Retrograde amnesia

A neurological syndrome characterized by complete or partial absence of memories of events that occurred hours, days, weeks, months, sometimes years before the injury or the onset of the disease is called retrograde amnesia. Sometimes the patient cannot remember a single fact of his life for a certain period, his name, people he knew well, often even his closest relatives. Some patients register partial memory lapses or memories are fragmentary, mixed, not corresponding to what happened. Typically, episodic memory (memories of events that occurred) suffers, while procedural memory (skills, conditioned reflexes) and semantic memory (meaning of words, semantic categories, rules of behavior, generalized prodstatements about the surrounding world) remain intact.

This state of memory makes it much more difficult to restore communication and establish new contacts, to plan, to perform a number of daily tasks at work and at home, because our lives are closely intertwined with events from the past memory. [1]

Epidemiology

Each year, amnesia of various types and origins is reported in 4% of the population worldwide. About half of memory loss is due to trauma, and among post-traumatic amnesias, just over a third (34%) last less than 60 minutes.

In patients with long-term memory loss developed from nutrient deficiencies, particularly vitamin B1, about 37% of cases are associated with alcohol abuse.

Transient amnesia affects 15% of epileptics, and nearly 40% of Alzheimer's patients in nursing homes have progressive amnesia.

Patients with retrograde amnesia may develop a clinical syndrome called transient global amnesia (TGA). Its main symptom is the loss of the ability to form new memories. The syndrome suddenly affects 5 people out of 100,000 of the world's population each year. The average age of primary patients is 61 years, the patient population ranges from 40 to 80 years old, and there is no sex predominance among them. Slightly more than half (55%) of patients suffering from TPA have vascular pathologies. [2]

Causes of the retrograde amnesia

How retrograde amnesia develops is not exactly clear. However, it is clear that there must be a disruption in the work of some parts of the brain. Many cerebral structures are involved in the realization of memory function, so any damage to them can become a trigger for the development of amnesia. First of all, it is a head injury with brain damage. And the trauma does not have to be obviously severe, a superficial blow may be enough, especially in the area of the forehead or temple, where the "storages" of information and structures involved in its reproduction are located. Retrograde amnesia in concussion, even if not very severe, may well develop. [3]

Not only surface structures are responsible for various memory functions, but also deep structures, in particular, the hippocampus. Emotions, processes of awareness, concentration, etc. Are involved in the formation of memories. The coordinated work of the system of cerebral structural elements can be disturbed not only because of trauma. Organic dysfunctions occur in:

• acute (heart attack, stroke) and chronic (CVH, encephalopathy, atherosclerosis) disorders of cerebral circulation;
• cerebral tumors;
• intoxications and infections;
• epilepsy and its treatment;
• brain degenerations (senile dementia, Alzheimer's disease);
• Long-term deficiency of certain vitamins and trace elements, in particular vitamin B1;
• prolonged use of certain medications.

In addition, retrograde amnesia of psychogenic nature develops after deeply traumatic events as a protective reaction of the body. The event that caused severe neuropsychiatric stress disappears from memory.

Sometimes the causes of amnesia remain unknown.

Risk factors

The etiology of retrograde amnesia in humans is very diverse. The following events can lead to the development of this condition.

1. Open and closed craniocerebral injuries resulting in impaired function of brain structures that process, store and accumulate information.
2. Pathological processes in the brain structures - ischemia, hemorrhages, necrosis, CVD, affecting the areas responsible for memory.
3. Diseases of the central nervous system - encephalopathy, epilepsy, Alzheimer's disease, Parkinson's disease, etc.
4. Mental illness and personality disorders - derealization, depression, PTSD, when the subconscious mind blocks memories of a traumatic event by scrubbing out past life episodes from memory that relate to a particular time.
5. Severe infectious diseases - Lyme disease, meningitis, encephalitis, brucellosis.
6. Toxemia, acute or chronic.
7. New neoplasms with localization in the head.
8. Electrocution with shock development.

Iatrogenic risk factors for retrograde amnesia are electroconvulsive therapy and the use of certain drugs, in particular, from the group of psychotropic drugs, myorelaxants, opioid anesthetics, as well as the antifungal antibiotic amphotericin B, which in overdose or prolonged use can cause respiratory arrest, or lithium salts. This undesirable effect is usually reversible and goes away on its own soon after completion of treatment.

