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==Overview==
==Overview==
Amnesia results from damage to different memory centers in the brain, such as the [[medial temporal lobe]] and the [[hippocampus]], which are involved in acquiring and restoring memory.
[[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==
==Pathophysiology==
Memory is disrupted by damage that may occur in different parts of the brain such as the [[medial temporal lobe]], the [[hippocampus]], the [[cortex]] and the [[frontal lobe]]. Injury to any of these areas may lead to specific disruptions in the processes of acquiring and recalling memories. For instance, damage to the medial [[temporal lobe]] and [[hippocampus]] can sharply reduce the ability to acquire new [[declarative memory]] whereas damage to the storage areas in the cortex can disrupt retrieval of old memories and interfere with the acquisition of new memories.
===Physiology===
===Anterograde Amnesia===
[[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]].<ref>Semon R. (1904). Die mneme [The mneme]. Edited by W. Engelmann. Leipzig</ref> [[Memory]] is divided into groups depending on the duration:
Anterograde amnesia can result from damage to the [[hippocampal formation|hippocampus]], [[Fornix of brain|fornix]], or [[mammillary bodies]], thus lending credence to the theory that these structures are primarily responsible for laying down long-term memories. However, the condition can also arise from damage to the [[basal forebrain]] (which produces [[acetylcholine]]) or a set of brain structures called the [[diencephalon]].  
*[[Sensory]] [[memory]]: Information from around us is stored as [[sensory]] [[memory]].<ref name="pmid28713278">{{cite journal| author=Camina E, Güell F| title=The Neuroanatomical, Neurophysiological and Psychological Basis of Memory: Current Models and Their Origins. | journal=Front Pharmacol | year= 2017 | volume= 8 | issue=  | pages= 438 | pmid=28713278 | doi=10.3389/fphar.2017.00438 | pmc=5491610 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28713278  }} </ref>
===Dissociative or Functional or Psychogenic Amnesia===
*Short-term [[memory]] are for short period of time and use existing [[neuronal]] network.
There are three types of memory – sensory, short-term, and long-term memory. Sensory memory lasts up to hundreds of milliseconds and short-term memory lasts from seconds to minutes while anything else longer than short-term memory is considered to be a long-term memory.<ref name = Markowitsch>{{cite journal |author=Markowitsch HJ |title=Psychogenic amnesia |journal=Neuroimage |volume=20 Suppl 1 |issue= |pages=S132–8 |year=2003 |pmid=14597306 |doi=}}</ref><ref name = Reinhold/>
*Long-term [[memory]] are long lasting and are formed by structural/functional changes in [[neuronal]] network.<ref name="pmid25301080">{{cite journal| author=Bisaz R, Travaglia A, Alberini CM| title=The neurobiological bases of memory formation: from physiological conditions to psychopathology. | journal=Psychopathology | year= 2014 | volume= 47 | issue= 6 | pages= 347-56 | pmid=25301080 | doi=10.1159/000363702 | pmc=4246028 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25301080  }} </ref>


The information obtained from the [[peripheral nervous system]] (PNS) is processed in four stages -encoding, consolidating, storage, and retrieval.<ref name = Markowitsch/> During encoding, the limbic system is responsible for bottlenecking or filtering information obtained from the PNS. According to the type of information given, the duration of consolidating stage varies drastically. Majority of consolidated information gets stored in the cerebral cortical networks where the limbic system record episodic-autobiographical events. These stored episodic and semantic memories can be obtained by triggering the uncinate fascicle that interconnects the regions of the temporofrontal junction area.
===Pathogenesis===


