Pathology of memory and attention. Memory impairment syndromes. Chapter VII memory pathology Syndromes with memory impairments

Pathological conditions brain are very often accompanied by memory impairment; however, until recently very little was known about what psychological characteristics memory impairments differ in brain lesions of different locations and what physiological mechanisms underlie them.

There are widely known facts indicating that, as a result of acute injuries or intoxications, the phenomena of retrograde and anterograde amnesia can occur. In these cases, patients, while retaining memories of long-past events, exhibit significant memory impairment current events, essentially exhausted the knowledge available to psychiatrists and neurologists who described memory changes during organic lesions brain These data are joined by facts indicating that lesions in the deep parts of the brain can lead to deep violations the ability to record traces and reproduce what is remembered, but the nature of these violations remains unclear.

Data obtained by numerous researchers over the past decades have significantly enriched our knowledge about the nature of memory impairment in lesions of various locations and have made it possible to clarify both the basic data on the role of individual brain structures in memory processes and the physiological mechanisms underlying its impairments.

Defeats deep parts of the brain - areas of the hippocampus and the system known as the “circle of Peipetz” (hippocampus, thalamus nuclei, mamillary bodies, amygdala), usually lead to massive memory impairments not limited to any one modality. Patients in this group, while retaining memories of distant events (long consolidated in the brain), are, however, unable to capture traces of current influences; in less pronounced cases they complain of bad memory, indicate that they are forced to write everything down so as not to forget. Massive lesions in this area cause severe amnesia for current events, sometimes leading to the fact that a person loses a clear idea of where he is and begins to experience significant difficulties in orienting himself in time, being unable to name the year, month, date, day weeks, and sometimes the time of day.

It is characteristic that memory impairments in these cases are not selective in nature and are equally manifested in difficulties in retaining visual and auditory, visual and verbal material. In cases where the lesion involves both hippocampi, these memory impairments are especially pronounced.

Detailed neuropsychological studies have made it possible to further characterize how psychological structure these memory defects, and approach the analysis physiological mechanisms underlying its violations.

It has been shown that in cases of relatively mild lesions of these areas of the brain, the disturbances are limited to defects in elementary, immediate memory, leaving the possibility of compensating for these defects through the semantic organization of the material. Patients who cannot remember a series of isolated words, pictures or actions are able to perform this task significantly better by resorting to aids and organizing memorized material into known semantic structures. Immediate memory impairment in these patients is not accompanied by any pronounced violation intelligence, and these patients, as a rule, do not show signs of dementia.

Essential facts were obtained by analyzing possible physiological memory impairments in these cases.

As these studies have shown, patients with lesions of the deep parts of the brain can retain relatively long series of words or actions and reproduce them after an interval of 1-1.5 minutes. However, a slight distraction by any interfering activity is enough to make the reproduction of a just memorized series of elements impossible. Physiological basis memory impairment in these cases turns out to be not so much the weakness of the traces as increased inhibition of traces by interfering influences. These mechanisms of memory impairment in the described cases are easily explained by the fact that persistent preservation of dominant foci and selective orienting reflexes is easily disrupted due to a decrease in cortical tone and separation from normal operation those primary apparatuses for comparing traces, which, as stated above, is a direct function of the hippocampus and related formations.

The picture of memory impairment changes significantly when damage to the deep parts of the brain is accompanied by damage frontal lobes(and especially their medial and basal sections). In these cases, the patient ceases to be critical of the shortcomings of his memory, is unable to compensate for its defects and loses the ability to distinguish between genuine performance and uncontrollably emerging associations. Confabulations and memory errors (“pseudo-reminiscences”) that appear in these patients join gross memory disorders (“Korsakoff syndrome”) and lead to those phenomena of confusion that stand on the borders of memory impairment and consciousness impairment.

Memory impairments that occur during local lesions external (convexital) surface of the brain.

Such lesions are never accompanied general violation memory and never lead to the emergence of “Korsakov syndrome” and, even more so, disturbances of consciousness with the disintegration of orientation in space and time.

