Amnesia pathophysiology: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
 
(31 intermediate revisions by the same user not shown)
Line 4: Line 4:
{{CMG}}; {{AE}} {{ZMalik}}
{{CMG}}; {{AE}} {{ZMalik}}
==Overview==
==Overview==
The exact pathogenesis of [disease name] is not fully understood.
[[Memory]] is the stored information in the [[hippocampal]] region of the [[brain]]. depending on the duration, [[memory]] is divided into short term and long term.
 
OR
 
It is thought that [disease name] is the result of / is mediated by / is produced by / is caused by either [hypothesis 1], [hypothesis 2], or [hypothesis 3].
 
OR
 
[Pathogen name] is usually transmitted via the [transmission route] route to the human host.
 
OR
 
Following transmission/ingestion, the [pathogen] uses the [entry site] to invade the [cell name] cell.
 
OR
 
 
[Disease or malignancy name] arises from [cell name]s, which are [cell type] cells that are normally involved in [function of cells].
 
OR
 
The progression to [disease name] usually involves the [molecular pathway].
 
OR
 
The pathophysiology of [disease/malignancy] depends on the histological subtype.
 
==Pathophysiology==
==Pathophysiology==
===Physiology===
===Physiology===
Line 44: Line 18:
! align="center" style="background: #4479BA; color: #FFFFFF| '''Pathogenesis'''
! align="center" style="background: #4479BA; color: #FFFFFF| '''Pathogenesis'''
  |-
  |-
  | [[Dissociative Amnesia]]        ||Temporary, [[episodic]] [[retrograde memory loss]]. Cause is [[psychological]] in origin. [[Dissociative Amnesia]] is also referred to as [[psychological]] amnesia. It has variable presentation:
  | [[Dissociative Amnesia]]        ||[[Psychological]] origin.  
*[[Repressed amnesia]] is seen in [[patients]] where they are unable to recall a stressful or traumatic incident from the past due to [[psychological]] [[defense mechanism]].
*[[Dissociative fugue]] has been observed in these [[patients]] where the identity and [[memory]] is lost. It is reversible and has variable time duration.<ref name="pmid18086739">{{cite journal| author=Bourget D, Whitehurst L| title=Amnesia and crime. | journal=J Am Acad Psychiatry Law | year= 2007 | volume= 35 | issue= 4 | pages= 469-80 | pmid=18086739 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18086739  }} </ref><ref name="pmid30311153">{{cite journal| author=Khalili M, Wong RJ| title=Underserved Does Not Mean Undeserved: Unfurling the HCV Care in the Safety Net. | journal=Dig Dis Sci | year= 2018 | volume= 63 | issue= 12 | pages= 3250-3252 | pmid=30311153 | doi=10.1007/s10620-018-5316-9 | pmc=6436636 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=30311153  }} </ref><ref> American Psychiatric Association (2013). Diagnostic and statistical manual of mental disorders : DSM-5</ref>
  |-
  |-
  | [[Post-traumatic Amnesia]] || Amnesia that follows [[head]] [[trauma]] could be temporary or permanent. The span of memory loss is uncertain it could present with retrograde, anterograde or combined. Extent of [[injury]] and duration of [[loss of consciousness]] are important [[prognostic]] factors in determining the severity of amnesia. <ref name="pmid11475324">{{cite journal| author=Leclerc S, Lassonde M, Delaney JS, Lacroix VJ, Johnston KM| title=Recommendations for grading of concussion in athletes. | journal=Sports Med | year= 2001 | volume= 31 | issue= 8 | pages= 629-36 | pmid=11475324 | doi=10.2165/00007256-200131080-00007 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11475324 }} </ref>
  |[[Transient global amnesia]] || Precipitated by [[brain]] [[ischemia]], [[migraine]], [[epileptic]] [[seizure]], [[venous]] [[congestion]], [[psychological]] [[trauma]].<ref name="pmid19031042">{{cite journal| author=Profice P, Rizzello V, Pennestrì F, Pilato F, Della Marca G, Sestito A | display-authors=etal| title=Transient global amnesia during transoesophageal echocardiogram. | journal=Neurol Sci | year= 2008 | volume= 29 | issue= 6 | pages= 477-9 | pmid=19031042 | doi=10.1007/s10072-008-1034-y | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19031042 }} </ref>
  |-
  |-
