}}

Transverse myelitis causes

2020-05-06T04:23:28Z

M Jahan:

__NOTOC__
{{Transverse myelitis}}

{{CMG}}; {{AE}} {{MMJ}}{{sali}}
==Overview==
 

==Causes==
===Life-threatening Causes===
*Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. There are no life-threatening causes of [[disease name]], however complications resulting from untreated [[disease name]] is common.
*Life-threatening causes of [symptom/manifestation] include [cause1], [cause2], and [cause3].
*[Cause] is a life-threatening cause of [disease].

===Common Causes===
Common causes of myelitis include may include:

*Various infectionsin in 30% to 60% of the cases:<ref name="pmid22379456">{{cite journal| author=Awad A, Stüve O| title=Idiopathic transverse myelitis and neuromyelitis optica: clinical profiles, pathophysiology and therapeutic choices. | journal=Curr Neuropharmacol | year= 2011 | volume= 9 | issue= 3 | pages= 417-28 | pmid=22379456 | doi=10.2174/157015911796557948 | pmc=3151596 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22379456 }} </ref><ref name="pmid8489410">{{cite journal| author=Jeffery DR, Mandler RN, Davis LE| title=Transverse myelitis. Retrospective analysis of 33 cases, with differentiation of cases associated with multiple sclerosis and parainfectious events. | journal=Arch Neurol | year= 1993 | volume= 50 | issue= 5 | pages= 532-5 | pmid=8489410 | doi=10.1001/archneur.1993.00540050074019 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8489410 }} </ref><ref name="pmid2375246">{{cite journal| author=Christensen PB, Wermuth L, Hinge HH, Bømers K| title=Clinical course and long-term prognosis of acute transverse myelopathy. | journal=Acta Neurol Scand | year= 1990 | volume= 81 | issue= 5 | pages= 431-5 | pmid=2375246 | doi=10.1111/j.1600-0404.1990.tb00990.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2375246 }} </ref><ref name="pmid14977560">{{cite journal| author=Krishnan C, Kaplin AI, Deshpande DM, Pardo CA, Kerr DA| title=Transverse Myelitis: pathogenesis, diagnosis and treatment. | journal=Front Biosci | year= 2004 | volume= 9 | issue= | pages= 1483-99 | pmid=14977560 | doi=10.2741/1351 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14977560 }} </ref><ref name="pmid13007166">{{cite journal| author=PAINE RS, BYERS RK| title=Transverse myelopathy in childhood. | journal=AMA Am J Dis Child | year= 1953 | volume= 85 | issue= 2 | pages= 151-63 | pmid=13007166 | doi=10.1001/archpedi.1953.02050070160004 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13007166 }} </ref><ref name="pmid697326">{{cite journal| author=Ropper AH, Poskanzer DC| title=The prognosis of acute and subacute transverse myelopathy based on early signs and symptoms. | journal=Ann Neurol | year= 1978 | volume= 4 | issue= 1 | pages= 51-9 | pmid=697326 | doi=10.1002/ana.410040110 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=697326 }} </ref><ref name="pmid9766742">{{cite journal| author=Knebusch M, Strassburg HM, Reiners K| title=Acute transverse myelitis in childhood: nine cases and review of the literature. | journal=Dev Med Child Neurol | year= 1998 | volume= 40 | issue= 9 | pages= 631-9 | pmid=9766742 | doi=10.1111/j.1469-8749.1998.tb15430.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9766742 }} </ref><ref name="pmid14048158">{{cite journal| author=ALTROCCHI PH| title=ACUTE TRANSVERSE MYELOPATHY. | journal=Arch Neurol | year= 1963 | volume= 9 | issue= | pages= 111-9 | pmid=14048158 | doi=10.1001/archneur.1963.00460080021002 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14048158 }} </ref><ref name="pmid4598176">{{cite journal| author=Lerer RJ, Kalavsky SM| title=Central nervous system disease associated with Mycoplasma pneumoniae infection: report of five cases and review of the literature. | journal=Pediatrics | year= 1973 | volume= 52 | issue= 5 | pages= 658-68 | pmid=4598176 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4598176 }} </ref><ref name="pmid10987731">{{cite journal| author=Salgado CD, Weisse ME| title=Transverse myelitis associated with probable cat-scratch disease in a previously healthy pediatric patient. | journal=Clin Infect Dis | year= 2000 | volume= 31 | issue= 2 | pages= 609-11 | pmid=10987731 | doi=10.1086/313986 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10987731 }} </ref>
**[[Herpesviridae]]
**[[Enterovirus|Enteroviruses]]
**[[Influenza virus|Influenza viruses]]
**[[Adenoviridae|Adenoviruses]]
**[[Coxsackievirus|Coxsackieviruses]]
**[[Echovirus|Enteric cytopathogenic human orphan (ECHO) virus]]
**[[Hepatitis A virus]]
**[[Lymphocytic choriomeningitis virus|Lymphocytic choriomeningitis virus (LCMV)]]
**[[Mumps virus]]
**[[Measles virus]]
**[[Rubella virus]]
**[[Poliovirus]]
**[[Rubeola|Rubeola virus]]
**[[Dengue virus]]
**[[Russian Spring Summer encephalitis virus|Russian spring-summer encephalitis virus]]
**[[Varicella virus]]
**[[Mycoplasma pneumonia|Mycoplasma pneumonia bacteria]]
**[[Legionella pneumophila|Legionella pneumonia bacteria]]
**[[Pulmonary tuberculosis]]
**[[Borrelia]] ([[Lyme disease]])
**[[Listeria]]
**[[Bartonella]] ([[cat scratch disease]])
*Vaccination<ref name="pmid22379456">{{cite journal| author=Awad A, Stüve O| title=Idiopathic transverse myelitis and neuromyelitis optica: clinical profiles, pathophysiology and therapeutic choices. | journal=Curr Neuropharmacol | year= 2011 | volume= 9 | issue= 3 | pages= 417-28 | pmid=22379456 | doi=10.2174/157015911796557948 | pmc=3151596 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22379456 }} </ref><ref name="pmid19880568">{{cite journal| author=Agmon-Levin N, Kivity S, Szyper-Kravitz M, Shoenfeld Y| title=Transverse myelitis and vaccines: a multi-analysis. | journal=Lupus | year= 2009 | volume= 18 | issue= 13 | pages= 1198-204 | pmid=19880568 | doi=10.1177/0961203309345730 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19880568 }} </ref>
**About 30% of pediatric cases are preceded with immunizations within one month of disease onset
*[Condition

OR

*[Disease name] is caused by an infection with [pathogen name].
*[Pathogen name] is caused by [pathogen name].

===Less Common Causes===
Less common causes of [disease name] include:
*[Cause1]
*[Cause2]
*[Cause3]

===Genetic Causes===
*[Disease name] is caused by a mutation in the [gene name] gene.

===Causes by Organ System===

{|style="width:80%; height:100px" border="1"
|style="height:100px"; style="width:25%" border="1" bgcolor="LightSteelBlue" |'''Cardiovascular'''
|style="height:100px"; style="width:75%" border="1" bgcolor="Beige" | No underlying causes
|-
|bgcolor="LightSteelBlue"| '''Chemical/Poisoning'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Dental'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Dermatologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Drug Side Effect'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Ear Nose Throat'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Endocrine'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Environmental'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Gastroenterologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Genetic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Hematologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Iatrogenic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Infectious Disease'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Musculoskeletal/Orthopedic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Neurologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Nutritional/Metabolic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Obstetric/Gynecologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Oncologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Ophthalmologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Overdose/Toxicity'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Psychiatric'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Pulmonary'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Renal/Electrolyte'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Rheumatology/Immunology/Allergy'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Sexual'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Trauma'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Urologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Miscellaneous'''
|bgcolor="Beige"| No underlying causes
|-
|}

===Causes in Alphabetical Order===
List the causes of the disease in alphabetical order:
<div style="-moz-column-count:3; column-count:3;">
* Cause 1
* Cause 2
* Cause 3
* Cause 4
* Cause 5
* Cause 6
* Cause 7
* Cause 8
* Cause 9
* Cause 10
</div>

==References==
{{Reflist|2}}

{{WH}}
{{WS}}
[[Category: (name of the system)]]

Restless legs syndrome

2020-05-06T04:22:27Z

M Jahan:

__NOTOC__
{{Infobox_Disease |
Name = Restless legs syndrome |
Image = RLS-Schlafmuster.jpg |
Caption = Sleep pattern of a Restless Legs Syndrome patient (red) vs. a healthy sleep pattern (blue). |
}}
{{Restless legs syndrome}}

{{CMG}}; {{AE}} {{MMJ}}{{sali}}
==[[Restless legs syndrome overview|Overview]]==

==[[Restless legs syndrome historical perspective|Historical Perspective]]==

==[[Restless legs syndrome classification|Classification]]==

==[[Restless legs syndrome pathophysiology|Pathophysiology]]==

==[[Restless legs syndrome causes|Causes]]==

==[[Restless legs syndrome differential diagnosis|Differentiating Restless legs syndrome from other Diseases]]==

==[[Restless legs syndrome epidemiology and demographics|Epidemiology and Demographics]]==

==[[Restless legs syndrome risk factors|Risk Factors]]==

==[[Restless legs syndrome screening|Screening]]==

==[[Restless legs syndrome natural history, complications and prognosis|Natural History, Complications and Prognosis]]==

==Diagnosis==
[[Restless legs syndrome diagnostic criteria|Diagnostic Criteria]] | [[Restless legs syndrome history and symptoms|History and Symptoms]] | [[Restless legs syndrome physical examination|Physical Examination]] | [[Restless legs syndrome laboratory findings|Laboratory Findings]] | [[Restless legs syndrome electrocardiogram|Electrocardiogram]] | [[Restless legs syndrome other diagnostic studies|Other Diagnostic Studies]]

==Treatment==
[[Restless legs syndrome medical therapy|Medical Therapy]] | [[Restless legs syndrome surgery | Surgery]] | [[Restless legs syndrome primary prevention|Primary Prevention]] | [[Restless legs syndrome secondary prevention|Secondary Prevention]] | [[Restless legs syndrome cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Restless legs syndrome future or investigational therapies|Future or Investigational Therapies]]

==Case Studies==
[[Restless legs syndrome case study one|Case #1]]

==Related Chapters==
*[[Actigraphy]]
*[[Parasomnia]]
*[[Disease mongering]]

{{Diseases of the nervous system|state=collapsed}}

[[Category:Sleep disorders]]
[[Category:Syndromes]]
[[Category:Neurology]]
[[Category:Primary care]]

[[ca:Síndrome de les cames neguitoses]]
[[de:Restless-Legs-Syndrom]]
[[es:Síndrome de las piernas inquietas]]
[[fr:Syndrome des jambes sans repos]]
[[ms:Sindrom kaki resah]]
[[ja:むずむず脚症候群]]
[[pl:Zespół niespokojnych nóg]]
[[pt:Síndrome das pernas inquietas]]
[[fi:Levottomat jalat]]
[[sv:Rastlösa ben]]

{{WH}}
{{WS}}

Transverse myelitis historical perspective

2020-05-06T04:21:18Z

M Jahan:

__NOTOC__
{{Transverse myelitis}}

{{CMG}}; {{AE}} {{MMJ}}{{sali}}

==Overview==
Transverse myelitis was first discovered by Dr. Suchett-Kaye, an English neurologist at St. Charles Hospital in London, utilized the term “acute transverse myelitis” in 1948. Cases of “acute myelitis” have been described earlier as cases of “acute myelitis” that have been described in association with or after infection and [[smallpox]] vaccination.

