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{{CMG}}; {{AE}} {{MKA}}, {{S.G.}}
===Differentiating [disease name] from other diseases on the basis of [symptom 1], [symptom 2], and [symptom 3]===
On the basis [symptom 1], [symptom 2], and [symptom 3], [disease name] must be differentiated from [disease 1], [disease 2], [disease 3], [disease 4], [disease 5], and [disease 6].
{|
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
! rowspan="4" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Diseases
| colspan="6" rowspan="1" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Clinical manifestations'''
! colspan="4" rowspan="2" |Para-clinical findings
| colspan="1" rowspan="4" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Gold standard'''
! rowspan="4" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Additional findings
|-
| colspan="3" rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Symptoms'''
| colspan="3" rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Physical examination'''
|-
! colspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Lab Findings'''
! colspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Imaging'''
|-
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Symptoms of DVT
! colspan="1" rowspan="1" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Symptoms of Pulmonary Embolism
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Symptoms of Myocardial Infarction
! colspan="1" rowspan="1" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Tenderness in extremities
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Edema in extremities
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Warmth in extremities
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |PT
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |aPTT
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Doppler ultrasound
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Chest CT scan
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Antithrombin III deficiency]]<ref name="pmid19141163">{{cite journal |vauthors=Patnaik MM, Moll S |title=Inherited antithrombin deficiency: a review |journal=Haemophilia |volume=14 |issue=6 |pages=1229–39 |date=November 2008 |pmid=19141163 |doi=10.1111/j.1365-2516.2008.01830.x |url=}}</ref><ref name="Al HadidiWu2017">{{cite journal|last1=Al Hadidi|first1=Samer|last2=Wu|first2=Kristi|last3=Aburahma|first3=Ahmed|last4=Alamarat|first4=Zain|title=Family with clots: antithrombin deficiency|journal=BMJ Case Reports|year=2017|pages=bcr-2017-221556|issn=1757-790X|doi=10.1136/bcr-2017-221556}}</ref><ref name="pmid21772860">{{cite journal |vauthors=Konecny F |title=Inherited trombophilic states and pulmonary embolism |journal=J Res Med Sci |volume=14 |issue=1 |pages=43–56 |date=January 2009 |pmid=21772860 |pmc=3129068 |doi= |url=}}</ref>
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | Normal
| style="background: #F5F5F5; padding: 5px;" |
* Normal
* Reduces the Increase in [[PTT]] after administration of [[heparin]]
| style="background: #F5F5F5; padding: 5px;" |
* Evidence of [[deep vein thrombosis]] ([[DVT]])
* Should be used for diagnosis and follow up
| style="background: #F5F5F5; padding: 5px;" |
* [[Occlusion]] of  [[brachiocephalic]] [[vein]]
* Large [[thrombus]] in [[superior vena cava]]
| style="background: #F5F5F5; padding: 5px;" |
* Decreased [[plasma]] [[Antithrombin III|antithrombin]] ([[AT III]]) activity
| style="background: #F5F5F5; padding: 5px;" |
* [[Nephrotic syndrome]]
* Decreased inhibition of [[factor II]] and Xa
* [[Antithrombin]] is a natural [[anticoagulant]] that is lost in the [[urine]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Factor V Leiden mutation]]<ref name="pmid20626623">{{cite journal |vauthors=Mannucci PM, Asselta R, Duga S, Guella I, Spreafico M, Lotta L, Merlini PA, Peyvandi F, Kathiresan S, Ardissino D |title=The association of factor V Leiden with myocardial infarction is replicated in 1880 patients with premature disease |journal=J. Thromb. Haemost. |volume=8 |issue=10 |pages=2116–21 |date=October 2010 |pmid=20626623 |doi=10.1111/j.1538-7836.2010.03982.x |url=}}</ref><ref name="pmid27797270">{{cite journal |vauthors=Campello E, Spiezia L, Simioni P |title=Diagnosis and management of factor V Leiden |journal=Expert Rev Hematol |volume=9 |issue=12 |pages=1139–1149 |date=December 2016 |pmid=27797270 |doi=10.1080/17474086.2016.1249364 |url=}}</ref><ref name="pmid15003896">{{cite journal |vauthors=Van Rooden CJ, Rosendaal FR, Meinders AE, Van Oostayen JA, Van Der Meer FJ, Huisman MV |title=The contribution of factor V Leiden and prothrombin G20210A mutation to the risk of central venous catheter-related thrombosis |journal=Haematologica |volume=89 |issue=2 |pages=201–6 |date=February 2004 |pmid=15003896 |doi= |url=}}</ref><ref name="pmid23615845">{{cite journal| author=Dentali F, Pomero F, Borretta V, Gianni M, Squizzato A, Fenoglio L et al.| title=Location of venous thrombosis in patients with FVL or prothrombin G20210A mutations: systematic review and meta-analysis. | journal=Thromb Haemost | year= 2013 | volume= 110 | issue= 1 | pages= 191-4 | pmid=23615845 | doi=10.1160/TH13-02-0163 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23615845  }}</ref><ref name="pmid12421138">{{cite journal |vauthors=Press RD, Bauer KA, Kujovich JL, Heit JA |title=Clinical utility of factor V leiden (R506Q) testing for the diagnosis and management of thromboembolic disorders |journal=Arch. Pathol. Lab. Med. |volume=126 |issue=11 |pages=1304–18 |date=November 2002 |pmid=12421138 |doi=10.1043/0003-9985(2002)126<1304:CUOFVL>2.0.CO;2 |url=}}</ref>
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" |N/A
| style="background: #F5F5F5; padding: 5px;" |↑
| style="background: #F5F5F5; padding: 5px;" |
* Recommended to do weekly
* [[Proximal]] [[DVT]] is more commonly observed as compared to [[distal]] [[DVT]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Pulmonary embolism]]
| style="background: #F5F5F5; padding: 5px;" |
* N/A
| style="background: #F5F5F5; padding: 5px;" |
* Inactivates factor Va and factor VIIIa
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Protein C deficiency]]<ref>{{Cite journal
| author = [[Bernard Khor]] & [[Elizabeth M. Van Cott]]
| title = Laboratory tests for protein C deficiency
| journal = [[American journal of hematology]]
| volume = 85
| issue = 6
| pages = 440–442
| year = 2010
| month = June
| doi = 10.1002/ajh.21679
| pmid = 20309856
}}</ref><ref name="pmid11336597">{{cite journal |vauthors=Pescatore SL |title=Clinical management of protein C deficiency |journal=Expert Opin Pharmacother |volume=2 |issue=3 |pages=431–9 |date=March 2001 |pmid=11336597 |doi=10.1517/14656566.2.3.431 |url=}}</ref><ref name=":0">{{Cite journal
| author = [[Gustavo A. Rodriguez-Leal]], [[Segundo Moran]], [[Roberto Corona-Cedillo]] & [[Rocio Brom-Valladares]]
| title = Portal vein thrombosis with protein C-S deficiency in a non-cirrhotic patient
| journal = [[World journal of hepatology]]
| volume = 6
| issue = 7
| pages = 532–537
| year = 2014
| month = July
| doi = 10.4254/wjh.v6.i7.532
| pmid = 25068006
}}</ref>
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | Normal
| style="background: #F5F5F5; padding: 5px;" |Normal / ↑
| style="background: #F5F5F5; padding: 5px;" |
* [[Hypercoagulation]]
* Recurrent [[venous thromboembolism]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Venous thromboembolism]]
* [[Pulmonary embolism]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Protein C]] functional [[assay]]
* [[ELISA]] [[assay]]: may produce [[false positive]] result in cross reaction with [[rheumatoid factor]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Factor VIII]] elevation in acute phase
* Functional [[assay]] should not be performed if patient is on [[warfarin]]
* [[Purpura fulminans]] ([[skin]] [[necrosis]]) could be a form of presentation
* Risk of [[thrombotic]] [[skin]] [[necrosis]] following [[warfarin]] administration
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Protein S deficiency]]<ref name=":0" /><ref>{{Cite journal
| author = [[Kristi J. Smock]], [[Elizabeth A. Plumhoff]], [[Piet Meijer]], [[Peihong Hsu]], [[Nicole D. Zantek]], [[Nahla M. Heikal]] & [[Elizabeth M. Van Cott]]
| title = Protein S testing in patients with protein S deficiency, factor V Leiden, and rivaroxaban by North American Specialized Coagulation Laboratories
| journal = [[Thrombosis and haemostasis]]
| volume = 116
| issue = 1
| pages = 50–57
| year = 2016
| month = July
| doi = 10.1160/TH15-12-0918
| pmid = 27075008
}}</ref><ref name="pmid21799399">{{cite journal |vauthors=Ji M, Yoon SN, Lee W, Jang S, Park SH, Kim DY, Chun S, Min WK |title=Protein S deficiency with a PROS1 gene mutation in a patient presenting with mesenteric venous thrombosis following total colectomy |journal=Blood Coagul. Fibrinolysis |volume=22 |issue=7 |pages=619–21 |date=October 2011 |pmid=21799399 |doi=10.1097/MBC.0b013e32834a0421 |url=}}</ref>
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" |Normal
| style="background: #F5F5F5; padding: 5px;" |Normal / ↑
| style="background: #F5F5F5; padding: 5px;" |
* [[Hypercoagulation]]
* Recurrent [[venous thromboembolism]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Pulmonary embolism]]
* [[Thrombosis]] of [[superior mesenteric vein]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Protein S]] free [[antigen]] [[assay]]
| style="background: #F5F5F5; padding: 5px;" |
* When performing the gold standard test, beware of interference from samples positive for [[Factor V]] [[mutation]], [[protein C deficiency]] and oral [[anticoagulants]] ([[rivaroxaban]])
* Risk of [[thrombotic]] [[skin]] [[necrosis]] following [[warfarin]] administration
* Suspected in patients with a strong family history of [[VTE]]
* [[Post phlebitic syndrome]] 
* [[Fetal]] loss
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Prothrombin gene mutation G20210A|Prothrombin gene mutation]]<ref name="pmid17474891">{{cite journal| author=Cooper PC, Rezende SM| title=An overview of methods for detection of factor V Leiden and the prothrombin G20210A mutations. | journal=Int J Lab Hematol | year= 2007 | volume= 29 | issue= 3 | pages= 153-62 | pmid=17474891 | doi=10.1111/j.1751-553X.2007.00892.x | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17474891  }}</ref><ref name="pmid12421139">{{cite journal| author=McGlennen RC, Key NS| title=Clinical and laboratory management of the prothrombin G20210A mutation. | journal=Arch Pathol Lab Med | year= 2002 | volume= 126 | issue= 11 | pages= 1319-25 | pmid=12421139 | doi=10.1043/0003-9985(2002)126<1319:CALMOT>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=12421139  }}</ref><ref name="pmid236158452">{{cite journal| author=Dentali F, Pomero F, Borretta V, Gianni M, Squizzato A, Fenoglio L et al.| title=Location of venous thrombosis in patients with FVL or prothrombin G20210A mutations: systematic review and meta-analysis. | journal=Thromb Haemost | year= 2013 | volume= 110 | issue= 1 | pages= 191-4 | pmid=23615845 | doi=10.1160/TH13-02-0163 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23615845  }}</ref>
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | -
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" |↑
| style="background: #F5F5F5; padding: 5px;" |N/A
| style="background: #F5F5F5; padding: 5px;" |
* [[Proximal]] [[DVT]] is more commonly observed as compared to [[distal]] [[DVT]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Pulmonary embolism]]
| style="background: #F5F5F5; padding: 5px;" |
* Detection of [[mutation]] using [[restriction enzyme]] and [[PCR]]
* [[DNA testing]] for [[prothrombin G20210A mutation]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Mutation]] causes increased production of [[prothrombin]]
* Increased [[blood]] levels of [[prothrombin]] lead to [[venous]] clots in the [[circulatory system]]
* [[Hormonal]] [[oral contraceptive pills]] can increase the risk of [[VTE]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Disseminated intravascular coagulation|Disseminated intravascular coagulation (DIC)]]<ref name="pmid25535423">{{cite journal |vauthors=Venugopal A |title=Disseminated intravascular coagulation |journal=Indian J Anaesth |volume=58 |issue=5 |pages=603–8 |date=September 2014 |pmid=25535423 |pmc=4260307 |doi=10.4103/0019-5049.144666 |url=}}</ref><ref name="pmid27276832">{{cite journal |vauthors=Makruasi N |title=Treatment of Disseminated Intravascular Coagulation |journal=J Med Assoc Thai |volume=98 Suppl 10 |issue= |pages=S45–51 |date=November 2015 |pmid=27276832 |doi= |url=}}</ref><ref name="pmid29178991">{{cite journal| author=Cui S, Fu Z, Feng Y, Xie X, Ma X, Liu T et al.| title=The disseminated intravascular coagulation score is a novel predictor for portal vein thrombosis in cirrhotic patients with hepatitis B. | journal=Thromb Res | year= 2018 | volume= 161 | issue=  | pages= 7-11 | pmid=29178991 | doi=10.1016/j.thromres.2017.11.010 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29178991  }}</ref>
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +/-
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" |↑
| style="background: #F5F5F5; padding: 5px;" |↑
| style="background: #F5F5F5; padding: 5px;" |
* [[Portal vein thrombosis]] is observed in patients with coexistent [[hepatitis B]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Pulmonary embolism]]
| style="background: #F5F5F5; padding: 5px;" |
* N/A
| style="background: #F5F5F5; padding: 5px;" |
* Elevated [[fibrin degradation products]] ([[D-dimers]])
* Decreased [[fibrinogen]]
* Decreased [[factor V]] and VIII
* Shistocytes (helmet [[cells]]) on [[peripheral blood smear]]
* [[Portal vein thrombosis]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Antiphospholipid  antibody syndrome]]<ref name="pmid24319251">{{cite journal |vauthors=Lim W |title=Antiphospholipid syndrome |journal=Hematology Am Soc Hematol Educ Program |volume=2013 |issue= |pages=675–80 |date=2013 |pmid=24319251 |doi=10.1182/asheducation-2013.1.675 |url=}}</ref><ref name="pmid19624461">{{cite journal |vauthors=Pengo V, Tripodi A, Reber G, Rand JH, Ortel TL, Galli M, De Groot PG |title=Update of the guidelines for lupus anticoagulant detection. Subcommittee on Lupus Anticoagulant/Antiphospholipid Antibody of the Scientific and Standardisation Committee of the International Society on Thrombosis and Haemostasis |journal=J. Thromb. Haemost. |volume=7 |issue=10 |pages=1737–40 |date=October 2009 |pmid=19624461 |doi=10.1111/j.1538-7836.2009.03555.x |url=}}</ref><ref name="pmid243192512">{{cite journal| author=Lim W| title=Antiphospholipid syndrome. | journal=Hematology Am Soc Hematol Educ Program | year= 2013 | volume= 2013 | issue=  | pages= 675-80 | pmid=24319251 | doi=10.1182/asheducation-2013.1.675 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=24319251  }}</ref><ref name="pmid29791828">{{cite journal| author=Garcia D, Erkan D| title=Diagnosis and Management of the Antiphospholipid Syndrome. | journal=N Engl J Med | year= 2018 | volume= 378 | issue= 21 | pages= 2010-2021 | pmid=29791828 | doi=10.1056/NEJMra1705454 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29791828  }}</ref><ref name="pmid23488294">{{cite journal| author=Kornacki J, Wirstlein P, Skrzypczak J| title=[Assessment of uterine arteries Doppler in the first half of pregnancy in women with thrombophilia]. | journal=Ginekol Pol | year= 2012 | volume= 83 | issue= 12 | pages= 916-21 | pmid=23488294 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23488294  }}</ref>
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +/-
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" | +
| style="background: #F5F5F5; padding: 5px;" |N/A
| style="background: #F5F5F5; padding: 5px;" |↑
| style="background: #F5F5F5; padding: 5px;" |
* Increased impedance of [[flow]] in [[uterine]] [[arteries]] at 12-20 weeks of [[gestation]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Pulmonary embolism]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Antiphospholipid antibody]]
* [[Anticardiolipin antibody]]
* [[Lupus anticoagulant]]
* Anti-β2GPI [[antibody]]
| style="background: #F5F5F5; padding: 5px;" |
* Both, [[arterial]] and [[venous]] [[thrombosis]] can occur
* History of [[spontaneous abortions]]
* [[False positive]] [[VDRL]]
* [[Stroke]] and [[transient ischemic attack]] ([[TIA]]) are most common forms of presentation of [[arterial thrombosis]]
|}
==References==
{{Reflist|2}}
{{WH}}
{{WS}}
[[Category: (name of the system)]]
__NOTOC__
__NOTOC__
{{Astrocytoma}}
{{CMG}}; {{AE}} {{Fs}}
==Overview==
On the basis of seizure, visual disturbance, and constitutional symptoms, astrocytoma must be differentiated from [[oligodendroglioma]], [[meningioma]], [[hemangioblastoma]], [[pituitary adenoma]], [[schwannoma]], [[Primary central nervous system lymphoma|primary CNS lymphoma]], [[medulloblastoma]], [[ependymoma]], [[craniopharyngioma]], [[pinealoma]], [[Arteriovenous malformation|AV malformation]], [[brain aneurysm]], [[bacterial]] [[brain]] [[abscess]], [[tuberculosis]], [[toxoplasmosis]], [[hydatid cyst]], [[CNS]] [[cryptococcosis]], [[CNS]] [[aspergillosis]], and [[brain metastasis]].
== Differentiating astrocytoma from other Diseases ==
=== Differentiating astrocytoma from other diseases on the basis of seizure, visual disturbance, and constitutional symptoms ===
On the basis of seizure, visual disturbance, and constitutional symptoms, astrocytoma must be differentiated from [[oligodendroglioma]], [[meningioma]], [[hemangioblastoma]], [[pituitary adenoma]], [[schwannoma]], [[Primary central nervous system lymphoma|primary CNS lymphoma]], [[medulloblastoma]], [[ependymoma]], [[craniopharyngioma]], [[pinealoma]], [[Arteriovenous malformation|AV malformation]], [[brain aneurysm]], [[bacterial]] [[brain]] [[abscess]], [[tuberculosis]], [[toxoplasmosis]], [[hydatid cyst]], [[CNS]] [[cryptococcosis]], [[CNS]] [[aspergillosis]], and [[brain metastasis]].
{|
|- style="background: #4479BA; color: #FFFFFF; text-align: center;"
! colspan="2" rowspan="4" |Diseases
| colspan="5" rowspan="1" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Clinical manifestations'''
! colspan="3" rowspan="2" |Para-clinical findings
| colspan="1" rowspan="4" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Gold<br>standard'''
! rowspan="4" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Additional findings
|-
| colspan="4" rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |'''Symptoms'''
! rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Physical examination
|-
! rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Lab Findings
! rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |MRI
! rowspan="2" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Immunohistopathology
|-
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Head-<br>ache
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Seizure
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Visual disturbance
! colspan="1" rowspan="1" style="background: #4479BA; color: #FFFFFF; text-align: center;" |Constitutional
! style="background: #4479BA; color: #FFFFFF; text-align: center;" |Focal neurological deficit
|-
| rowspan="7" style="background: #DCDCDC; padding: 5px; text-align: center;" |Adult primary brain tumors
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Glioblastoma multiforme]]<br><ref name="pmid17964028">{{cite journal |vauthors=Sathornsumetee S, Rich JN, Reardon DA |title=Diagnosis and treatment of high-grade astrocytoma |journal=Neurol Clin |volume=25 |issue=4 |pages=1111–39, x |date=November 2007 |pmid=17964028 |doi=10.1016/j.ncl.2007.07.004 |url=}}</ref><ref name="pmid22819718">{{cite journal |vauthors=Pedersen CL, Romner B |title=Current treatment of low grade astrocytoma: a review |journal=Clin Neurol Neurosurg |volume=115 |issue=1 |pages=1–8 |date=January 2013 |pmid=22819718 |doi=10.1016/j.clineuro.2012.07.002 |url=}}</ref><ref name=":0">{{cite book | last = Mattle | first = Heinrich | title = Fundamentals of neurology : an illustrated guide | publisher = Thieme | location = Stuttgart New York | year = 2017 | isbn = 9783131364524 }}</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;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" |−
| style="background: #F5F5F5; padding: 5px;" |
* [[Supratentorial]]
* Irregular ring-nodular enhancing lesions
* Central [[necrosis]]
* Surrounding [[vasogenic edema]]
* Cross [[corpus callosum]] ([[butterfly glioma]])
| style="background: #F5F5F5; padding: 5px;" |
* [[Astrocyte]] origin
* [[Pleomorphism|Pleomorphic]] cell
* Pseudopalisading appearance
* [[GFAP]] +
* [[Necrosis]] +
* [[Hemorrhage]] +
* [[Vascular]] prolifration +
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* Highest [[incidence]] in fifth and sixth decades of life
* Most of the time, focal [[neurological]] deficit is the presenting [[Sign (medical)|sign]].
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[oligodendroglioma]]<br><ref name="pmid26849038">{{cite journal |vauthors=Smits M |title=Imaging of oligodendroglioma |journal=Br J Radiol |volume=89 |issue=1060 |pages=20150857 |date=2016 |pmid=26849038 |pmc=4846213 |doi=10.1259/bjr.20150857 |url=}}</ref><ref name="pmid25943885">{{cite journal |vauthors=Wesseling P, van den Bent M, Perry A |title=Oligodendroglioma: pathology, molecular mechanisms and markers |journal=Acta Neuropathol. |volume=129 |issue=6 |pages=809–27 |date=June 2015 |pmid=25943885 |pmc=4436696 |doi=10.1007/s00401-015-1424-1 |url=}}</ref><ref name="pmid26478444">{{cite journal |vauthors=Kerkhof M, Benit C, Duran-Pena A, Vecht CJ |title=Seizures in oligodendroglial tumors |journal=CNS Oncol |volume=4 |issue=5 |pages=347–56 |date=2015 |pmid=26478444 |pmc=6082346 |doi=10.2217/cns.15.29 |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;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* Almost always in [[Cerebral hemisphere|cerebral hemisphers]] ([[Frontal lobe|frontal lobes]])
* Hypointense on T1
* Hyperintense on T2
* [[Calcification]]
* Chicken wire capillary pattern
| style="background: #F5F5F5; padding: 5px;" |
* [[Oligodendrocyte]] origin
* [[Calcification]] +
* Fried egg cell appearance
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* Highest [[incidence]] is between 40 and 50 years of age.
* Most of the time, [[epileptic seizure]] is the presenting [[Sign (medicine)|sign]].
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Meningioma]]<br><ref name="pmid1642904">{{cite journal |vauthors=Zee CS, Chin T, Segall HD, Destian S, Ahmadi J |title=Magnetic resonance imaging of meningiomas |journal=Semin. Ultrasound CT MR |volume=13 |issue=3 |pages=154–69 |date=June 1992 |pmid=1642904 |doi= |url=}}</ref><ref name="pmid25744347">{{cite journal |vauthors=Shibuya M |title=Pathology and molecular genetics of meningioma: recent advances |journal=Neurol. Med. Chir. (Tokyo) |volume=55 |issue=1 |pages=14–27 |date=2015 |pmid=25744347 |doi=10.2176/nmc.ra.2014-0233 |url=}}</ref><ref name="pmid17509660">{{cite journal |vauthors=Begnami MD, Palau M, Rushing EJ, Santi M, Quezado M |title=Evaluation of NF2 gene deletion in sporadic schwannomas, meningiomas, and ependymomas by chromogenic in situ hybridization |journal=Hum. Pathol. |volume=38 |issue=9 |pages=1345–50 |date=September 2007 |pmid=17509660 |pmc=2094208 |doi=10.1016/j.humpath.2007.01.027 |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;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* Well circumscribed
* Extra-axial [[mass]]
* [[Meninges|Dural]] attachment
* [[CSF]] [[vascular]] cleft sign
* Sunburst appearance of the [[Vessel|vessels]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Arachnoid]] origin
* [[Psammoma body|Psammoma bodies]]
* Whorled spindle cell pattern
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* Highest [[incidence]] is between 40 and 50 years of age.
* Most of the time, focal [[neurological]] deficit and [[epileptic seizure]] are the presenting [[signs]].
* May be associated with [[Neurofibromatosis type II|NF-2]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Hemangioblastoma]]<br><ref name="pmid24579662">{{cite journal |vauthors=Lonser RR, Butman JA, Huntoon K, Asthagiri AR, Wu T, Bakhtian KD, Chew EY, Zhuang Z, Linehan WM, Oldfield EH |title=Prospective natural history study of central nervous system hemangioblastomas in von Hippel-Lindau disease |journal=J. Neurosurg. |volume=120 |issue=5 |pages=1055–62 |date=May 2014 |pmid=24579662 |pmc=4762041 |doi=10.3171/2014.1.JNS131431 |url=}}</ref><ref name="pmid17877533">{{cite journal |vauthors=Hussein MR |title=Central nervous system capillary haemangioblastoma: the pathologist's viewpoint |journal=Int J Exp Pathol |volume=88 |issue=5 |pages=311–24 |date=October 2007 |pmid=17877533 |pmc=2517334 |doi=10.1111/j.1365-2613.2007.00535.x |url=}}</ref><ref name="pmid2704812">{{cite journal |vauthors=Lee SR, Sanches J, Mark AS, Dillon WP, Norman D, Newton TH |title=Posterior fossa hemangioblastomas: MR imaging |journal=Radiology |volume=171 |issue=2 |pages=463–8 |date=May 1989 |pmid=2704812 |doi=10.1148/radiology.171.2.2704812 |url=}}</ref><ref name="pmid945331">{{cite journal |vauthors=Perks WH, Cross JN, Sivapragasam S, Johnson P |title=Supratentorial haemangioblastoma with polycythaemia |journal=J. Neurol. Neurosurg. Psychiatry |volume=39 |issue=3 |pages=218–20 |date=March 1976 |pmid=945331 |doi= |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;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* [[Infratentorial]]
* [[Cyst|Cystic]] lesion with a solid enhancing mural [[nodule]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Blood vessel]] origin
* [[Capillary|Capillaries]] with thin walls
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* Might secret [[erythropoietin]] and cause [[polycythemia]]
* May be associated with [[Von Hippel-Lindau Disease|von hippel-lindau syndrome]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Pituitary adenoma]]<br><ref name="pmid3786729">{{cite journal |vauthors=Kucharczyk W, Davis DO, Kelly WM, Sze G, Norman D, Newton TH |title=Pituitary adenomas: high-resolution MR imaging at 1.5 T |journal=Radiology |volume=161 |issue=3 |pages=761–5 |date=December 1986 |pmid=3786729 |doi=10.1148/radiology.161.3.3786729 |url=}}</ref><ref name="pmid22584705">{{cite journal |vauthors=Syro LV, Scheithauer BW, Kovacs K, Toledo RA, Londoño FJ, Ortiz LD, Rotondo F, Horvath E, Uribe H |title=Pituitary tumors in patients with MEN1 syndrome |journal=Clinics (Sao Paulo) |volume=67 Suppl 1 |issue= |pages=43–8 |date=2012 |pmid=22584705 |pmc=3328811 |doi= |url=}}</ref><ref name=":0" />
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | + [[Bitemporal hemianopia]]
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* [[Endocrine]] abnormalities as a result of [[Pituitary adenoma|functional adenomas]] or pressure effect of non-functional [[Adenoma|adenomas]]
| style="background: #F5F5F5; padding: 5px;" |
* Isointense to normal [[pituitary gland]] in T1
| style="background: #F5F5F5; padding: 5px;" |
* [[Endocrine]] cell [[hyperplasia]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* It is associated with [[MEN1]] disease.
* Initialy presents with upper bitemporal quadrantanopsia followed by [[Bitemporal hemianopia|bitemporal hemianopsia]] (pressure on [[Optic chiasm|optic chiasma]] from below)
*
*
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Schwannoma]]<br><ref name="DonnellyDaly2007">{{cite journal|last1=Donnelly|first1=Martin J.|last2=Daly|first2=Carmel A.|last3=Briggs|first3=Robert J. S.|title=MR imaging features of an intracochlear acoustic schwannoma|journal=The Journal of Laryngology & Otology|volume=108|issue=12|year=2007|issn=0022-2151|doi=10.1017/S0022215100129056}}</ref><ref name="pmid9639114">{{cite journal |vauthors=Feany MB, Anthony DC, Fletcher CD |title=Nerve sheath tumours with hybrid features of neurofibroma and schwannoma: a conceptual challenge |journal=Histopathology |volume=32 |issue=5 |pages=405–10 |date=May 1998 |pmid=9639114 |doi= |url=}}</ref><ref name="pmid28710469">{{cite journal |vauthors=Chen H, Xue L, Wang H, Wang Z, Wu H |title=Differential NF2 Gene Status in Sporadic Vestibular Schwannomas and its Prognostic Impact on Tumour Growth Patterns |journal=Sci Rep |volume=7 |issue=1 |pages=5470 |date=July 2017 |pmid=28710469 |doi=10.1038/s41598-017-05769-0 |url=}}</ref><ref name="HardellHansson Mild2003">{{cite journal|last1=Hardell|first1=Lennart|last2=Hansson Mild|first2=Kjell|last3=Sandström|first3=Monica|last4=Carlberg|first4=Michael|last5=Hallquist|first5=Arne|last6=Påhlson|first6=Anneli|title=Vestibular Schwannoma, Tinnitus and Cellular Telephones|journal=Neuroepidemiology|volume=22|issue=2|year=2003|pages=124–129|issn=0251-5350|doi=10.1159/000068745}}</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;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* Split-fat sign
* Fascicular sign
* Often have areas of [[hemosiderin]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Schwann cell]] origin
* S100+
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* It causes [[hearing loss]] and [[tinnitus]]


