Amnesia pathophysiology

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

## Overview[edit | edit source]

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[edit | edit source]

### Physiology[edit | edit source]

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:

* Sensory memory: Information from around us is stored as sensory memory.[2]
* Short-term memory are for short period of time and use existing neuronal network.
* Long-term memory are long lasting and are formed by structural/functional changes in neuronal network.[3]

### Pathogenesis[edit | edit source]

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[edit | edit source]

* Alzheimer's disease:[12]
* 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.
* 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.[13]

## Gross Pathology[edit | edit source]

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[edit | edit source]

* Korsakoff's syndrome:[15]
* 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.[14]

## References[edit | edit source]

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.CS1 maint: Multiple names: authors list (link)
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.CS1 maint: Multiple names: authors list (link)
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.CS1 maint: Multiple names: authors list (link)
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.CS1 maint: Multiple names: authors list (link)
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.CS1 maint: Multiple names: authors list (link)
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.CS1 maint: Multiple names: authors list (link)
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.

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