==Historical Perspective==

===Discovery===

*Transverse myelitis was first discovered by Dr. Suchett-Kaye, an English neurologist at St. Charles Hospital in London, utilized the term “acute transverse myelitis” in 1948.<ref name="pmid28798719">{{cite journal| author=Hsam NBO, Angstwurm K, Peters S, Fuchs K, Schuierer G, Bogdahn U | display-authors=etal| title=Fulminant Acute Ascending Hemorrhagic Myelitis Treated with Eculizumab. | journal=Front Neurol | year= 2017 | volume= 8 | issue= | pages= 345 | pmid=28798719 | doi=10.3389/fneur.2017.00345 | pmc=5529383 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28798719 }} </ref>

*Cases of “acute myelitis” have been described earlier as cases of “acute myelitis” that have been described in association with or after infection and [[smallpox]] vaccination.<ref name="pmid15956176">{{cite journal| author=Krishnan C, Kerr DA| title=Idiopathic transverse myelitis. | journal=Arch Neurol | year= 2005 | volume= 62 | issue= 6 | pages= 1011-3 | pmid=15956176 | doi=10.1001/archneur.62.6.1011 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15956176 }} </ref>

==References==
{{Reflist|2}}

{{WH}}
{{WS}}

Transverse myelitis pathophysiology

2020-05-06T04:19:47Z

M Jahan:

__NOTOC__
{{Transverse myelitis}}

{{CMG}}; {{AE}} {{MMJ}}{{sali}}
==Overview==

* In the pathogenesis of transverse myelitis, a variety of immunological mechanisms may cause pathological substrate and dysfunction of [[Neural|neural cells]] within the [[spinal cord]].

* Transverse myelitis is the result of progressive [[demyelination]] and [[axonal]] loss in addition to [[Grey matter|gray matter]] involvement, [[necrosis]] and [[cavitation]].
* It is understood that [[infections]] may cause transverse myelitis by:
** Direct tissue damage
** Immune-mediated infection-triggered tissue damage
* [[Multiple sclerosis]] is the other cause to the transverse myelitis and it sometimes transverse myelitis can appear as the first symptom of [[Multiple sclerosis]].
* Acute partial transverse myelitis may be predictive of a subsequent diagnosis of [[multiple sclerosis]] in children.
* Invariable histopathological findings of transverse myelitis include:
** Perivascular spread of [[Monocyte|monocytes]]
** Focal areas of [[Lymphocyte|lymphocytes]] infiltrating
** [[Astroglia|Astroglial]] and [[Microglia|microglial]] activation

* Other histopathological findings of transverse myelitis include:
** Infiltration of [[CD4+ T cells|CD4+]] and [[CD8+ T cells|CD8+ T-lymphocytes]]
** Typically preservation of the subpial parenchyma suggesting ischemia as the ultimate cause of the cord lesions in transverse myelitis

Conditions that may cause transverse myelitis include:

* Various infectionsin 30% to 60% of the cases:
** [[Herpesviridae]]
** [[Enterovirus|Enteroviruses]]
** [[Influenza virus|Influenza viruses]]
** [[Adenoviridae|Adenoviruses]]
** [[Coxsackievirus|Coxsackieviruses]]
** [[Echovirus|Enteric cytopathogenic human orphan (ECHO) virus]]
** [[Hepatitis A virus]]
** [[Lymphocytic choriomeningitis virus|Lymphocytic choriomeningitis virus (LCMV)]]
** [[Mumps virus]]
** [[Measles virus]]
** [[Rubella virus]]
** [[Poliovirus]]
** [[Rubeola|Rubeola virus]]
** [[Dengue virus]]
** [[Russian Spring Summer encephalitis virus|Russian spring-summer encephalitis virus]]
** [[Varicella virus]]
** [[Mycoplasma pneumonia|Mycoplasma pneumonia bacteria]]
** [[Legionella pneumophila|Legionella pneumonia bacteria]]
** [[Pulmonary tuberculosis]]
** [[Borrelia]] ([[Lyme disease]])
** [[Listeria]]
** [[Bartonella]] ([[cat scratch disease]])
* Vaccination
** About 30% of pediatric cases are preceded with [[immunization]]<nowiki/>s within one month of disease onset

[[Infections]] can cause transverse myelitis through two main mechanisms:

# Direct tissue damage
# Immune-mediated infection-triggered tissue damage which may be due to: [[Molecular mimicry]] or [[Superantigen|superantigen effect]]

* This immune response may be caused either by [[Cell-mediated immunity|T-cell mediated immune response]] or by [[Humoral immunity|antibody-mediated immune response]].

A non-microbial related immune dysfunction by the presence of autoantibodies has been also proposed in the immunopathogenesis of transverse myelitis.

In the spinal fluid of patients with transverse myelitis, [[Interleukin 6|Interleukin 6 (IL-6)]] levels were also markedly elevated.

 

==Pathophysiology==
===Physiology ===

* The lesions in acute transverse myelitis are invariably limited to the [[spinal cord]].<ref name="pmid22379456" /><ref name="pmid29696041">{{cite journal| author=Tavasoli A, Tabrizi A| title=Acute Transverse Myelitis in Children, Literature Review. | journal=Iran J Child Neurol | year= 2018 | volume= 12 | issue= 2 | pages= 7-16 | pmid=29696041 | doi= | pmc=5904733 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29696041 }} </ref>
* There is no involvement of other structures in the [[central nervous system]].<ref name="pmid22379456" />
*The [[spinal cord]] involvement in patients with transverse myelitis is usually central, uniform and symmetric but in patients with [[multiple sclerosis]] it typically affects the [[spinal cord]] in a patchy way and the lesions are usually peripheral.
*
*
*
*
*
*
*
*
*
*
*
*
*
*

===Pathogenesis===

* In the pathogenesis of transverse myelitis, a variety of immunological mechanisms may cause pathological substrate and dysfunction of [[Neural|neural cells]] within the [[spinal cord]].<ref name="pmid12045735">{{cite journal| author=Kerr DA, Ayetey H| title=Immunopathogenesis of acute transverse myelitis. | journal=Curr Opin Neurol | year= 2002 | volume= 15 | issue= 3 | pages= 339-47 | pmid=12045735 | doi=10.1097/00019052-200206000-00019 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12045735 }} </ref>

*Transverse myelitis is the result of progressive [[demyelination]] and [[axonal]] loss in addition to [[Grey matter|gray matter]] involvement, [[necrosis]] and [[cavitation]].<ref name="pmid22379456">{{cite journal| author=Awad A, Stüve O| title=Idiopathic transverse myelitis and neuromyelitis optica: clinical profiles, pathophysiology and therapeutic choices. | journal=Curr Neuropharmacol | year= 2011 | volume= 9 | issue= 3 | pages= 417-28 | pmid=22379456 | doi=10.2174/157015911796557948 | pmc=3151596 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22379456 }} </ref>
*It is understood that [[infections]] may cause transverse myelitis by: <ref name="pmid22379456">{{cite journal| author=Awad A, Stüve O| title=Idiopathic transverse myelitis and neuromyelitis optica: clinical profiles, pathophysiology and therapeutic choices. | journal=Curr Neuropharmacol | year= 2011 | volume= 9 | issue= 3 | pages= 417-28 | pmid=22379456 | doi=10.2174/157015911796557948 | pmc=3151596 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22379456 }} </ref>
**Direct tissue damage
**Immune-mediated infection-triggered tissue damage
*[[Multiple sclerosis]] is the other cause to the transverse myelitis and it sometimes transverse myelitis can appear as the first symptom of [[Multiple sclerosis]].<ref name="pmid22379456">{{cite journal| author=Awad A, Stüve O| title=Idiopathic transverse myelitis and neuromyelitis optica: clinical profiles, pathophysiology and therapeutic choices. | journal=Curr Neuropharmacol | year= 2011 | volume= 9 | issue= 3 | pages= 417-28 | pmid=22379456 | doi=10.2174/157015911796557948 | pmc=3151596 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22379456 }} </ref>
*Acute partial transverse myelitis may be predictive of a subsequent diagnosis of [[multiple sclerosis]] in children.<ref name="pmid24619933">{{cite journal| author=Meyer P, Leboucq N, Molinari N, Roubertie A, Carneiro M, Walther-Louvier U | display-authors=etal| title=Partial acute transverse myelitis is a predictor of multiple sclerosis in children. | journal=Mult Scler | year= 2014 | volume= 20 | issue= 11 | pages= 1485-93 | pmid=24619933 | doi=10.1177/1352458514526943 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24619933 }} </ref>
*Invariable histopathological findings of transverse myelitis include:<ref name="pmid22379456" />
**Perivascular spread of [[Monocyte|monocytes]]
**Focal areas of [[Lymphocyte|lymphocytes]] infiltrating
**[[Astroglia|Astroglial]] and [[Microglia|microglial]] activation

* Other histopathological findings of transverse myelitis include:<ref name="pmid22379456" /><ref name="pmid24503658">{{cite journal| author=Moulignier A, Lescure FX, Savatovsky J, Campa P| title=CD8 transverse myelitis in a patient with HIV-1 infection. | journal=BMJ Case Rep | year= 2014 | volume= 2014 | issue= | pages= | pmid=24503658 | doi=10.1136/bcr-2013-201073 | pmc=3918629 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24503658 }} </ref>
** Infiltration of [[CD4+ T cells|CD4+]] and [[CD8+ T cells|CD8+ T-lymphocytes]]
** Typically preservation of the subpial parenchyma suggesting ischemia as the ultimate cause of the cord lesions in transverse myelitis

Conditions that may cause transverse myelitis include:

*Various infectionsin 30% to 60% of the cases:<ref name="pmid22379456">{{cite journal| author=Awad A, Stüve O| title=Idiopathic transverse myelitis and neuromyelitis optica: clinical profiles, pathophysiology and therapeutic choices. | journal=Curr Neuropharmacol | year= 2011 | volume= 9 | issue= 3 | pages= 417-28 | pmid=22379456 | doi=10.2174/157015911796557948 | pmc=3151596 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22379456 }} </ref><ref name="pmid8489410">{{cite journal| author=Jeffery DR, Mandler RN, Davis LE| title=Transverse myelitis. Retrospective analysis of 33 cases, with differentiation of cases associated with multiple sclerosis and parainfectious events. | journal=Arch Neurol | year= 1993 | volume= 50 | issue= 5 | pages= 532-5 | pmid=8489410 | doi=10.1001/archneur.1993.00540050074019 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8489410 }} </ref><ref name="pmid2375246">{{cite journal| author=Christensen PB, Wermuth L, Hinge HH, Bømers K| title=Clinical course and long-term prognosis of acute transverse myelopathy. | journal=Acta Neurol Scand | year= 1990 | volume= 81 | issue= 5 | pages= 431-5 | pmid=2375246 | doi=10.1111/j.1600-0404.1990.tb00990.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2375246 }} </ref><ref name="pmid14977560">{{cite journal| author=Krishnan C, Kaplin AI, Deshpande DM, Pardo CA, Kerr DA| title=Transverse Myelitis: pathogenesis, diagnosis and treatment. | journal=Front Biosci | year= 2004 | volume= 9 | issue= | pages= 1483-99 | pmid=14977560 | doi=10.2741/1351 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14977560 }} </ref><ref name="pmid13007166">{{cite journal| author=PAINE RS, BYERS RK| title=Transverse myelopathy in childhood. | journal=AMA Am J Dis Child | year= 1953 | volume= 85 | issue= 2 | pages= 151-63 | pmid=13007166 | doi=10.1001/archpedi.1953.02050070160004 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13007166 }} </ref><ref name="pmid697326">{{cite journal| author=Ropper AH, Poskanzer DC| title=The prognosis of acute and subacute transverse myelopathy based on early signs and symptoms. | journal=Ann Neurol | year= 1978 | volume= 4 | issue= 1 | pages= 51-9 | pmid=697326 | doi=10.1002/ana.410040110 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=697326 }} </ref><ref name="pmid9766742">{{cite journal| author=Knebusch M, Strassburg HM, Reiners K| title=Acute transverse myelitis in childhood: nine cases and review of the literature. | journal=Dev Med Child Neurol | year= 1998 | volume= 40 | issue= 9 | pages= 631-9 | pmid=9766742 | doi=10.1111/j.1469-8749.1998.tb15430.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9766742 }} </ref><ref name="pmid14048158">{{cite journal| author=ALTROCCHI PH| title=ACUTE TRANSVERSE MYELOPATHY. | journal=Arch Neurol | year= 1963 | volume= 9 | issue= | pages= 111-9 | pmid=14048158 | doi=10.1001/archneur.1963.00460080021002 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14048158 }} </ref><ref name="pmid4598176">{{cite journal| author=Lerer RJ, Kalavsky SM| title=Central nervous system disease associated with Mycoplasma pneumoniae infection: report of five cases and review of the literature. | journal=Pediatrics | year= 1973 | volume= 52 | issue= 5 | pages= 658-68 | pmid=4598176 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4598176 }} </ref><ref name="pmid10987731">{{cite journal| author=Salgado CD, Weisse ME| title=Transverse myelitis associated with probable cat-scratch disease in a previously healthy pediatric patient. | journal=Clin Infect Dis | year= 2000 | volume= 31 | issue= 2 | pages= 609-11 | pmid=10987731 | doi=10.1086/313986 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10987731 }} </ref>
**[[Herpesviridae]]
**[[Enterovirus|Enteroviruses]]
**[[Influenza virus|Influenza viruses]]
**[[Adenoviridae|Adenoviruses]]
**[[Coxsackievirus|Coxsackieviruses]]
**[[Echovirus|Enteric cytopathogenic human orphan (ECHO) virus]]
**[[Hepatitis A virus]]
**[[Lymphocytic choriomeningitis virus|Lymphocytic choriomeningitis virus (LCMV)]]
**[[Mumps virus]]
**[[Measles virus]]
**[[Rubella virus]]
**[[Poliovirus]]
**[[Rubeola|Rubeola virus]]
**[[Dengue virus]]
**[[Russian Spring Summer encephalitis virus|Russian spring-summer encephalitis virus]]
**[[Varicella virus]]
**[[Mycoplasma pneumonia|Mycoplasma pneumonia bacteria]]
**[[Legionella pneumophila|Legionella pneumonia bacteria]]
**[[Pulmonary tuberculosis]]
**[[Borrelia]] ([[Lyme disease]])
**[[Listeria]]
**[[Bartonella]] ([[cat scratch disease]])
*Vaccination<ref name="pmid22379456">{{cite journal| author=Awad A, Stüve O| title=Idiopathic transverse myelitis and neuromyelitis optica: clinical profiles, pathophysiology and therapeutic choices. | journal=Curr Neuropharmacol | year= 2011 | volume= 9 | issue= 3 | pages= 417-28 | pmid=22379456 | doi=10.2174/157015911796557948 | pmc=3151596 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22379456 }} </ref><ref name="pmid19880568">{{cite journal| author=Agmon-Levin N, Kivity S, Szyper-Kravitz M, Shoenfeld Y| title=Transverse myelitis and vaccines: a multi-analysis. | journal=Lupus | year= 2009 | volume= 18 | issue= 13 | pages= 1198-204 | pmid=19880568 | doi=10.1177/0961203309345730 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19880568 }} </ref>
**About 30% of pediatric cases are preceded with [[immunization]]<nowiki/>s within one month of disease onset

