Amnesia pathophysiology: Difference between revisions
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| [[Neurological]] Amnesia||[[Alzheimer's Disease]], [[Pick's Disease]] | | [[Neurological]] Amnesia||[[Alzheimer's Disease]], [[Pick's Disease]] | ||
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| 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]].<ref>Kolb, Bryan, and Ian Q. Whishaw. Fundamentals of human neuropsychology. New York, NY: Worth Publishers, 2003. Print.</ref> | | 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> | ||
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| [[Selective Amnesia]] || | | [[Selective Amnesia]] || | ||
Revision as of 14:07, 15 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
The exact pathogenesis of [disease name] is not fully understood.
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
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 | Temporary, episodic retrograde memory loss. Cause is psychological in origin. Dissociative Amnesia is also referred to as psychological amnesia. It has variable presentation:
|
| 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. [7] |
| 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.[8] |
| 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.[9] 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. |
| 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.[10] |
| Selective Amnesia | |
| Epileptic Amnesia | |
| Lacunar amnesia |
Genetics
[Disease name] is transmitted in [mode of genetic transmission] pattern.
OR
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
On gross pathology, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
Microscopic Pathology
On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].
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.
- ↑ Bourget D, Whitehurst L (2007). "Amnesia and crime". J Am Acad Psychiatry Law. 35 (4): 469–80. PMID 18086739.
- ↑ Khalili M, Wong RJ (2018). "Underserved Does Not Mean Undeserved: Unfurling the HCV Care in the Safety Net". Dig Dis Sci. 63 (12): 3250–3252. doi:10.1007/s10620-018-5316-9. PMC 6436636. PMID 30311153.
- ↑ American Psychiatric Association (2013). Diagnostic and statistical manual of mental disorders : DSM-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.
- ↑ 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.