Patients with local lesions of the convexital parts of the brain may exhibit private disorder of mnestic activity, usually worn modal-specific character, in other words, manifesting themselves in one particular area.

Thus, patients with lesions left temporal region show signs of impairment auditory-verbal memory, cannot hold any long series of syllables or words. However, they may not show any defects in visual memory and in some cases, relying on the latter, they can compensate for their defects by logical organization of the material being fixed.

Patients with local lesions of the left parieto-occipital region may exhibit impairment of visual-spatial memory, but, as a rule, they retain auditory-verbal memory to a much greater extent.

Patients with lesions frontal lobes of the brain, as a rule, they do not lose memory, but their mnestic activity may be significantly hampered pathological inertia once stereotypes arise and difficult switching from one link of the memorized system to another; attempts to actively remember the material proposed to them are also complicated by the pronounced inactivity of such patients, and any memorization of a long series of elements, requiring intense work on the memorized material, turns into a passive repetition of those links in the series that are remembered immediately, without any effort. Therefore, the “memory curve,” which normally has a distinct progressive nature, ceases to increase in them, continuing to remain at the same level, and begins to have the character of a “plateau,” reflecting the inactivity of their mnestic activity. It is characteristic that local lesions of the right (subdominant) hemisphere can occur without noticeable disturbances in mnestic activity.

Research conducted over the past decades has made it possible to come closer to the characteristics of those memory impairments that arise when general cerebral violations mental activity.

If these disorders cause weakness and instability of excitations in the cerebral cortex (and this can occur with various vascular lesions, internal hydrocephalus and cerebral hypertension), memory impairments can be expressed in a general decrease in memory capacity, difficulty in learning and easy inhibition of traces by interfering influences; they lead to sharp exhaustion of the patient, as a result of which memorization becomes very difficult and the “learning curve” begins to not increase, and even decreases with subsequent repetitions.

Analysis of the “learning curve” can be of great diagnostic value, making it possible to distinguish between different syndromes of changes in mental processes with brain lesions of different nature.

Characteristic features of memory impairment are: organic dementia ( Pick's disease, Alzheimer's disease) and in cases of mental retardation.

The central location for such lesions is usually is a violation higher forms memory, and above all logical memory. Such patients are unable to apply necessary techniques semantic organization of the memorized material and reveal especially pronounced defects in experiments with indirect memorization.

It is typical that in cases mental retardation(oligophrenia), these violations of logical memory can sometimes appear against the background of well-preserved mechanical memory, which in some cases can be satisfactory in its volume.

Memory research is very great importance to clarify the symptoms of brain diseases and their diagnosis.

Pathological conditions of the brain are very often accompanied by memory impairment; However, until recently, very little was known about what psychological features distinguish memory impairments in brain lesions of different locations and what physiological mechanisms underlie them.

There are widely known facts indicating that, as a result of acute injuries or intoxications, the phenomena of retrograde and anterograde amnesia can occur. In these cases, patients, retaining memories of long-past events, reveal significant memory impairments for current events, essentially exhausting the knowledge that psychiatrists and neurologists had at their disposal when describing memory changes in organic brain lesions. These data are joined by evidence indicating that lesions in the deep parts of the brain can lead to profound impairments in the ability to record traces and reproduce what is remembered, but the nature of these impairments remains unclear.

Lesions of the deep parts of the brain - the region of the hippocampus and the system known as the “circle of Peipetz” (hippocampus, thalamus nuclei, mammillary bodies, amygdala) usually lead to massive memory impairments that are not limited to any one modality . Patients in this group, while retaining memories of distant events (long consolidated in the brain), are, however, unable to capture traces of current influences; in less pronounced cases, they complain of poor memory and indicate that they are forced to write everything down so as not to forget. Massive lesions in this area cause severe amnesia for current events, sometimes leading to the fact that a person loses a clear idea of where he is and begins to experience significant difficulties in orienting himself in time, being unable to name the year, month, date, day weeks, and sometimes the time of day.

Detailed neuropsychological studies made it possible to further characterize both the psychological structure of these memory defects and to approach the analysis of the physiological mechanisms underlying its disorders.