[[Infections]] can cause transverse myelitis through two main mechanisms:<ref name="pmid22379456">{{cite journal| author=Awad A, Stüve O| title=Idiopathic transverse myelitis and neuromyelitis optica: clinical profiles, pathophysiology and therapeutic choices. | journal=Curr Neuropharmacol | year= 2011 | volume= 9 | issue= 3 | pages= 417-28 | pmid=22379456 | doi=10.2174/157015911796557948 | pmc=3151596 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22379456 }} </ref><ref name="pmid10987731">{{cite journal| author=Salgado CD, Weisse ME| title=Transverse myelitis associated with probable cat-scratch disease in a previously healthy pediatric patient. | journal=Clin Infect Dis | year= 2000 | volume= 31 | issue= 2 | pages= 609-11 | pmid=10987731 | doi=10.1086/313986 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10987731 }} </ref><ref name="pmid10378139">{{cite journal| author=Giobbia M, Carniato A, Scotton PG, Marchiori GC, Vaglia A| title=Cytomegalovirus-associated transverse myelitis in a non-immunocompromised patient. | journal=Infection | year= 1999 | volume= 27 | issue= 3 | pages= 228-30 | pmid=10378139 | doi=10.1007/bf02561538 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10378139 }} </ref>

# Direct tissue damage
# Immune-mediated infection-triggered tissue damage which may be due to: [[Molecular mimicry]] or [[Superantigen|superantigen effect]]

*This immune response may be caused either by [[Cell-mediated immunity|T-cell mediated immune response]] or by [[Humoral immunity|antibody-mediated immune response]].

A non-microbial related immune dysfunction by the presence of autoantibodies has been also proposed in the immunopathogenesis of transverse myelitis.<ref name="pmid22379456" /><ref name="pmid2027486">{{cite journal| author=Tippett DS, Fishman PS, Panitch HS| title=Relapsing transverse myelitis. | journal=Neurology | year= 1991 | volume= 41 | issue= 5 | pages= 703-6 | pmid=2027486 | doi=10.1212/wnl.41.5.703 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2027486 }} </ref><ref name="pmid8609515">{{cite journal| author=Pandit L, Rao S| title=Recurrent myelitis. | journal=J Neurol Neurosurg Psychiatry | year= 1996 | volume= 60 | issue= 3 | pages= 336-8 | pmid=8609515 | doi=10.1136/jnnp.60.3.336 | pmc=1073861 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8609515 }} </ref><ref name="pmid11064439">{{cite journal| author=Bashir K, Whitaker JN| title=Importance of paraclinical and CSF studies in the diagnosis of MS in patients presenting with partial cervical transverse myelopathy and negative cranial MRI. | journal=Mult Scler | year= 2000 | volume= 6 | issue= 5 | pages= 312-6 | pmid=11064439 | doi=10.1177/135245850000600503 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11064439 }} </ref>

In the spinal fluid of patients with transverse myelitis, [[Interleukin 6|Interleukin 6 (IL-6)]] levels were also markedly elevated.<ref name="pmid22379456" /><ref name="pmid14977560">{{cite journal| author=Krishnan C, Kaplin AI, Deshpande DM, Pardo CA, Kerr DA| title=Transverse Myelitis: pathogenesis, diagnosis and treatment. | journal=Front Biosci | year= 2004 | volume= 9 | issue= | pages= 1483-99 | pmid=14977560 | doi=10.2741/1351 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14977560 }} </ref><ref name="pmid16184194">{{cite journal| author=Kaplin AI, Deshpande DM, Scott E, Krishnan C, Carmen JS, Shats I | display-authors=etal| title=IL-6 induces regionally selective spinal cord injury in patients with the neuroinflammatory disorder transverse myelitis. | journal=J Clin Invest | year= 2005 | volume= 115 | issue= 10 | pages= 2731-41 | pmid=16184194 | doi=10.1172/JCI25141 | pmc=1224298 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16184194 }} </ref>
==Associated Conditions==
Conditions associated with transverse myelitis include:<ref name="pmid21621005">{{cite journal| author=Borchers AT, Gershwin ME| title=Transverse myelitis. | journal=Autoimmun Rev | year= 2012 | volume= 11 | issue= 3 | pages= 231-48 | pmid=21621005 | doi=10.1016/j.autrev.2011.05.018 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21621005 }} </ref><ref name="pmid19662820">{{cite journal| author=Tristano AG| title=[Autoimmune diseases associated with transverse myelitis. Review]. | journal=Invest Clin | year= 2009 | volume= 50 | issue= 2 | pages= 251-70 | pmid=19662820 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19662820 }} </ref><ref name="pmid22379456">{{cite journal| author=Awad A, Stüve O| title=Idiopathic transverse myelitis and neuromyelitis optica: clinical profiles, pathophysiology and therapeutic choices. | journal=Curr Neuropharmacol | year= 2011 | volume= 9 | issue= 3 | pages= 417-28 | pmid=22379456 | doi=10.2174/157015911796557948 | pmc=3151596 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22379456 }} </ref><ref name="pmid12045735">{{cite journal| author=Kerr DA, Ayetey H| title=Immunopathogenesis of acute transverse myelitis. | journal=Curr Opin Neurol | year= 2002 | volume= 15 | issue= 3 | pages= 339-47 | pmid=12045735 | doi=10.1097/00019052-200206000-00019 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12045735 }} </ref><ref name="pmid24090445">{{cite journal| author=Cobo Calvo A, Mañé Martínez MA, Alentorn-Palau A, Bruna Escuer J, Romero Pinel L, Martínez-Yélamos S| title=Idiopathic acute transverse myelitis: outcome and conversion to multiple sclerosis in a large series. | journal=BMC Neurol | year= 2013 | volume= 13 | issue= | pages= 135 | pmid=24090445 | doi=10.1186/1471-2377-13-135 | pmc=3856522 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24090445 }} </ref>

*Various infections
*Systemic autoimmune diseases like:
**[[Lupus erythematosus]]
**[[Sjögren's syndrome]]
**[[Sarcoidosis]]
**[[Optic neuritis]]
**[[multiple sclerosis]]

==Microscopic Pathology==
Findings on microscopic histopathological analysis of transverse myelitis include:<ref name="pmid16635433">{{cite journal| author=Krishnan C, Kaplin AI, Pardo CA, Kerr DA, Keswani SC| title=Demyelinating disorders: update on transverse myelitis. | journal=Curr Neurol Neurosci Rep | year= 2006 | volume= 6 | issue= 3 | pages= 236-43 | pmid=16635433 | doi=10.1007/s11910-006-0011-1 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16635433 }} </ref><ref name="pmid1763730">{{cite journal| author=Mirich DR, Kucharczyk W, Keller MA, Deck J| title=Subacute necrotizing myelopathy: MR imaging in four pathologically proved cases. | journal=AJNR Am J Neuroradiol | year= 1991 | volume= 12 | issue= 6 | pages= 1077-83 | pmid=1763730 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1763730 }} </ref>

* [[Perivascular cell|Perivascular]] [[Lymphocytic|lymphocytic infiltrates]]
* [[Axonal|Axonal injury]]
* [[Necrosis]] and [[demyelination]]

==References==
{{Reflist|2}}

{{WH}}
{{WS}}
[[Category: (name of the system)]]

Transverse myelitis

2020-05-06T04:18:40Z

M Jahan:

__NOTOC__
{{Transverse myelitis}}
'''For patient information, click [[Transverse myelitis (patient information)|here]]'''

{{CMG}}; {{AE}}{{MMJ}}{{sali}}

{{SK}}

==[[Transverse myelitis overview|Overview]]==

==[[Transverse myelitis historical perspective|Historical Perspective]]==

==[[Transverse myelitis classification|Classification]]==

==[[Transverse myelitis pathophysiology|Pathophysiology]]==

==[[Transverse myelitis causes|Causes]]==

==[[Transverse myelitis differential diagnosis|Differentiating Transverse myelitis from other Diseases]]==

==[[Transverse myelitis epidemiology and demographics|Epidemiology and Demographics]]==

==[[Transverse myelitis risk factors|Risk Factors]]==

==[[Transverse myelitis screening|Screening]]==

==[[Transverse myelitis natural history, complications and prognosis|Natural History, Complications and Prognosis]]==

==Diagnosis==
[[Transverse myelitis diagnostic study of choice|Diagnostic study of choice]] | [[Transverse myelitis history and symptoms|History and Symptoms]] | [[Transverse myelitis physical examination|Physical Examination]] | [[Transverse myelitis laboratory findings|Laboratory Findings]] | [[Transverse myelitis electrocardiogram|Electrocardiogram]] | [[Transverse myelitis x ray|X-Ray Findings]] | [[Transverse myelitis echocardiography and ultrasound|Echocardiography and Ultrasound]] | [[Transverse myelitis CT scan|CT-Scan Findings]] | [[Transverse myelitis MRI|MRI Findings]] | [[Transverse myelitis other imaging findings|Other Imaging Findings]] | [[Transverse myelitis other diagnostic studies|Other Diagnostic Studies]]

==Treatment==
[[Transverse myelitis medical therapy|Medical Therapy]] | [[Transverse myelitis interventions|Interventions]] | [[Transverse myelitis surgery|Surgery]] | [[Transverse myelitis primary prevention|Primary Prevention]] | [[Transverse myelitis secondary prevention|Secondary Prevention]] | [[Transverse myelitis cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Transverse myelitis future or investigational therapies|Future or Investigational Therapies]]

==Case Studies==
[[Transverse myelitis case study one|Case #1]]

[[Category: (name of the system)]]

Sandbox:Vthonda

2020-05-05T18:52:12Z

M Jahan: Created blank page

Template:Vthonda

2020-05-05T18:32:15Z

M Jahan: Created page with "Vishwanath Thondamala, MBBS[mailto:visu.medico@gmail.com]"

[[User:Vthondamala|Vishwanath Thondamala, MBBS]][mailto:visu.medico@gmail.com]

Transverse myelitis differential diagnosis

2020-04-28T14:18:09Z

M Jahan:

__NOTOC__
[[Image:Home_logo1.png|right|250px|link=https://www.wikidoc.org/index.php/Transverse_myelitis]]
{{CMG}}; {{AE}}{{TarekNafee}} {{MMJ}}
==Overview==
Transverse myelitis must be differentiated from other diseases that cause [[hypotonia]], [[muscle weakness]], or [[paralysis]] such as: Adult [[botulism]], infant [[botulism]], [[Guillian-Barre syndrome]], [[Eaton lambert syndrome|Eaton Lambert syndrome]], [[myasthenia gravis]], [[electrolyte disturbance]], [[Organophosphate poisoning|organophosphate toxicity]], [[tick paralysis]], [[stroke]][[tetrodotoxin]] poisoning, [[poliomyelitis]], [[Neurosyphilis (patient information)|neurosyphilis,]] [[muscular dystrophy]][[Muscular dystrophy|,]] [[multiple sclerosis]] exacerbation, [[amyotrophic lateral sclerosis]] and [[Myositis|inflammatory myopathy]].

