Amnesia

Amnesia is a partial or complete inability to reproduce information received in the past. It can be a consequence of craniocerebral trauma, degenerative processes, metabolic disorders, epilepsy or psychological disorders. The diagnosis is based on clinical symptoms, results of neuropsychological and radiological (CT, MRI) studies. Treatment of amnesia is aimed at the underlying cause of the disease.

Memory processing involves registration (receiving new information), encoding (forming connections, time stamps, and other processes necessary for information retrieval), and retrieval. Disruption of any of these steps can cause amnesia.

Amnesia can be classified as retrograde (loss of memory for events before the injury), anterograde (loss of memory for events that occurred after the injury), or global (loss of the ability to remember new information and loss of memory for recent events). Amnesia can be transient (e.g., after brain injury), permanent (e.g., after severe illnesses such as encephalitis, total cerebral ischemia, or cardiac arrest), or progressive (e.g., in degenerative dementias such as Alzheimer's disease).

In case of declarative memory disorder (for events and facts), the patient forgets familiar words and faces, losing access to past individual experience; in case of procedural (implicit) memory disorder, the patient is unable to use previously acquired skills.

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Causes of amnesia

Amnesia can be caused by psychological and organic factors. Organic amnesia can be divided into:

• An "amnestic" syndrome with focal pathological lesions of the brain. Pathological examination reveals brain damage, particularly in the mammillary body, the posterior hypothalamus, and the gray matter in the area of the third and fourth ventricles and the aqueductus cerebri. Bilateral hippocampal lesions are sometimes found. Focal damage may be caused by tumors, thiamine deficiency (as in Wernicke's encephalopathy and Korsakoff's psychosis), and infarctions. It is expressed by the inability to store new memories after an event or incident (anterograde amnesia) and by the loss of old memories (retrograde amnesia), in the absence of symptoms such as confusion or inability to concentrate.
• Amnesia due to diffuse brain damage, such as in dementia (e.g., Alzheimer's disease), toxic-induced confusional states, head trauma, or hypoglycemia.

Amnesia may result from diffuse brain damage or bilateral focal or multifocal lesions involving structures involved in information storage and retrieval. Neural pathways involved in declarative memory are located in the hippocampus and parahippocampus, the inferior medial temporal lobes, the orbital surface of the frontal lobes, and the diencephalon. The most important structures are the hippocampus, hypothalamus, basal forebrain nuclei, and dorsomedial thalamic nuclei. The amygdala contributes to emotional memory enhancement, and the intralaminar nuclei of the thalamus and the reticular activating formation of the brainstem stimulate the fixation of new information in memory. Bilateral damage to the medial and posterior thalamus, brainstem reticular formation, and adrenergic system results in decreased/loss of recent memory and the ability to learn new information, most commonly due to thiamine deficiency, hypothalamic tumors, and ischemia. Bilateral damage to the medial temporal lobes, especially the hippocampus, is usually associated with transient declarative memory impairment.

Severe, irreversible memory loss usually accompanies degenerative dementias, severe brain injury, cerebral hypoxia or ischemia, malnutrition in alcoholism (eg, Wernicke's encephalopathy, Korsakoff's psychosis), and various drug intoxications (amphotericin B or lithium, chronic solvent poisoning).

Retrograde and anterograde amnesia for the periods immediately before and after a concussion or more severe traumatic brain injury also appears to be due to damage to the medial temporal lobe. More extensive brain damage may involve other structures involved in storing and retrieving information, as is seen in many diseases that lead to dementia.

Excessive psychological trauma or stress can cause memory disorders of psychological origin.

Many older adults gradually develop difficulty remembering things – first names, then events and dates, and sometimes spatial relationships. This common condition, called benign senile forgetfulness, has no proven link to degenerative dementia, although some similarities are hard to miss. The presence of subjective memory problems and poorer performance on objective tests, combined with intact cognitive and daily functioning, can be categorized as amnestic mild cognitive decline, or mild cognitive impairment (MCI). People with the more severe memory problems of MCI are more likely to develop Alzheimer's disease later in life than their peers without memory problems.