  | [[Infantile]] Amnesia|| Also known as childhood amnesia. Early childhood memory is lost, usually up to the age of fours year. Influenced by cultural norms and [[sexual]] [[repression]].<ref name="pmid12653489">{{cite journal| author=Wang Q| title=Infantile amnesia reconsidered: a cross-cultural analysis. | journal=Memory | year= 2003 | volume= 11 | issue= 1 | pages= 65-80 | pmid=12653489 | doi=10.1080/741938173 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12653489 }} </ref>
  | [[Post-traumatic Amnesia]] || Amnesia that follows [[head]] [[trauma]] could be temporary or permanent.<ref name="pmid11475324">{{cite journal| author=Leclerc S, Lassonde M, Delaney JS, Lacroix VJ, Johnston KM| title=Recommendations for grading of concussion in athletes. | journal=Sports Med | year= 2001 | volume= 31 | issue= 8 | pages= 629-36 | pmid=11475324 | doi=10.2165/00007256-200131080-00007 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11475324 }} </ref>
  |-
  |-
  | [[Drug]]-Induced Amnesia||[[Benzodiazepine]] are the most common group of [[drugs]] that can cause [[drug]]-induced amnesia, especially if used with [[alcohol]]. [[Memory]] loss could be long term or short term.<ref> Sadock, Benjamin J., and Virginia A. Sadock. Kaplan & Sadock's concise textbook of clinical psychiatry. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins, 2008. Print</ref> Amnesia is anterograde from the time the drug was introduced and patient has impairment in forming new memories. It is reversible upon discontinuation of the [[drug]].
  | [[Infantile]] Amnesia|| Influenced by cultural norms and [[sexual]] [[repression]].<ref name="pmid12653489">{{cite journal| author=Wang Q| title=Infantile amnesia reconsidered: a cross-cultural analysis. | journal=Memory | year= 2003 | volume= 11 | issue= 1 | pages= 65-80 | pmid=12653489 | doi=10.1080/741938173 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12653489  }} </ref>
  |-
  |-
  | [[Neurological]] Amnesia||[[Alzheimer's Disease]], [[Pick's Disease]]
  | [[Drug]]-Induced Amnesia||[[Benzodiazepine]] are the most common group of [[drugs]] that can cause [[drug]]-induced amnesia, especially if used with [[alcohol]].<ref> Sadock, Benjamin J., and Virginia A. Sadock. Kaplan & Sadock's concise textbook of clinical psychiatry. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins, 2008. Print</ref>
  |-
  |-
  | Amnesia in [[Korsakoff’s Syndrome]]|| Caused by [[thiamine]] [[deficiency]] due to prolonged [[alcohol]] use. [[Deficiency]] of [[thiamine]] damages medial [[thalamus]], [[mammillary bodies]] and causes [[cerebral atrophy]] due to lack of [[pyruvate]] [[decarboxylation]].
  | [[Neurologically]] Derived Amnesia|| [[Brain]] regions involved are the [[hippocampus]] and the [[medial]] [[temporal lobes]].<ref name="pmid29623196">{{cite journal| author=Allen RJ| title=Classic and recent advances in understanding amnesia. | journal=F1000Res | year= 2018 | volume= 7 | issue=  | pages= 331 | pmid=29623196 | doi=10.12688/f1000research.13737.1 | pmc=5861508 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=29623196  }} </ref>
  |-
  |-
  | [[Selective Amnesia]] ||  
  | Amnesia in [[Korsakoff’s Syndrome]]|| Caused by [[thiamine]] [[deficiency]] due to prolonged [[alcohol]] use or severe [[malnutrition]]. [[Deficiency]] of [[thiamine]] damages medial [[thalamus]], [[mammillary bodies]] and causes [[cerebral atrophy]] due to lack of [[pyruvate]] [[decarboxylation]].<ref>Kolb, Bryan, and Ian Q. Whishaw. Fundamentals of human neuropsychology. New York, NY: Worth Publishers, 2003. Print.</ref>
  |-
  |-
  |[[Epileptic]] Amnesia||
  |[[Epileptic]] Amnesia|| Rare, episodic amnesia seen in [[patients]] with [[temporal lobe]] [[epilepsy]].<ref name="pmid21262589">{{cite journal| author=Walsh RD, Wharen RE, Tatum WO| title=Complex transient epileptic amnesia. | journal=Epilepsy Behav | year= 2011 | volume= 20 | issue= 2 | pages= 410-3 | pmid=21262589 | doi=10.1016/j.yebeh.2010.12.026 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21262589  }} </ref>
  |-
  |-
  |[[Lacunar amnesia]]||
  |[[Lacunar amnesia]]|| Occurs due to [[brain]] damage. These [[patients]] have a gap in [[memory]].<ref name="pmid747264">{{cite journal| author=Benezech M, Leyssenne JP| title=[Lacunar amnesia and criminal behaviour : realities and medico-legal consequences]. | journal=Ann Med Psychol (Paris) | year= 1978 | volume= 136 | issue= 6-8 | pages= 918-29 | pmid=747264 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=747264  }} </ref>
|}
|}