==Differential Diagnosis==
Transverse myelitis must be differentiated from other diseases that may cause [[hypotonia]], [[muscle weakness]], or [[paralysis]]:<ref name="pmid29433111">{{cite journal |vauthors=Kira R |title=[Acute Flaccid Myelitis] |language=Japanese |journal=Brain Nerve |volume=70 |issue=2 |pages=99–112 |date=February 2018 |pmid=29433111 |doi=10.11477/mf.1416200962 |url=}}</ref><ref name="pmid29433111">{{cite journal |vauthors=Kira R |title=[Acute Flaccid Myelitis] |language=Japanese |journal=Brain Nerve |volume=70 |issue=2 |pages=99–112 |date=February 2018 |pmid=29433111 |doi=10.11477/mf.1416200962 |url=}}</ref><ref name="pmid29181601">{{cite journal |vauthors=Hopkins SE |title=Acute Flaccid Myelitis: Etiologic Challenges, Diagnostic and Management Considerations |journal=Curr Treat Options Neurol |volume=19 |issue=12 |pages=48 |date=November 2017 |pmid=29181601 |doi=10.1007/s11940-017-0480-3 |url=}}</ref><ref name="pmid27422805">{{cite journal |vauthors=Messacar K, Schreiner TL, Van Haren K, Yang M, Glaser CA, Tyler KL, Dominguez SR |title=Acute flaccid myelitis: A clinical review of US cases 2012-2015 |journal=Ann. Neurol. |volume=80 |issue=3 |pages=326–38 |date=September 2016 |pmid=27422805 |pmc=5098271 |doi=10.1002/ana.24730 |url=}}</ref><ref name="pmid29028962">{{cite journal |vauthors=Chong PF, Kira R, Mori H, Okumura A, Torisu H, Yasumoto S, Shimizu H, Fujimoto T, Hanaoka N, Kusunoki S, Takahashi T, Oishi K, Tanaka-Taya K |title=Clinical Features of Acute Flaccid Myelitis Temporally Associated With an Enterovirus D68 Outbreak: Results of a Nationwide Survey of Acute Flaccid Paralysis in Japan, August-December 2015 |journal=Clin. Infect. Dis. |volume=66 |issue=5 |pages=653–664 |date=February 2018 |pmid=29028962 |pmc=5850449 |doi=10.1093/cid/cix860 |url=}}</ref><ref name="pmid29482893">{{cite journal |vauthors=Messacar K, Asturias EJ, Hixon AM, Van Leer-Buter C, Niesters HGM, Tyler KL, Abzug MJ, Dominguez SR |title=Enterovirus D68 and acute flaccid myelitis-evaluating the evidence for causality |journal=Lancet Infect Dis |volume=18 |issue=8 |pages=e239–e247 |date=August 2018 |pmid=29482893 |doi=10.1016/S1473-3099(18)30094-X |url=}}</ref><ref name="pmid30200066">{{cite journal |vauthors=Chen IJ, Hu SC, Hung KL, Lo CW |title=Acute flaccid myelitis associated with enterovirus D68 infection: A case report |journal=Medicine (Baltimore) |volume=97 |issue=36 |pages=e11831 |date=September 2018 |pmid=30200066 |pmc=6133480 |doi=10.1097/MD.0000000000011831 |url=}}</ref><ref name="urlBotulism | Botulism | CDC">{{cite web |url=https://www.cdc.gov/botulism/index.html |title=Botulism | Botulism | CDC |format= |work= |accessdate=}}</ref><ref name="pmid3290234">{{cite journal |vauthors=McCroskey LM, Hatheway CL |title=Laboratory findings in four cases of adult botulism suggest colonization of the intestinal tract |journal=J. Clin. Microbiol. |volume=26 |issue=5 |pages=1052–4 |date=May 1988 |pmid=3290234 |pmc=266519 |doi= |url=}}</ref><ref name="pmid16614251">{{cite journal |vauthors=Lindström M, Korkeala H |title=Laboratory diagnostics of botulism |journal=Clin. Microbiol. Rev. |volume=19 |issue=2 |pages=298–314 |date=April 2006 |pmid=16614251 |pmc=1471988 |doi=10.1128/CMR.19.2.298-314.2006 |url=}}</ref><ref name="pmid17224901">{{cite journal |vauthors=Brook I |title=Botulism: the challenge of diagnosis and treatment |journal=Rev Neurol Dis |volume=3 |issue=4 |pages=182–9 |date=2006 |pmid=17224901 |doi= |url=}}</ref><ref name="pmid23642721">{{cite journal |vauthors=Dimachkie MM, Barohn RJ |title=Guillain-Barré syndrome and variants |journal=Neurol Clin |volume=31 |issue=2 |pages=491–510 |date=May 2013 |pmid=23642721 |pmc=3939842 |doi=10.1016/j.ncl.2013.01.005 |url=}}</ref><ref name="pmid23418763">{{cite journal |vauthors=Walling AD, Dickson G |title=Guillain-Barré syndrome |journal=Am Fam Physician |volume=87 |issue=3 |pages=191–7 |date=February 2013 |pmid=23418763 |doi= |url=}}</ref><ref name="pmid21969911">{{cite journal |vauthors=Gilhus NE |title=Lambert-eaton myasthenic syndrome; pathogenesis, diagnosis, and therapy |journal=Autoimmune Dis |volume=2011 |issue= |pages=973808 |date=2011 |pmid=21969911 |pmc=3182560 |doi=10.4061/2011/973808 |url=}}</ref><ref name="pmid14977560">{{cite journal |vauthors=Krishnan C, Kaplin AI, Deshpande DM, Pardo CA, Kerr DA |title=Transverse Myelitis: pathogenesis, diagnosis and treatment |journal=Front. Biosci. |volume=9 |issue= |pages=1483–99 |date=May 2004 |pmid=14977560 |doi= |url=}}</ref><ref name="pmid24305450">{{cite journal |vauthors=Amato AA, Greenberg SA |title=Inflammatory myopathies |journal=Continuum (Minneap Minn) |volume=19 |issue=6 Muscle Disease |pages=1615–33 |date=December 2013 |pmid=24305450 |doi=10.1212/01.CON.0000440662.26427.bd |url=}}</ref><ref name="pmid24365430">{{cite journal |vauthors=Berger JR, Dean D |title=Neurosyphilis |journal=Handb Clin Neurol |volume=121 |issue= |pages=1461–72 |date=2014 |pmid=24365430 |doi=10.1016/B978-0-7020-4088-7.00098-5 |url=}}</ref>
{|
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
! rowspan="2" |Diseases
! colspan="8" |History and Physical
! colspan="2" |Diagnostic tests
! rowspan="2" |Other Findings
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
!Motor Deficit
!Sensory deficit
!Cranial nerve Involvement
!Autonomic dysfunction
!Proximal/Distal/Generalized
!Ascending/Descending/Systemic
!Unilateral (UL)
or Bilateral (BL)

or

No Lateralization (NL)
!Onset
!Lab or Imaging Findings
!Specific test
|-
| style="background: #DCDCDC; padding: 5px; text-align:center;" |Transverse myelitis
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>+</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Proximal > Distal
| style="background: #F5F5F5; padding: 5px; text-align:center" |Systemic
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL or UL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Sudden
| style="background: #F5F5F5; padding: 5px; text-align:center" |MRI & [[Lumbar puncture]]
| style="background: #F5F5F5; padding: 5px; text-align:center" |MRI
| style="background: #F5F5F5; padding: 5px; text-align:center" |History of chronic viral or autoimmune disease (e.g. [[HIV]])
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Botulism|Adult Botulism]]
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>+</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Generalized
| style="background: #F5F5F5; padding: 5px; text-align:center" |Descending
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Sudden
| style="background: #F5F5F5; padding: 5px; text-align:center" |Toxin test
| style="background: #F5F5F5; padding: 5px; text-align:center" |Blood, Wound, or Stool culture
| style="background: #F5F5F5; padding: 5px; text-align:center" |[[Diplopia]], [[Hyporeflexia|Hyporeflexia,]] [[Hypotonia]], possible respiratory paralysis
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |Infant [[Botulism]]
| style="background: #F5F5F5; padding: 5px; text-align:center" |+
| style="background: #F5F5F5; padding: 5px; text-align:center" |-
| style="background: #F5F5F5; padding: 5px; text-align:center" |+
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>+</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Generalized
| style="background: #F5F5F5; padding: 5px; text-align:center" |Descending
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Sudden
| style="background: #F5F5F5; padding: 5px; text-align:center" |Toxin test
| style="background: #F5F5F5; padding: 5px; text-align:center" |Blood, Wound, or Stool culture
| style="background: #F5F5F5; padding: 5px; text-align:center" |[[Flaccid paralysis]] ([[Floppy baby syndrome]]), possible respiratory paralysis
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" | [[Guillian-Barre syndrome]]<ref name="pmid22081202">{{cite journal| author=Talukder RK, Sutradhar SR, Rahman KM, Uddin MJ, Akhter H| title=Guillian-Barre syndrome. | journal=Mymensingh Med J | year= 2011 | volume= 20 | issue= 4 | pages= 748-56 | pmid=22081202 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22081202 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>-</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Generalized
| style="background: #F5F5F5; padding: 5px; text-align:center" |Ascending
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Insidious
| style="background: #F5F5F5; padding: 5px; text-align:center" |CSF: ↑Protein

