Table of contents:
- Definition of Amnestic Disorders
- Types of Amnesia
- Amnesic syndrome
- Mental disorders with identified organic etiology
- Organic personality change
- Organic delusional disorder
Amnesic symptoms can appear in a multitude of disorders, but the difference with amnesic disorders is that amnesia is the main symptom and that its organic etiology has been demonstrated. In 1953 Sconville bilaterally excised HM's hippocampus, which caused him to retain memories but not be able to store new information. Amnesic disorder is characterized by memory impairment in the absence of other significant cognitive impairments. Amnestic disorders are listed according to their presumed etiology: amnestic disorder due to a general medical condition, persistent substance-induced amnestic disorder, or unspecified amnestic disorder.
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- Types of Amnesia
- Amnesic syndrome
- Mental disorders with identified organic etiology
- Organic personality change
- Organic delusional disorder
Definition of Amnestic Disorders
Subjects with an amnesic disorder have impaired ability to learn new information and are unable to recall past events or previously learned information. Memory impairment may be severe enough to cause marked impairment in work or social activity and may represent a significant decline in previous level of activity. Memory impairment does not appear exclusively during delirium or dementia.
The ability to recall new information is always impaired, but the difficulty in recalling previously learned information is more variable, depending on the location and severity of the brain injury. The memory deficit is most apparent in tasks that require spontaneous recall and may be evident when the examiner provides stimuli to the subject to recall later.
The deficits can be predominantly related to verbal or visual stimuli depending on the area of the brain specifically affected. In some forms of amnesic disorder, the subject is better able to recall very remote things from the past than more recent events (e.g., a subject recalls a stay in hospital a decade ago, with details that are vividly expressed, without realizing that currently is in that same hospital). The diagnosis is not made if memory impairment occurs exclusively in the course of delirium (eg, if it occurs only in the context of reduced ability to maintain or direct attention).
In amnesic disorder, the ability to immediately repeat a sequence of information (eg, digits) is not impaired. When it is, one should suspect the presence of a disturbance in attention, which may be indicative of delirium. Amnestic disorder is diagnosed if there are other cognitive deficits characteristic of dementia (eg, aphasia, agnosia, impaired ability to perform).
Individuals with amnesic disorder may experience serious impairments in their personal or social capacity as a result of their memory deficits, requiring daily supervision to ensure their diet and minimal care. Amnestic disorder is often preceded by a clinical picture of confusion and disorientation, and possible attention problems that suggest delirium (eg, amnestic disorder due to thiamine deficiency). During the initial stages of the disorder, confabulation is frequent, often evidenced by the narration of imaginary events that seek to fill the memory gaps, but it tends to disappear with time.
For this reason, it is important to collect information from relatives or close friends. Deep amnesia can lead to temporal and spatial disorientation, but autopsychic disorientation is rare and is common in individuals with dementia but not with amnesic disorder. Most individuals with severe amnesic disorder lack the judgment to recognize their memory deficits and can explicitly deny the presence of their severe impairment, despite evidence to the contrary. This lack of judgment can lead to accusations of others or, in exceptional cases, agitation.
Some individuals recognize that they have a problem and appear not to be concerned. There may be some suggestive changes of personality alteration, such as apathy, lack of initiative and emotional fragility. Subjects may appear superficially friendly and agreeable, but have narrow or poor emotional expressiveness. Often times, transient global amnesia gives individuals with it an appearance of perplexity and bewilderment. Minor deficits in other cognitive functions may be seen, but by definition they are not severe enough to cause clinically significant impairment. Quantitative neuropsychological tests often demonstrate specific memory deficits, with the absence of other cognitive impairments.
Depending on the extent or nature of the deficits, the results of standardized tests that assess recall of known historical events or of public persons are variable. Memory impairment is also a symptom of deliriumand dementia. In delirium, memory dysfunction is associated with impaired consciousness, with reduced ability to focus, maintain, or direct attention. In dementia, memory impairment must be accompanied by multiple cognitive deficits (eg, aphasia, apraxia, agnosia, or impaired performance), leading to clinically significant impairment. Amnestic disorder must be distinguished from dissociative amnesia and from amnesia that occurs in the context of other dissociative disorders (eg, dissociative identity disorder).