==Genetics==
==Genetics==
[Disease name] is transmitted in [mode of genetic transmission] pattern.
*[[Alzheimer's disease]]:<ref name="pmid21045163">{{cite journal| author=Bekris LM, Yu CE, Bird TD, Tsuang DW| title=Genetics of Alzheimer disease. | journal=J Geriatr Psychiatry Neurol | year= 2010 | volume= 23 | issue= 4 | pages= 213-27 | pmid=21045163 | doi=10.1177/0891988710383571 | pmc=3044597 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21045163  }} </ref>
 
**Late-onset: Apolipoprotein E (APOE) [[gene]] on [[chromosome]] 19. This [[gene]] has variable risk of developing [[Alzheimer's disease]] depending on the [[allele]]. APOE ε4 increases the risk, APOE ε3 neither increases nor decreases and APOE ε2 [[allele]] provides some protection against the [[disease]].
OR
**Early-onset: [[Amyloid precursor protein]] (APP) on [[chromosome 21]], [[presenilin 1]] (PSEN1) on [[chromosome 14]] and [[presenilin 2]] (PSEN2) on [[chromosome 1]] are associated with early-onset [[Alzheimer's disease]].
 
*[[Deficiency]] of RbAp48 [[protein]] encoded by RBBP4 [[gene]] have been co-related to [[memory]] loss.<ref name="pmid23986399">{{cite journal| author=Pavlopoulos E, Jones S, Kosmidis S, Close M, Kim C, Kovalerchik O | display-authors=etal| title=Molecular mechanism for age-related memory loss: the histone-binding protein RbAp48. | journal=Sci Transl Med | year= 2013 | volume= 5 | issue= 200 | pages= 200ra115 | pmid=23986399 | doi=10.1126/scitranslmed.3006373 | pmc=4940031 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23986399  }} </ref>
Genes involved in the pathogenesis of [disease name] include:
*[Gene1]
*[Gene2]
*[Gene3]
 
OR
 
The development of [disease name] is the result of multiple genetic mutations such as:
 
*[Mutation 1]
*[Mutation 2]
*[Mutation 3]
 
==Associated Conditions==
Conditions associated with [disease name] include:
 
*[Condition 1]
*[Condition 2]
*[Condition 3]


==Gross Pathology==
==Gross Pathology==
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
On gross pathology, generalized [[cortical atrophy]], more pronounced in [[hippocampus]] and [[medial temporal lobe]] is seen in [[patients]] with [[Alzheimer's disease]].<ref name="pmid31375134">{{cite journal| author=DeTure MA, Dickson DW| title=The neuropathological diagnosis of Alzheimer's disease. | journal=Mol Neurodegener | year= 2019 | volume= 14 | issue= 1 | pages= 32 | pmid=31375134 | doi=10.1186/s13024-019-0333-5 | pmc=6679484 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31375134  }} </ref>