↓Cells

| style="background: #F5F5F5; padding: 5px; text-align:center" |Clinical & Lumbar Puncture
| style="background: #F5F5F5; padding: 5px; text-align:center" |Progressive [[ascending paralysis]] following infection, possible respiratory paralysis
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" | [[Eaton lambert syndrome|Eaton Lambert syndrome]]<ref name="pmid27412406">{{cite journal| author=Merino-Ramírez MÁ, Bolton CF| title=Review of the Diagnostic Challenges of Lambert-Eaton Syndrome Revealed Through Three Case Reports. | journal=Can J Neurol Sci | year= 2016 | volume= 43 | issue= 5 | pages= 635-47 | pmid=27412406 | doi=10.1017/cjn.2016.268 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27412406 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>+</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Generalized
| style="background: #F5F5F5; padding: 5px; text-align:center" |Systemic
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Intermittent
| style="background: #F5F5F5; padding: 5px; text-align:center" | [[EMG]], repetitive nerve stimulation test (RNS)
| style="background: #F5F5F5; padding: 5px; text-align:center" |[[Voltage gated calcium channel|Voltage gated calcium channe]]<nowiki/>l<nowiki/> (VGCC) antibody
| style="background: #F5F5F5; padding: 5px; text-align:center" |[[Diplopia]], [[ptosis]], improves with movement (as the day progresses)
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Myasthenia gravis]]<ref name="pmid28029925">{{cite journal| author=Gilhus NE| title=Myasthenia Gravis. | journal=N Engl J Med | year= 2016 | volume= 375 | issue= 26 | pages= 2570-2581 | pmid=28029925 | doi=10.1056/NEJMra1602678 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28029925 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>+</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Generalized
| style="background: #F5F5F5; padding: 5px; text-align:center" |Systemic
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Intermittent
| style="background: #F5F5F5; padding: 5px; text-align:center" | [[Electromyography|EMG]], [[Edrophonium|Edrophonium test]]
| style="background: #F5F5F5; padding: 5px; text-align:center" |[[Acetylcholine receptor|Ach receptor]] antibody
| style="background: #F5F5F5; padding: 5px; text-align:center" |[[Diplopia]], [[ptosis]], worsening with movement (as the day progresses)
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Electrolyte disturbance]]<ref name="pmid26813501">{{cite journal| author=Ozono K| title=[Diagnostic criteria for vitamin D-deficient rickets and hypocalcemia-]. | journal=Clin Calcium | year= 2016 | volume= 26 | issue= 2 | pages= 215-22 | pmid=26813501 | doi=CliCa1602215222 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26813501 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>-</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Generalized
| style="background: #F5F5F5; padding: 5px; text-align:center" |Systemic
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Insidious
| style="background: #F5F5F5; padding: 5px; text-align:center" | Electrolyte panel
| style="background: #F5F5F5; padding: 5px; text-align:center" |↓Ca++, ↓Mg++, ↓K+
| style="background: #F5F5F5; padding: 5px; text-align:center" |Possible [[arrhythmia]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Organophosphate poisoning|Organophosphate toxicity]]<ref name="pmid15020723">{{cite journal| author=Kamanyire R, Karalliedde L| title=Organophosphate toxicity and occupational exposure. | journal=Occup Med (Lond) | year= 2004 | volume= 54 | issue= 2 | pages= 69-75 | pmid=15020723 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15020723 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>+</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Generalized
| style="background: #F5F5F5; padding: 5px; text-align:center" |Ascending
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Sudden
| style="background: #F5F5F5; padding: 5px; text-align:center" | Clinical diagnosis: physical exam & history
| style="background: #F5F5F5; padding: 5px; text-align:center" |Clinical suspicion confirmed with RBC AchE activity
| style="background: #F5F5F5; padding: 5px; text-align:center" |History of exposure to i[[Insecticide|nsecticide]] or living in farming environment. with : [[Diarrhea]], [[Urination]], [[Miosis]], [[Bradycardia]], [[Lacrimation]], [[Emesis]], [[Salivation]], [[Sweating]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Tick paralysis]] ([[Dermacentor andersoni|Dermacentor tick]])<ref name="pmid23677663">{{cite journal| author=Pecina CA| title=Tick paralysis. | journal=Semin Neurol | year= 2012 | volume= 32 | issue= 5 | pages= 531-2 | pmid=23677663 | doi=10.1055/s-0033-1334474 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23677663 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>-</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Generalized
| style="background: #F5F5F5; padding: 5px; text-align:center" |Ascending
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Insidious
| style="background: #F5F5F5; padding: 5px; text-align:center" | Clinical diagnosis: physical exam & history
| style="background: #F5F5F5; padding: 5px; text-align:center" |-
| style="background: #F5F5F5; padding: 5px; text-align:center" |History of outdoor activity in Northeastern United States. The tick is often still latched to the patient at presentation (often in head and neck area)
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Tetrodotoxin]] poisoning<ref name="pmid24566728">{{cite journal| author=Bane V, Lehane M, Dikshit M, O'Riordan A, Furey A| title=Tetrodotoxin: chemistry, toxicity, source, distribution and detection. | journal=Toxins (Basel) | year= 2014 | volume= 6 | issue= 2 | pages= 693-755 | pmid=24566728 | doi=10.3390/toxins6020693 | pmc=3942760 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24566728 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>+</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Generalized
| style="background: #F5F5F5; padding: 5px; text-align:center" |Systemic
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Sudden
| style="background: #F5F5F5; padding: 5px; text-align:center" | Clinical diagnosis: physical exam & dietary history
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" | History of consumption of puffer fish species.
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Stroke]]<ref name="pmid8848683">{{cite journal| author=Kuntzer T, Hirt L, Bogousslavsky J| title=[Neuromuscular involvement and cerebrovascular accidents]. | journal=Rev Med Suisse Romande | year= 1996 | volume= 116 | issue= 8 | pages= 605-9 | pmid=8848683 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8848683 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" | +/-
| style="background: #F5F5F5; padding: 5px; text-align:center" | +/-
| style="background: #F5F5F5; padding: 5px; text-align:center" | +/-
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>+/-</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Generalized
| style="background: #F5F5F5; padding: 5px; text-align:center" |Systemic
| style="background: #F5F5F5; padding: 5px; text-align:center" |UL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Sudden
| style="background: #F5F5F5; padding: 5px; text-align:center" | MRI +ve for ischemia or hemorrhage
| style="background: #F5F5F5; padding: 5px; text-align:center" |MRI
| style="background: #F5F5F5; padding: 5px; text-align:center" |Sudden unilateral motor and sensory deficit in a patient with a history of [[Atherosclerosis|atherosclero]]<nowiki/>tic risk factors (diabetes, hypertension, smoking) or [[Atrial fibrillation|atrial fibrillation.]]
|-
| style="background: #DCDCDC; padding: 5px; text-align:center;" | [[Poliomyelitis]]<ref name="pmid19944665">{{cite journal| author=Laffont I, Julia M, Tiffreau V, Yelnik A, Herisson C, Pelissier J| title=Aging and sequelae of poliomyelitis. | journal=Ann Phys Rehabil Med | year= 2010 | volume= 53 | issue= 1 | pages= 24-33 | pmid=19944665 | doi=10.1016/j.rehab.2009.10.002 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19944665 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" |+
| style="background: #F5F5F5; padding: 5px; text-align:center" |+
| style="background: #F5F5F5; padding: 5px; text-align:center" |+
| style="background: #F5F5F5; padding: 5px; text-align:center" |+/-
| style="background: #F5F5F5; padding: 5px; text-align:center" |Proximal > Distal
| style="background: #F5F5F5; padding: 5px; text-align:center" |Systemic
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL or UL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Sudden
| style="background: #F5F5F5; padding: 5px; text-align:center" |
| style="background: #F5F5F5; padding: 5px; text-align:center" |PCR of CSF
| style="background: #F5F5F5; padding: 5px; text-align:center" |Asymmetric paralysis following a flu-like syndrome.
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Neurosyphilis]]<ref name="pmid22482824">{{cite journal| author=Liu LL, Zheng WH, Tong ML, Liu GL, Zhang HL, Fu ZG et al.| title=Ischemic stroke as a primary symptom of neurosyphilis among HIV-negative emergency patients. | journal=J Neurol Sci | year= 2012 | volume= 317 | issue= 1-2 | pages= 35-9 | pmid=22482824 | doi=10.1016/j.jns.2012.03.003 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22482824 }} </ref><ref name="pmid24365430">{{cite journal |vauthors=Berger JR, Dean D |title=Neurosyphilis |journal=Handb Clin Neurol |volume=121 |issue= |pages=1461–72 |year=2014 |pmid=24365430 |doi=10.1016/B978-0-7020-4088-7.00098-5 |url=}}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" | +/-
| style="background: #F5F5F5; padding: 5px; text-align:center" |Generalized
| style="background: #F5F5F5; padding: 5px; text-align:center" |Systemic
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Insidious<nowiki/>
| style="background: #F5F5F5; padding: 5px; text-align:center" |MRI & [[Lumbar puncture]]
| style="background: #F5F5F5; padding: 5px; text-align:center" |CSF [[VDRL]]-specifc
CSF [[FTA-ABS|FTA-Ab]] -sensitive<ref name="pmid22421697">{{cite journal| author=Ho EL, Marra CM| title=Treponemal tests for neurosyphilis--less accurate than what we thought? | journal=Sex Transm Dis | year= 2012 | volume= 39 | issue= 4 | pages= 298-9 | pmid=22421697 | doi=10.1097/OLQ.0b013e31824ee574 | pmc=3746559 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22421697 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" |History of unprotected sex or multiple sexual partners.

History of [[genital ulcer]] ([[chancre]]), diffuse [[Maculopapular rash|maculopapular ras]]<nowiki/>h.
|-
| style="background: #DCDCDC; padding: 5px; text-align:center;" |[[Muscular dystrophy]]<ref name="pmid26457695">{{cite journal| author=Falzarano MS, Scotton C, Passarelli C, Ferlini A| title=Duchenne Muscular Dystrophy: From Diagnosis to Therapy. | journal=Molecules | year= 2015 | volume= 20 | issue= 10 | pages= 18168-84 | pmid=26457695 | doi=10.3390/molecules201018168 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26457695 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>-</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Proximal > Distal
| style="background: #F5F5F5; padding: 5px; text-align:center" |Systemic
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Insidious
| style="background: #F5F5F5; padding: 5px; text-align:center" | Genetic testing
| style="background: #F5F5F5; padding: 5px; text-align:center" |[[Muscle biopsy]]
| style="background: #F5F5F5; padding: 5px; text-align:center" |Progressive proximal lower limb weakness with calf pseudohypertrophy in early childhood. [[Gowers' sign|Gower sign]] positive.
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Multiple sclerosis]] exacerbation<ref name="pmid27432676">{{cite journal| author=Filippi M, Preziosa P, Rocca MA| title=Multiple sclerosis. | journal=Handb Clin Neurol | year= 2016 | volume= 135 | issue= | pages= 399-423 | pmid=27432676 | doi=10.1016/B978-0-444-53485-9.00020-9 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27432676 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>+</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Generalized
| style="background: #F5F5F5; padding: 5px; text-align:center" |Systemic
| style="background: #F5F5F5; padding: 5px; text-align:center" |NL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Sudden
| style="background: #F5F5F5; padding: 5px; text-align:center" |'''[[CSF|↑]]'''[[CSF]] [[IgG]] levels
(monoclonal)
| style="background: #F5F5F5; padding: 5px; text-align:center" |Clinical assessment and [[MRI]] <ref name="pmid8274111">{{cite journal| author=Giang DW, Grow VM, Mooney C, Mushlin AI, Goodman AD, Mattson DH et al.| title=Clinical diagnosis of multiple sclerosis. The impact of magnetic resonance imaging and ancillary testing. Rochester-Toronto Magnetic Resonance Study Group. | journal=Arch Neurol | year= 1994 | volume= 51 | issue= 1 | pages= 61-6 | pmid=8274111 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8274111 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" |[[Blurred vision|Blurry vision]], [[urinary incontinence]], [[fatigue]]
|-
| style="background: #DCDCDC; padding: 5px; text-align:center" |[[Amyotrophic lateral sclerosis]]<ref name="pmid27025851">{{cite journal| author=Riva N, Agosta F, Lunetta C, Filippi M, Quattrini A| title=Recent advances in amyotrophic lateral sclerosis. | journal=J Neurol | year= 2016 | volume= 263 | issue= 6 | pages= 1241-54 | pmid=27025851 | doi=10.1007/s00415-016-8091-6 | pmc=4893385 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27025851 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>-</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Generalized
| style="background: #F5F5F5; padding: 5px; text-align:center" |Systemic
| style="background: #F5F5F5; padding: 5px; text-align:center" |BL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Insidious
| style="background: #F5F5F5; padding: 5px; text-align:center" | Normal [[Lumbar puncture|LP]] (to rule out DDx)
| style="background: #F5F5F5; padding: 5px; text-align:center" |MRI & [[Lumbar puncture|LP]]
| style="background: #F5F5F5; padding: 5px; text-align:center" |Patient initially presents with [[upper motor neuron]] deficit ([[spasticity]]) followed by [[lower motor neuron]] deficit ([[flaccidity]]).
|-
| style="background: #DCDCDC; padding: 5px; text-align:center;" |[[Myositis|Inflammatory myopathy]]<ref name="pmid26290112">{{cite journal| author=Michelle EH, Mammen AL| title=Myositis Mimics. | journal=Curr Rheumatol Rep | year= 2015 | volume= 17 | issue= 10 | pages= 63 | pmid=26290112 | doi=10.1007/s11926-015-0541-0 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=26290112 }}</ref>
| style="background: #F5F5F5; padding: 5px; text-align:center" | +
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" | -
| style="background: #F5F5F5; padding: 5px; text-align:center" |<nowiki>-</nowiki>
| style="background: #F5F5F5; padding: 5px; text-align:center" |Proximal > Distal
| style="background: #F5F5F5; padding: 5px; text-align:center" |Systemic
| style="background: #F5F5F5; padding: 5px; text-align:center" |UL or BL
| style="background: #F5F5F5; padding: 5px; text-align:center" |Insidious
| style="background: #F5F5F5; padding: 5px; text-align:center" |Elevated [[Creatine kinase|CK]] & [[Aldolase]]
| style="background: #F5F5F5; padding: 5px; text-align:center" |[[Muscle biopsy]]
| style="background: #F5F5F5; padding: 5px; text-align:center" |Progressive proximal muscle weakness in 3rd to 5th decade of life. With or without skin manifestations.
|-
|}

== References ==
{{reflist|2}}
{{WH}}
{{WS}}

Transverse myelitis electrocardiogram

2020-04-28T04:12:06Z

M Jahan:

__NOTOC__
{{Transverse myelitis}}
{{CMG}}; {{AE}} {{MMJ}}

==Overview==
 

==Electrocardiogram==

There are no ECG findings associated with [disease name].