{{CMG}}; {{AE}}
* May be associated with [[Neurofibromatosis type II|NF-2]] (bilateral [[Schwannoma|schwannomas]])
==Overview==
|-
The pathogenesis of alcoholic liver disease is complex and still remains unclear, the metabolites of the oxidative metabolism in the liver; acetaldehyde and reactive oxygen species are thought to be involved in the toxic effects of ethanol on the liver.<ref name="pmid25548474">{{cite journal |vauthors=Ceni E, Mello T, Galli A |title=Pathogenesis of alcoholic liver disease: role of oxidative metabolism |journal=World J. Gastroenterol. |volume=20 |issue=47 |pages=17756–72 |year=2014 |pmid=25548474 |pmc=4273126 |doi=10.3748/wjg.v20.i47.17756 |url=}}</ref>
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Primary central nervous system lymphoma|Primary CNS lymphoma]]<br><ref name="pmid7480733">{{cite journal |vauthors=Chinn RJ, Wilkinson ID, Hall-Craggs MA, Paley MN, Miller RF, Kendall BE, Newman SP, Harrison MJ |title=Toxoplasmosis and primary central nervous system lymphoma in HIV infection: diagnosis with MR spectroscopy |journal=Radiology |volume=197 |issue=3 |pages=649–54 |date=December 1995 |pmid=7480733 |doi=10.1148/radiology.197.3.7480733 |url=}}</ref><ref name="Paulus19992">{{cite journal|last1=Paulus|first1=Werner|journal=Journal of Neuro-Oncology|title=Classification, Pathogenesis and Molecular Pathology of Primary CNS Lymphomas|volume=43|issue=3|year=1999|pages=203–208|issn=0167594X|doi=10.1023/A:1006242116122}}</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;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* Usually deep in the [[white matter]]
 