By definition, amnesic disorder is due to the direct physiological effects of a general medical condition or substance use. Furthermore, amnesia in dissociative disorders does not imply a deficit in learning and remembering new information, but rather that the subjects present a circumscribed inability to recall content of a traumatic or stressful nature.
For memory disturbances present only during intoxication or withdrawal from a drug of abuse, the appropriate diagnoses will be substance intoxication or withdrawal from substances, and a separate diagnosis of amnestic disorder should not be made. For memory disorders associated with drug use, unspecified side effects of medication should be noted.
The presumed etiology of the amnestic disorder determines the diagnosis (the description and diagnostic criteria for each amnestic disorder are described separately later in this section). If the memory impairment is believed to be the consequence of direct physiological effects of a general medical condition (including head trauma), an Amnesic Disorder Due to General Medical Condition will be diagnosed.
If the memory impairment is the result of the persistent effects of a substance (eg, drug of abuse, medications, or toxic exposure), a persistent substance-induced amnesic disorder will be diagnosed. Both diagnoses should be made when both a substance (eg, alcohol) or a general medical condition (eg, head injury) have played an etiological role in the development of the memory impairment. If a specific etiology cannot be established (eg, dissociative, substance-induced, or due to a general medical condition), an unspecified amnesic disorder will be diagnosed.
Amnesic disorder must be distinguished from simulation and factitious disorder. Systematic memory tests (which often provide inconsistent results in simulation and factitious disorder) as well as the absence of a general medical condition or substance use believed to be related to impaired memory can help to make this difficult distinction. memory. Amnestic disorder must be distinguished from the memory impairment characteristic of age-related cognitive deficit, in which there is a physiological loss in relation to age. Criteria for the diagnosis of Amnestic Disorder due to… (indicate general medical condition):
- Memory impairment is manifested by a deficit in the ability to learn new information or by the inability to recall previously learned information.
- Memory impairment causes a significant deterioration in work or social activity and represents a significant decrease in the previous level of activity.
- Memory impairment does not appear exclusively during delirium or dementia.
- Demonstration, through history, physical examination, or laboratory tests, that the disturbance is a direct effect of the general medical condition (including physical trauma).
Specify if:
- Transient: if memory impairment lasts less than 1 month
- Chronic: if memory impairment lasts more than 1 month
As areas related to amnesia we find areas of the diencephalon, mammillary bodies and dorsomedial nuclei of the thalamus. Amnesic deterioration can be explained based on the deficit of certain processes:
- Coding or storage deficit (in the amnesiac, deep processing would not be carried out and his memory would be worse
- Storage deficit: The problem of amnesiacs would be of transfer to long-term memory and consolidation of information.
- Retention deficit: Forgetfulness is extremely fast
- Recovery deficit: What is impaired in the amnesiac is the ability to intentionally access stored information.
This hypothesis is supported by authors such as Jacoby (intentional or incidental recovery), Schacter (implicit / explicit memory) and Graf's experiment (facilitation effect).
Other hypotheses:
- Hirst and the coherence model: The subject takes the words as a continuous list and the deficit would be located in the coding phase.
- Another hypothesis is that of Mayes and the hypothesis of the memory deficit of the context of Mayes, which states that there is a disproportionate deterioration of the context.
Tulving places importance on memory and proposes a direct connection between consciousness and memory. "Autonoetic" (self-knowledge) consciousness noetic (semantic system) and anoetic (system of procedures)
Types of Amnesia
TRANSITORY GLOBAL AMNESIA
Transient global amnesia (TGA) is a clinical syndrome that appears in mature and elderly people, characterized by episodes of anterograde amnesia and profound confusion lasting several hours and with full recovery. The attacks are not accompanied by seizure activity or impaired consciousness and are based on amnesia for the recognition of attitudes and the recent past.
