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==Overview==
==Overview==
Amnesia can be divided into two broad groups, [[retrograde amnesia]] and [[anterograde amnesia]]
Amnesia can be divided into two broad groups, [[retrograde amnesia]] and [[anterograde amnesia]]. [[Retrograde amnesia]] is the loss of [[memory]] prior to the onset of amnesia and [[anterograde amnesia]] is the inability to form new [[memory]]. [[Memory]] can also be divided into two groups depending on the duration, short-term [[memory]] and long-term [[memory]]. Other types of amnesia are [[Psychological]] including [[repressive amnesia]] and [[dissociative fugue]], [[infantile]] amnesia, [[neurological]] amnesia ([[Alzheimer's disease]], [[Pick's disease]]), post-[[traumatic]] Amnesia, [[drug]]-Induced Amnesia, [[transient global amnesia]], amnesia due to [[nutritional]] [[deficiency]] ([[thiamine]], [[vitamin B12]]). Richard Semon in 1904 described that experiences cause some changes in the [[neurons]] and these changes are referred to as ''engram'' and they form [[memory]] of the particular experience in those [[neurons]]. Reactivation of these [[neurons]] occur when [[patient]] tries to recall those [[memories]]. 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. Common causes of amnesia include [[medications]], [[head trauma]], [[depression]] and [[aging]]. Less common cause of amnesia are childhood [[sexual]] [[abuse]], traumatic incident, [[hypoxia]], [[psychological]] [[trauma]], [[thiamine]] [[deficiency]], [[alcohol]] [[abuse]], [[Alzheimer's disease]], [[Pick's disease]], [[Parkinson's disease]], [[benzodiazepines]], [[hypoglycemia]], [[stroke]], [[electroconvulsive therapy]]. The underlying [[etiology]] of memory loss must be differentiated on the basis of duration of [[memory]] loss, presence of [[anterograde amnesia]] or [[retrograde amnesia]], associated features, and [[cognitive impairment]]. [[Memory]] impairment tends to increase with [[age]]. Forty percent of the [[population]] over [[age]] sixty have some degree of [[memory]] loss. Amnesia and mild [[cognitive impairment]] is more [[prevalent]] in middle-aged to older Non-[[Hispanic]] Black and older [[Latino]] as compared to non-[[Hispanic]] Whites. [[Aging]], [[depression]], [[chronic]] [[stress]], [[head]] [[trauma]], [[chronic]] [[sleep deprivation]] and [[medications]] are [[risk factors]] ​for amnesia. Amnesia may progress slowly or suddenly, and maybe transient or permanent. The natural history and [[prognosis]] depends upon the underlying [[etiology]]. [[Patients]] with [[memory]] loss could suffer from [[depression]] and [[grief]] long term. [[Quality of life]] and activities of daily living are difficult to maintain which causes decreased socialization and a decline in [[cognitive]] functions in the [[elderly]].Amnesia is largely a clinical [[diagnosis]], a detailed history of [[memory]] impairment and associated [[symptoms]] should be obtained. Focal [[examination]] including [[vital signs]], [[altered mental status]], [[mini mental status exam]] ([[MMSE]]), [[Glasgow Coma Scale]], [[nystagmus]], [[papilledema]], [[gait]], [[instruments of daily activities]] should be assessed. [[Head]] [[CT scan]] and [[MRI]] may be helpful in identifying structural and functional abnormalities including [[bleeding]], [[stroke]], [[tumor]], [[atrophy]] or any changes suggestive of amnesia. [[Positron emission tomography]] [[PET]] may show [[hypometabolism]] in areas of [[brain]] associated with [[memory]] in [[patients]] with history of amnesia but with no visible structural or functional [[brain]] damage on [[CT scan]] or [[MRI]]. Other [[diagnostic]] studies helpful in the diagnosis of the cause amnesia are [[EEG]] for [[epilepsy]], [[CSF]] fluid analysis for [[encephalitis]].[[Treatment]] can be offered in cases of reversible conditions. If not, provision of supportive care can help to improve a [[patient's]] condition. [[Etiology]] specific [[treatment]] plan should be followed to improve [[memory]] and delay [[progression]]. [[Surgical]] intervention is not recommended for the management of [[memory]] loss. Measures for the [[primary prevention]] of amnesia include preventing [[brain]] [[trauma]], managing [[stress]], avoid [[alcohol]] [[abuse]], manage [[stroke]] [[risk factors]], good [[sleep]] [[habits]], social integration, optimum [[nutrition]] and [[exercise]] routine. Effective measures for the [[secondary prevention]] of [[memory]] loss include, sustainable daily routine, healthy eating habits, social integration, [[exercise]] routine, reduce and manage [[stress]], adequate [[sleep]], reading and playing strategic games like puzzles and word games.