It has been shown that in cases of relatively mild lesions of these areas of the brain, the disturbances are limited to defects in elementary, immediate memory, leaving the possibility of compensating for these defects through the semantic organization of the material. Patients who cannot remember a series of isolated words, pictures or actions are able to perform this task much better by resorting to auxiliary means and organizing the memorized material into known semantic structures. The impairment of immediate memory in these patients is not accompanied by any significant impairment of intelligence, and these patients, as a rule, do not show signs of dementia.

Essential facts were obtained by analyzing possible physiological memory impairments in these cases.

As these studies have shown, patients with lesions of the deep parts of the brain can retain relatively long series of words or actions and reproduce them after an interval of 1-1.5 minutes. However, a slight distraction by any interfering activity is enough to make the reproduction of a just memorized series of elements impossible. The physiological basis of memory impairment in these cases is not so much the weakness of traces as the increased inhibition of traces by interfering influences. These mechanisms of memory impairment in the described cases are easily explained by the fact that the persistent preservation of dominant foci and selective orientation reflexes is easily disrupted due to a decrease in the tone of the cortex and the isolation from the normal functioning of those primary trace comparison apparatuses, which, as stated above, is a direct function of the hippocampus and related entities.

The picture of memory impairment changes significantly when damage to the deep parts of the brain is accompanied by damage to the frontal lobes (and especially their medial and basal parts).

In these cases, the patient ceases to be critical of the shortcomings of his memory, is unable to compensate for its defects and loses the ability to distinguish between genuine performance and uncontrollably emerging associations. Confabulations and memory errors (“pseudo-reminiscences”) that appear in these patients join gross memory disorders (“Korsakov’s syndrome”) and lead to those phenomena of confusion that stand on the borders of memory impairment and impairment of consciousness.

Memory impairments that occur with local lesions of the outer (convexital) surface of the brain differ significantly from all variants of the picture described above.

Such lesions are never accompanied by a general memory impairment and never lead to the emergence of “Korsakov’s syndrome,” much less disturbances of consciousness with the disintegration of orientation in space and time.

Patients with local lesions of the convexital parts of the brain may exhibit a partial disturbance of mnestic activity, usually of a modality-specific nature, in other words, manifesting itself in one particular area.

Thus, patients with damage to the left temporal region show signs of impaired auditory-verbal memory and cannot retain any long series of syllables or words. However, they may not show any defects in visual memory and in some cases, relying on the latter, they can compensate for their defects by logical organization of the material being fixed.

Patients with local lesions of the left parieto-occipital region may exhibit impaired visual-spatial memory, but, as a rule, retain auditory-verbal memory to a much greater extent.

Patients with damage to the frontal lobes of the brain, as a rule, do not lose memory, but their mnestic activity can be significantly hampered by the pathological inertia of once formed stereotypes and difficult switching from one link of the memorized system to another; attempts to actively remember the material proposed to them are also complicated by the pronounced inactivity of such patients, and any memorization of a long series of elements, requiring intense work on the memorized material, turns into a passive repetition of those links in the series that are remembered immediately, without any effort. Therefore, the “memory curve,” which normally has a distinct progressive nature, ceases to increase in them, continuing to remain at the same level, and begins to have the character of a “plateau,” reflecting the inactivity of their mnestic activity. It is characteristic that local lesions of the right (subdominant) hemisphere can occur without noticeable disturbances in mnestic activity.

Research conducted over the past decades has made it possible to come closer to the characteristics of those memory impairments that arise from general cerebral disorders of mental activity.

Characteristic features are distinguished by memory impairment in organic dementia (Pick's disease, Alzheimer's disease) and in cases of mental retardation.

Central to such lesions is usually a violation of higher forms of memory, and especially logical memory. Such patients are unable to apply the necessary techniques for the semantic organization of memorized material and exhibit particularly pronounced defects in experiments with indirect memorization.

It is characteristic that in cases of mental retardation (oligophrenia), these violations of logical memory can sometimes appear against the background of well-preserved mechanical memory, which in some cases can be satisfactory in its volume.