OR

An ECG may be helpful in the diagnosis of [disease name]. Findings on an ECG suggestive of/diagnostic of [disease name] include
*[Finding 1]
*[Finding 2]
*[Finding 3]

==References==
{{Reflist|2}}

{{WH}}
{{WS}}

Transverse myelitis electrocardiogram

2020-04-28T04:11:28Z

M Jahan: Created page with "__NOTOC__ {{Transverse myelitis}} {{CMG}}; {{AE}} {{MMJ}} ==Overview== There are no ECG findings associated with [disease name]. OR An ECG may be helpful in the diagnosis o..."

__NOTOC__
{{Transverse myelitis}}
{{CMG}}; {{AE}} {{MMJ}}

==Overview==
There are no ECG findings associated with [disease name].

OR

An ECG may be helpful in the diagnosis of [disease name]. Findings on an ECG suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

==Electrocardiogram==

There are no ECG findings associated with [disease name].

OR

An ECG may be helpful in the diagnosis of [disease name]. Findings on an ECG suggestive of/diagnostic of [disease name] include
*[Finding 1]
*[Finding 2]
*[Finding 3]

==References==
{{Reflist|2}}

{{WH}}
{{WS}}

Transverse myelitis diagnostic study of choice

2020-04-27T02:41:48Z

M Jahan: Created page with "__NOTOC__ {{Transverse myelitis}} {{CMG}}; {{AE}} {{MMJ}} == Overview == == Diagnostic Study of Choice == === Study of choice === [Name of the investigation] is the gold sta..."

__NOTOC__
{{Transverse myelitis}}
{{CMG}}; {{AE}} {{MMJ}}
== Overview ==

== Diagnostic Study of Choice ==

=== Study of choice ===
[Name of the investigation] is the gold standard test for the diagnosis of [disease name].

OR

The following result of [gold standard test] is confirmatory of [disease name]:
* [Result 1]
* [Result 2]

OR

[Name of the investigation] must be performed when:
* The patient presents with [symptom/sign 1], [symptom/sign 2], and [symptom/sign 3].
* A [name of test] is positive for [sign 1], [sign 2], and [sign 3] in the patient.

OR

[Name of the investigation] is the gold standard test for the diagnosis of [disease name].

OR

The diagnostic study of choice for [disease name] is [name of the investigation].

OR

There is no single diagnostic study of choice for the diagnosis of [disease name].

OR

There is no single diagnostic study of choice for the diagnosis of [disease name], but [disease name] can be diagnosed based on [name of the investigation 1] and [name of the investigation 2].

OR

[Disease name] is primarily diagnosed based on the clinical presentation.

OR

Investigations:
* Among the patients who present with clinical signs of [disease name], the [investigation name] is the most specific test for the diagnosis.
* Among the patients who present with clinical signs of [disease name], the [investigation name] is the most sensitive test for diagnosis.
* Among the patients who present with clinical signs of [disease name], the [investigation name] is the most efficient test for diagnosis.

==== The comparison of various diagnostic studies for [disease name] ====
{|
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
! style="background: #4479BA; color: #FFFFFF; text-align: center;" | Test
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Sensitivity
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Specificity
|-
! style="background: #696969; color: #FFFFFF; text-align: center;" |Test 1
| style="background: #DCDCDC; padding: 5px; text-align: center;" |...%
| style="background: #DCDCDC; padding: 5px; text-align: center;" |...%
|-
! style="background: #696969; color: #FFFFFF; text-align: center;" |Test 2
| style="background: #DCDCDC; padding: 5px; text-align: center;" |...%
| style="background: #DCDCDC; padding: 5px; text-align: center;" |...%
|}
 [Name of test with higher sensitivity and specificity] is the preferred investigation based on the sensitivity and specificity

===== Diagnostic results =====
The following finding(s) on performing [investigation name] is(are) confirmatory for [disease name]:
* [Finding 1]
* [Finding 2]

===== Sequence of Diagnostic Studies =====
The [name of the investigation] must be performed when:
* The patient presented with symptoms/signs 1, 2, and 3 as the first step of diagnosis.
* A positive [test] is detected in the patient, to confirm the diagnosis.

OR

The various investigations must be performed in the following order:
* [Initial investigation]
* [2nd investigation]

=== Name of Diagnostic Criteria ===

'''It is recommended that you include the criteria in a table. Make sure you always cite the source of the content and whether the table has been adapted from another source.'''

[Disease name] is primarily diagnosed based on clinical presentation. There are no established criteria for the diagnosis of [disease name].

OR

There is no single diagnostic study of choice for [disease name], though [disease name] may be diagnosed based on [name of criteria] established by [...].

OR

The diagnosis of [disease name] is made when at least [number] of the following [number] diagnostic criteria are met: [criterion 1], [criterion 2], [criterion 3], and [criterion 4].

OR

The diagnosis of [disease name] is based on the [criteria name] criteria, which includes [criterion 1], [criterion 2], and [criterion 3].

OR

[Disease name] may be diagnosed at any time if one or more of the following criteria are met:
* Criteria 1
* Criteria 2
* Criteria 3

OR

'''IF there are clear, established diagnostic criteria'''

The diagnosis of [disease name] is made when at least [number] of the following [number] diagnostic criteria are met: [criterion 1], [criterion 2], [criterion 3], and [criterion 4].

OR

The diagnosis of [disease name] is based on the [criteria name] criteria, which include [criterion 1], [criterion 2], and [criterion 3].

OR

The diagnosis of [disease name] is based on the [definition name] definition, which includes [criterion 1], [criterion 2], and [criterion 3].

OR

'''IF there are no established diagnostic criteria'''

There are no established criteria for the diagnosis of [disease name].

==References==
{{Reflist|2}}
{{WH}}
{{WS}}

Transverse myelitis pathophysiology

2020-04-22T18:44:45Z

M Jahan: /* Overview */

__NOTOC__
{{Transverse myelitis}}

{{CMG}}; {{AE}} {{MMJ}}
==Overview==

* In the pathogenesis of transverse myelitis, a variety of immunological mechanisms may cause pathological substrate and dysfunction of [[Neural|neural cells]] within the [[spinal cord]].

* Transverse myelitis is the result of progressive [[demyelination]] and [[axonal]] loss in addition to [[Grey matter|gray matter]] involvement, [[necrosis]] and [[cavitation]].
* It is understood that [[infections]] may cause transverse myelitis by:
** Direct tissue damage
** Immune-mediated infection-triggered tissue damage
* [[Multiple sclerosis]] is the other cause to the transverse myelitis and it sometimes transverse myelitis can appear as the first symptom of [[Multiple sclerosis]].
* Acute partial transverse myelitis may be predictive of a subsequent diagnosis of [[multiple sclerosis]] in children.
* Invariable histopathological findings of transverse myelitis include:
** Perivascular spread of [[Monocyte|monocytes]]
** Focal areas of [[Lymphocyte|lymphocytes]] infiltrating
** [[Astroglia|Astroglial]] and [[Microglia|microglial]] activation

* Other histopathological findings of transverse myelitis include:
** Infiltration of [[CD4+ T cells|CD4+]] and [[CD8+ T cells|CD8+ T-lymphocytes]]
** Typically preservation of the subpial parenchyma suggesting ischemia as the ultimate cause of the cord lesions in transverse myelitis

Conditions that may cause transverse myelitis include:

* Various infectionsin 30% to 60% of the cases:
** [[Herpesviridae]]
** [[Enterovirus|Enteroviruses]]
** [[Influenza virus|Influenza viruses]]
** [[Adenoviridae|Adenoviruses]]
** [[Coxsackievirus|Coxsackieviruses]]
** [[Echovirus|Enteric cytopathogenic human orphan (ECHO) virus]]
** [[Hepatitis A virus]]
** [[Lymphocytic choriomeningitis virus|Lymphocytic choriomeningitis virus (LCMV)]]
** [[Mumps virus]]
** [[Measles virus]]
** [[Rubella virus]]
** [[Poliovirus]]
** [[Rubeola|Rubeola virus]]
** [[Dengue virus]]
** [[Russian Spring Summer encephalitis virus|Russian spring-summer encephalitis virus]]
** [[Varicella virus]]
** [[Mycoplasma pneumonia|Mycoplasma pneumonia bacteria]]
** [[Legionella pneumophila|Legionella pneumonia bacteria]]
** [[Pulmonary tuberculosis]]
** [[Borrelia]] ([[Lyme disease]])
** [[Listeria]]
** [[Bartonella]] ([[cat scratch disease]])
* Vaccination
** About 30% of pediatric cases are preceded with [[immunization]]<nowiki/>s within one month of disease onset

[[Infections]] can cause transverse myelitis through two main mechanisms:

# Direct tissue damage
# Immune-mediated infection-triggered tissue damage which may be due to: [[Molecular mimicry]] or [[Superantigen|superantigen effect]]

* This immune response may be caused either by [[Cell-mediated immunity|T-cell mediated immune response]] or by [[Humoral immunity|antibody-mediated immune response]].

A non-microbial related immune dysfunction by the presence of autoantibodies has been also proposed in the immunopathogenesis of transverse myelitis.

In the spinal fluid of patients with transverse myelitis, [[Interleukin 6|Interleukin 6 (IL-6)]] levels were also markedly elevated.