* Single [[mass]] with ring enhancement
| style="background: #F5F5F5; padding: 5px;" |
* [[B cell]] origin
 
* Similar to [[Non-Hodgkin lymphoma|non hodgkin lymphoma]] ([[Diffuse large B cell lymphoma|diffuse large B cell]])
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* Usually in young [[immunocompromised]] patients ([[HIV]]) or old [[immunocompetent]] person.


==Pathophysiology==
*
|-
| rowspan="5" style="background: #DCDCDC; padding: 5px; text-align: center;" |Childhood primary brain tumors
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Pilocytic astrocytoma]]<br><ref name="pmid179640282">{{cite journal |vauthors=Sathornsumetee S, Rich JN, Reardon DA |title=Diagnosis and treatment of high-grade astrocytoma |journal=Neurol Clin |volume=25 |issue=4 |pages=1111–39, x |date=November 2007 |pmid=17964028 |doi=10.1016/j.ncl.2007.07.004 |url=}}</ref><ref name="pmid228197182">{{cite journal |vauthors=Pedersen CL, Romner B |title=Current treatment of low grade astrocytoma: a review |journal=Clin Neurol Neurosurg |volume=115 |issue=1 |pages=1–8 |date=January 2013 |pmid=22819718 |doi=10.1016/j.clineuro.2012.07.002 |url=}}</ref><ref name=":02">{{cite book | last = Mattle | first = Heinrich | title = Fundamentals of neurology : an illustrated guide | publisher = Thieme | location = Stuttgart New York | year = 2017 | isbn = 9783131364524 }}</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;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* [[Infratentorial]]


===Pathogenesis===
* Solid and [[Cyst|cystic]] component
*Ethanol metabolism in the liver is carried out mainly by two enzymes; alcohol dehydrogenase and aldehyde dehydrogenase. Both of these enzymes use NAD+ as a cofactor. Alcohol is converted to acetaldehyde and acetaldehyde is then further oxidized to acetate. Acetaldehyde is the toxic metabolite in this process.<ref name="pmid25548474">{{cite journal |vauthors=Ceni E, Mello T, Galli A |title=Pathogenesis of alcoholic liver disease: role of oxidative metabolism |journal=World J. Gastroenterol. |volume=20 |issue=47 |pages=17756–72 |year=2014 |pmid=25548474 |pmc=4273126 |doi=10.3748/wjg.v20.i47.17756 |url=}}</ref>
* Mostly in [[posterior fossa]]
*The metabolism of alcohol in the liver ends up producing an excess of reduced nicotinamide adenine dinucleotide(NADH). This changes the reduction-oxidation potential in the liver and inhibits key metabolic processes in the liver such as, the tricarboxylic acid cycle and the oxidation of fatty acids and thereby ends up promoting lipogenesis.<ref name="pmid15194557">{{cite journal |vauthors=You M, Crabb DW |title=Recent advances in alcoholic liver disease II. Minireview: molecular mechanisms of alcoholic fatty liver |journal=Am. J. Physiol. Gastrointest. Liver Physiol. |volume=287 |issue=1 |pages=G1–6 |year=2004 |pmid=15194557 |doi=10.1152/ajpgi.00056.2004 |url=}}</ref>
* Usually in [[Cerebellar hemisphere|cerebellar hemisphers]] and [[Cerebellar vermis|vermis]]
*Since acetaldehyde has an electrophilic nature it can form covalent chemical bonds with proteins, lipids and DNA. These covalent bonds that are formed are extremely pathogenic, as they have the ability to alter cell environments, protein structures and they can enable DNA damage and mutation.<ref name="pmid16088993">{{cite journal |vauthors=Freeman TL, Tuma DJ, Thiele GM, Klassen LW, Worrall S, Niemelä O, Parkkila S, Emery PW, Preedy VR |title=Recent advances in alcohol-induced adduct formation |journal=Alcohol. Clin. Exp. Res. |volume=29 |issue=7 |pages=1310–6 |year=2005 |pmid=16088993 |doi= |url=}}</ref><ref name="pmid17590995">{{cite journal |vauthors=Niemelä O |title=Acetaldehyde adducts in circulation |journal=Novartis Found. Symp. |volume=285 |issue= |pages=183–92; discussion 193–7 |year=2007 |pmid=17590995 |doi= |url=}}</ref><ref name="pmid11841919">{{cite journal |vauthors=Tuma DJ |title=Role of malondialdehyde-acetaldehyde adducts in liver injury |journal=Free Radic. Biol. Med. |volume=32 |issue=4 |pages=303–8 |year=2002 |pmid=11841919 |doi= |url=}}</ref><ref name="pmid15540799">{{cite journal |vauthors=Tuma DJ, Casey CA |title=Dangerous byproducts of alcohol breakdown--focus on adducts |journal=Alcohol Res Health |volume=27 |issue=4 |pages=285–90 |year=2003 |pmid=15540799 |doi= |url=}}</ref><ref name="pmid16054980">{{cite journal |vauthors=Brooks PJ, Theruvathu JA |title=DNA adducts from acetaldehyde: implications for alcohol-related carcinogenesis |journal=Alcohol |volume=35 |issue=3 |pages=187–93 |year=2005 |pmid=16054980 |doi=10.1016/j.alcohol.2005.03.009 |url=}}</ref><ref name="pmid17718399">{{cite journal |vauthors=Seitz HK, Becker P |title=Alcohol metabolism and cancer risk |journal=Alcohol Res Health |volume=30 |issue=1 |pages=38–41, 44–7 |year=2007 |pmid=17718399 |pmc=3860434 |doi= |url=}}</ref><ref name="pmid9857222">{{cite journal |vauthors=Biewald J, Nilius R, Langner J |title=Occurrence of acetaldehyde protein adducts formed in various organs of chronically ethanol fed rats: an immunohistochemical study |journal=Int. J. Mol. Med. |volume=2 |issue=4 |pages=389–96 |year=1998 |pmid=9857222 |doi= |url=}}</ref><ref name="pmid17543846">{{cite journal |vauthors=Seitz HK, Meier P |title=The role of acetaldehyde in upper digestive tract cancer in alcoholics |journal=Transl Res |volume=149 |issue=6 |pages=293–7 |year=2007 |pmid=17543846 |doi=10.1016/j.trsl.2006.12.002 |url=}}</ref>
| style="background: #F5F5F5; padding: 5px;" |
* [[Glial cell]] origin
*Solid and [[Cyst|cystic]] component


*The cytochrome P450 enzymes (CYP) are a part of the microsomal ethanol oxidizing system. These are a large group of enzymes involved in numerous oxidizing reactions on different substrates. They catalyze many different reactions in order to make them in to more polar metabolites that are easier to excrete.<ref name="pmid3678578">{{cite journal |vauthors=Guengerich FP, Beaune PH, Umbenhauer DR, Churchill PF, Bork RW, Dannan GA, Knodell RG, Lloyd RS, Martin MV |title=Cytochrome P-450 enzymes involved in genetic polymorphism of drug oxidation in humans |journal=Biochem. Soc. Trans. |volume=15 |issue=4 |pages=576–8 |year=1987 |pmid=3678578 |doi= |url=}}</ref>
* [[GFAP]] +
| style="background: #F5F5F5; padding: 5px;" |
* [[Biopsy]]
| style="background: #F5F5F5; padding: 5px;" |
* Most of the time, [[Cerebellum|cerebellar]] dysfunction is the presenting [[signs]].
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Medulloblastoma]]<br><ref name="DorwartWara1981">{{cite journal|last1=Dorwart|first1=R H|last2=Wara|first2=W M|last3=Norman|first3=D|last4=Levin|first4=V A|title=Complete myelographic evaluation of spinal metastases from medulloblastoma.|journal=Radiology|volume=139|issue=2|year=1981|pages=403–408|issn=0033-8419|doi=10.1148/radiology.139.2.7220886}}</ref><ref name="Fruehwald-PallamarPuchner2011">{{cite journal|last1=Fruehwald-Pallamar|first1=Julia|last2=Puchner|first2=Stefan B.|last3=Rossi|first3=Andrea|last4=Garre|first4=Maria L.|last5=Cama|first5=Armando|last6=Koelblinger|first6=Claus|last7=Osborn|first7=Anne G.|last8=Thurnher|first8=Majda M.|title=Magnetic resonance imaging spectrum of medulloblastoma|journal=Neuroradiology|volume=53|issue=6|year=2011|pages=387–396|issn=0028-3940|doi=10.1007/s00234-010-0829-8}}</ref><ref name="BurgerGrahmann1987">{{cite journal|last1=Burger|first1=P. C.|last2=Grahmann|first2=F. C.|last3=Bliestle|first3=A.|last4=Kleihues|first4=P.|title=Differentiation in the medulloblastoma|journal=Acta Neuropathologica|volume=73|issue=2|year=1987|pages=115–123|issn=0001-6322|doi=10.1007/BF00693776}}</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;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
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* [[Infratentorial]]