==Historical Perspective==
==Historical Perspective==
Richard Semon in 1904 described that experiences cause some changes in the [[neurons]] and these changes are referred to as ''engram'' and they form [[memory]] of the particular experience in those [[neurons]]. Reactivation of these [[neurons]] occur when [[patient]] tries to recall those [[memories]]. Theodule-Armand Ribot, a [[French]] [[psychologist]] determined that [[memory]] loss affects recent [[memories]] first. [[Memories]] are lost in reverse order of their [[development]].


==Classification==
==Classification==
Amnesia can be divided into two broad groups, [[retrograde amnesia]] and [[anterograde amnesia]]. [[Retrograde amnesia]] is the loss of [[memory]] prior to the onset of amnesia and [[anterograde amnesia]] is the inability to form new [[memory]].
Amnesia can be divided into two broad groups, [[retrograde amnesia]] and [[anterograde amnesia]]. [[Retrograde amnesia]] is the loss of [[memory]] prior to the onset of amnesia and [[anterograde amnesia]] is the inability to form new [[memory]]. Other types of amnesia are [[Psychological]] including [[repressive amnesia]] and [[dissociative fugue]], [[infantile]] amnesia, [[neurological]] amnesia ([[Alzheimer's disease]], [[Pick's disease]]), post-[[traumatic]] Amnesia, [[drug]]-Induced Amnesia, [[transient global amnesia]]. [[Memory]] can also be divided into two groups depending on the duration, short-term [[memory]] and long-term [[memory]].


==Pathophysiology==
==Pathophysiology==
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.
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]].


==Causes==
==Causes==
Common causes of amnesia include medications, [[head trauma]], [[depression]] and aging.
Common causes of amnesia include [[medications]], [[head trauma]], [[depression]] and [[aging]]. Less common cause of amnesia are childhood [[sexual]] [[abuse]], traumatic incident, [[hypoxia]], [[psychological]] [[trauma]], [[thiamine]] [[deficiency]], [[alcohol]] [[abuse]], [[Alzheimer's disease]], [[Pick's disease]], [[Parkinson's disease]], [[benzodiazepines]], [[hypoglycemia]], [[stroke]], [[electroconvulsive therapy]].
 
==Differentiating Amnesia from other Diseases==
The underlying [[etiology]] of memory loss must be differentiated on the basis of duration of [[memory]] loss, presence of [[anterograde amnesia]] or [[retrograde amnesia]], associated features, and [[cognitive impairment]].
 
==Epidemiology and Demographics==
[[Memory]] impairment tends to increase with [[age]]. Forty percent of the [[population]] over [[age]] sixty have some degree of [[memory]] loss. Amnesia and mild [[cognitive impairment]] is more [[prevalent]] in middle-aged to older Non-[[Hispanic]] Black and older [[Latino]] as compared to non-[[Hispanic]] Whites.


==Risk Factors==
==Risk Factors==
[[Aging]], [[depression]] and [[medications]] (both prescription and non-prescription) are risk factors for amnesia.
[[Aging]], [[depression]], [[chronic]] [[stress]], [[head]] [[trauma]], [[chronic]] [[sleep deprivation]] and [[medications]] are [[risk factors]] ​for amnesia.
 
==Natural History, Complications and Prognosis==
Amnesia may progress slowly or suddenly, and maybe transient or permanent. The natural history and [[prognosis]] depends upon the underlying [[etiology]]. [[Patients]] with [[memory]] loss could suffer from [[depression]] and [[grief]] long term. [[Quality of life]] and activities of daily living are difficult to maintain which causes decreased socialization and a decline in [[cognitive]] functions in the [[elderly]].


==Diagnosis==
==Diagnosis==
===Diagnostic Study of Choice===
There is no [[diagnostic]] study of choice to [[diagnose]] amnesia. The best approach is to obtain a detailed history followed by a focused [[physical examination]].
===History and Symptoms===
===History and Symptoms===
It is critical to perform a formal and exhaustive assessment of the patient to look for any indications of memory disorders and to hear any subjective complaints. With this information, preventative measures and care can be specifically addressed to the patient's needs.
It is critical to perform a formal and exhaustive assessment of the [[patient]] to look for any indications of [[memory]] [[disorders]] and to hear any subjective complaints. With this information, [[preventative]] measures and care can be specifically addressed to the [[patient's]] needs. A detailed history of [[memory]] loss and associated [[symptoms]] is crucial for understanding the [[etiology]] of amnesia.