Emotion seems to play an important role in memory processing in structures like the cingulated gyrus, the septal nuclei, and the amygdala that is primarily involved in emotional memories.<ref name = Markowitsch /><ref name = Yang>{{cite journal |author=Yang JC, Jeong GW, Lee MS, ''et al'' |title=Functional MR imaging of psychogenic amnesia: a case report |journal=Korean J Radiol |volume=6 |issue=3 |pages=196–9 |year=2005 |pmid=16145296 |doi=}}</ref> Functional imaging of normal patients reveal that right-hemispheric amygdala and ventral prefrontal regions are activated when they were retrieving autobiographical information and events. Additionally, the hippocampal region is known to be linked to recognizing faces. Researchers have found that emotional memories can be suppressed in non-mentally ill individuals via the [[prefrontal cortex]] in two stages - an initial suppression of the sensory aspects of the memory, followed by a suppression of the [[emotion]]al aspect.<ref>{{cite journal |author=Depue BE, Curran T, Banich MT |title=Prefrontal regions orchestrate suppression of emotional memories via a two-phase process |journal=Science |volume=317 |issue=5835 |pages=215–9 |year=2007 |pmid=17626877 |doi=10.1126/science.1139560}}</ref> It has also been proposed that [[glucocorticoid]]s can impair memory retrieval, though to date this has only been tested in rats.<ref>{{cite journal |author=Roozendaal B, de Quervain DJ, Schelling G, McGaugh JL |title=A systemically administered beta-adrenoceptor antagonist blocks corticosterone-induced impairment of contextual memory retrieval in rats |journal=Neurobiol Learn Mem |volume=81 |issue=2 |pages=150–4 |year=2004 |pmid=14990235 |doi=10.1016/j.nlm.2003.10.001}}</ref>
{| class="wikitable"
!align="center" style="background: #4479BA; color: #FFFFFF | '''Types of Amnesia'''
! align="center" style="background: #4479BA; color: #FFFFFF| '''Pathogenesis'''
|-
| [[Dissociative Amnesia]]        ||[[Psychological]] origin.
|-
|[[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>
|-
| [[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>
|-
| [[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>
|-
| [[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>
|-
| [[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>
|-
| 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|| 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]]|| 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>
|}


Traumas can interfere with several memory functions. Dr. Bessel van der Kolk divided these functional disturbances into four sets, traumatic amnesia, global memory impairment, dissociative processes and traumatic memories' sensorimotor organization. Traumatic amnesia involves the loss of remembering traumatic experiences. The younger the subject and the longer the traumatic event is, the greater the chance of significant amnesia. Global memory impairment makes it difficult for these subjects to construct an accurate account of their present and past history. Dissociation refers to memories being stored as fragments and not as unitary wholes. Not being able to integrate traumatic memories seems to be the main element which leads to PTSD. In the sensorimotor organization of traumatic memories, sensations are fragmented into different sensory components.<ref name="pmid8564271">{{cite journal |author=van der Kolk BA, Fisler R |title=Dissociation and the fragmentary nature of traumatic memories: overview and exploratory study |journal=J Trauma Stress |volume=8 |issue=4 |pages=505–25 |year=1995 |pmid=8564271 |doi= |url=http://www.trauma-pages.com/a/vanderk2.php | accessdate = 2008-03-22}}</ref>
==Genetics==
*[[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]].
**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>


Psychogenic amnesia is far from being completely understood and while several explanations have been proposed, none of them have been verified as the mechanism that fits all types of psychogenic amnesia. Different theories include:
==Gross Pathology==
* [[Psychoanalysis|Freudian psychology]] states that psychogenic amnesia is an act of self-preservation, an alternative to suicide.<ref name = Brandt>{{cite journal |author=Brandt J, Van Gorp WG |title=Functional ("psychogenic") amnesia |journal=Semin Neurol |volume=26 |issue=3 |pages=331–40 |year=2006 |pmid=16791779 |doi=10.1055/s-2006-945519}}</ref>
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>
* [[Cognitive psychology|Cognitive]] point-of-view states that this disorder utilizes the body’s personal semantic belief system to repress unwanted memories from entering the consciousness by altering [[neuropeptide]]s and [[neurotransmitter]]s released during stressful events, affecting the formation and recall of memory.<ref name = Brandt/>
* "Betrayal trauma theory suggests that psychogenic amnesia is an adaptive response to childhood abuse. When a parent or other powerful figure violates a fundamental ethic of human relationships, victims may need to remain unaware of the trauma not to reduce suffering but rather to promote survival. Amnesia enables the child to maintain an attachment with a figure vital to survival, development, and thriving. Analysis of evolutionary pressures, mental modules, social cognitions, and developmental needs suggests that the degree to which the most fundamental human ethics are violated can influence the nature, form, and processes of trauma and responses to trauma."<ref>{{cite journal |last=Freyd |first=J. |year=1994 |title=Betrayal Trauma: Traumatic Amnesia as an Adaptive Response to Childhood Abuse. |journal= Ethics & Behavior |volume=4 |issue=4 |pages=307–330 |url=http://www.questia.com/read/95814385 |accessdate= 2008-01-13 |doi=10.1207/s15327019eb0404_1}}</ref> 
*Normal autobiographical memory processing is blocked by imbalance or altered release of [[stress hormone]]s such as [[glucocorticoid]]s and [[mineralocorticoid]]s in the brain.<ref name = Markowitsch/><ref name = Yang/>  The regions of expanded [[limbic system]] in the [[Cerebral hemisphere|right hemisphere]] are more vulnerable to stress and trauma, affecting the body's [[opioid]]s, [[hormone]]s, and neurotransmitters such as [[norepinephrine]] [[serotonin]], and [[neuropeptide Y]].<ref name = Reinhold>{{cite journal | author = Reinhold, N | coauthors = Kuehnel, S, Brand, M & Markowitsch, HJ | title = Functional neuroimaging in memory and memory disturbances | journal = Current Medical Imaging Reviews | volume = 2 | issue = 1 | pages = 35–57 | year = 2006 | url = http://www.ingentaconnect.com/content/ben/cmir/2006/00000002/00000001/art00004 | accessdate = 2007-12-05 | doi = 10.2174/157340506775541668 }}</ref> Increased levels of glucocorticoid and mineralocorticoid receptor density may affect the anterior temporal, [[orbitofrontal cortex]], [[Hippocampus|hippocampal]], and [[amygdala]]r regions. These morphological changes may be caused by loss of regulation of [[gene expression]]s in those receptors along with inhibition of neurotrophic factors during chronic stress conditions.
*[[Stress (medicine)|Stress]] may directly affect the medial [[Temporal lobe|temporal]]/[[Diencephalon|diencephalic]] system, inhibiting the retrieval of autobiographical memories and producing a loss of personal identity. [[Negative feedback]] produced by this system may dampen the patient's emotions, giving a perplexed or 'flat' appearance.<ref name = Kopelman>{{cite journal |author=Kopelman MD |title=Disorders of memory |journal=Brain |volume=125 |issue=Pt 10 |pages=2152–90 |year=2002 |pmid=12244076 |doi=|url = http://brain.oxfordjournals.org/cgi/content/full/125/10/2152 | accessdate = 2008-04-05}}</ref>