*There is an ethanol inducible form of CYP enzymes that is working in a small amount under normal physiological conditions. This enzyme CYP2E1 is converting ethanol to acetaldehyde and then to acetate. When there is chronic alcohol abuse, there is induction of the microsomal system and there is an increase in the expression of CYP2E1. This increase in CYP2E1 expression under chronic ethanol consumption can be hazardous, as this oxidation reaction can produces many different ROS; O<sub>2</sub><sup>-</sup>, H<sub>2</sub>O<sub>2</sub>, OH<sup>-</sup> and hydroxyethyl radical (HER).<ref name="pmid36785782">{{cite journal |vauthors=Guengerich FP, Beaune PH, Umbenhauer DR, Churchill PF, Bork RW, Dannan GA, Knodell RG, Lloyd RS, Martin MV |title=Cytochrome P-450 enzymes involved in genetic polymorphism of drug oxidation in humans |journal=Biochem. Soc. Trans. |volume=15 |issue=4 |pages=576–8 |year=1987 |pmid=3678578 |doi= |url=}}</ref><ref name="pmid5009602">{{cite journal |vauthors=Lieber CS |title=Metabolism of ethanol and alcoholism: racial and acquired factors |journal=Ann. Intern. Med. |volume=76 |issue=2 |pages=326–7 |year=1972 |pmid=5009602 |doi= |url=}}</ref><ref name="pmid4402282">{{cite journal |vauthors=Lieber CS, DeCarli LM |title=The role of the hepatic microsomal ethanol oxidizing system (MEOS) for ethanol metabolism in vivo |journal=J. Pharmacol. Exp. Ther. |volume=181 |issue=2 |pages=279–87 |year=1972 |pmid=4402282 |doi= |url=}}</ref><ref name="pmid9114822">{{cite journal |vauthors=Lieber CS |title=Cytochrome P-4502E1: its physiological and pathological role |journal=Physiol. Rev. |volume=77 |issue=2 |pages=517–44 |year=1997 |pmid=9114822 |doi= |url=}}</ref><ref name="pmid2333153">{{cite journal |vauthors=Hansson T, Tindberg N, Ingelman-Sundberg M, Köhler C |title=Regional distribution of ethanol-inducible cytochrome P450 IIE1 in the rat central nervous system |journal=Neuroscience |volume=34 |issue=2 |pages=451–63 |year=1990 |pmid=2333153 |doi= |url=}}</ref><ref name="pmid17760783">{{cite journal |vauthors=Donohue TM, Cederbaum AI, French SW, Barve S, Gao B, Osna NA |title=Role of the proteasome in ethanol-induced liver pathology |journal=Alcohol. Clin. Exp. Res. |volume=31 |issue=9 |pages=1446–59 |year=2007 |pmid=17760783 |doi=10.1111/j.1530-0277.2007.00454.x |url=}}</ref><ref name="pmid17854134">{{cite journal |vauthors=Osna NA, Donohue TM |title=Implication of altered proteasome function in alcoholic liver injury |journal=World J. Gastroenterol. |volume=13 |issue=37 |pages=4931–7 |year=2007 |pmid=17854134 |pmc=4434615 |doi= |url=}}</ref><ref name="pmid18078827">{{cite journal |vauthors=Lu Y, Cederbaum AI |title=CYP2E1 and oxidative liver injury by alcohol |journal=Free Radic. Biol. Med. |volume=44 |issue=5 |pages=723–38 |year=2008 |pmid=18078827 |pmc=2268632 |doi=10.1016/j.freeradbiomed.2007.11.004 |url=}}</ref><ref name="pmid1545775">{{cite journal |vauthors=Yun YP, Casazza JP, Sohn DH, Veech RL, Song BJ |title=Pretranslational activation of cytochrome P450IIE during ketosis induced by a high fat diet |journal=Mol. Pharmacol. |volume=41 |issue=3 |pages=474–9 |year=1992 |pmid=1545775 |doi= |url=}}</ref><ref name="pmid2005876">{{cite journal |vauthors=Raucy JL, Lasker JM, Kraner JC, Salazar DE, Lieber CS, Corcoran GB |title=Induction of cytochrome P450IIE1 in the obese overfed rat |journal=Mol. Pharmacol. |volume=39 |issue=3 |pages=275–80 |year=1991 |pmid=2005876 |doi= |url=}}</ref><ref name="pmid11826398">{{cite journal |vauthors=Woodcroft KJ, Hafner MS, Novak RF |title=Insulin signaling in the transcriptional and posttranscriptional regulation of CYP2E1 expression |journal=Hepatology |volume=35 |issue=2 |pages=263–73 |year=2002 |pmid=11826398 |doi=10.1053/jhep.2002.30691 |url=}}</ref><ref name="pmid7700245">{{cite journal |vauthors=De Waziers I, Garlatti M, Bouguet J, Beaune PH, Barouki R |title=Insulin down-regulates cytochrome P450 2B and 2E expression at the post-transcriptional level in the rat hepatoma cell line |journal=Mol. Pharmacol. |volume=47 |issue=3 |pages=474–9 |year=1995 |pmid=7700245 |doi= |url=}}</ref><ref name="pmid9765518">{{cite journal |vauthors=Peng HM, Coon MJ |title=Regulation of rabbit cytochrome P450 2E1 expression in HepG2 cells by insulin and thyroid hormone |journal=Mol. Pharmacol. |volume=54 |issue=4 |pages=740–7 |year=1998 |pmid=9765518 |doi= |url=}}</ref><ref name="pmid1822117">{{cite journal |vauthors=Terelius Y, Norsten-Höög C, Cronholm T, Ingelman-Sundberg M |title=Acetaldehyde as a substrate for ethanol-inducible cytochrome P450 (CYP2E1) |journal=Biochem. Biophys. Res. Commun. |volume=179 |issue=1 |pages=689–94 |year=1991 |pmid=1822117 |doi= |url=}}</ref><ref name="pmid9726291">{{cite journal |vauthors=Wu YS, Salmela KS, Lieber CS |title=Microsomal acetaldehyde oxidation is negligible in the presence of ethanol |journal=Alcohol. Clin. Exp. Res. |volume=22 |issue=5 |pages=1165–9 |year=1998 |pmid=9726291 |doi= |url=}}</ref><ref name="pmid9309320">{{cite journal |vauthors=Brooks PJ |title=DNA damage, DNA repair, and alcohol toxicity--a review |journal=Alcohol. Clin. Exp. Res. |volume=21 |issue=6 |pages=1073–82 |year=1997 |pmid=9309320 |doi= |url=}}</ref>
* Mostly in [[cerebellum]]


*Ethanol metabolism additionally promotes lipogenesis through the inhibition of peroxisome proliferator activated receptor α (PPAR-α) and AMP kinase, as well as the stimulation of sterol regulatory element binding protein 1, which is a membrane bound transcription factor. The sequence of all these events results in a fat storing metabolic remodeling of the liver.<ref name="pmid12791698">{{cite journal |vauthors=Fischer M, You M, Matsumoto M, Crabb DW |title=Peroxisome proliferator-activated receptor alpha (PPARalpha) agonist treatment reverses PPARalpha dysfunction and abnormalities in hepatic lipid metabolism in ethanol-fed mice |journal=J. Biol. Chem. |volume=278 |issue=30 |pages=27997–8004 |year=2003 |pmid=12791698 |doi=10.1074/jbc.M302140200 |url=}}</ref><ref name="pmid15578517">{{cite journal |vauthors=You M, Matsumoto M, Pacold CM, Cho WK, Crabb DW |title=The role of AMP-activated protein kinase in the action of ethanol in the liver |journal=Gastroenterology |volume=127 |issue=6 |pages=1798–808 |year=2004 |pmid=15578517 |doi= |url=}}</ref><ref name="pmid16879892">{{cite journal |vauthors=Ji C, Chan C, Kaplowitz N |title=Predominant role of sterol response element binding proteins (SREBP) lipogenic pathways in hepatic steatosis in the murine intragastric ethanol feeding model |journal=J. Hepatol. |volume=45 |issue=5 |pages=717–24 |year=2006 |pmid=16879892 |doi=10.1016/j.jhep.2006.05.009 |url=}}</ref>
* Non communicating [[hydrocephalus]]
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* [[Neuroectoderm]] origin


*Based on animal studies, 2 key factors that play an important role in the inflammatory process that leads to the alcohol mediated liver injury are endotoxin and gut permeability. Endotoxin is associated to the lipopolysaccharide (LPS) component of the outer wall of gram-negative bacteria and is thought to be the key trigger in this inflammatory process. Gut permeability is the factor that is either enabling or preventing the transfer of the LPS-endotoxin from the intestinal lumen into the portal circulation, it is seen to be altered in response to long term exposure to alcohol. This fact has been observed in humans as gut permeability and LPS-endotoxin levels have been found to be elevated in patients with alcoholic liver injury.<ref name="pmid6433728">{{cite journal |vauthors=Tsukamoto H, Reidelberger RD, French SW, Largman C |title=Long-term cannulation model for blood sampling and intragastric infusion in the rat |journal=Am. J. Physiol. |volume=247 |issue=3 Pt 2 |pages=R595–9 |year=1984 |pmid=6433728 |doi= |url=}}</ref><ref name="pmid11431739">{{cite journal |vauthors=Uesugi T, Froh M, Arteel GE, Bradford BU, Thurman RG |title=Toll-like receptor 4 is involved in the mechanism of early alcohol-induced liver injury in mice |journal=Hepatology |volume=34 |issue=1 |pages=101–8 |year=2001 |pmid=11431739 |doi=10.1053/jhep.2001.25350 |url=}}</ref><ref name="pmid15723320">{{cite journal |vauthors=Wiest R, Garcia-Tsao G |title=Bacterial translocation (BT) in cirrhosis |journal=Hepatology |volume=41 |issue=3 |pages=422–33 |year=2005 |pmid=15723320 |doi=10.1002/hep.20632 |url=}}</ref><ref name="pmid8171045">{{cite journal |vauthors=Nanji AA, Khettry U, Sadrzadeh SM |title=Lactobacillus feeding reduces endotoxemia and severity of experimental alcoholic liver (disease) |journal=Proc. Soc. Exp. Biol. Med. |volume=205 |issue=3 |pages=243–7 |year=1994 |pmid=8171045 |doi= |url=}}</ref><ref name="pmid7806045">{{cite journal |vauthors=Adachi Y, Moore LE, Bradford BU, Gao W, Thurman RG |title=Antibiotics prevent liver injury in rats following long-term exposure to ethanol |journal=Gastroenterology |volume=108 |issue=1 |pages=218–24 |year=1995 |pmid=7806045 |doi= |url=}}</ref><ref name="pmid6141332">{{cite journal |vauthors=Bjarnason I, Peters TJ, Wise RJ |title=The leaky gut of alcoholism: possible route of entry for toxic compounds |journal=Lancet |volume=1 |issue=8370 |pages=179–82 |year=1984 |pmid=6141332 |doi= |url=}}</ref><ref name="pmid11236841">{{cite journal |vauthors=Urbaschek R, McCuskey RS, Rudi V, Becker KP, Stickel F, Urbaschek B, Seitz HK |title=Endotoxin, endotoxin-neutralizing-capacity, sCD14, sICAM-1, and cytokines in patients with various degrees of alcoholic liver disease |journal=Alcohol. Clin. Exp. Res. |volume=25 |issue=2 |pages=261–8 |year=2001 |pmid=11236841 |doi= |url=}}</ref>
* Homer wright rosettes
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* [[Biopsy]]
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* [[Drop metastasis]] ([[metastasis]] through [[CSF]])
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Ependymoma]]<br><ref name="YuhBarkovich2009">{{cite journal|last1=Yuh|first1=E. L.|last2=Barkovich|first2=A. J.|last3=Gupta|first3=N.|title=Imaging of ependymomas: MRI and CT|journal=Child's Nervous System|volume=25|issue=10|year=2009|pages=1203–1213|issn=0256-7040|doi=10.1007/s00381-009-0878-7}}</ref><ref name=":0" />
| 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;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
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* [[Infratentorial]]