Pathogenesis

In our brain, memory is not localized in any one center. It is "distributed" in accordance with the functions of the zones of the cerebral cortex of the cerebral hemispheres throughout the brain: in the motor zone - the storage of memory of movements, in the cortical centers of analyzers - about the characteristics of the signals perceived by them, etc. In the zone of primary centers of analyzers and directly in the motor zone specific memories are stored: information about individual movements of certain muscles or specific features of signals. The structures responsible for complex abstract perception - recognition, comparison, planning of actions, application of skills, which is provided by the cerebellum and the basal ganglia - are located at a distance from these primary centers; information of semantic (generalized knowledge) memory is stored in the anterior part of the temporal lobe, of episodic memory (specific memories of events that took place) - in the medial zone of the temporal lobe. In addition, semantic memory, especially verbal memory, is predominantly connected with the left (dominant) hemisphere of the brain, while episodic memory is connected with the right hemisphere. Memorization of information read by analyzers and stored in declarative memory, i.e. Such information that can be potentially put into words, expounded, is carried out by the hippocampus. Hypothetically, this brain structure provides some kind of "coding" of new information and establishes its connection with the existing information, builds cognitive maps and mental models of their relationships - spatial, temporal, etc. [4]

Retrograde amnesia is one of the possible quantitative disorders of long-term declarative memory. The above is a very brief and primitive model of declarative memory operation, which makes it clear that disruption of the functions of virtually any structural element of the brain can entail an amnesic disorder.

Information processing can be divided into three stages:

• registration - receiving new information and perceiving it;
• encoding - comparing and linking it with the memories already available in the "storages" of the brain, with abstract mental images, knowledge in order to extract deeper and more generalized information, which, abstracted from the context, will be further stored in the all-mental memory (only the most significant and emotionally vivid for a person memories will remain in the episodic memory);
• retrieval from memory - replaying past events.

Obviously, in retrograde amnesia, disorders must occur in the structures that provide the third stage of information processing. This is damage to the temporal and frontal lobes (etiological prerequisites and risk factors are listed above). But everything is not so simple. The storage of memories and their retrieval are influenced by emotions, they are linked to the already existing ones. The limbic system is responsible for this. Its part, the hippocampus, which encodes information (stage 2), links memories with emotions that people experienced at the time of memory formation. Without this, the reproduction of past events is blocked. That is, disruption of the structures of the limbic system can also entail the development of retrograde amnesia. And the presence of memory loss about the past in some cases prevents the formation of memories from newly acquired information.

Certain areas in the brainstem that provide concentration and awareness are also involved in memory formation, and damage to them impairs memory function.

The pathogenesis of retrograde amnesia cannot yet be accurately described by modern medicine. It is still under study. Modern methods of neuroimaging, such as functional magnetic resonance imaging, make it possible to register activity in the structures that search, retrieve, and reproduce memories during memory testing. In addition, observations of patients with isolated lesions of brain structures in these localizations confirm that each type of memory has its own relatively independent neurophysiological basis. However, a complete picture of all processes and their interrelation has not yet been established.

Symptoms of the retrograde amnesia

The main sign of retrograde amnesia is the inability to recall some or all events that occurred before the injury, information about people, places or facts familiar in the past. Familiar routes disappear from memory, the names of loved ones and the patient himself may be forgotten. Episodes of memory loss may last from a few hours to days or months.

Patients usually have difficulty with daily life because they can no longer rely on memory of the past, which is necessary on a daily basis to perform daily tasks and plan for the future. The person appears lost and disoriented, unable to take care of himself properly. Trying to recover his memory, he asks many questions, interrogating the interlocutor several times. Mental strain is very difficult for patients, and they often feel as if they have lost their ability to think.

Non-existent, false memories may occur - confabulations. This is especially characteristic of patients with amnesia of intoxication origin or eating disorders (Korsakov amnesic syndrome). In this case, a mix of nonexistent memories is formed in the patient's memory and such memories, which, although they contain real events, but they are not correctly correlated with time and place or with other events. At the same time, the volume of memory remains the same. [5]

In some cases, retrograde amnesia is not immediately apparent when a person wakes up after a period of impaired consciousness; at first, the person still remembers events that occurred before the injury or illness, but after a period of time, these memories disappear from memory. This is called retarded or delayed retrograde amnesia.

Classify the pathology by the reason for its development on:

• organic, arising after brain injury, CNS diseases, various kinds of intoxications and deficiencies, tumors;
• psychogenic, developed after severe stress;
• iatrogenic, as a consequence of treatment;
• idiopathic-- no known cause.

Depending on the cause of retrograde amnesia and on the course of the pathological process can be distinguished:

• temporary or acute - usually of traumatic, intoxication, infectious, psychogenic origin;
• permanent - usually after acute and chronic CVD, severe infections and trauma;
• progressive - growing neoplasms, malignant degenerative process (e.g. Alzheimer's disease).

In progressive amnesia, the destruction of memory follows the law of Ribaud, a French physician who described this pattern back in the late XIX century: first disappear less firmly fixed memories (newer and fresher), later - more old, i.e. Firmly fixed. Progressive amnesia develops in the direction:

• from recent memories to early memories - the recent past is forgotten first, and the events of youth and childhood are forgotten last;
• from specifics to generalities;
• from emotionally neutral (first we forget everything that left us indifferent) to emotionally important (last we forget what caused a storm of emotions).

This law also works in physiological aging. When the patient's memory returns, the process is reversed. The most emotionally significant events are recalled first, and so on.

In terms of the amount of memories lost, retrograde amnesia can be complete or partial.