Memory research is very important for clarifying the symptoms of brain diseases and their diagnosis.

1) Amnesia, a significant decrease or absence of memory. They can be observed not only with local brain lesions, but also as general cerebral symptoms that accompany almost all disorders with brain lesions.

Fixation amnesia - insufficient fixation of impressions in the CP or DP.
For example, Korsakov's syndrome - the patient is capable of reproducing past experiences, but not today's events. This is due to interference caused by disruption of limbic structures and the cortical-thalamic region.
Retrograde amnesia - in relation to the events of a certain period preceding another event.
Anterograde amnesia - for events after shock, trauma, psychological change.
Progressive amnesia - memory for events is consistently impaired from modern to past and from diffuse to clear.

Luria divides amnesia into
1) modally nonspecific memory impairments - poor imprinting (reproduction -?) of information of any modality. They occur when various levels of midline nonspecific brain structures are affected.
- level of the medulla oblongata
- diencephalic level
- level of the limbic system
- level of the medial and basal parts of the frontal lobes of the brain

2) modality-specific memory impairments are associated only with stimuli of a certain modality and apply only to stimuli addressed to a single analyzer
- impairment of auditory-verbal memory in acoustic-mnestic aphasia
- violations of visual-speech memory in optical-mnestic aphasia
- violations auditory memory with lesions of the right hemisphere
- visual memory impairments with lesions of the right hemisphere
2) Hypermnesia
A sharp increase in the volume and strength of memorization of material compared to average indicators. Possible both congenital and acquired - with local brain lesions, for example, pituitary lesions. It may be the result of a shock or trauma - the patient remembers something that he himself did not specifically remember.
3) Hypomnesia
Memory impairment that may be associated with age-related changes, be congenital or appear as a result of a brain disease. As a rule, they are characterized by weakening of all types of memory.
4) Paramnesia
“False recognition” is a special condition when a person experiences a feeling of familiarity when encountering unfamiliar objects (deja vu). Confabulations, “filling in holes,” are possible, for example: in Korsakov’s syndrome. Associated with changes in state of consciousness.
5) Pseudoamnesia
Pseudoamnesia is a memory disorder activities. It occurs with massive lesions of the frontal lobes of the brain, when the process of forming intentions, plans and behavioral programs is grossly disrupted, and among the consequences is a violation of voluntary memorization.

Memory disorder is a violation or loss of the ability to remember, store, recognize or reproduce information.

The classification of memory disorders is presented in table. 2.3.

Hypermnesia is an involuntary revival of memory, increased ability to reproduce, memories of long-forgotten events of the past, insignificant and of little relevance for a person in the present.

Increased recall is often combined with weakened memorization of current information, especially voluntary. Hypermnesia occurs with a facilitated, sometimes chaotic flow of simple mental associations, is associated with an increase in mechanical memory, but is accompanied, however, by a significant deterioration of logical-semantic memory, and difficulties in reproducing complex abstract associations.

Hypermnesia occurs in manic and hypomanic states (within affective syndromes), in case of intoxication with certain narcotic substances, clouding of consciousness of infectious and psychogenic origin, in some cases special conditions consciousness.

Hypomnesia is a partial loss from memory of events, facts, and phenomena. This is a violation of the ability to remember, retain, reproduce certain events and facts or their individual parts.

Table 23

Classification of memory disorders (diamnesias)


Hynermnesia
Hypomnesia
	By genesis: - organic; - psychogenic. In relation to the period of illness: - retro grade; - anterograde; - fixation
Paramnesia	Pseudo-reminiscences. Cryptomnsii. Confabulation

Hypomnesia is most often observed in vascular, degenerative and other organic diseases of the brain, with the consequences of traumatic brain injury, etc.

With a progressive pathological process, in particular neurodegenerative diseases (Pick's and Alzheimer's diseases), with disorders old age etc., hypomnesia can turn into more serious violation memory - amnesia.

Amnesia is a complete loss from memory of events, facts, phenomena that take place in a certain time period, or loss from memory of a particular situation.

