Amnesia

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

Memory management involves recording (receiving new information), coding (linking, time stamping and other processes necessary to find information) and retrieving information. Violation of any of these stages can cause amnesia.

Amnesia can be classified as retrograde (loss of events from memory to trauma), anterograde (loss of memory of events that occurred after trauma), global (loss of ability to remember new information and loss of recent events). Amnesia can be transient (for example, after a brain injury), permanent (after severe illnesses such as encephalitis, total cerebral ischemia or cardiac arrest) or progressive (with degenerative dementia, eg Alzheimer's disease).

In the disorder of declarative memory (on events and facts), the patient forgets familiar words, faces, losing access to past individual experience; if the procedural (implicit) memory is broken the patient is not able to use the skills acquired earlier.

[1]

Causes of amnesia

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

• "Amnestic" syndrome with focal pathological lesions of the brain. Pathological studies reveal brain damage, especially in the mamillary body, the posterior part of the hypothalamus, as well as in the gray matter in the third and fourth ventricles, and aqueductus cerebri. Occasionally, bilateral hippocampal lesions are detected. The causes of such focal damage may be tumors, thiamine deficiency (as in Wernicke's encephalopathy and Korsakov's psychosis) and infarctions. It is expressed in the inability to postpone new memories after an event or incident (anterograde amnesia) and in the loss of old memories (retrograde amnesia), in the absence of such symptoms as confusion or inability to concentrate.
• Amnesia due to diffuse brain damage, such as in dementia (for example, Alzheimer's disease), in states of confusion caused by toxic substances, with head injuries or hypoglycemia.

Amnesia can occur as a result of diffuse brain damage or bilateral focal or multifocal lesions involving structures involved in the storage and reproduction of information. Nerve pathways related to declarative memory are localized in the hippocampus and para-hippocampus regions, the lower medial part of the temporal lobes, the orbital surface of the frontal lobes, and the intermediate brain. The most important structures are the hippocampus, the hypothalamus, the nuclei of the basal forebrain and the dorsomedial nuclei of the thalamus. The almond-shaped nucleus contributes to the emotional enhancement of memory, intralaminar nuclei of the thalamus and activating the reticular formation of the trunk stimulate the fixation of new information in memory. Two-sided damage to the medial and posterior thalamus, the reticular formation of the brainstem and the adrenergic system leads to a decrease / loss of memory for recent events and the ability to memorize new information, most often due to thiamine deficiency, hypothalamic tumor, and ischemia. Two-sided damage to the medial parts of the temporal lobes, especially the hippocampus, is usually accompanied by a transient disturbance of the declarative memory.

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

Retrograde and anterograde amnesia for periods immediately before and after concussion of the brain or a more severe craniocerebral trauma are also apparently caused by damage to the medial parts of the temporal lobe. As a result of more extensive brain damage, other structures involved in the storage and reproduction of information may be involved, as is the case with many diseases leading to dementia.

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

Many older people are gradually developing difficulties with the memory - first names, then events and dates and sometimes - spatial relationships. This widespread condition - the so-called benign senile forgetfulness - has no proven connection with degenerative dementia, although it is difficult not to notice some of the similarities. Presence of subjective memory problems and less confident performance of objective tests in combination with the preservation of cognitive and everyday functions can be categorized as an amnestic soft cognitive decline, or moderate cognitive impairment (RBM). In people with more serious memory impairment with RBM, the likelihood of developing Alzheimer's disease in the future is higher than that of peers who do not have memory problems.

[2], [3], [4], [5]

Diagnosis of amnesia

Simple tests at the patient's bed (for example, a test for memorizing three items, locating hidden objects) and formal tests (for example, word list tests such as the California test for acoustical memory and the "Buschka test for selective memorization") help to identify memory loss by words. To explore and evaluate other types of memory (figurative, visual, auditory) is more difficult; In everyday practice, tests for memorizing visual images or a number of tones are available. The need for additional tests is established during the clinical examination.