===Physical Examination===
===Physical Examination===
The physical examination includes a detailed test of thinking and memory ([[mental status examination]] or neurocognitive test), and an examination of the nervous system. Recent, intermediate, and long-term memory should be tested.
[[Patients]] with amnesia may have variable [[general appearance]] depending on the underlying cause of [[memory]] loss. Amnesia is largely a clinical [[diagnosis]]. Focal [[examination]] including [[vital signs]], [[altered mental status]], [[mini mental status exam]] ([[MMSE]]), [[Glasgow Coma Scale]], [[nystagmus]], [[papilledema]], [[gait]], [[instruments of daily activities]] should be assessed.
 
===Laboratory Findings===
There is no [[laboratory]] test to [[diagnose]] memory loss. however, it is important to obtain [[toxicology screening]], [[alcohol]], [[glucose]], [[electrolytes]] level.
 
===Electrocardiogram===
There are no [[ECG]] findings associated with amnesia.
===X-ray===
There are no [[x-ray]] findings associated with amnesia.
 
===Echocardiography and Ultrasound===
There are no [[echocardiography]]/[[ultrasound]] findings associated with amnesia. Although a case of [[transient global amnesia]] has been reported in a patient undergoing a [[transesophageal echocardiogram]] ([[TEE]]).
 
===CT===
[[Head]] [[CT scan]] may be helpful in the [[diagnosis]] of the cause of amnesia. Structural and functional abnormalities are identified to detect any [[bleeding]], [[stroke]], [[tumor]], [[atrophy]] or any changes suggestive of amnesia.
===MRI===
===MRI===
Psychogenic amnesia is defined by the lack of structural damage to the brain, but upon [[Medical imaging|functional imaging]], abnormal brain activity can be seen. Tests using [[functional magnetic resonance imaging]] suggest that patients with psychogenic amnesia are unable to retrieve emotional memories normally during the amnesic period, suggesting that changes in the limbic functions are related to the symptoms of psychogenic amnesia.<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>
[[Head]] [[MRI]] may be helpful in the [[diagnosis]] of the cause of amnesia in some cases including, [[Alzheimer's disease]], or [[brain]] [[trauma]]. In majority of the cases of amnesia the [[brain]] appears normal on [[MRI]].


===Other Imaging Findings===
===Other Imaging Findings===
By performing a [[positron emission tomography]] activation study on psychogenic amnesic patients with [[Face perception|face recognition]], it was found that activation of the right anterior medial [[Temporal lobe|temporal region]] including the [[amygdala]] was increased in the patient whereas bilateral [[Hippocampus|hippocampal]] regions increased only in the control subjects, demonstrating again that [[Limbic system|limbic]] and limbic-[[Cortex|cortical]] functions are related to the symptoms of psychogenic amnesia.<ref name = Yasuno>{{cite journal |author=Yasuno F, Nishikawa T, Nakagawa Y, ''et al'' |title=Functional anatomical study of psychogenic amnesia |journal=Psychiatry Res |volume=99 |issue=1 |pages=43–57 |year=2000 |pmid=10891648 |doi=}}</ref> Transient global amnesia is distinct in that abnormalities in the [[hippocampus]] can sometimes be visualized using a special form of [[magnetic resonance imaging]] of the brain known as [[diffusion-weighted imaging]] (DWI).
[[Positron emission tomography]] [[PET]] may show [[hypometabolism]] in areas of [[brain]] associated with [[memory]] in [[patients]] with history of amnesia but with no visible structural or functional [[brain]] damage on [[CT scan]] or [[MRI]].
 
===Other Diagnostic study===
Other [[diagnostic]] studies helpful in the diagnosis of the cause amnesia are [[EEG]] for [[epilepsy]], [[CSF]] fluid analysis for [[encephalitis]].


==Treatment==
==Treatment==


===Medical Therapy===
===Medical Therapy===
Treatment can be offered in cases of reversible conditions. If not, provision of supportive care can help to improve a patient's condition.
[[Treatment]] can be offered in cases of reversible conditions. If not, provision of supportive care can help to improve a [[patient's]] condition. [[Etiology]] specific [[treatment]] plan should be followed to improve [[memory]] and delay [[progression]]. When [[memory]] loss is a [[symptom]] of a more severe [[disease]], it may be reversed as soon as the underlying condition is identified and cured. [[Memory]] loss due to [[aging]] cannot be cured, but the symptoms may be improved by [[preventative]] measures.
 