In the event of a steady deterioration in memory productivity due to pathological processes in the brain they talk about progressive amnesia. With progressive amnesia, memory decay occurs in accordance with Ribot's law. This process proceeds in the reverse order of memory formation. The memory of the most recently captured events and facts disappears first, and the earlier ones disappear last.

Progressive amnesia has a number of stages. The very first manifestations are forgetfulness, difficulties in memorizing and recalling dates, names, everyday information, planned events, etc. Subsequently, everything begins to fall out of memory larger number current events and facts. Then the process gradually begins to spread to the memory of the past, first capturing a close period, and then more and more distant periods of time.

First of all, the “memory of time” suffers while the “memory of content” is preserved. Patients remember individual events and facts, but have difficulty determining them in time and sequence. Only then does the “memory of content” gradually fade.

As periods of the recent or less distant past fade from memory, memories of ancient events (childhood, adolescence) emerge quite vividly in the memory. Often these memories become the main content of the patients’ consciousness.

With further progression of amnesia, an increasing amount of information disappears from memory. First of all, the most mature, but at the same time less organized knowledge (scientific, knowledge foreign languages and so on.). What was acquired in youth was repeated many times in life, became more stable, automatic, and is the last thing to disappear. An almost complete loss of “memory of facts” may occur, but the so-called “memory of the affective tone of relationships”, or “memory of emotional and moral-ethical reactions”, which is embedded in early childhood and is therefore characterized by high durability. Subsequently, this type of memory gradually weakens and disappears, but the “memory of the simplest skills” still remains - praxis, which disappears last with the formation of apraxia.

It should be noted that amnesia is not always progressive in nature and in some cases (depending on the genesis and severity of the disorder that caused amnesia) can be reversible.

Variants of amnesia but genesis:

organic - disorders in which loss of events, facts and phenomena from memory is associated with brain damage (due to injuries, organic diseases of the central nervous system, intoxications, etc.);
psychogenic - disorders (mostly reversible), in which loss of events, facts and phenomena from memory is associated with the influence of traumatic factors. Memory gaps arise psychogenically, through the mechanism of repressing affectively saturated individually unpleasant and unacceptable impressions and events. With strong mental shocks, it is also possible to repress all events (even indifferent ones) that coincided in time with mental trauma. Variant of psychogenic amnesia - hysterical amnesia, in which individual unpleasant events and facts that are subjectively unacceptable to the patient and present him in an unfavorable light (for example, autobiographical facts or features of social status that do not satisfy the patient) are selectively removed from memory. The combined tendency to overestimate one’s own personality, efficiency and egocentrism often lead to the fact that memory gaps are replaced by fictitious events and facts with a touch of grotesqueness, exaggeration, and fantasticality.

Variants of amnesia in relation to the period of illness:

retrograde - loss from memory of impressions preceding the acute period of the disease. At the same time, the duration of the period of time covered by amnesia varies: from several minutes to several days, weeks. Retrograde amnesia occurs when severe intoxications and hypoxia, brain injuries;
anterograde - loss of memories of events, experiences, facts corresponding to the period following the acute stage of the disease. In this case, as a rule, the functions of memorizing and storing information suffer. Often the basis of this disorder is the remaining after acute period diseases of impaired consciousness in mild degree. With anterograde amnesia, the behavior of patients is orderly, correct, they critically assess the situation, which indicates the preservation of short-term memory. Can be observed in severe alcoholism, due to traumatic brain injury, severe infectious diseases and etc.;
fixation - a sharp weakening or loss of the ability to remember (record) current events, while maintaining the ability to fully recall previously acquired experience and facts. The inability to capture current events and facts in memory leads to difficulties in orientation in place and time. With fixation amnesia, the ability to adapt to the conditions of everyday life, to navigate the surrounding world (on the street, in the apartment), events, and people significantly suffers. Patients with this variant of amnesia retain a clear memory of events past life without losing professional knowledge and skills, are unable to remember new information: new people, new surroundings, events happening during the day, errands, etc. Fixation amnesia most often develops as a complication against the background of severe alcoholism.