==Microscopic Pathology==
==Microscopic Pathology==
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
*[[Korsakoff's syndrome]]:<ref name="pmid19066199">{{cite journal| author=Sullivan EV, Pfefferbaum A| title=Neuroimaging of the Wernicke-Korsakoff syndrome. | journal=Alcohol Alcohol | year= 2009 | volume= 44 | issue= 2 | pages= 155-65 | pmid=19066199 | doi=10.1093/alcalc/agn103 | pmc=2724861 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=19066199  }} </ref>
 
**[[Gliosis]] and [[microhemorrhages]] found in [[periaqueductal]] and [[paraventricular]] region.,  
 
**[[Mamillary bodies]] [[atrophy]] and
**[[Atrophy]] seen in [[thalamus]]
*[[Microscopic]] features seen in [[Alzheimer's disease]] are, [[amyloid plaques]], [[intracellular]] [[neurofibrillary tangles]], [[tau]]-positive [[neuropil threads]], [[dystrophic]] [[neurites]], activated [[microglia]], reactive [[astrocytes]], [[eosinophilic]] [[Hirano bodies]], [[granulovacuolar]] [[degeneration]] and [[cerebral]] [[amyloid]] [[angiopathy]].<ref name="pmid31375134">{{cite journal| author=DeTure MA, Dickson DW| title=The neuropathological diagnosis of Alzheimer's disease. | journal=Mol Neurodegener | year= 2019 | volume= 14 | issue= 1 | pages= 32 | pmid=31375134 | doi=10.1186/s13024-019-0333-5 | pmc=6679484 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=31375134  }} </ref>


==References==
==References==

Latest revision as of 02:53, 25 March 2021

Amnesia Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Amnesia from other Diseases

Epidemiology and Demographics

Risk Factors

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

Echocardiography and Ultrasound

CT

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Amnesia pathophysiology On the Web

Most recent articles

cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Amnesia pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Amnesia pathophysiology

CDC on Amnesia pathophysiology

Amnesia pathophysiology in the news

Blogs on Amnesia pathophysiology

Directions to Hospitals Treating Amnesia

Risk calculators and risk factors for Amnesia pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Zehra Malik, M.B.B.S[2]

Overview

Memory is the stored information in the hippocampal region of the brain. depending on the duration, memory is divided into short term and long term.

Pathophysiology

Physiology

Memory is the stored information in the hippocampal region of the brain. According to Richard Semon (1904), experiences cause some structural and functional changes in the neurons and these changes are referred to as engram and they form memory of that experience. Reactivation of these neurons occur when patient tries to recall those memories.[1] Memory is divided into groups depending on the duration:

Pathogenesis

Types of Amnesia Pathogenesis
Dissociative Amnesia Psychological origin.
Transient global amnesia Precipitated by brain ischemia, migraine, epileptic seizure, venous congestion, psychological trauma.[4]
Post-traumatic Amnesia Amnesia that follows head trauma could be temporary or permanent.[5]
Infantile Amnesia Influenced by cultural norms and sexual repression.[6]
Drug-Induced Amnesia Benzodiazepine are the most common group of drugs that can cause drug-induced amnesia, especially if used with alcohol.[7]
Neurologically Derived Amnesia Brain regions involved are the hippocampus and the medial temporal lobes.[8]
Amnesia in Korsakoff’s Syndrome Caused by thiamine deficiency due to prolonged alcohol use or severe malnutrition. Deficiency of thiamine damages medial thalamus, mammillary bodies and causes cerebral atrophy due to lack of pyruvate decarboxylation.[9]
Epileptic Amnesia Rare, episodic amnesia seen in patients with temporal lobe epilepsy.[10]
Lacunar amnesia Occurs due to brain damage. These patients have a gap in memory.[11]