===Surgery===
[[Surgical]] intervention is not recommended for the management of [[memory]] loss.


===Primary Prevention===
===Primary Prevention===

Latest revision as of 03:05, 25 March 2021

Amnesia Microchapters

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Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Amnesia from other Diseases

Epidemiology and Demographics

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Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

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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

Amnesia can be divided into two broad groups, retrograde amnesia and anterograde amnesia. Retrograde amnesia is the loss of memory prior to the onset of amnesia and anterograde amnesia is the inability to form new memory. Memory can also be divided into two groups depending on the duration, short-term memory and long-term memory. Other types of amnesia are Psychological including repressive amnesia and dissociative fugue, infantile amnesia, neurological amnesia (Alzheimer's disease, Pick's disease), post-traumatic Amnesia, drug-Induced Amnesia, transient global amnesia, amnesia due to nutritional deficiency (thiamine, vitamin B12). Richard Semon in 1904 described that experiences cause some changes in the neurons and these changes are referred to as engram and they form memory of the particular experience in those neurons. Reactivation of these neurons occur when patient tries to recall those memories. 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. Common causes of amnesia include medications, head trauma, depression and aging. Less common cause of amnesia are childhood sexual abuse, traumatic incident, hypoxia, psychological trauma, thiamine deficiency, alcohol abuse, Alzheimer's disease, Pick's disease, Parkinson's disease, benzodiazepines, hypoglycemia, stroke, electroconvulsive therapy. The underlying etiology of memory loss must be differentiated on the basis of duration of memory loss, presence of anterograde amnesia or retrograde amnesia, associated features, and cognitive impairment. Memory impairment tends to increase with age. Forty percent of the population over age sixty have some degree of memory loss. Amnesia and mild cognitive impairment is more prevalent in middle-aged to older Non-Hispanic Black and older Latino as compared to non-Hispanic Whites. Aging, depression, chronic stress, head trauma, chronic sleep deprivation and medications are risk factors ​for amnesia. Amnesia may progress slowly or suddenly, and maybe transient or permanent. The natural history and prognosis depends upon the underlying etiology. Patients with memory loss could suffer from depression and grief long term. Quality of life and activities of daily living are difficult to maintain which causes decreased socialization and a decline in cognitive functions in the elderly.Amnesia is largely a clinical diagnosis, a detailed history of memory impairment and associated symptoms should be obtained. Focal examination including vital signs, altered mental status, mini mental status exam (MMSE), Glasgow Coma Scale, nystagmus, papilledema, gait, instruments of daily activities should be assessed. Head CT scan and MRI may be helpful in identifying structural and functional abnormalities including bleeding, stroke, tumor, atrophy or any changes suggestive of amnesia. Positron emission tomography PET may show hypometabolism in areas of brain associated with memory in patients with history of amnesia but with no visible structural or functional brain damage on CT scan or MRI. Other diagnostic studies helpful in the diagnosis of the cause amnesia are EEG for epilepsy, CSF fluid analysis for encephalitis.Treatment can be offered in cases of reversible conditions. If not, provision of supportive care can help to improve a patient's condition. Etiology specific treatment plan should be followed to improve memory and delay progression. Surgical intervention is not recommended for the management of memory loss. Measures for the primary prevention of amnesia include preventing brain trauma, managing stress, avoid alcohol abuse, manage stroke risk factors, good sleep habits, social integration, optimum nutrition and exercise routine. Effective measures for the secondary prevention of memory loss include, sustainable daily routine, healthy eating habits, social integration, exercise routine, reduce and manage stress, adequate sleep, reading and playing strategic games like puzzles and word games.

Historical Perspective

Richard Semon in 1904 described that experiences cause some changes in the neurons and these changes are referred to as engram and they form memory of the particular experience in those neurons. Reactivation of these neurons occur when patient tries to recall those memories. Theodule-Armand Ribot, a French psychologist determined that memory loss affects recent memories first. Memories are lost in reverse order of their development.

Classification

Amnesia can be divided into two broad groups, retrograde amnesia and anterograde amnesia. Retrograde amnesia is the loss of memory prior to the onset of amnesia and anterograde amnesia is the inability to form new memory. Other types of amnesia are Psychological including repressive amnesia and dissociative fugue, infantile amnesia, neurological amnesia (Alzheimer's disease, Pick's disease), post-traumatic Amnesia, drug-Induced Amnesia, transient global amnesia. Memory can also be divided into two groups depending on the duration, short-term memory and long-term memory.