Paramnesia is a memory disorder manifested in false memories.

Main types of paramnesia:

pseudoremipiscence -“illusions of memory”, erroneous memories. Memories of events that actually took place are related to patients in a different time period. The replay of events is usually carried out from the past to the present, in which it replaces memory failures that arise as a result of fixation or progressive amnesia. Pseudo-reminiscences are usually quite stable in content, are repeatedly stated by patients, and have ordinary content. Their variety is ecmnesia - a shift of the situation into the past (“life in the past”), when the time line between past and present is erased, and long-standing events are transferred to the present. This transfer does not affect individual facts or events, but entire, often quite significant, periods of life. Pseudo-reminiscences can be observed in organic diseases of the brain, senile dementia;
cryptomnesia - memory distortions in which alienation or appropriation of memories occurs:
- - associated memories- painful appropriation to personal experience of what was once heard or seen, while what was read, seen in a dream, in a movie, on stage is remembered by the patient as something that happened in reality, as something experienced or imagined (invented). This option includes true cryotomnesia (pathological plagiarism) - a memory pathology that leads the patient to assign to himself the authorship of various scientific ideas, works of art, etc.;
- - false associated memories - painful alienation personal experience, in which real events from life in memories appear to the patient as having happened to someone else, as heard, read, seen in a dream, in a movie or on stage;
confabulation(“fictions of memory”, “hallucinations of memory”, “delirium of the imagination”) - vivid, imaginative false memories, combined with a person’s pathological conviction of their truth. The patient remembers events and facts that supposedly took place in his life, when in reality they did not happen. Basic confabulation options:
- substituting - false memories that fill in gaps in memory. They are characterized by ordinary content, most often have a professional-everyday character, and are unstable in plot. They arise, as a rule, during a conversation with the patient, and as the questioning progresses, the plot often acquires new details that are “remembered” by the patient. Replacement confabulations can be observed in severe alcoholism, organic brain diseases, senile dementia;
- fantastic - false memories of incredible fantastic events that supposedly took place in the distant or recent past (for example, absurd love stories, meetings with great people). Their content is usually quite stable, combined with monothematic delusions of grandeur, erotic delirium, delusions of other (high) origin, etc. May be detected in severe delusional disorders.

Memory is a special type of mental activity associated with the perception (reception), retention (retention) and reproduction (reproduction) of information. Memory is an integral part of the processes of thinking and learning. In memory mechanisms, predominant importance is given to ribonucleic acid (RNA), in the molecule of which information is encoded, encrypted and stored.

The memory possibilities are endless. It is known that Julius Caesar, Seneca, and Alexander the Great had phenomenal memory. There are mechanical and semantic memory. Mechanical memory is the ability to remember this or that material, regardless of its content. Semantic, or associative, memory is characterized by the fact that the elements of what is remembered are associated with each other associatively, that is, they enter into internal connections with previous or former information.

When studying memory, short-term (short-term) memory is also distinguished, associated with the hippocampus, and long-term memory, associated with certain areas of the cerebral cortex.

Short memory refers to the ability to memorize, retain and reproduce information through relatively a short time after her admission. If there is no consolidation, this information disappears. With the constant maintenance of information and its emotional or intellectual significance, long term memory. This, by the way, is demonstrated in the famous school thesis: repetition is the mother of learning.

Memory pathology, called general term dysmnesia, in psychiatric practice it is expressed in hypermnesia, hypomnesia, amnesia and paramnesia.

Hypermnesia - short-term enhancement, memory sharpening. The patient, to his surprise, recalls long-forgotten rather large episodes of his childhood or youth in the smallest detail, reproduces by heart entire pages of once read, but long forgotten works. The state of hypermnesia is observed when manic syndrome, with some delusional states, drug addictions and in exceptional conditions, for example before death, when a person’s whole life instantly flashes before his eyes. Once the painful state has passed, hypermnesia goes away.

Hypomnesia - memory loss is the lot of all people in old age. The development of hypomnesia obeys the Ribot-Jackson law (reverse progression of memory), when information accumulated over a lifetime is gradually lost in an order inversely proportional to its acquisition, i.e. from the present to the past. First of all, mechanical memory for names, phone numbers, exact dates, and important life events suffers.