===Childhood Amnesia===
==Microscopic Pathology==
Since Miles first officially documented childhood amnesia as a psychological phenomenon, many theories of its causes and character have been developed. Some of the most notable are described here to aid in understanding what childhood amnesia may be. It is worth noting that many of these theories are highly controversial and the true nature of childhood amnesia is still being debated.
*[[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>
====Freud’s Trauma Explanation====
**[[Gliosis]] and [[microhemorrhages]] found in [[periaqueductal]] and [[paraventricular]] region.,  
Sigmund Freud’s theories of [[psychosexual development]] are highly intertwined with childhood experiences, and Freud’s explanation of childhood amnesia is one of the most controversial. In what is now published as The Standard Edition of the Complete Psychological Works of Sigmund Freud, Freud theorized that childhood amnesia is the result of the mind’s attempt to repress memories of [[Psychological trauma|traumatic events]] that, according to Freud, necessarily occur in the psychosexual development of every child. This would lead to the [[Memory inhibition|repression]] of the majority of the first years of life (Gleitman, et al., 2004). Some evidence has been found that could support the repression theory. In one study, high school and college students were asked to recall the nature of their earliest memory. In the first phase, high school students were found to have much later earliest retrievable memories, many of which featured traumatic events. In a retest several months later, 42% of the high school students reported a different earliest memory, and many of these new memories were markedly less traumatic than the ones they had recalled the first time (Kihlstrom, et al., 1982). At the same time, Freudian theory, including his explanation for childhood amnesia, has been severely criticized. One criticism is actually about the evidence, often [[Anecdotal evidence|anecdotal]] rather than purely [[Scientific evidence|scientific]], and said to frequently permit multiple interpretations (Gleitman, et al., 2004). Criticism specifically of the Kihlstrom experiment includes the observation that no part of the study actually involved children, but rather adolescents and young adults (Bauer, 2004).
**[[Mamillary bodies]] [[atrophy]] and  
====Physical Development Explanation====
**[[Atrophy]] seen in [[thalamus]]
Another often-cited explanation of childhood amnesia is that the infant’s mind is not mentally mature enough to create long-lasting autobiographical memories. In particular, it is not until the age 3 or 4 that toddlers have a mature [[hippocampus]] and [[prefrontal cortex]]. These regions of the [[Human brain|brain]] are known to be associated with the formation of autobiographical memories of the type notably missing from adult recollection of early childhood (Gleitman, 2004; Newcombe, et al., 2000).
*[[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>
====Language Explanation====
The incomplete development of [[language]] in young children may be a cause of childhood amnesia in that infants do not have the language capacity to encode autobiographical memories in a manner that their language-based adult selves can interpret correctly. Indeed, the typical schedule of [[language development]] seems to support this theory. Babies of one year old tend to be limited to one word utterances, and childhood amnesia predicts that adults have very few, if any, memories of this time. By the age of three, however, children are capable of two or three word phrases, and by age five their speech already resembles adult speech. This language development seems to very much correspond to childhood amnesia because it is around the age of three to four that is the time of most adults’ earliest recallable memory (Gleitman, et al., 2004).
====Emotion Explanation====
One explanation notes the connections between the [[emotion]] or [[amygdala]]-governed memory pathway and the autobiographical or hippocampus- governed pathway. While these two memory systems do have much independence, it is also known that emotions and the amygdala play a role in the encoding of memories typically associated with the hippocampus (Phelps, 2004). Knowing this, it has been suggested that the differences between the emotions experienced by infants and adults may be a cause of childhood amnesia (West, et al., 1999). One problem with this explanation, however, is that one of the most widely proclaimed examples of emotion influencing memory, the "[[flashbulb memory]]" mechanism, may not exist at all. If so, it would be unlikely for emotion and memory to be so intertwined as to cause an inability to recall the first several years of memories (McCloskey, et al., 1988).
====Context Explanation====
The difference in perspective that children and adults experience of the world may be a cause of childhood amnesia. For children, their physical perception of objects and their understanding of people and events are very different from the world of the adult. Moreover, an infant’s basic understanding of the universe, like object permanence or occlusion effects, is not innate at birth. This leads to a disparity in retrieval cues used by the adult and those used by the infant, who will encode memories without many of these principles that are ingrained in the mind of the adult trying to recollect. This different context could lead to the inability of the adult to remember his earliest years at all (Gleitman, et al., 2004). For example, one study showed that an infant’s development of a [[theory of mind]] is linked to his ability to form [[Episodic memory|episodic memories]]. The conclusion was that the context explanation may be justified, especially since infants develop the ability to perceive the world as adults do around the age of 3 to 5, when many people also have their earliest retrievable memory (Perner, et al., 1995).
 
