Amnesia pathophysiology: Difference between revisions
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**[[Mamillary bodies]] [[atrophy]] and | **[[Mamillary bodies]] [[atrophy]] and | ||
**[[Atrophy]] seen in [[thalamus]] | **[[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]]. | *[[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]]. | ||
==References== | ==References== | ||
Revision as of 02:57, 21 March 2021
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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
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:
- 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
| Types of Amnesia | Pathogenesis |
|---|---|
| Dissociative Amnesia | Psychological origin. |
| Post-traumatic Amnesia | Amnesia that follows head trauma could be temporary or permanent.[4] |
| Infantile Amnesia | Influenced by cultural norms and sexual repression.[5] |
| Drug-Induced Amnesia | Benzodiazepine are the most common group of drugs that can cause drug-induced amnesia, especially if used with alcohol.[6] |
| Neurological Amnesia | Alzheimer's Disease, Pick's Disease |
| 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.[7] |
| Epileptic Amnesia | Rare, episodic amnesia seen in patients with temporal lobe epilepsy.[8] |
| Lacunar amnesia | Occurs due to brain damage. These patients have a gap in memory.[9] |
Genetics
- Alzheimer's disease:[10]
- 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.
Gross Pathology
On gross pathology, generalized cortical atrophy, more pronounced in hippocampus and medial temporal lobe is seen in patients with Alzheimer's disease.[11]
Microscopic Pathology
- Korsakoff's syndrome:[12]
- 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.
References
- ↑ Semon R. (1904). Die mneme [The mneme]. Edited by W. Engelmann. Leipzig
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ Wang Q (2003). "Infantile amnesia reconsidered: a cross-cultural analysis". Memory. 11 (1): 65–80. doi:10.1080/741938173. PMID 12653489.
- ↑ Sadock, Benjamin J., and Virginia A. Sadock. Kaplan & Sadock's concise textbook of clinical psychiatry. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins, 2008. Print
- ↑ Kolb, Bryan, and Ian Q. Whishaw. Fundamentals of human neuropsychology. New York, NY: Worth Publishers, 2003. Print.
- ↑ 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.
- ↑ 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.
- ↑ 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.
- ↑ 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. - ↑ 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.