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Diagnosis of amnesia

Simple bedside tests (e.g., three-item recall, hidden object location) and formal tests (e.g., word list recall tests such as the California Verbal Memory Test and the Buschke Selective Memory Test) can help identify memory loss for words. Other types of memory (figurative, visual, auditory) are more difficult to assess; visual memory or tone recall tests are available in routine practice. The need for additional testing is determined by clinical examination.

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Treatment of amnesia

The underlying disease should be treated or psychological problems should be eliminated. Sometimes, with acute amnesia, recovery occurs without any intervention. Diseases that caused such a memory disorder as amnesia (Alzheimer's disease, Korsakov's psychosis, herpes encephalitis) should also be treated, but this is not a fact that it will lead to an improvement in memory. If the treatment does not improve memory, no other methods will speed up recovery or change the outcome for the better.

Amnesia and the Law

The association of amnesia with the commission of violent crimes is well known. In particular, this concerns amnesia due to drug or alcohol intoxication and the degree of violence used. The latter is supported by data showing that victims of violent crimes suffer more often from memory loss regarding the details of the crime than victims of non-violent crimes. It is also known that persons who commit murder more often have amnesia for the act of murder. In a number of studies of homicides, the frequency of amnesia varies from 25 to 45%. In such cases, it is often found that although the initial cause of memory loss is organic (often alcohol intoxication), amnesia is maintained by psychogenic factors, often as a result of an unconscious reluctance to remember the crime committed, especially if a spouse or other family members were killed.

Taylor described the following factors associated with amnesia for the act of committing a crime:

• the violent nature of the crime, especially in the case of homicide;
• excessive emotional arousal during the commission of a crime;
• alcohol abuse and intoxication;
• depressed mood of the criminal.

The latter was noted in a study of the prevalence of amnesia among pretrial detainees.

However, the presence of amnesia does not in itself render the accused incompetent to stand trial, nor does it prove the absence of the mens rea necessary to commit the crime. However, in both these situations, amnesia, although not in itself a defense, if it is a symptom of an underlying organic disease such as dementia, brain damage, or epileptic automatism, it may be a significant factor in declaring the accused incompetent to stand trial or in demonstrating the absence of the mens rea. This is especially true in cases of anterograde amnesia.

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Description of a case of amnesia

Mr. V is 50 years old and is charged with the attempted murder of his estranged wife. They had been married for five years and one of the reasons his wife left was because she was violent. Mr. V has no history of psychiatric treatment and no history of conflict with the law. He attempted to kill them both by tying his wife up in her car and running a hose connected to the exhaust pipe of the car. He locked himself in the car with his wife and started the engine. Both passed out, but then the engine stalled and they were discovered by neighbors. Mr. V was taken unconscious to hospital and a CT scan revealed increased cerebrospinal fluid in the ventricles of the brain and an infarction in the cerebellum. He did not regain consciousness for two weeks. His wife regained consciousness quickly and suffered minor carbon monoxide poisoning. Mr. V spent eight months in a rehabilitation unit.

Psychometric testing one year later revealed that Mr. V. had severe short-term memory deficits. He was only able to retain information for a few minutes. He also had poor memory of the previous 10 to 15 years, but could recall important events from a more distant past. He had clear abnormalities in the functioning of the frontal regions of the brain, with impairment of executive functions, particularly the ability to plan, solve problems, and perform sequential actions. Mr. V.'s personality also changed: he became apathetic, passive, and emotionally flat.

On the recommendation of two psychiatrists and a neuropsychologist, Mr V was found unfit to stand trial. This was because he was unable to understand the evidence adduced in court, was unable to retain information, and could only remember what he heard or read for a few minutes. He was found incapable of participating to the extent necessary in the trial. The trial found that he had committed the offence. He was placed under guardianship under section 37 of the Mental Health Act. He was placed with friends who provided him with full care.

Mr. V. was unable to participate in the trial not so much because of the severity of his retrograde amnesia as because of his anterograde amnesia. Anterograde amnesia of this severity affects a person's ability to understand what has been said and therefore renders him incapable of making objections. There was no doubt about the genuineness of the anterograde amnesia in this case. This is despite the often used assertion that the inability to retain new information is characteristic of psychogenic amnesia. It is now generally recognized that the rigid distinction between psychogenic and organic amnesia, which was previously considered correct, is artificial.

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