POST-TRAUMATIC AMNESIA
Usually caused by a head injury (fall, blow to the head) that does not penetrate the skull. It is frequently transitory; the duration of amnesia is related to the degree of damage caused and can give an indication of prognosis for the recovery of other functions. A slight trauma, such as a car accident that results in no more than a slight whiplash, can cause the occupant to not remember the events that occurred just before the accident due to a brief interruption in the short-to-long-term memory transfer mechanism. This mechanism is known as Memory Consolidation and it consists of molecular changes based on protein synthesis that form fixed representations in the brain.The person who suffers from post-traumatic amnesia can also present a coma that can last from seconds to weeks, depending on the severity of the trauma. After the coma state there is a period of confusion. The person will present anterograde amnesia of the events that occurred in the period of confusion. Period of amnesia between the brain injury responsible for memory loss and the point at which memory-related functions are restored.The period of amnesia between the brain injury responsible for memory loss and the point at which memory-related functions are restored.The period of amnesia between the brain injury responsible for memory loss and the point at which memory-related functions are restored.
Ribot's Law is given (the information is forgotten in the opposite sense to how it was learned. Poor memory and recognition of later events and closer to the beginning of the disorder. It does not show what the law shows.
AMNESIA DUE TO ELECTROCONVULSIVE THERAPY
After the seizures, a confusional state appears followed by retrograde and anterograde amnesia. Memory gradually recovers over the next 6 months.
Amnesic syndrome
KORSAKOFF SYNDROME
The acute phase is the Wernicke phase and the chronic phase is the Korsakoff phase. It is a brain disorder due to thiamine deficiency.
Causes, incidence, and risk factors Wernicke's encephalopathy and Korsakoff syndrome are thought to be different conditions, both due to brain damage caused by a lack of vitamin B1 (thiamine). Lack of vitamin B1 is common in people who suffer from alcoholism. It is also common in people whose bodies do not absorb food properly (malabsorption), as occurs sometimes after obesity surgery. Korsakoff syndrome or psychosis tends to develop as the symptoms of Wernicke syndrome disappear. Wernicke encephalopathy causes brain damage in lower parts of the brain called the thalamus and hypothalamus. Korsakoff psychosis results from damage to areas of the brain involved with memory.
Symptoms of KORSAKOFF SYNDROME
Symptoms of Wernicke encephalopathy:
- Confusion
- Loss of muscle coordination (ataxia) tremor in the legs
- Vision changes abnormal eye movements (movements from side to side called nystagmus) double vision drooping of the eyelids
Korsakoff syndrome symptoms
- Inability to form new memories
- Memory loss which can be serious
- Make up stories (conspiracy)
- Seeing or hearing things that are not really there (hallucinations) Note: There may also be symptoms of alcohol withdrawal.
Signs and tests
Examination of the nervous and muscular system may show damage to multiple nervous systems:
- Abnormal eye movements
- Abnormal or decreased reflexes
- Rapid pulse (heart rate)
- Low blood pressure
- Low body temperature
- Muscle weakness and atrophy (loss of tissue mass)
- Gait and coordination problems The person may appear undernourished.
The following tests are used to check the nutritional level of the person:
- Serum albumin (related to the general nutrition of the person)
- Serum levels of vitamin B1
- Red blood cell transketolase activity (reduced in people with thiamine deficiency)
- Urine or blood alcohol levels and liver enzymes may be high in people with a history of chronic alcohol use.
Other chronic conditions that can cause a thiamine deficiency include, but are not limited to:
- AIDS Cancers that have spread throughout the body
- Vomiting and extreme nausea during pregnancy (hyperemesis gravidarum)
- Heart failure (when treated with long-term diuretic therapy)
- Long periods of intravenous (IV) therapy without receiving thiamine supplements
- Prolonged dialysis
- Very high levels of thyroid hormone (thyrotoxicosis)
An MRI of the brain can show changes in brain tissue, but if Wernicke-Korsakoff syndrome is suspected, treatment should be started immediately. An MRI of the brain is usually not needed.