Hypomnesia is especially characteristic for vascular, traumatic and atrophic processes of the brain.

Amnesia - lack of memory - occupies a more significant place than hyper- and hypomnesia in the clinic of mental illness. Amnesia can be general, spreading over a fairly large period of time, or partial, when it concerns only some specific memories (for example, a translator of oriental languages completely forgot for six months after a skull injury Japanese, which he freely owned before, but which he openly did not like; his beloved Korean language was not affected at all; V in this case we can only talk about partial amnesia). Acquired special knowledge and skills, such as the ability to draw or drive a car, can also be affected by amnesia. There are several types of amnesia.

Retrograde amnesia - lack of memory for the period before the onset of the disease. For example, a patient who has received a skull injury may forget everything that happened to him during the week before the injury.

Anterograde amnesia - loss of memory for the period after the onset of the disease. The duration of both retro- and anterograde amnesia can vary from several hours to several months.

Retroanterograde amnesia covers a more or less long period of memory loss before and after, for example, a skull injury.

Fixation amnesia is the patient’s inability to retain and record incoming information. Everything that is told to him, what is happening around him, is perceived adequately, but is not retained in memory (there is no fixation of incoming information) and after a few minutes, or even seconds, the patient completely forgets about it.

Progressive amnesia is characterized, like hypomnesia, by a gradual weakening of memory according to the Ribot-Jackson law from the present to the past.

Total amnesia is the loss from memory of all information that the patient had, including even information about himself. Such a patient does not know his name, how old he is, where he lives, whether he has parents, in other words, he does not remember anything. Total amnesia can occur with severe skull trauma, especially in military conditions; it is less common with functional diseases(in severe stressful situations).

Palimpsest- loss of memory of individual events while intoxicated.

Hysterical amnesia - lapses in memory regarding unpleasant, unfavorable facts and events for the patient. It develops according to the type of repression not only in patients, but also in healthy individuals who are accentuated by the hysterical type. If memory loss of the hysterical type occurs in a subject who does not have hysterical features in the premorbid, such dysmnesia is called scotomization.

Paramnesia - this is a deception, a memory failure, which is filled with various information that determines the type of paramnesia. There are four types of this pathology: confabulation, pseudoreminiscence, cryptomnesia and echonesia.

The most common type of paramnesia is confabulation- this is the replacement of memory lapses with fiction of a fantastic nature, in which the patient absolutely believes.

Pseudo-reminiscences- is the replacement of memory lapses with information and real facts from the patient’s life, but significantly shifted in time. For example, a patient with senile dementia, who has been in the hospital for about six months, who was an excellent mathematics teacher before his illness, claims that he had just taught trigonometry classes in the Xth grade. Sometimes in the literature, instead of this term, the concept of “substituting confabulations” is used.

Cryptomnesia(assigned memories) - memory gaps filled with information, the source of which the patient forgets: he does not remember whether this or that event happened in reality or in a dream, and considers thoughts read in books or heard from someone to be his own.

Cryptomnesia also includes the so-called alienated memory which consists in the fact that he subsequently perceives the events that happened in the patient’s life not as real, but as read in a book, seen in a movie or theater, heard on the radio, from interlocutors or experienced in dreams.

Some researchers refer to paramnesia and echonesia(reduplicating memories). This is a special type of memory deception in which events occurring now seem to have already happened before.

With a certain degree of convention, this group of disorders also includes ecmnesia, in which the distant past is experienced as the present. With ecmnesia, very elderly people consider themselves youths and begin to prepare for the wedding. Concentrated complex memory impairment is especially pronounced in the so-called Korsakoff syndrome.

Korsakoff's syndrome includes a triad of symptoms: fixation amnesia, paramnesia and amnestic disorientation in time or place. This syndrome was described by S.S. Korsakov in 1887 for alcoholic polyneuritic psychosis. It received the name of its discoverer and was identified by many mental illness except for schizophrenia.