*Experimental studies in animals have led to a better understanding of the disease process and how the factors mentioned above contribute to these processes. After the entry of LPS-endotoxin in to the portal circulation it binds to the LPS-binding protein, this is a key step in the inflammatory and histopathological response to alcohol ingestion.The LPS-Lps binding protein complex binds to the CD14 receptor on the cell surface membrane of the Kupffer cells in the liver. Activation of these Kupffer cells requires 3 main cellular proteins: CD 14 (monocyte differentiation antigen), toll-like receptor 4 (TLR4) and a protein known as MD2, this protein binds TLR4 with LPS-LPS binding protein. The TLR4 then signals activation of early growth response 1 (EGR1), which is an early gene-zinc-finger transcription factor. The nuclear factor-kB (NF-kB) and the TLR4 adapter also play an important role in the activation of the kupffer cells. EGR1 plays the pivotal role in lipopolysaccharide-stimulated TNF-α production; in mice the absence of EGR1 prevents alcohol induced liver injury.<ref name="pmid11884468">{{cite journal |vauthors=Uesugi T, Froh M, Arteel GE, Bradford BU, Wheeler MD, Gäbele E, Isayama F, Thurman RG |title=Role of lipopolysaccharide-binding protein in early alcohol-induced liver injury in mice |journal=J. Immunol. |volume=168 |issue=6 |pages=2963–9 |year=2002 |pmid=11884468 |doi= |url=}}</ref><ref name="pmid8045507">{{cite journal |vauthors=Adachi Y, Bradford BU, Gao W, Bojes HK, Thurman RG |title=Inactivation of Kupffer cells prevents early alcohol-induced liver injury |journal=Hepatology |volume=20 |issue=2 |pages=453–60 |year=1994 |pmid=8045507 |doi= |url=}}</ref><ref name="pmid11477402">{{cite journal |vauthors=Akira S, Takeda K, Kaisho T |title=Toll-like receptors: critical proteins linking innate and acquired immunity |journal=Nat. Immunol. |volume=2 |issue=8 |pages=675–80 |year=2001 |pmid=11477402 |doi=10.1038/90609 |url=}}</ref><ref name="pmid11254735">{{cite journal |vauthors=Yin M, Bradford BU, Wheeler MD, Uesugi T, Froh M, Goyert SM, Thurman RG |title=Reduced early alcohol-induced liver injury in CD14-deficient mice |journal=J. Immunol. |volume=166 |issue=7 |pages=4737–42 |year=2001 |pmid=11254735 |doi= |url=}}</ref><ref name="pmid15940638">{{cite journal |vauthors=McMullen MR, Pritchard MT, Wang Q, Millward CA, Croniger CM, Nagy LE |title=Early growth response-1 transcription factor is essential for ethanol-induced fatty liver injury in mice |journal=Gastroenterology |volume=128 |issue=7 |pages=2066–76 |year=2005 |pmid=15940638 |pmc=1959407 |doi= |url=}}</ref><ref name="pmid18713975">{{cite journal |vauthors=Zhao XJ, Dong Q, Bindas J, Piganelli JD, Magill A, Reiser J, Kolls JK |title=TRIF and IRF-3 binding to the TNF promoter results in macrophage TNF dysregulation and steatosis induced by chronic ethanol |journal=J. Immunol. |volume=181 |issue=5 |pages=3049–56 |year=2008 |pmid=18713975 |pmc=3690475 |doi= |url=}}</ref><ref name="pmid18792393">{{cite journal |vauthors=Hritz I, Mandrekar P, Velayudham A, Catalano D, Dolganiuc A, Kodys K, Kurt-Jones E, Szabo G |title=The critical role of toll-like receptor (TLR) 4 in alcoholic liver disease is independent of the common TLR adapter MyD88 |journal=Hepatology |volume=48 |issue=4 |pages=1224–31 |year=2008 |pmid=18792393 |doi=10.1002/hep.22470 |url=}}</ref>
* Usually found in [[Fourth ventricle|4th ventricle]]
* Mixed [[Cyst|cystic]]/solid [[lesion]]


*Ethanol administration stimulates the release of mitochondrial cytochrome c and the expression of the Fas ligand, this leads to hepatic cell apoptosis mediated by the cascade-3 activation pathway. The cumulative effect of TNF-α and Fas-mediated apoptotic signals make the hepatocytes more susceptible to injury by stimulating an increase in natural killer T cells in the liver.<ref name="pmid11438480">{{cite journal |vauthors=Zhou Z, Sun X, Kang YJ |title=Ethanol-induced apoptosis in mouse liver: Fas- and cytochrome c-mediated caspase-3 activation pathway |journal=Am. J. Pathol. |volume=159 |issue=1 |pages=329–38 |year=2001 |pmid=11438480 |pmc=1850406 |doi=10.1016/S0002-9440(10)61699-9 |url=}}</ref><ref name="pmid15131799">{{cite journal |vauthors=Minagawa M, Deng Q, Liu ZX, Tsukamoto H, Dennert G |title=Activated natural killer T cells induce liver injury by Fas and tumor necrosis factor-alpha during alcohol consumption |journal=Gastroenterology |volume=126 |issue=5 |pages=1387–99 |year=2004 |pmid=15131799 |doi= |url=}}</ref>
* Hydrocephalus
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* [[Ependymal cell]] origin


==Genetics==
* Peri[[vascular]] pseudorosette
*[Disease name] is transmitted in [mode of genetic transmission] pattern.
| style="background: #F5F5F5; padding: 5px;" |
*Genes involved in the pathogenesis of [disease name] include [gene1], [gene2], and [gene3].
* [[Biopsy]]
*The development of [disease name] is the result of multiple genetic mutations.
| style="background: #F5F5F5; padding: 5px;" |
* Causes an unusually persistent, continuous [[headache]] in children.
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Craniopharyngioma]]<br><ref name="pmid12407316">{{cite journal |vauthors=Brunel H, Raybaud C, Peretti-Viton P, Lena G, Girard N, Paz-Paredes A, Levrier O, Farnarier P, Manera L, Choux M |title=[Craniopharyngioma in children: MRI study of 43 cases] |language=French |journal=Neurochirurgie |volume=48 |issue=4 |pages=309–18 |date=September 2002 |pmid=12407316 |doi= |url=}}</ref><ref name="PrabhuBrown2005">{{cite journal|last1=Prabhu|first1=Vikram C.|last2=Brown|first2=Henry G.|title=The pathogenesis of craniopharyngiomas|journal=Child's Nervous System|volume=21|issue=8-9|year=2005|pages=622–627|issn=0256-7040|doi=10.1007/s00381-005-1190-9}}</ref><ref name="pmid766825">{{cite journal |vauthors=Kennedy HB, Smith RJ |title=Eye signs in craniopharyngioma |journal=Br J Ophthalmol |volume=59 |issue=12 |pages=689–95 |date=December 1975 |pmid=766825 |pmc=1017436 |doi= |url=}}</ref><ref name=":0" />
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | + [[Bitemporal hemianopia]]
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px; text-align: center;" | +
| style="background: #F5F5F5; padding: 5px;" |
* [[Hypopituitarism]] as a result of pressure effect on [[pituitary gland]]
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* [[Calcification]]
* Lobulated contour
* Motor-oil like fluid within [[tumor]]
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* [[Ectoderm|Ectodermal]] origin ([[Rathke's pouch|Rathkes pouch]])