===Blackout (Alcohol Related Amnesia)===
Various studies have proven links between general alcohol consumption and its effects on memory creation.<ref>PARKER, E.S.; BIRNBAUM, I.M.; AND NOBLE, E.P. Alcohol and memory: Storage and state dependency. Journal of Verbal Learning and Verbal Behaviour 15:691-702, 1976.</ref> Particularly, these studies had shown that associations made between words and objects when intoxicated are less easily recalled than associations made when not intoxicated. Later blackout-specific studies have indicated that alcohol specifically impairs the brain's ability to take short-term memories and experiences and transfer them to long-term memory.<ref>ACHESON, S.; STEIN, R.; AND SWARTZWELDER, H.S. Impairment of semantic and figural memory by acute ethanol: Age-dependent effects. Alcoholism: Clinical and Experimental Research 22:1437-1442, 1998.</ref> This was shown by the ability to recall associations made while intoxicated being affected over time; it is strongly indicated that memories can be easily recalled for 2-3 minutes before the permanent inability to recall them in the future. Blackouts are quite often associated with the consumption of large amounts of alcohol, however surveys of drinkers who have experienced blackouts have indicated that blacking out is not directly related to the amount of alcohol consumed. Respondents reported they frequently recalled having "had drunk as much or more without memory loss," compared to instances of blacking out.<ref>GOODWIN, D.W; CRANE, J.B.; AND GUZE, S.B. Alcoholic "blackouts": A review and clinical study of 100 alcoholics. American Journal of Psychiatry 126:191-198, 1969.</ref> Subsequent research has indicated that blackouts are most likely caused by a rapid increase in a person's [[Blood alcohol content |blood-alcohol concentration]]. One study, in particular, resulted in subjects being stratified easily into two groups, those who consumed alcohol very quickly, and blacked out, and those who did not black out by drinking alcohol slowly, despite being extremely intoxicated by the end of the study.<ref>RYBACK, R.S. Alcohol amnesia: Observations in seven drinking inpatient alcoholics. Quarterly Journal of Studies on Alcohol 31:616-632, 1970.</ref> Hence, in order to prevent a blackout, alcohol should not be consumed in large gulps, and should most likely not be drunk on an empty stomach.


==References==
==References==

Latest revision as of 02:53, 25 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:

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.

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