 

==Pathophysiology==
===Physiology ===

* The lesions in acute transverse myelitis are invariably limited to the [[spinal cord]].<ref name="pmid22379456" /><ref name="pmid29696041">{{cite journal| author=Tavasoli A, Tabrizi A| title=Acute Transverse Myelitis in Children, Literature Review. | journal=Iran J Child Neurol | year= 2018 | volume= 12 | issue= 2 | pages= 7-16 | pmid=29696041 | doi= | pmc=5904733 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29696041 }} </ref>
* There is no involvement of other structures in the [[central nervous system]].<ref name="pmid22379456" />
*The [[spinal cord]] involvement in patients with transverse myelitis is usually central, uniform and symmetric but in patients with [[multiple sclerosis]] it typically affects the [[spinal cord]] in a patchy way and the lesions are usually peripheral.
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===Pathogenesis===

* In the pathogenesis of transverse myelitis, a variety of immunological mechanisms may cause pathological substrate and dysfunction of [[Neural|neural cells]] within the [[spinal cord]].<ref name="pmid12045735">{{cite journal| author=Kerr DA, Ayetey H| title=Immunopathogenesis of acute transverse myelitis. | journal=Curr Opin Neurol | year= 2002 | volume= 15 | issue= 3 | pages= 339-47 | pmid=12045735 | doi=10.1097/00019052-200206000-00019 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12045735 }} </ref>

*Transverse myelitis is the result of progressive [[demyelination]] and [[axonal]] loss in addition to [[Grey matter|gray matter]] involvement, [[necrosis]] and [[cavitation]].<ref name="pmid22379456">{{cite journal| author=Awad A, Stüve O| title=Idiopathic transverse myelitis and neuromyelitis optica: clinical profiles, pathophysiology and therapeutic choices. | journal=Curr Neuropharmacol | year= 2011 | volume= 9 | issue= 3 | pages= 417-28 | pmid=22379456 | doi=10.2174/157015911796557948 | pmc=3151596 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22379456 }} </ref>
*It is understood that [[infections]] may cause transverse myelitis by: <ref name="pmid22379456">{{cite journal| author=Awad A, Stüve O| title=Idiopathic transverse myelitis and neuromyelitis optica: clinical profiles, pathophysiology and therapeutic choices. | journal=Curr Neuropharmacol | year= 2011 | volume= 9 | issue= 3 | pages= 417-28 | pmid=22379456 | doi=10.2174/157015911796557948 | pmc=3151596 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22379456 }} </ref>
**Direct tissue damage
**Immune-mediated infection-triggered tissue damage
*[[Multiple sclerosis]] is the other cause to the transverse myelitis and it sometimes transverse myelitis can appear as the first symptom of [[Multiple sclerosis]].<ref name="pmid22379456">{{cite journal| author=Awad A, Stüve O| title=Idiopathic transverse myelitis and neuromyelitis optica: clinical profiles, pathophysiology and therapeutic choices. | journal=Curr Neuropharmacol | year= 2011 | volume= 9 | issue= 3 | pages= 417-28 | pmid=22379456 | doi=10.2174/157015911796557948 | pmc=3151596 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22379456 }} </ref>
*Acute partial transverse myelitis may be predictive of a subsequent diagnosis of [[multiple sclerosis]] in children.<ref name="pmid24619933">{{cite journal| author=Meyer P, Leboucq N, Molinari N, Roubertie A, Carneiro M, Walther-Louvier U | display-authors=etal| title=Partial acute transverse myelitis is a predictor of multiple sclerosis in children. | journal=Mult Scler | year= 2014 | volume= 20 | issue= 11 | pages= 1485-93 | pmid=24619933 | doi=10.1177/1352458514526943 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24619933 }} </ref>
*Invariable histopathological findings of transverse myelitis include:<ref name="pmid22379456" />
**Perivascular spread of [[Monocyte|monocytes]]
**Focal areas of [[Lymphocyte|lymphocytes]] infiltrating
**[[Astroglia|Astroglial]] and [[Microglia|microglial]] activation

* Other histopathological findings of transverse myelitis include:<ref name="pmid22379456" /><ref name="pmid24503658">{{cite journal| author=Moulignier A, Lescure FX, Savatovsky J, Campa P| title=CD8 transverse myelitis in a patient with HIV-1 infection. | journal=BMJ Case Rep | year= 2014 | volume= 2014 | issue= | pages= | pmid=24503658 | doi=10.1136/bcr-2013-201073 | pmc=3918629 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24503658 }} </ref>
** Infiltration of [[CD4+ T cells|CD4+]] and [[CD8+ T cells|CD8+ T-lymphocytes]]
** Typically preservation of the subpial parenchyma suggesting ischemia as the ultimate cause of the cord lesions in transverse myelitis

Conditions that may cause transverse myelitis include:

*Various infectionsin 30% to 60% of the cases:<ref name="pmid22379456">{{cite journal| author=Awad A, Stüve O| title=Idiopathic transverse myelitis and neuromyelitis optica: clinical profiles, pathophysiology and therapeutic choices. | journal=Curr Neuropharmacol | year= 2011 | volume= 9 | issue= 3 | pages= 417-28 | pmid=22379456 | doi=10.2174/157015911796557948 | pmc=3151596 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22379456 }} </ref><ref name="pmid8489410">{{cite journal| author=Jeffery DR, Mandler RN, Davis LE| title=Transverse myelitis. Retrospective analysis of 33 cases, with differentiation of cases associated with multiple sclerosis and parainfectious events. | journal=Arch Neurol | year= 1993 | volume= 50 | issue= 5 | pages= 532-5 | pmid=8489410 | doi=10.1001/archneur.1993.00540050074019 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8489410 }} </ref><ref name="pmid2375246">{{cite journal| author=Christensen PB, Wermuth L, Hinge HH, Bømers K| title=Clinical course and long-term prognosis of acute transverse myelopathy. | journal=Acta Neurol Scand | year= 1990 | volume= 81 | issue= 5 | pages= 431-5 | pmid=2375246 | doi=10.1111/j.1600-0404.1990.tb00990.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2375246 }} </ref><ref name="pmid14977560">{{cite journal| author=Krishnan C, Kaplin AI, Deshpande DM, Pardo CA, Kerr DA| title=Transverse Myelitis: pathogenesis, diagnosis and treatment. | journal=Front Biosci | year= 2004 | volume= 9 | issue= | pages= 1483-99 | pmid=14977560 | doi=10.2741/1351 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14977560 }} </ref><ref name="pmid13007166">{{cite journal| author=PAINE RS, BYERS RK| title=Transverse myelopathy in childhood. | journal=AMA Am J Dis Child | year= 1953 | volume= 85 | issue= 2 | pages= 151-63 | pmid=13007166 | doi=10.1001/archpedi.1953.02050070160004 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13007166 }} </ref><ref name="pmid697326">{{cite journal| author=Ropper AH, Poskanzer DC| title=The prognosis of acute and subacute transverse myelopathy based on early signs and symptoms. | journal=Ann Neurol | year= 1978 | volume= 4 | issue= 1 | pages= 51-9 | pmid=697326 | doi=10.1002/ana.410040110 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=697326 }} </ref><ref name="pmid9766742">{{cite journal| author=Knebusch M, Strassburg HM, Reiners K| title=Acute transverse myelitis in childhood: nine cases and review of the literature. | journal=Dev Med Child Neurol | year= 1998 | volume= 40 | issue= 9 | pages= 631-9 | pmid=9766742 | doi=10.1111/j.1469-8749.1998.tb15430.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9766742 }} </ref><ref name="pmid14048158">{{cite journal| author=ALTROCCHI PH| title=ACUTE TRANSVERSE MYELOPATHY. | journal=Arch Neurol | year= 1963 | volume= 9 | issue= | pages= 111-9 | pmid=14048158 | doi=10.1001/archneur.1963.00460080021002 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14048158 }} </ref><ref name="pmid4598176">{{cite journal| author=Lerer RJ, Kalavsky SM| title=Central nervous system disease associated with Mycoplasma pneumoniae infection: report of five cases and review of the literature. | journal=Pediatrics | year= 1973 | volume= 52 | issue= 5 | pages= 658-68 | pmid=4598176 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4598176 }} </ref><ref name="pmid10987731">{{cite journal| author=Salgado CD, Weisse ME| title=Transverse myelitis associated with probable cat-scratch disease in a previously healthy pediatric patient. | journal=Clin Infect Dis | year= 2000 | volume= 31 | issue= 2 | pages= 609-11 | pmid=10987731 | doi=10.1086/313986 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10987731 }} </ref>
**[[Herpesviridae]]
**[[Enterovirus|Enteroviruses]]
**[[Influenza virus|Influenza viruses]]
**[[Adenoviridae|Adenoviruses]]
**[[Coxsackievirus|Coxsackieviruses]]
**[[Echovirus|Enteric cytopathogenic human orphan (ECHO) virus]]
**[[Hepatitis A virus]]
**[[Lymphocytic choriomeningitis virus|Lymphocytic choriomeningitis virus (LCMV)]]
**[[Mumps virus]]
**[[Measles virus]]
**[[Rubella virus]]
**[[Poliovirus]]
**[[Rubeola|Rubeola virus]]
**[[Dengue virus]]
**[[Russian Spring Summer encephalitis virus|Russian spring-summer encephalitis virus]]
**[[Varicella virus]]
**[[Mycoplasma pneumonia|Mycoplasma pneumonia bacteria]]
**[[Legionella pneumophila|Legionella pneumonia bacteria]]
**[[Pulmonary tuberculosis]]
**[[Borrelia]] ([[Lyme disease]])
**[[Listeria]]
**[[Bartonella]] ([[cat scratch disease]])
*Vaccination<ref name="pmid22379456">{{cite journal| author=Awad A, Stüve O| title=Idiopathic transverse myelitis and neuromyelitis optica: clinical profiles, pathophysiology and therapeutic choices. | journal=Curr Neuropharmacol | year= 2011 | volume= 9 | issue= 3 | pages= 417-28 | pmid=22379456 | doi=10.2174/157015911796557948 | pmc=3151596 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22379456 }} </ref><ref name="pmid19880568">{{cite journal| author=Agmon-Levin N, Kivity S, Szyper-Kravitz M, Shoenfeld Y| title=Transverse myelitis and vaccines: a multi-analysis. | journal=Lupus | year= 2009 | volume= 18 | issue= 13 | pages= 1198-204 | pmid=19880568 | doi=10.1177/0961203309345730 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19880568 }} </ref>
**About 30% of pediatric cases are preceded with [[immunization]]<nowiki/>s within one month of disease onset

[[Infections]] can cause transverse myelitis through two main mechanisms:<ref name="pmid22379456">{{cite journal| author=Awad A, Stüve O| title=Idiopathic transverse myelitis and neuromyelitis optica: clinical profiles, pathophysiology and therapeutic choices. | journal=Curr Neuropharmacol | year= 2011 | volume= 9 | issue= 3 | pages= 417-28 | pmid=22379456 | doi=10.2174/157015911796557948 | pmc=3151596 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22379456 }} </ref><ref name="pmid10987731">{{cite journal| author=Salgado CD, Weisse ME| title=Transverse myelitis associated with probable cat-scratch disease in a previously healthy pediatric patient. | journal=Clin Infect Dis | year= 2000 | volume= 31 | issue= 2 | pages= 609-11 | pmid=10987731 | doi=10.1086/313986 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10987731 }} </ref><ref name="pmid10378139">{{cite journal| author=Giobbia M, Carniato A, Scotton PG, Marchiori GC, Vaglia A| title=Cytomegalovirus-associated transverse myelitis in a non-immunocompromised patient. | journal=Infection | year= 1999 | volume= 27 | issue= 3 | pages= 228-30 | pmid=10378139 | doi=10.1007/bf02561538 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10378139 }} </ref>

# Direct tissue damage
# Immune-mediated infection-triggered tissue damage which may be due to: [[Molecular mimicry]] or [[Superantigen|superantigen effect]]

*This immune response may be caused either by [[Cell-mediated immunity|T-cell mediated immune response]] or by [[Humoral immunity|antibody-mediated immune response]].