==Associated Conditions==
* [[Calcification]] +
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* [[Biopsy]]
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* Initialy presents with lower bitemporal quadrantanopsia followed by [[Bitemporal hemianopia|bitemporal hemianopsia]] (pressure on [[Optic chiasm|optic chiasma]] from above)
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Pinealoma]]<br><ref name="pmid6625640">{{cite journal |vauthors=Ahmed SR, Shalet SM, Price DA, Pearson D |title=Human chorionic gonadotrophin secreting pineal germinoma and precocious puberty |journal=Arch. Dis. Child. |volume=58 |issue=9 |pages=743–5 |date=September 1983 |pmid=6625640 |doi= |url=}}</ref><ref name="Sano1976">{{cite journal|last1=Sano|first1=Keiji|title=Pinealoma in Children|journal=Pediatric Neurosurgery|volume=2|issue=1|year=1976|pages=67–72|issn=1016-2291|doi=10.1159/000119602}}</ref><ref name="Baggenstoss1939">{{cite journal|last1=Baggenstoss|first1=Archie H.|title=PINEALOMAS|journal=Archives of Neurology And Psychiatry|volume=41|issue=6|year=1939|pages=1187|issn=0096-6754|doi=10.1001/archneurpsyc.1939.02270180115011}}</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;" | + vertical gaze palsy
| style="background: #F5F5F5; padding: 5px;" |
* B-hCG rise leads to [[precocious puberty]] in [[Male|males]]
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* [[Hydrocephalus]] (compression of [[cerebral aqueduct]])
| style="background: #F5F5F5; padding: 5px;" |
* Similar to [[testicular seminoma]]
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* [[Biopsy]]
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* May cause prinaud syndrome ([[Vertical gaze center|vertical gaze]] palsy, pupillary light-near dissociation, lid retraction and convergence-retraction [[nystagmus]]
|-
| rowspan="2" style="background: #DCDCDC; padding: 5px; text-align: center;" |Vascular
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Arteriovenous malformation|AV malformation]]<br><ref name="KucharczykLemme-Pleghos1985">{{cite journal|last1=Kucharczyk|first1=W|last2=Lemme-Pleghos|first2=L|last3=Uske|first3=A|last4=Brant-Zawadzki|first4=M|last5=Dooms|first5=G|last6=Norman|first6=D|title=Intracranial vascular malformations: MR and CT imaging.|journal=Radiology|volume=156|issue=2|year=1985|pages=383–389|issn=0033-8419|doi=10.1148/radiology.156.2.4011900}}</ref><ref name="FleetwoodSteinberg2002">{{cite journal|last1=Fleetwood|first1=Ian G|last2=Steinberg|first2=Gary K|title=Arteriovenous malformations|journal=The Lancet|volume=359|issue=9309|year=2002|pages=863–873|issn=01406736|doi=10.1016/S0140-6736(02)07946-1}}</ref><ref name=":0" />
| 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;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* [[Supratentorial]]: ~85%
* Flow voids on T2 weighted images
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* We do not perform [[biopsy]] for [[AVM]]
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* [[Angiography]]
| style="background: #F5F5F5; padding: 5px;" |
* We may see bag of worms appearance in [[CT angiography]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Brain aneurysm]]<br><ref name="ChapmanRubinstein1992">{{cite journal|last1=Chapman|first1=Arlene B.|last2=Rubinstein|first2=David|last3=Hughes|first3=Richard|last4=Stears|first4=John C.|last5=Earnest|first5=Michael P.|last6=Johnson|first6=Ann M.|last7=Gabow|first7=Patricia A.|last8=Kaehny|first8=William D.|title=Intracranial Aneurysms in Autosomal Dominant Polycystic Kidney Disease|journal=New England Journal of Medicine|volume=327|issue=13|year=1992|pages=916–920|issn=0028-4793|doi=10.1056/NEJM199209243271303}}</ref><ref name="pmid25632331">{{cite journal |vauthors=Castori M, Voermans NC |title=Neurological manifestations of Ehlers-Danlos syndrome(s): A review |journal=Iran J Neurol |volume=13 |issue=4 |pages=190–208 |date=October 2014 |pmid=25632331 |pmc=4300794 |doi= |url=}}</ref><ref name="SchievinkRaissi2010">{{cite journal|last1=Schievink|first1=W. I.|last2=Raissi|first2=S. S.|last3=Maya|first3=M. M.|last4=Velebir|first4=A.|title=Screening for intracranial aneurysms in patients with bicuspid aortic valve|journal=Neurology|volume=74|issue=18|year=2010|pages=1430–1433|issn=0028-3878|doi=10.1212/WNL.0b013e3181dc1acf}}</ref><ref name="pmid28486967">{{cite journal |vauthors=Germain DP |title=Pseudoxanthoma elasticum |journal=Orphanet J Rare Dis |volume=12 |issue=1 |pages=85 |date=May 2017 |pmid=28486967 |pmc=5424392 |doi=10.1186/s13023-017-0639-8 |url=}}</ref><ref name="pmid27162847">{{cite journal |vauthors=Farahmand M, Farahangiz S, Yadollahi M |title=Diagnostic Accuracy of Magnetic Resonance Angiography for Detection of Intracranial Aneurysms in Patients with Acute Subarachnoid Hemorrhage; A Comparison to Digital Subtraction Angiography |journal=Bull Emerg Trauma |volume=1 |issue=4 |pages=147–51 |date=October 2013 |pmid=27162847 |pmc=4789449 |doi= |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;" | +/−
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* In [[magnetic resonance angiography]], we may see [[aneurysm]] mostly in anterior circulation (~85%)
| style="background: #F5F5F5; padding: 5px;" |
* We do not perform [[biopsy]] for [[brain aneurysm]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Magnetic resonance angiography]]  and [[CT angiography]] ([[Angiography]] is reserved for patients who have negative [[Magnetic resonance angiography|MAR]] and [[CT angiography|CTA]])
| style="background: #F5F5F5; padding: 5px;" |
* It is associated with [[autosomal dominant polycystic kidney disease]], [[Ehlers-Danlos syndrome]], [[pseudoxanthoma elasticum]] and [[Bicuspid aortic valve]]
|-
| rowspan="6" style="background: #DCDCDC; padding: 5px; text-align: center;" |Infectious
| style="background: #DCDCDC; padding: 5px; text-align: center;" |Bacterial [[brain abscess]]<br><ref name="HaimesZimmerman1989">{{cite journal|last1=Haimes|first1=AB|last2=Zimmerman|first2=RD|last3=Morgello|first3=S|last4=Weingarten|first4=K|last5=Becker|first5=RD|last6=Jennis|first6=R|last7=Deck|first7=MD|title=MR imaging of brain abscesses|journal=American Journal of Roentgenology|volume=152|issue=5|year=1989|pages=1073–1085|issn=0361-803X|doi=10.2214/ajr.152.5.1073}}</ref><ref name="BrouwerTunkel2014">{{cite journal|last1=Brouwer|first1=Matthijs C.|last2=Tunkel|first2=Allan R.|last3=McKhann|first3=Guy M.|last4=van de Beek|first4=Diederik|title=Brain Abscess|journal=New England Journal of Medicine|volume=371|issue=5|year=2014|pages=447–456|issn=0028-4793|doi=10.1056/NEJMra1301635}}</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;" | +
| style="background: #F5F5F5; padding: 5px;" |
* [[Leukocytosis]]
* Elevated [[ESR]]
* [[Blood culture]] may be positive for underlying [[organism]]
| style="background: #F5F5F5; padding: 5px;" |
* Central hypodense signal and surrounding ring-enhancement in T1
* Central hyperintense area surrounded by a well-defined hypointense capsule with surrounding [[edema]] in T2
| style="background: #F5F5F5; padding: 5px;" |
* We do not perform [[biopsy]] for [[brain abscess]]
| style="background: #F5F5F5; padding: 5px;" |
* Clinical presentation/ imaging
| style="background: #F5F5F5; padding: 5px;" |
* The most common causes of [[brain abscess]] are [[Streptococcus]] and [[Staphylococcus]].
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Tuberculosis]]<br><ref name="MorgadoRuivo2005">{{cite journal|last1=Morgado|first1=Carlos|last2=Ruivo|first2=Nuno|title=Imaging meningo-encephalic tuberculosis|journal=European Journal of Radiology|volume=55|issue=2|year=2005|pages=188–192|issn=0720048X|doi=10.1016/j.ejrad.2005.04.017}}</ref><ref name=":0" /><ref name="pmid19275620">{{cite journal |vauthors=Be NA, Kim KS, Bishai WR, Jain SK |title=Pathogenesis of central nervous system tuberculosis |journal=Curr. Mol. Med. |volume=9 |issue=2 |pages=94–9 |date=March 2009 |pmid=19275620 |pmc=4486069 |doi= |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;" | +
| style="background: #F5F5F5; padding: 5px;" |
* Positive [[acid-fast bacilli]] ([[AFB]]) smear in [[CSF]] specimen
* Positive [[CSF]] [[nucleic acid]] amplification testing
* [[Hyponatremia]] (inappropriate secretion of [[antidiuretic hormone]])
* Mild [[anemia]]
* [[Leukocytosis]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Hydrocephalus]] combined with marked basilar [[Meninges|meningeal]] enhancement
| style="background: #F5F5F5; padding: 5px;" |
* We do not perform [[biopsy]] for [[brain]] [[tuberculosis]]
| style="background: #F5F5F5; padding: 5px;" |
* [[CSF]] analysis/ Imaging
| style="background: #F5F5F5; padding: 5px;" |
* It is associated with [[HIV]] [[infection]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Toxoplasmosis]]<br><ref name="pmid74807332">{{cite journal |vauthors=Chinn RJ, Wilkinson ID, Hall-Craggs MA, Paley MN, Miller RF, Kendall BE, Newman SP, Harrison MJ |title=Toxoplasmosis and primary central nervous system lymphoma in HIV infection: diagnosis with MR spectroscopy |journal=Radiology |volume=197 |issue=3 |pages=649–54 |date=December 1995 |pmid=7480733 |doi=10.1148/radiology.197.3.7480733 |url=}}</ref><ref name="pmid27348541">{{cite journal |vauthors=Helton KJ, Maron G, Mamcarz E, Leventaki V, Patay Z, Sadighi Z |title=Unusual magnetic resonance imaging presentation of post-BMT cerebral toxoplasmosis masquerading as meningoencephalitis and ventriculitis |journal=Bone Marrow Transplant. |volume=51 |issue=11 |pages=1533–1536 |date=November 2016 |pmid=27348541 |doi=10.1038/bmt.2016.168 |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;" | +
| style="background: #F5F5F5; padding: 5px;" |
* Normal [[CSF]]
| style="background: #F5F5F5; padding: 5px;" |
* Multifocal [[Mass|masses]] with ring enhancement
* Mostly in [[basal ganglia]], [[thalami]], and corticomedullary junction.
| style="background: #F5F5F5; padding: 5px;" |
* We do not perform [[biopsy]] for brain [[toxoplasmosis]]
| style="background: #F5F5F5; padding: 5px;" |
* Clinical presentation/ imaging
| style="background: #F5F5F5; padding: 5px;" |
* It is associated with [[HIV]] [[infection]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Hydatid cyst]]<br><ref name="pmid27620198">{{cite journal |vauthors=Taslakian B, Darwish H |title=Intracranial hydatid cyst: imaging findings of a rare disease |journal=BMJ Case Rep |volume=2016 |issue= |pages= |date=September 2016 |pmid=27620198 |pmc=5030532 |doi=10.1136/bcr-2016-216570 |url=}}</ref><ref name=":0" />
| 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;" | +
| style="background: #F5F5F5; padding: 5px; text-align: left;" |
* Positive [[serology]] ([[Antibody]] detection for [[E. granulosus]]'')''
| style="background: #F5F5F5; padding: 5px;" |
* Honeycomb appearance
* [[Necrotic]] area
| style="background: #F5F5F5; padding: 5px;" |
* We do not perform [[biopsy]] for [[Hydatid cyst|hydatid cysts]]
| style="background: #F5F5F5; padding: 5px;" |
* Imaging
| style="background: #F5F5F5; padding: 5px;" |
* [[Brain]], [[eye]], and [[Spleen|splenic]] [[Cyst|cysts]] may not produce detectable amount of [[antibodies]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[CNS]] [[cryptococcosis]]<br><ref name="pmid25006721">{{cite journal |vauthors=McCarthy M, Rosengart A, Schuetz AN, Kontoyiannis DP, Walsh TJ |title=Mold infections of the central nervous system |journal=N. Engl. J. Med. |volume=371 |issue=2 |pages=150–60 |date=July 2014 |pmid=25006721 |pmc=4840461 |doi=10.1056/NEJMra1216008 |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;" | +
| style="background: #F5F5F5; padding: 5px;" |
* Positive [[CSF]] [[antigen]] testing ([[coccidioidomycosis]])
* [[CSF]] [[Lymphocyte|lymphocytic]] [[pleocytosis]]
* Elevated [[CSF]] [[Protein|proteins]] and [[lactate]]
* Low [[CSF]] [[glucose]]
*
| style="background: #F5F5F5; padding: 5px;" |
* Dilated peri[[vascular]] spaces
* [[Basal ganglia]] [[Pseudocyst|pseudocysts]]


==Gross Pathology==
* Soap bubble brain lesions ([[cryptococcus neoformans]])
*On gross pathology, characteristic findings of alcoholic liver disease include:<ref name="pmid24739823">{{cite journal |vauthors=Agrawal P, Vaiphei K |title=Histomorphological features of pancreas and liver in chronic alcoholics--an analytical study in 390 autopsy cases |journal=Indian J Pathol Microbiol |volume=57 |issue=1 |pages=2–8 |year=2014 |pmid=24739823 |doi=10.4103/0377-4929.130842 |url=}}</ref>
*  
**Hepatomegaly
| style="background: #F5F5F5; padding: 5px;" |
**Nodules
* We may see numerous acutely branching septate [[Hypha|hyphae]]
***Macronodules
| style="background: #F5F5F5; padding: 5px;" |
***Micronodules
* [[Laboratory|Lab]] data/ Imaging
**Firm in consistency
* since [[brain]] [[Biopsy|biopsies]] are highly invasive and may may cause [[neurological]] deficits, we [[diagnose]] [[CNS]] [[fungal]] [[Infection|infections]] based on [[laboratory]] and imaging findings
**Portal vein dilation
| style="background: #F5F5F5; padding: 5px;" |
* It is the most common [[brain]] [[fungal infection]]


==Microscopic Pathology==
* It is associated with [[HIV]], [[Immunosuppressive therapy|immunosuppressive therapies]], and [[Organ transplant|organ transplants]]
*On microscopic histopathological analysis, steatosis (macrovesicular steatosis-the cytoplasm of hepatocytes is occupied by large lipid droplets that end up displacing the nucleus and other organelles peripherally), proliferation of the smooth endoplasmic reticulum, distortion of the mitochondria (giant mitochondria) and hepatocyte balooning (Mallory-Denk bodies) are characteristic findings of alcoholic liver disease.<ref name="pmid15763228">{{cite journal |vauthors=Lefkowitch JH |title=Morphology of alcoholic liver disease |journal=Clin Liver Dis |volume=9 |issue=1 |pages=37–53 |year=2005 |pmid=15763228 |doi=10.1016/j.cld.2004.11.001 |url=}}</ref><ref name="pmid5641156">{{cite journal |vauthors=Rubin E, Lieber CS |title=Alcohol-induced hepatic injury in nonalcoholic volunteers |journal=N. Engl. J. Med. |volume=278 |issue=16 |pages=869–76 |year=1968 |pmid=5641156 |doi=10.1056/NEJM196804182781602 |url=}}</ref><ref name="pmid7806041">{{cite journal |vauthors=Fromenty B, Grimbert S, Mansouri A, Beaugrand M, Erlinger S, Rötig A, Pessayre D |title=Hepatic mitochondrial DNA deletion in alcoholics: association with microvesicular steatosis |journal=Gastroenterology |volume=108 |issue=1 |pages=193–200 |year=1995 |pmid=7806041 |doi= |url=}}</ref><ref name="pmid3699404">{{cite journal |vauthors=Chedid A, Mendenhall CL, Tosch T, Chen T, Rabin L, Garcia-Pont P, Goldberg SJ, Kiernan T, Seeff LB, Sorrell M |title=Significance of megamitochondria in alcoholic liver disease |journal=Gastroenterology |volume=90 |issue=6 |pages=1858–64 |year=1986 |pmid=3699404 |doi= |url=}}</ref><ref name="pmid6700382">{{cite journal |vauthors=Uchida T, Kronborg I, Peters RL |title=Giant mitochondria in the alcoholic liver diseases--their identification, frequency and pathologic significance |journal=Liver |volume=4 |issue=1 |pages=29–38 |year=1984 |pmid=6700382 |doi= |url=}}</ref>
* In may happen in [[immunocompetent]] patients undergoing invasive procedures ( [[neurosurgery]]) or exposed to [[Contamination|contaminated]] devices or [[drugs]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[CNS]] [[aspergillosis]]<br><ref name="pmid250067212">{{cite journal |vauthors=McCarthy M, Rosengart A, Schuetz AN, Kontoyiannis DP, Walsh TJ |title=Mold infections of the central nervous system |journal=N. Engl. J. Med. |volume=371 |issue=2 |pages=150–60 |date=July 2014 |pmid=25006721 |pmc=4840461 |doi=10.1056/NEJMra1216008 |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;" | +
| style="background: #F5F5F5; padding: 5px;" |
* Positive [[galactomannan]] [[antigen]] testing ([[aspergillosis]])
* [[CSF]] [[Lymphocyte|lymphocytic]] [[pleocytosis]]
* Elevated [[CSF]] [[Protein|proteins]] and [[lactate]]
* Low [[CSF]] [[glucose]]
| style="background: #F5F5F5; padding: 5px;" |
* Multiple [[Abscess|abscesses]]
* Ring enhancement
* Peripheral low signal intensity on T2
| style="background: #F5F5F5; padding: 5px;" |
* We may see numerous acutely branching septate [[Hypha|hyphae]]
| style="background: #F5F5F5; padding: 5px;" |
* [[Laboratory|Lab]] data/ Imaging
* since [[brain]] [[Biopsy|biopsies]] are highly invasive and may may cause [[neurological]] deficits, we [[diagnose]] [[CNS]] [[fungal]] [[Infection|infections]] based on [[laboratory]] and imaging findings
| style="background: #F5F5F5; padding: 5px;" |
* It is associated with [[HIV]], [[Immunosuppressive therapy|immunosuppressive therapies]], and [[Organ transplant|organ transplants]]
* In may happen in [[immunocompetent]] patients undergoing invasive procedures ( [[neurosurgery]]) or exposed to [[Contamination|contaminated]] devices or [[drugs]]
|-
| style="background: #DCDCDC; padding: 5px; text-align: center;" |Other
| style="background: #DCDCDC; padding: 5px; text-align: center;" |[[Brain metastasis]]<br><ref name="pmid29307364">{{cite journal |vauthors=Pope WB |title=Brain metastases: neuroimaging |journal=Handb Clin Neurol |volume=149 |issue= |pages=89–112 |date=2018 |pmid=29307364 |pmc=6118134 |doi=10.1016/B978-0-12-811161-1.00007-4 |url=}}</ref><ref name=":0" />
| 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;" | +
| style="background: #F5F5F5; padding: 5px; text-align: center;" | −
| style="background: #F5F5F5; padding: 5px;" |
* Multiple [[Lesion|lesions]]
* [[Vasogenic edema]]
*
| style="background: #F5F5F5; padding: 5px;" |
* Based on the primary [[cancer]] type we may have different immunohistopathology findings.
| style="background: #F5F5F5; padding: 5px;" |
* History/ imaging
* If there is any uncertainty about [[etiology]], [[biopsy]] should be performed
| style="background: #F5F5F5; padding: 5px;" |
* Most common primary [[Tumor|tumors]] that [[metastasis]] to [[brain]]:
** [[Lung cancer]]
** [[Renal cell carcinoma]]
** [[Breast cancer]]
** [[Melanoma]]
** [[Gastrointestinal tract]]
|}
'''ABBREVIATIONS'''