Treatment The goals of treatment are to control symptoms as much as possible and to prevent the disease from getting worse. Some people may need hospitalization early in the condition to help control symptoms. Proper surveillance and care of the disease may be required if the person is: Comatose Lethargic Unconscious Thiamine (vitamin B1) can be given by intravenous or intramuscular injection or by mouth. It can improve symptoms of:
- Confusion or delirium
- Difficulties with vision and eye movement
- Lack of muscle coordination
- Thiamine generally does not improve the loss of memory and brainpower that occurs with Korsakoff psychosis.
Stopping alcohol consumption can prevent further loss of brain function and nerve damage. Eating a nutritious and well-balanced diet can help, but it is not a substitute for quitting alcohol. Expectations (prognosis) Without treatment, Wernicke-Korsakoff syndrome is constantly getting worse and is life threatening. With treatment, symptoms such as poor coordination and visual difficulties can be controlled, as well as reduced or prevented from getting worse. Some symptoms, particularly loss of memory and cognitive skills, can be permanent. Other disorders related to excessive alcohol use can also occur.
Complications
- Alcohol withdrawal
- Difficulties in relationships with people or in social interaction
- Injuries from falls
- Permanent alcoholic neuropathy
- Permanent loss of cognitive skills
- Permanent memory loss
- Shortened life span
In people who are at risk, Wernicke's encephalopathy can be caused by carbohydrate loading or glucose infusion. Thiamine supplements should always be given before glucose infusion to prevent this.
AMNESIC SYNDROME
Amnesic syndrome has been defined as a permanent, stable and global memory disorder, due to an organic brain disorder in the absence of other perceptual or cognitive deficits. The responsible etiology is wide and includes, cerebral infarcts, subarachnoid hemorrhages, hypoxia, tumors, head trauma (TBI), metabolic diseases, herpes simplex encephalitis, etc. According to Parkin and Leng, the characteristics that define amnesic syndrome are the following:
- there is no evidence of immediate memory deficits assessed by tasks such as digit span;
- semantic memory and other intellectual functions measured by standard tests are largely preserved;
- severe and permanent anterograde amnesia, clearly evident in evocation and recognition tests;
- a certain degree of retrograde amnesia, which is extremely variable from one patient to another; preserved procedural memory, good motor skills, and some evidence that the subject has the ability to form new procedural memories
- preserved procedural memory, good motor skills and some type of evidence that the subject has the capacity to form new procedural memories.
Mental disorders with identified organic etiology
COMMON DIAGNOSTIC CRITERIA
- Demonstration that the alteration is a direct physiological effect of a medical disease
- The alteration is not better explained by the presence of another mental disorder
- It does not appear exclusively in the course of a delirium.
Organic catatonic disorder
A disorder characterized by decreased (stupor) or increased (agitation) psychomotor activity, which is accompanied by catatonic symptoms. Both poles of psychomotor disorders can alternate. It is unknown whether the full range of catatonic disorders described in schizophrenia can present in these organic conditions. Nor has it been conclusively clarified whether an organic catatonic state can present itself with a clear state of consciousness or whether it is always a manifestation of a delirium, with a subsequent total or partial amnesia. This implies caution in diagnosing such a condition and carefully evaluating the guidelines for the diagnosis of delirium.It is generally accepted that encephalitis and carbon monoxide poisoning give rise to this syndrome more frequently than other organic causes. Guidelines for diagnosis.
The general guidelines for accepting an organic etiology, outlined in F06, must be met. In addition, one of the following symptoms should be present:
- Stupor (decrease or total absence of spontaneous movements with partial or total silence, negativism and rigid postures maintained).
- Agitation (frank motor restlessness with or without aggressive tendencies).
- Both states (going rapidly and unexpectedly from hiccups to hyperactivity).