Genetics

Gross Pathology

On gross pathology, generalized cortical atrophy, more pronounced in hippocampus and medial temporal lobe is seen in patients with Alzheimer's disease.[14]

Microscopic Pathology

References

  1. ↑ Semon R. (1904). Die mneme [The mneme]. Edited by W. Engelmann. Leipzig
  2. ↑ Camina E, Güell F (2017). "The Neuroanatomical, Neurophysiological and Psychological Basis of Memory: Current Models and Their Origins". Front Pharmacol. 8: 438. doi:10.3389/fphar.2017.00438. PMC 5491610. PMID 28713278.
  3. ↑ Bisaz R, Travaglia A, Alberini CM (2014). "The neurobiological bases of memory formation: from physiological conditions to psychopathology". Psychopathology. 47 (6): 347–56. doi:10.1159/000363702. PMC 4246028. PMID 25301080.
  4. ↑ Profice P, Rizzello V, Pennestrì F, Pilato F, Della Marca G, Sestito A; et al. (2008). "Transient global amnesia during transoesophageal echocardiogram". Neurol Sci. 29 (6): 477–9. doi:10.1007/s10072-008-1034-y. PMID 19031042.
  5. ↑ Leclerc S, Lassonde M, Delaney JS, Lacroix VJ, Johnston KM (2001). "Recommendations for grading of concussion in athletes". Sports Med. 31 (8): 629–36. doi:10.2165/00007256-200131080-00007. PMID 11475324.
  6. ↑ Wang Q (2003). "Infantile amnesia reconsidered: a cross-cultural analysis". Memory. 11 (1): 65–80. doi:10.1080/741938173. PMID 12653489.
  7. ↑ Sadock, Benjamin J., and Virginia A. Sadock. Kaplan & Sadock's concise textbook of clinical psychiatry. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins, 2008. Print
  8. ↑ Allen RJ (2018). "Classic and recent advances in understanding amnesia". F1000Res. 7: 331. doi:10.12688/f1000research.13737.1. PMC 5861508. PMID 29623196.
  9. ↑ Kolb, Bryan, and Ian Q. Whishaw. Fundamentals of human neuropsychology. New York, NY: Worth Publishers, 2003. Print.
  10. ↑ Walsh RD, Wharen RE, Tatum WO (2011). "Complex transient epileptic amnesia". Epilepsy Behav. 20 (2): 410–3. doi:10.1016/j.yebeh.2010.12.026. PMID 21262589.
  11. ↑ Benezech M, Leyssenne JP (1978). "[Lacunar amnesia and criminal behaviour : realities and medico-legal consequences]". Ann Med Psychol (Paris). 136 (6–8): 918–29. PMID 747264.
  12. ↑ Bekris LM, Yu CE, Bird TD, Tsuang DW (2010). "Genetics of Alzheimer disease". J Geriatr Psychiatry Neurol. 23 (4): 213–27. doi:10.1177/0891988710383571. PMC 3044597. PMID 21045163.
  13. ↑ Pavlopoulos E, Jones S, Kosmidis S, Close M, Kim C, Kovalerchik O; et al. (2013). "Molecular mechanism for age-related memory loss: the histone-binding protein RbAp48". Sci Transl Med. 5 (200): 200ra115. doi:10.1126/scitranslmed.3006373. PMC 4940031. PMID 23986399.
  14. ↑ 14.0 14.1 DeTure MA, Dickson DW (2019). "The neuropathological diagnosis of Alzheimer's disease". Mol Neurodegener. 14 (1): 32. doi:10.1186/s13024-019-0333-5. PMC 6679484 Check |pmc= value (help). PMID 31375134.
  15. ↑ Sullivan EV, Pfefferbaum A (2009). "Neuroimaging of the Wernicke-Korsakoff syndrome". Alcohol Alcohol. 44 (2): 155–65. doi:10.1093/alcalc/agn103. PMC 2724861. PMID 19066199.

Template:WH Template:WS

Retrieved from "https://www.wikidoc.org/index.php?title=Amnesia_pathophysiology&oldid=1695353"