*A cirrhotic liver will show fibrous septae that are made up of collagen surrounding the hepatocytes which results in pseudo lobule formation. This produces a nodular appearance of the liver and then progresses from micro nodular to macro nodular cirrhosis with time. Proliferation of the bile ducts may also be seen.<ref name="pmid6629323">{{cite journal |vauthors=Fauerholdt L, Schlichting P, Christensen E, Poulsen H, Tygstrup N, Juhl E |title=Conversion of micronodular cirrhosis into macronodular cirrhosis |journal=Hepatology |volume=3 |issue=6 |pages=928–31 |year=1983 |pmid=6629323 |doi= |url=}}</ref><ref name="pmid649765">{{cite journal |vauthors=Anthony PP, Ishak KG, Nayak NC, Poulsen HE, Scheuer PJ, Sobin LH |title=The morphology of cirrhosis. Recommendations on definition, nomenclature, and classification by a working group sponsored by the World Health Organization |journal=J. Clin. Pathol. |volume=31 |issue=5 |pages=395–414 |year=1978 |pmid=649765 |pmc=1145292 |doi= |url=}}</ref><ref name="pmid2466751">{{cite journal |vauthors=Van Eyken P, Sciot R, Desmet VJ |title=A cytokeratin immunohistochemical study of alcoholic liver disease: evidence that hepatocytes can express 'bile duct-type' cytokeratins |journal=Histopathology |volume=13 |issue=6 |pages=605–17 |year=1988 |pmid=2466751 |doi= |url=}}</ref>
CNS=Central nervous system, AV=Arteriovenous, CSF=Cerebrospinal fluid, NF-2=Neurofibromatosis type 2, MEN-1=Multiple endocrine neoplasia, GFAP=Glial fibrillary acidic protein, HIV=Human immunodeficiency virus, BhCG=Human chorionic gonadotropin, ESR=Erythrocyte sedimentation rate, AFB=Acid fast bacilli


==References==
==References==
Line 50: Line 746:
{{WH}}
{{WH}}
{{WS}}
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[[Category:Disease]]
[[Category:Neurology]]
[[Category:Neurosurgery]]
[[Category:Pathology]]
[[Category:Up-To-Date]]
[[Category:Oncology]]
[[Category:Medicine]]

Latest revision as of 18:31, 30 January 2019

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: M. Khurram Afzal, MD [2], Sogand Goudarzi, MD [3]

Differentiating [disease name] from other diseases on the basis of [symptom 1], [symptom 2], and [symptom 3]

On the basis [symptom 1], [symptom 2], and [symptom 3], [disease name] must be differentiated from [disease 1], [disease 2], [disease 3], [disease 4], [disease 5], and [disease 6].

Diseases Clinical manifestations Para-clinical findings Gold standard Additional findings
Symptoms Physical examination
Lab Findings Imaging
Symptoms of DVT Symptoms of Pulmonary Embolism Symptoms of Myocardial Infarction Tenderness in extremities Edema in extremities Warmth in extremities PT aPTT Doppler ultrasound Chest CT scan
Antithrombin III deficiency[1][2][3] + + - + + + Normal
  • Normal
  • Reduces the Increase in PTT after administration of heparin
Factor V Leiden mutation[4][5][6][7][8] + + + + + + N/A ↑
  • N/A
  • Inactivates factor Va and factor VIIIa
Protein C deficiency[9][10][11] + + - + + + Normal Normal / ↑
Protein S deficiency[11][12][13] + + - + + + Normal Normal / ↑
Prothrombin gene mutation[14][15][16] + + - + + + ↑ N/A
Disseminated intravascular coagulation (DIC)[17][18][19] + + +/- + + + ↑ ↑
  • N/A
Antiphospholipid antibody syndrome[20][21][22][23][24] + + +/- + + + N/A ↑

References

  1. ↑ Patnaik MM, Moll S (November 2008). "Inherited antithrombin deficiency: a review". Haemophilia. 14 (6): 1229–39. doi:10.1111/j.1365-2516.2008.01830.x. PMID 19141163.
  2. ↑ Al Hadidi, Samer; Wu, Kristi; Aburahma, Ahmed; Alamarat, Zain (2017). "Family with clots: antithrombin deficiency". BMJ Case Reports: bcr-2017–221556. doi:10.1136/bcr-2017-221556. ISSN 1757-790X.
  3. ↑ Konecny F (January 2009). "Inherited trombophilic states and pulmonary embolism". J Res Med Sci. 14 (1): 43–56. PMC 3129068. PMID 21772860.
  4. ↑ Mannucci PM, Asselta R, Duga S, Guella I, Spreafico M, Lotta L, Merlini PA, Peyvandi F, Kathiresan S, Ardissino D (October 2010). "The association of factor V Leiden with myocardial infarction is replicated in 1880 patients with premature disease". J. Thromb. Haemost. 8 (10): 2116–21. doi:10.1111/j.1538-7836.2010.03982.x. PMID 20626623.
  5. ↑ Campello E, Spiezia L, Simioni P (December 2016). "Diagnosis and management of factor V Leiden". Expert Rev Hematol. 9 (12): 1139–1149. doi:10.1080/17474086.2016.1249364. PMID 27797270.
  6. ↑ Van Rooden CJ, Rosendaal FR, Meinders AE, Van Oostayen JA, Van Der Meer FJ, Huisman MV (February 2004). "The contribution of factor V Leiden and prothrombin G20210A mutation to the risk of central venous catheter-related thrombosis". Haematologica. 89 (2): 201–6. PMID 15003896.
  7. ↑ Dentali F, Pomero F, Borretta V, Gianni M, Squizzato A, Fenoglio L; et al. (2013). "Location of venous thrombosis in patients with FVL or prothrombin G20210A mutations: systematic review and meta-analysis". Thromb Haemost. 110 (1): 191–4. doi:10.1160/TH13-02-0163. PMID 23615845.
  8. ↑ Press RD, Bauer KA, Kujovich JL, Heit JA (November 2002). "Clinical utility of factor V leiden (R506Q) testing for the diagnosis and management of thromboembolic disorders". Arch. Pathol. Lab. Med. 126 (11): 1304–18. doi:10.1043/0003-9985(2002)126<1304:CUOFVL>2.0.CO;2. PMID 12421138.
  9. ↑ Bernard Khor & Elizabeth M. Van Cott (2010). "Laboratory tests for protein C deficiency". American journal of hematology. 85 (6): 440–442. doi:10.1002/ajh.21679. PMID 20309856. Unknown parameter |month= ignored (help)
  10. ↑ Pescatore SL (March 2001). "Clinical management of protein C deficiency". Expert Opin Pharmacother. 2 (3): 431–9. doi:10.1517/14656566.2.3.431. PMID 11336597.
  11. ↑ 11.0 11.1 Gustavo A. Rodriguez-Leal, Segundo Moran, Roberto Corona-Cedillo & Rocio Brom-Valladares (2014). "Portal vein thrombosis with protein C-S deficiency in a non-cirrhotic patient". World journal of hepatology. 6 (7): 532–537. doi:10.4254/wjh.v6.i7.532. PMID 25068006. Unknown parameter |month= ignored (help)
  12. ↑ Kristi J. Smock, Elizabeth A. Plumhoff, Piet Meijer, Peihong Hsu, Nicole D. Zantek, Nahla M. Heikal & Elizabeth M. Van Cott (2016). "Protein S testing in patients with protein S deficiency, factor V Leiden, and rivaroxaban by North American Specialized Coagulation Laboratories". Thrombosis and haemostasis. 116 (1): 50–57. doi:10.1160/TH15-12-0918. PMID 27075008. Unknown parameter |month= ignored (help)
  13. ↑ Ji M, Yoon SN, Lee W, Jang S, Park SH, Kim DY, Chun S, Min WK (October 2011). "Protein S deficiency with a PROS1 gene mutation in a patient presenting with mesenteric venous thrombosis following total colectomy". Blood Coagul. Fibrinolysis. 22 (7): 619–21. doi:10.1097/MBC.0b013e32834a0421. PMID 21799399.
  14. ↑ Cooper PC, Rezende SM (2007). "An overview of methods for detection of factor V Leiden and the prothrombin G20210A mutations". Int J Lab Hematol. 29 (3): 153–62. doi:10.1111/j.1751-553X.2007.00892.x. PMID 17474891.
  15. ↑ McGlennen RC, Key NS (2002). "Clinical and laboratory management of the prothrombin G20210A mutation". Arch Pathol Lab Med. 126 (11): 1319–25. doi:10.1043/0003-9985(2002)126<1319:CALMOT>2.0.CO;2. PMID 12421139.
  16. ↑ Dentali F, Pomero F, Borretta V, Gianni M, Squizzato A, Fenoglio L; et al. (2013). "Location of venous thrombosis in patients with FVL or prothrombin G20210A mutations: systematic review and meta-analysis". Thromb Haemost. 110 (1): 191–4. doi:10.1160/TH13-02-0163. PMID 23615845.
  17. ↑ Venugopal A (September 2014). "Disseminated intravascular coagulation". Indian J Anaesth. 58 (5): 603–8. doi:10.4103/0019-5049.144666. PMC 4260307. PMID 25535423.
  18. ↑ Makruasi N (November 2015). "Treatment of Disseminated Intravascular Coagulation". J Med Assoc Thai. 98 Suppl 10: S45–51. PMID 27276832.
  19. ↑ Cui S, Fu Z, Feng Y, Xie X, Ma X, Liu T; et al. (2018). "The disseminated intravascular coagulation score is a novel predictor for portal vein thrombosis in cirrhotic patients with hepatitis B." Thromb Res. 161: 7–11. doi:10.1016/j.thromres.2017.11.010. PMID 29178991.
  20. ↑ Lim W (2013). "Antiphospholipid syndrome". Hematology Am Soc Hematol Educ Program. 2013: 675–80. doi:10.1182/asheducation-2013.1.675. PMID 24319251.
  21. ↑ Pengo V, Tripodi A, Reber G, Rand JH, Ortel TL, Galli M, De Groot PG (October 2009). "Update of the guidelines for lupus anticoagulant detection. Subcommittee on Lupus Anticoagulant/Antiphospholipid Antibody of the Scientific and Standardisation Committee of the International Society on Thrombosis and Haemostasis". J. Thromb. Haemost. 7 (10): 1737–40. doi:10.1111/j.1538-7836.2009.03555.x. PMID 19624461.
  22. ↑ Lim W (2013). "Antiphospholipid syndrome". Hematology Am Soc Hematol Educ Program. 2013: 675–80. doi:10.1182/asheducation-2013.1.675. PMID 24319251.
  23. ↑ Garcia D, Erkan D (2018). "Diagnosis and Management of the Antiphospholipid Syndrome". N Engl J Med. 378 (21): 2010–2021. doi:10.1056/NEJMra1705454. PMID 29791828.
  24. ↑ Kornacki J, Wirstlein P, Skrzypczak J (2012). "[Assessment of uterine arteries Doppler in the first half of pregnancy in women with thrombophilia]". Ginekol Pol. 83 (12): 916–21. PMID 23488294.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [4]; Associate Editor(s)-in-Chief: Fahimeh Shojaei, M.D.

Overview

On the basis of seizure, visual disturbance, and constitutional symptoms, astrocytoma must be differentiated from oligodendroglioma, meningioma, hemangioblastoma, pituitary adenoma, schwannoma, primary CNS lymphoma, medulloblastoma, ependymoma, craniopharyngioma, pinealoma, AV malformation, brain aneurysm, bacterial brain abscess, tuberculosis, toxoplasmosis, hydatid cyst, CNS cryptococcosis, CNS aspergillosis, and brain metastasis.

Differentiating astrocytoma from other Diseases

Differentiating astrocytoma from other diseases on the basis of seizure, visual disturbance, and constitutional symptoms

On the basis of seizure, visual disturbance, and constitutional symptoms, astrocytoma must be differentiated from oligodendroglioma, meningioma, hemangioblastoma, pituitary adenoma, schwannoma, primary CNS lymphoma, medulloblastoma, ependymoma, craniopharyngioma, pinealoma, AV malformation, brain aneurysm, bacterial brain abscess, tuberculosis, toxoplasmosis, hydatid cyst, CNS cryptococcosis, CNS aspergillosis, and brain metastasis.