Pathophysiology

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.

Causes

Common causes of amnesia include medications, head trauma, depression and aging. Less common cause of amnesia are childhood sexual abuse, traumatic incident, hypoxia, psychological trauma, thiamine deficiency, alcohol abuse, Alzheimer's disease, Pick's disease, Parkinson's disease, benzodiazepines, hypoglycemia, stroke, electroconvulsive therapy.

Differentiating Amnesia from other Diseases

The underlying etiology of memory loss must be differentiated on the basis of duration of memory loss, presence of anterograde amnesia or retrograde amnesia, associated features, and cognitive impairment.

Epidemiology and Demographics

Memory impairment tends to increase with age. Forty percent of the population over age sixty have some degree of memory loss. Amnesia and mild cognitive impairment is more prevalent in middle-aged to older Non-Hispanic Black and older Latino as compared to non-Hispanic Whites.

Risk Factors

Aging, depression, chronic stress, head trauma, chronic sleep deprivation and medications are risk factors ​for amnesia.

Natural History, Complications and Prognosis

Amnesia may progress slowly or suddenly, and maybe transient or permanent. The natural history and prognosis depends upon the underlying etiology. Patients with memory loss could suffer from depression and grief long term. Quality of life and activities of daily living are difficult to maintain which causes decreased socialization and a decline in cognitive functions in the elderly.

Diagnosis

Diagnostic Study of Choice

There is no diagnostic study of choice to diagnose amnesia. The best approach is to obtain a detailed history followed by a focused physical examination.

History and Symptoms

It is critical to perform a formal and exhaustive assessment of the patient to look for any indications of memory disorders and to hear any subjective complaints. With this information, preventative measures and care can be specifically addressed to the patient's needs. A detailed history of memory loss and associated symptoms is crucial for understanding the etiology of amnesia.

Physical Examination

Patients with amnesia may have variable general appearance depending on the underlying cause of memory loss. Amnesia is largely a clinical diagnosis. Focal examination including vital signs, altered mental status, mini mental status exam (MMSE), Glasgow Coma Scale, nystagmus, papilledema, gait, instruments of daily activities should be assessed.

Laboratory Findings

There is no laboratory test to diagnose memory loss. however, it is important to obtain toxicology screening, alcohol, glucose, electrolytes level.

Electrocardiogram

There are no ECG findings associated with amnesia.

X-ray

There are no x-ray findings associated with amnesia.

Echocardiography and Ultrasound

There are no echocardiography/ultrasound findings associated with amnesia. Although a case of transient global amnesia has been reported in a patient undergoing a transesophageal echocardiogram (TEE).

CT

Head CT scan may be helpful in the diagnosis of the cause of amnesia. Structural and functional abnormalities are identified to detect any bleeding, stroke, tumor, atrophy or any changes suggestive of amnesia.

MRI

Head MRI may be helpful in the diagnosis of the cause of amnesia in some cases including, Alzheimer's disease, or brain trauma. In majority of the cases of amnesia the brain appears normal on MRI.

Other Imaging Findings

Positron emission tomography PET may show hypometabolism in areas of brain associated with memory in patients with history of amnesia but with no visible structural or functional brain damage on CT scan or MRI.

Other Diagnostic study

Other diagnostic studies helpful in the diagnosis of the cause amnesia are EEG for epilepsy, CSF fluid analysis for encephalitis.

Treatment

Medical Therapy

Treatment can be offered in cases of reversible conditions. If not, provision of supportive care can help to improve a patient's condition. Etiology specific treatment plan should be followed to improve memory and delay progression. When memory loss is a symptom of a more severe disease, it may be reversed as soon as the underlying condition is identified and cured. Memory loss due to aging cannot be cured, but the symptoms may be improved by preventative measures.

Surgery

Surgical intervention is not recommended for the management of memory loss.

Primary Prevention

Measures for the primary prevention of amnesia include preventing brain trauma, managing stress, avoid alcohol abuse, manage stroke risk factors, good sleep habits, social integration, optimum nutrition and exercise routine.

Secondary Prevention

Effective measures for the secondary prevention of memory loss include, sustainable daily routine, healthy eating habits, social integration, exercise routine, reduce and manage stress, adequate sleep, reading and playing strategic games like puzzles and word games.

References


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