[6], [7], [8]

Treatment of amnesia

It is necessary to treat the underlying disease or eliminate psychological problems. Sometimes, with acute amnesia, recovery occurs without any intervention. It is also necessary to treat diseases that caused such a memory disorder as amnesia (Alzheimer's disease, Korsak's psychosis, herpetic encephalitis), but not the fact that this will entail better memory. If the treatment does not improve memory, no other methods will speed up the recovery and change the outcome for the better.

Amnesia and law

The connection of amnesia with the commission of violent crimes is well known. In particular, this applies to amnesia due to drug or alcohol intoxication and the degree of violence used. The latter is confirmed by the data that victims of violent crimes are more likely to suffer loss of memory regarding the details of the crime than victims of non-violent crimes. It is also known that the perpetrators of murder are more likely to have amnesia of the act of murder. In a number of homicidal studies, the incidence of amnesia varies from 25 to 45%. In such cases, it is often found that although the original cause of memory loss is organic (often alcohol intoxication), amnesia is supported by psychogenic factors, often as a result of an unconscious unwillingness to recall a committed crime, especially if the spouse, or spouse, or other family members were killed.

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

• the violent nature of the crime, especially in the case of homicide;
• excessive emotional agitation 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 people in pre-trial detention.

However, the presence of amnesia does not in itself make the accused incapable of participating in the trial, nor does it prove the absence of mens gaa necessary for the commission of the crime. However, in both of these situations, amnesia, although in itself can not serve as a basis for protection, if it is a symptom of deep organic disease, such as, for example, dementia, cerebral damage or epileptic automatism, it can be significant factor in declaring an accused incapable of participating in a trial or demonstrating the absence of a mens gea. This is especially true of cases of anterograde amnesia.

[9], [10], [11], [12],

Description of the case of amnesia

Mr. V. Is 50 years old, and he is accused of attempting to kill the wife who left him. They were married for five years, and one of the reasons for the wife's departure was violence from her husband. Mr. V. Does not have a history of contacting a psychiatrist; he has no history of friction with the law. He attempted to kill both of them by tying his wife in the car and bringing the hose connected to the exhaust pipe of the car inside. He closed himself in the car with his wife and started the engine. Both lost consciousness, but then the motor died down, and they were discovered by neighbors. In an unconscious state, Mr. V. Was taken to the hospital, and a computerized tomography showed him an increased amount of cerebrospinal fluid in the ventricles of the brain and a heart attack in the cerebellum. He did not regain consciousness for two weeks. The wife regained consciousness quickly and slightly affected by carbon monoxide poisoning. Mr. V. Spent eight months in the rehabilitation department.

According to psychometric testing a year later, Mr. V. Marked a severe short-term memory deficit. He was able to save information only for a few minutes. He also poorly remembered the preceding 10-15 years, but could recall important events from a more remote past. He has clear anomalies in the functioning of the frontal parts of the brain with the defeat of executive functions, in particular the ability to plan, solve problems and perform a sequence of actions. Personality of Mr. V has also changed: he became apathetic, passive and emotionally flattened.

On the recommendation of two psychiatrists and a neuropsychologist, Mr. V. Was declared incapable of participating in the trial. This was done because he was not able to understand the evidence given in court, could not store information in memory, since he remembered what he had heard or read in just a few minutes. He was found incapable of participating in the necessary degree in judicial proceedings. During the judicial consideration of the facts, the commission of the aforementioned act was recognized. In accordance with Art. 37 of the Mental Health Act, he was placed under guardianship. He began to live with friends who fully provided care for him.

Mr. V. Was unable to participate in the trial, not so much because of pronounced retrograde amnesia, but because of anterograde amnesia. Anterograde amnesia of this severity affects the ability of a person to understand what has been said and, therefore, makes him unable to make objections. This case did not cause any doubts as to the authenticity of anterograde amnesia. And this despite the often used statement that the inability to store new information in memory is characteristic of psychogenic amnesia. It is now generally accepted that the rigid separation of psychogenic and organic amnesia, which was considered correct earlier, is of an artificial nature.

[13], [14], [15], [16]