Other catatonic phenomena that increase the reliability of the diagnosis are: stereotypies, waxy flexibility and impulsive acts. Excludes: catatonic schizophrenia (F20.2). Dissociative stupor (F44.2). Unspecified stupor (R40.1).
Organic personality change
Long-lasting personality alteration, which represents a change in the previous characteristics of the subject's personality pattern (in children it is expressed by a marked deviation from the normal development pattern, or by a significant change from the habitual behavior pattern, and which is maintained at least one year)
DSM IV Diagnostic Criteria for Personality Change Due to Medical Condition.
- Persistent personality alteration that represents a change from the individual's previous characteristic personality pattern. (In children, the alteration includes a marked deviation in the habitual patterns of behavior of the child with a minimum duration of one year).
- There is evidence from history, physical examination, or laboratory findings that the disturbance is a direct physiological consequence of a general medical condition.
- The disturbance is not better explained by another mental disorder (including another mental disorder due to a general medical condition).
- The alteration does not occur exclusively during the course of a delirium and does not meet the criteria for dementia.
- The disturbance is the cause of significant clinical distress or impairment in social, occupational, or other important areas of functioning.
Specify type:
- Labile type: If the predominant characteristic is affective lability.
- Disinhibited type: If the predominant characteristic is poor impulse control such as sexual indiscretions, etc.
- Aggressive type: If the predominant characteristic is aggressive behavior.
- Apathetic type: If the predominant characteristic is marked apathy and indifference.
- Paranoid type: If the predominant characteristic is suspicion or paranoid ideation.
- Other Type: If the predominant characteristic is none of those mentioned, for example: personality change associated with epilepsy.
- Combined type: If more than one of the characteristics predominate in the clinical picture.
- Unspecified type.
Organic delusional disorder
The criteria for accepting an organic etiology must be met. In addition, delusions must be presented. Hallucinations, thought disorders, or isolated catatonic phenomena may also be present.
Organic dissociative disorder
Picture similar to the primary dissociative pictures (dissociative amnesia, dissociative figa, dissociative identity disorder, etc.) but in which there is a demonstration of organic etiology.
Organic mood disorders
A disorder characterized by depressed mood, decreased vitality, and activity. The only criterion for the inclusion of this state in the organic section is a presumed direct causal relationship with a brain or somatic disorder whose presence must be demonstrated.
Organic anxiety disorder
Table characterized by the essential features of a generalized anxiety disorder, panic disorder, or a combination of both.
Organic sleep disorder
Prominent sleep disturbance, severe enough to require independent clinical care
Post-concussion disorder
It is caused by a TBI. Existence of objective evidence of impairment in attention or memory.
Organic sexual disorder
Clinically significant sexual disorder, causing marked discomfort, or difficulty in interpersonal relationships as predominant clinical features.
Post-encephalic disorder
Changes in behavior that occur after viral or bacterial encephalitis.
Mild cognitive disorder
Cognitive evaluations in epidemiological studies allow the elderly to be separated into three groups: dementia carriers (that is, with a deterioration of different cognitive areas that alters daily functioning), without dementia and not classifiable.
This last group includes patients who have alterations in a specific cognitive area (mainly memory), but maintain a good functioning in daily life and a normal general intellectual level. After receiving different names in the literature, this group has recently been defined as mild cognitive impairment. The criteria for mild cognitive impairment were validated by Peterson in 1999. This author published a comparative study between patients with Alzheimer's disease, mild cognitive impairment, and healthy subjects. The work showed that patients with mild cognitive impairment do not have significant alterations in the results of global cognitive assessment tests such as the Wechsler intelligence scale or "minimental" test (MMSE).
Consistent with the diagnostic criteria, patients with mild cognitive impairment have memory test results (including learning word lists, paragraphs, non-verbal materials, and semantic memory) below 1.5 standard deviations from the expected value for age. Although these are the most widely accepted criteria, it is important to mention that this is still an area that is under review. Some authors suggest including as non-amnesic mild cognitive impairment patients who present some cognitive impairment in an area other than memory.
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