A non-microbial related immune dysfunction by the presence of autoantibodies has been also proposed in the immunopathogenesis of transverse myelitis.<ref name="pmid22379456" /><ref name="pmid2027486">{{cite journal| author=Tippett DS, Fishman PS, Panitch HS| title=Relapsing transverse myelitis. | journal=Neurology | year= 1991 | volume= 41 | issue= 5 | pages= 703-6 | pmid=2027486 | doi=10.1212/wnl.41.5.703 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2027486 }} </ref><ref name="pmid8609515">{{cite journal| author=Pandit L, Rao S| title=Recurrent myelitis. | journal=J Neurol Neurosurg Psychiatry | year= 1996 | volume= 60 | issue= 3 | pages= 336-8 | pmid=8609515 | doi=10.1136/jnnp.60.3.336 | pmc=1073861 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8609515 }} </ref><ref name="pmid11064439">{{cite journal| author=Bashir K, Whitaker JN| title=Importance of paraclinical and CSF studies in the diagnosis of MS in patients presenting with partial cervical transverse myelopathy and negative cranial MRI. | journal=Mult Scler | year= 2000 | volume= 6 | issue= 5 | pages= 312-6 | pmid=11064439 | doi=10.1177/135245850000600503 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11064439 }} </ref>

In the spinal fluid of patients with transverse myelitis, [[Interleukin 6|Interleukin 6 (IL-6)]] levels were also markedly elevated.<ref name="pmid22379456" /><ref name="pmid14977560">{{cite journal| author=Krishnan C, Kaplin AI, Deshpande DM, Pardo CA, Kerr DA| title=Transverse Myelitis: pathogenesis, diagnosis and treatment. | journal=Front Biosci | year= 2004 | volume= 9 | issue= | pages= 1483-99 | pmid=14977560 | doi=10.2741/1351 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14977560 }} </ref><ref name="pmid16184194">{{cite journal| author=Kaplin AI, Deshpande DM, Scott E, Krishnan C, Carmen JS, Shats I | display-authors=etal| title=IL-6 induces regionally selective spinal cord injury in patients with the neuroinflammatory disorder transverse myelitis. | journal=J Clin Invest | year= 2005 | volume= 115 | issue= 10 | pages= 2731-41 | pmid=16184194 | doi=10.1172/JCI25141 | pmc=1224298 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16184194 }} </ref>
==Associated Conditions==
Conditions associated with transverse myelitis include:<ref name="pmid21621005">{{cite journal| author=Borchers AT, Gershwin ME| title=Transverse myelitis. | journal=Autoimmun Rev | year= 2012 | volume= 11 | issue= 3 | pages= 231-48 | pmid=21621005 | doi=10.1016/j.autrev.2011.05.018 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21621005 }} </ref><ref name="pmid19662820">{{cite journal| author=Tristano AG| title=[Autoimmune diseases associated with transverse myelitis. Review]. | journal=Invest Clin | year= 2009 | volume= 50 | issue= 2 | pages= 251-70 | pmid=19662820 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19662820 }} </ref><ref name="pmid22379456">{{cite journal| author=Awad A, Stüve O| title=Idiopathic transverse myelitis and neuromyelitis optica: clinical profiles, pathophysiology and therapeutic choices. | journal=Curr Neuropharmacol | year= 2011 | volume= 9 | issue= 3 | pages= 417-28 | pmid=22379456 | doi=10.2174/157015911796557948 | pmc=3151596 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22379456 }} </ref><ref name="pmid12045735">{{cite journal| author=Kerr DA, Ayetey H| title=Immunopathogenesis of acute transverse myelitis. | journal=Curr Opin Neurol | year= 2002 | volume= 15 | issue= 3 | pages= 339-47 | pmid=12045735 | doi=10.1097/00019052-200206000-00019 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12045735 }} </ref><ref name="pmid24090445">{{cite journal| author=Cobo Calvo A, Mañé Martínez MA, Alentorn-Palau A, Bruna Escuer J, Romero Pinel L, Martínez-Yélamos S| title=Idiopathic acute transverse myelitis: outcome and conversion to multiple sclerosis in a large series. | journal=BMC Neurol | year= 2013 | volume= 13 | issue= | pages= 135 | pmid=24090445 | doi=10.1186/1471-2377-13-135 | pmc=3856522 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24090445 }} </ref>

*Various infections
*Systemic autoimmune diseases like:
**[[Lupus erythematosus]]
**[[Sjögren's syndrome]]
**[[Sarcoidosis]]
**[[Optic neuritis]]
**[[multiple sclerosis]]

==Microscopic Pathology==
Findings on microscopic histopathological analysis of transverse myelitis include:<ref name="pmid16635433">{{cite journal| author=Krishnan C, Kaplin AI, Pardo CA, Kerr DA, Keswani SC| title=Demyelinating disorders: update on transverse myelitis. | journal=Curr Neurol Neurosci Rep | year= 2006 | volume= 6 | issue= 3 | pages= 236-43 | pmid=16635433 | doi=10.1007/s11910-006-0011-1 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=16635433 }} </ref><ref name="pmid1763730">{{cite journal| author=Mirich DR, Kucharczyk W, Keller MA, Deck J| title=Subacute necrotizing myelopathy: MR imaging in four pathologically proved cases. | journal=AJNR Am J Neuroradiol | year= 1991 | volume= 12 | issue= 6 | pages= 1077-83 | pmid=1763730 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1763730 }} </ref>

* [[Perivascular cell|Perivascular]] [[Lymphocytic|lymphocytic infiltrates]]
* [[Axonal|Axonal injury]]
* [[Necrosis]] and [[demyelination]]

==References==
{{Reflist|2}}

{{WH}}
{{WS}}
[[Category: (name of the system)]]

Transverse myelitis causes

2020-04-22T18:42:33Z

M Jahan: /* Common Causes */

__NOTOC__
{{Transverse myelitis}}

{{CMG}}; {{AE}} {{MMJ}}
==Overview==
 

==Causes==
===Life-threatening Causes===
*Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated. There are no life-threatening causes of [[disease name]], however complications resulting from untreated [[disease name]] is common.
*Life-threatening causes of [symptom/manifestation] include [cause1], [cause2], and [cause3].
*[Cause] is a life-threatening cause of [disease].

===Common Causes===
Common causes of myelitis include may include:

*Various infectionsin in 30% to 60% of the cases:<ref name="pmid22379456">{{cite journal| author=Awad A, Stüve O| title=Idiopathic transverse myelitis and neuromyelitis optica: clinical profiles, pathophysiology and therapeutic choices. | journal=Curr Neuropharmacol | year= 2011 | volume= 9 | issue= 3 | pages= 417-28 | pmid=22379456 | doi=10.2174/157015911796557948 | pmc=3151596 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22379456 }} </ref><ref name="pmid8489410">{{cite journal| author=Jeffery DR, Mandler RN, Davis LE| title=Transverse myelitis. Retrospective analysis of 33 cases, with differentiation of cases associated with multiple sclerosis and parainfectious events. | journal=Arch Neurol | year= 1993 | volume= 50 | issue= 5 | pages= 532-5 | pmid=8489410 | doi=10.1001/archneur.1993.00540050074019 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8489410 }} </ref><ref name="pmid2375246">{{cite journal| author=Christensen PB, Wermuth L, Hinge HH, Bømers K| title=Clinical course and long-term prognosis of acute transverse myelopathy. | journal=Acta Neurol Scand | year= 1990 | volume= 81 | issue= 5 | pages= 431-5 | pmid=2375246 | doi=10.1111/j.1600-0404.1990.tb00990.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2375246 }} </ref><ref name="pmid14977560">{{cite journal| author=Krishnan C, Kaplin AI, Deshpande DM, Pardo CA, Kerr DA| title=Transverse Myelitis: pathogenesis, diagnosis and treatment. | journal=Front Biosci | year= 2004 | volume= 9 | issue= | pages= 1483-99 | pmid=14977560 | doi=10.2741/1351 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14977560 }} </ref><ref name="pmid13007166">{{cite journal| author=PAINE RS, BYERS RK| title=Transverse myelopathy in childhood. | journal=AMA Am J Dis Child | year= 1953 | volume= 85 | issue= 2 | pages= 151-63 | pmid=13007166 | doi=10.1001/archpedi.1953.02050070160004 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=13007166 }} </ref><ref name="pmid697326">{{cite journal| author=Ropper AH, Poskanzer DC| title=The prognosis of acute and subacute transverse myelopathy based on early signs and symptoms. | journal=Ann Neurol | year= 1978 | volume= 4 | issue= 1 | pages= 51-9 | pmid=697326 | doi=10.1002/ana.410040110 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=697326 }} </ref><ref name="pmid9766742">{{cite journal| author=Knebusch M, Strassburg HM, Reiners K| title=Acute transverse myelitis in childhood: nine cases and review of the literature. | journal=Dev Med Child Neurol | year= 1998 | volume= 40 | issue= 9 | pages= 631-9 | pmid=9766742 | doi=10.1111/j.1469-8749.1998.tb15430.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9766742 }} </ref><ref name="pmid14048158">{{cite journal| author=ALTROCCHI PH| title=ACUTE TRANSVERSE MYELOPATHY. | journal=Arch Neurol | year= 1963 | volume= 9 | issue= | pages= 111-9 | pmid=14048158 | doi=10.1001/archneur.1963.00460080021002 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=14048158 }} </ref><ref name="pmid4598176">{{cite journal| author=Lerer RJ, Kalavsky SM| title=Central nervous system disease associated with Mycoplasma pneumoniae infection: report of five cases and review of the literature. | journal=Pediatrics | year= 1973 | volume= 52 | issue= 5 | pages= 658-68 | pmid=4598176 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=4598176 }} </ref><ref name="pmid10987731">{{cite journal| author=Salgado CD, Weisse ME| title=Transverse myelitis associated with probable cat-scratch disease in a previously healthy pediatric patient. | journal=Clin Infect Dis | year= 2000 | volume= 31 | issue= 2 | pages= 609-11 | pmid=10987731 | doi=10.1086/313986 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10987731 }} </ref>
**[[Herpesviridae]]
**[[Enterovirus|Enteroviruses]]
**[[Influenza virus|Influenza viruses]]
**[[Adenoviridae|Adenoviruses]]
**[[Coxsackievirus|Coxsackieviruses]]
**[[Echovirus|Enteric cytopathogenic human orphan (ECHO) virus]]
**[[Hepatitis A virus]]
**[[Lymphocytic choriomeningitis virus|Lymphocytic choriomeningitis virus (LCMV)]]
**[[Mumps virus]]
**[[Measles virus]]
**[[Rubella virus]]
**[[Poliovirus]]
**[[Rubeola|Rubeola virus]]
**[[Dengue virus]]
**[[Russian Spring Summer encephalitis virus|Russian spring-summer encephalitis virus]]
**[[Varicella virus]]
**[[Mycoplasma pneumonia|Mycoplasma pneumonia bacteria]]
**[[Legionella pneumophila|Legionella pneumonia bacteria]]
**[[Pulmonary tuberculosis]]
**[[Borrelia]] ([[Lyme disease]])
**[[Listeria]]
**[[Bartonella]] ([[cat scratch disease]])
*Vaccination<ref name="pmid22379456">{{cite journal| author=Awad A, Stüve O| title=Idiopathic transverse myelitis and neuromyelitis optica: clinical profiles, pathophysiology and therapeutic choices. | journal=Curr Neuropharmacol | year= 2011 | volume= 9 | issue= 3 | pages= 417-28 | pmid=22379456 | doi=10.2174/157015911796557948 | pmc=3151596 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=22379456 }} </ref><ref name="pmid19880568">{{cite journal| author=Agmon-Levin N, Kivity S, Szyper-Kravitz M, Shoenfeld Y| title=Transverse myelitis and vaccines: a multi-analysis. | journal=Lupus | year= 2009 | volume= 18 | issue= 13 | pages= 1198-204 | pmid=19880568 | doi=10.1177/0961203309345730 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19880568 }} </ref>
**About 30% of pediatric cases are preceded with immunizations within one month of disease onset
*[Condition

OR

*[Disease name] is caused by an infection with [pathogen name].
*[Pathogen name] is caused by [pathogen name].

===Less Common Causes===
Less common causes of [disease name] include:
*[Cause1]
*[Cause2]
*[Cause3]

===Genetic Causes===
*[Disease name] is caused by a mutation in the [gene name] gene.

===Causes by Organ System===

{|style="width:80%; height:100px" border="1"
|style="height:100px"; style="width:25%" border="1" bgcolor="LightSteelBlue" |'''Cardiovascular'''
|style="height:100px"; style="width:75%" border="1" bgcolor="Beige" | No underlying causes
|-
|bgcolor="LightSteelBlue"| '''Chemical/Poisoning'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Dental'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Dermatologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Drug Side Effect'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Ear Nose Throat'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Endocrine'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Environmental'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Gastroenterologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Genetic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Hematologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Iatrogenic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Infectious Disease'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Musculoskeletal/Orthopedic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Neurologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Nutritional/Metabolic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Obstetric/Gynecologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Oncologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Ophthalmologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Overdose/Toxicity'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Psychiatric'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Pulmonary'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Renal/Electrolyte'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Rheumatology/Immunology/Allergy'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Sexual'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Trauma'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Urologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Miscellaneous'''
|bgcolor="Beige"| No underlying causes
|-
|}

===Causes in Alphabetical Order===
List the causes of the disease in alphabetical order:
<div style="-moz-column-count:3; column-count:3;">
* Cause 1
* Cause 2
* Cause 3
* Cause 4
* Cause 5
* Cause 6
* Cause 7
* Cause 8
* Cause 9
* Cause 10
</div>

==References==
{{Reflist|2}}

{{WH}}
{{WS}}
[[Category: (name of the system)]]