Diseases Clinical manifestations Para-clinical findings Gold
standard 		Additional findings
Symptoms Physical examination
Lab Findings MRI Immunohistopathology
Head-
ache 		Seizure Visual disturbance Constitutional Focal neurological deficit
Adult primary brain tumors Glioblastoma multiforme
[1][2][3] 		+ +/− +/− − + −
  • Pseudopalisading appearance
oligodendroglioma
[4][5][6] 		+ + +/− − + −
  • Chicken wire capillary pattern
  • Fried egg cell appearance
Meningioma
[7][8][9] 		+ +/− +/− − + −
  • Well circumscribed
  • Extra-axial mass
  • Whorled spindle cell pattern
  • May be associated with NF-2
Hemangioblastoma
[10][11][12][13] 		+ +/− +/− − + −
Pituitary adenoma
[14][15][3] 		− − + Bitemporal hemianopia − −
  • It is associated with MEN1 disease.
Schwannoma
[16][17][18][19] 		− − − − + −
  • Split-fat sign
  • Fascicular sign
  • Often have areas of hemosiderin
  • S100+
Primary CNS lymphoma
[20][21] 		+ +/− +/− − + −
  • Single mass with ring enhancement
Childhood primary brain tumors Pilocytic astrocytoma
[22][23][24] 		+ +/− +/− − + −
Medulloblastoma
[25][26][27] 		+ +/− +/− − + −
  • Homer wright rosettes
Ependymoma
[28][3] 		+ +/− +/− − + −
  • Hydrocephalus
  • Causes an unusually persistent, continuous headache in children.
Craniopharyngioma
[29][30][31][3] 		+ +/− + Bitemporal hemianopia − +
Pinealoma
[32][33][34] 		+ +/− +/− − + vertical gaze palsy
  • May cause prinaud syndrome (vertical gaze palsy, pupillary light-near dissociation, lid retraction and convergence-retraction nystagmus
Vascular AV malformation
[35][36][3] 		+ + +/− − +/− −
Brain aneurysm
[37][38][39][40][41] 		+ +/− +/− − +/− −
Infectious Bacterial brain abscess
[42][43] 		+ +/− +/− + +
  • Central hypodense signal and surrounding ring-enhancement in T1
  • Central hyperintense area surrounded by a well-defined hypointense capsule with surrounding edema in T2
  • Clinical presentation/ imaging
Tuberculosis
[44][3][45] 		+ +/− +/− + +
  • CSF analysis/ Imaging
Toxoplasmosis
[46][47] 		+ +/− +/− − +
  • Clinical presentation/ imaging
Hydatid cyst
[48][3] 		+ +/− +/− +/− +
  • Imaging
CNS cryptococcosis
[49] 		+ +/− +/− + +
  • We may see numerous acutely branching septate hyphae
CNS aspergillosis
[50] 		+ +/− +/− + +
  • Multiple abscesses
  • Ring enhancement
  • Peripheral low signal intensity on T2
  • We may see numerous acutely branching septate hyphae
Other Brain metastasis
[51][3] 		+ +/− +/− + + −
  • Based on the primary cancer type we may have different immunohistopathology findings.
  • History/ imaging
  • If there is any uncertainty about etiology, biopsy should be performed

ABBREVIATIONS

CNS=Central nervous system, AV=Arteriovenous, CSF=Cerebrospinal fluid, NF-2=Neurofibromatosis type 2, MEN-1=Multiple endocrine neoplasia, GFAP=Glial fibrillary acidic protein, HIV=Human immunodeficiency virus, BhCG=Human chorionic gonadotropin, ESR=Erythrocyte sedimentation rate, AFB=Acid fast bacilli

References

  1. ↑ Sathornsumetee S, Rich JN, Reardon DA (November 2007). "Diagnosis and treatment of high-grade astrocytoma". Neurol Clin. 25 (4): 1111–39, x. doi:10.1016/j.ncl.2007.07.004. PMID 17964028.
  2. ↑ Pedersen CL, Romner B (January 2013). "Current treatment of low grade astrocytoma: a review". Clin Neurol Neurosurg. 115 (1): 1–8. doi:10.1016/j.clineuro.2012.07.002. PMID 22819718.
  3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 Mattle, Heinrich (2017). Fundamentals of neurology : an illustrated guide. Stuttgart New York: Thieme. ISBN 9783131364524.
  4. ↑ Smits M (2016). "Imaging of oligodendroglioma". Br J Radiol. 89 (1060): 20150857. doi:10.1259/bjr.20150857. PMC 4846213. PMID 26849038.
  5. ↑ Wesseling P, van den Bent M, Perry A (June 2015). "Oligodendroglioma: pathology, molecular mechanisms and markers". Acta Neuropathol. 129 (6): 809–27. doi:10.1007/s00401-015-1424-1. PMC 4436696. PMID 25943885.
  6. ↑ Kerkhof M, Benit C, Duran-Pena A, Vecht CJ (2015). "Seizures in oligodendroglial tumors". CNS Oncol. 4 (5): 347–56. doi:10.2217/cns.15.29. PMC 6082346. PMID 26478444.
  7. ↑ Zee CS, Chin T, Segall HD, Destian S, Ahmadi J (June 1992). "Magnetic resonance imaging of meningiomas". Semin. Ultrasound CT MR. 13 (3): 154–69. PMID 1642904.
  8. ↑ Shibuya M (2015). "Pathology and molecular genetics of meningioma: recent advances". Neurol. Med. Chir. (Tokyo). 55 (1): 14–27. doi:10.2176/nmc.ra.2014-0233. PMID 25744347.
  9. ↑ Begnami MD, Palau M, Rushing EJ, Santi M, Quezado M (September 2007). "Evaluation of NF2 gene deletion in sporadic schwannomas, meningiomas, and ependymomas by chromogenic in situ hybridization". Hum. Pathol. 38 (9): 1345–50. doi:10.1016/j.humpath.2007.01.027. PMC 2094208. PMID 17509660.
  10. ↑ Lonser RR, Butman JA, Huntoon K, Asthagiri AR, Wu T, Bakhtian KD, Chew EY, Zhuang Z, Linehan WM, Oldfield EH (May 2014). "Prospective natural history study of central nervous system hemangioblastomas in von Hippel-Lindau disease". J. Neurosurg. 120 (5): 1055–62. doi:10.3171/2014.1.JNS131431. PMC 4762041. PMID 24579662.
  11. ↑ Hussein MR (October 2007). "Central nervous system capillary haemangioblastoma: the pathologist's viewpoint". Int J Exp Pathol. 88 (5): 311–24. doi:10.1111/j.1365-2613.2007.00535.x. PMC 2517334. PMID 17877533.
  12. ↑ Lee SR, Sanches J, Mark AS, Dillon WP, Norman D, Newton TH (May 1989). "Posterior fossa hemangioblastomas: MR imaging". Radiology. 171 (2): 463–8. doi:10.1148/radiology.171.2.2704812. PMID 2704812.
  13. ↑ Perks WH, Cross JN, Sivapragasam S, Johnson P (March 1976). "Supratentorial haemangioblastoma with polycythaemia". J. Neurol. Neurosurg. Psychiatry. 39 (3): 218–20. PMID 945331.
  14. ↑ Kucharczyk W, Davis DO, Kelly WM, Sze G, Norman D, Newton TH (December 1986). "Pituitary adenomas: high-resolution MR imaging at 1.5 T". Radiology. 161 (3): 761–5. doi:10.1148/radiology.161.3.3786729. PMID 3786729.
  15. ↑ Syro LV, Scheithauer BW, Kovacs K, Toledo RA, Londoño FJ, Ortiz LD, Rotondo F, Horvath E, Uribe H (2012). "Pituitary tumors in patients with MEN1 syndrome". Clinics (Sao Paulo). 67 Suppl 1: 43–8. PMC 3328811. PMID 22584705.
  16. ↑ Donnelly, Martin J.; Daly, Carmel A.; Briggs, Robert J. S. (2007). "MR imaging features of an intracochlear acoustic schwannoma". The Journal of Laryngology & Otology. 108 (12). doi:10.1017/S0022215100129056. ISSN 0022-2151.
  17. ↑ Feany MB, Anthony DC, Fletcher CD (May 1998). "Nerve sheath tumours with hybrid features of neurofibroma and schwannoma: a conceptual challenge". Histopathology. 32 (5): 405–10. PMID 9639114.
  18. ↑ Chen H, Xue L, Wang H, Wang Z, Wu H (July 2017). "Differential NF2 Gene Status in Sporadic Vestibular Schwannomas and its Prognostic Impact on Tumour Growth Patterns". Sci Rep. 7 (1): 5470. doi:10.1038/s41598-017-05769-0. PMID 28710469.
  19. ↑ Hardell, Lennart; Hansson Mild, Kjell; Sandström, Monica; Carlberg, Michael; Hallquist, Arne; Påhlson, Anneli (2003). "Vestibular Schwannoma, Tinnitus and Cellular Telephones". Neuroepidemiology. 22 (2): 124–129. doi:10.1159/000068745. ISSN 0251-5350.
  20. ↑ Chinn RJ, Wilkinson ID, Hall-Craggs MA, Paley MN, Miller RF, Kendall BE, Newman SP, Harrison MJ (December 1995). "Toxoplasmosis and primary central nervous system lymphoma in HIV infection: diagnosis with MR spectroscopy". Radiology. 197 (3): 649–54. doi:10.1148/radiology.197.3.7480733. PMID 7480733.
  21. ↑ Paulus, Werner (1999). "Classification, Pathogenesis and Molecular Pathology of Primary CNS Lymphomas". Journal of Neuro-Oncology. 43 (3): 203–208. doi:10.1023/A:1006242116122. ISSN 0167-594X.
  22. ↑ Sathornsumetee S, Rich JN, Reardon DA (November 2007). "Diagnosis and treatment of high-grade astrocytoma". Neurol Clin. 25 (4): 1111–39, x. doi:10.1016/j.ncl.2007.07.004. PMID 17964028.
  23. ↑ Pedersen CL, Romner B (January 2013). "Current treatment of low grade astrocytoma: a review". Clin Neurol Neurosurg. 115 (1): 1–8. doi:10.1016/j.clineuro.2012.07.002. PMID 22819718.
  24. ↑ Mattle, Heinrich (2017). Fundamentals of neurology : an illustrated guide. Stuttgart New York: Thieme. ISBN 9783131364524.
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  26. ↑ Fruehwald-Pallamar, Julia; Puchner, Stefan B.; Rossi, Andrea; Garre, Maria L.; Cama, Armando; Koelblinger, Claus; Osborn, Anne G.; Thurnher, Majda M. (2011). "Magnetic resonance imaging spectrum of medulloblastoma". Neuroradiology. 53 (6): 387–396. doi:10.1007/s00234-010-0829-8. ISSN 0028-3940.
  27. ↑ Burger, P. C.; Grahmann, F. C.; Bliestle, A.; Kleihues, P. (1987). "Differentiation in the medulloblastoma". Acta Neuropathologica. 73 (2): 115–123. doi:10.1007/BF00693776. ISSN 0001-6322.
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  40. ↑ Germain DP (May 2017). "Pseudoxanthoma elasticum". Orphanet J Rare Dis. 12 (1): 85. doi:10.1186/s13023-017-0639-8. PMC 5424392. PMID 28486967.
  41. ↑ Farahmand M, Farahangiz S, Yadollahi M (October 2013). "Diagnostic Accuracy of Magnetic Resonance Angiography for Detection of Intracranial Aneurysms in Patients with Acute Subarachnoid Hemorrhage; A Comparison to Digital Subtraction Angiography". Bull Emerg Trauma. 1 (4): 147–51. PMC 4789449. PMID 27162847.
  42. ↑ Haimes, AB; Zimmerman, RD; Morgello, S; Weingarten, K; Becker, RD; Jennis, R; Deck, MD (1989). "MR imaging of brain abscesses". American Journal of Roentgenology. 152 (5): 1073–1085. doi:10.2214/ajr.152.5.1073. ISSN 0361-803X.
  43. ↑ Brouwer, Matthijs C.; Tunkel, Allan R.; McKhann, Guy M.; van de Beek, Diederik (2014). "Brain Abscess". New England Journal of Medicine. 371 (5): 447–456. doi:10.1056/NEJMra1301635. ISSN 0028-4793.
  44. ↑ Morgado, Carlos; Ruivo, Nuno (2005). "Imaging meningo-encephalic tuberculosis". European Journal of Radiology. 55 (2): 188–192. doi:10.1016/j.ejrad.2005.04.017. ISSN 0720-048X.
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  46. ↑ Chinn RJ, Wilkinson ID, Hall-Craggs MA, Paley MN, Miller RF, Kendall BE, Newman SP, Harrison MJ (December 1995). "Toxoplasmosis and primary central nervous system lymphoma in HIV infection: diagnosis with MR spectroscopy". Radiology. 197 (3): 649–54. doi:10.1148/radiology.197.3.7480733. PMID 7480733.
  47. ↑ Helton KJ, Maron G, Mamcarz E, Leventaki V, Patay Z, Sadighi Z (November 2016). "Unusual magnetic resonance imaging presentation of post-BMT cerebral toxoplasmosis masquerading as meningoencephalitis and ventriculitis". Bone Marrow Transplant. 51 (11): 1533–1536. doi:10.1038/bmt.2016.168. PMID 27348541.
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  49. ↑ McCarthy M, Rosengart A, Schuetz AN, Kontoyiannis DP, Walsh TJ (July 2014). "Mold infections of the central nervous system". N. Engl. J. Med. 371 (2): 150–60. doi:10.1056/NEJMra1216008. PMC 4840461. PMID 25006721.
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  51. ↑ Pope WB (2018). "Brain metastases: neuroimaging". Handb Clin Neurol. 149: 89–112. doi:10.1016/B978-0-12-811161-1.00007-4. PMC 6118134. PMID 29307364.

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