Complications and consequences

Retrograde amnesia, especially complete amnesia, renders a person quite helpless, especially in the first time after discharge from the hospital, when he or she is faced with the need to solve everyday problems. In addition, people with retrograde amnesia may develop transient global amnesia syndrome.

The main complications are directly related to the cause of memory loss. In severe and massive brain damage, amnesia may be irreversible, and in extensive degeneration, it may be progressive. In addition, traumatic injuries can lead to cerebral edema or hemorrhage and, as a consequence, coma.

Complications of neurological diseases of any origin are partial and complete paralysis, motor and speech disorders, cognitive disorders. [6]

Diagnostics of the retrograde amnesia

First of all, a patient with memory loss is examined and interviewed by a doctor. During the interview, it is determined for what period of time memories are missing, whether they have completely disappeared or partially disappeared; the patient is offered to take a test. For example, the Galverston test is used in post-traumatic amnesia. It contains a number of questions concerning the facts of the patient's biography, his orientation in time and space. Testing is carried out daily and the results are compared in dynamics. Comparison allows you to determine whether the memory is restored. If the patient scores 78 points or higher (maximum 100) three times in a row, it means that the amnestic period is coming to an end.

In addition, a neurological examination is performed and the preservation of other higher brain activities is checked. The condition of the CNS can be assessed by tests for attention, preservation of the ability to think, speak coherently, and coordinate movements. Hardware diagnostic methods are used to determine the root cause of memory loss.

The most informative are computed tomography and echoencephalography, which allow to detect many typical foci. Magnetic resonance tomography and spectrography provide more detailed information about the state of nervous tissue in ischemia zones; functional activity of the brain is assessed by echoencephalography with stress tests and in the state of artificial chronic sleep deprivation.

If meningitis or other infections are suspected, a lumbar puncture may be ordered.

Differential diagnosis is made with other types of time-limited amnesia.

Retrograde and anterograde amnesia are differentiated. In the first case, memory lapses are fixed in the interval preceding the event that caused the disturbance of consciousness (e.g., a victim of a traffic accident, waking up, cannot report anything about the circumstances of the accident), in the second - in the subsequent period, when the patient, after regaining consciousness, cannot remember the facts of his current life - where he is, where he went, what he has just done.

If the patient does not remember anything at all that happened before and after the injury (disease), he is diagnosed with retroanterograde (combined) amnesia.

A distinction is also made between congrade and retrograde amnesia. Congrade memory loss concerns only the period of disturbed consciousness. It can be partial, when a person, being out of reality, is at least somewhat accessible - answers some simple questions, knows who he/she is, but does not fully regain consciousness. Also congradational amnesia can be complete, when a person during the period of disturbed consciousness is inaccessible to communication, and coming to consciousness - absolutely nothing remembers only about the period of disturbed consciousness. The rest of the time the memories are preserved.

The differentiation is also made with global amnesia, when the patient does not remember anything at all. In typical cases, the diagnosis is not difficult, however, it is often not immediately possible to determine the underlying cause, especially since it is practically impossible to interview a patient even with limited amnesia, especially retrograde amnesia. It is often necessary to perform differential diagnosis of the underlying cause: transient ischemic attacks and strokes, differentiate infectious from metabolic lesions of the brain. [7]

Treatment of the retrograde amnesia

Treatment of amnesias is based on measures to eliminate or maximally compensate for the cause of their occurrence. Most patients are treated in hospital for some time after treatment, in the first days often in the intensive care unit (after trauma, stroke, toxic shock, surgical treatment), where they receive etiopathogenetic therapy. For example, patients after a stroke are prescribed drugs to thin the blood and prevent the formation of blood clots, in toxemia detoxification, in infectious diseases prescribe antibacterial, antiviral, antifungal drugs. In acute traumas, emergency surgery is often necessary, in neoplasms - planned.

Once the patient's condition has stabilized, comprehensive neurorehabilitation is performed. This stage of treatment is aimed at preventing secondary damage to cerebral structures and restoring mental functions, which contributes to a more favorable prognosis for the patient.

During the neurorehabilitation phase, the following are commonly used:

• drugs that inhibit the body's pain, inflammatory and immune responses, most commonly the familiar non-steroidal anti-inflammatory drugs that inhibit the cyclooxygenase enzyme and relieve symptoms; monoclonal antibody therapy may be used to reduce the production of harmful cytokines;
• antioxidant therapy - drug binding of free radicals, inhibition of their synthesis, stimulation of activity of protective enzymes - all this increases resistance to hypoxia in brain areas;

• nootropics and calcium channel blockers that prevent brain cell death and improve higher mental functioning;
• physiotherapy treatments to stimulate the cortex;
• activities designed to strengthen memory.

Surgical treatment may be prescribed for patients with brain injuries, neoplasms, and to remove hematomas after a stroke.

In case of amnesia of psychogenic genesis, individual psychocorrection is carried out, sometimes against the background of drug therapy. Also, sessions with a psychologist may be necessary for patients after traumas or diseases, as they help to get rid of complications caused by the underlying disease and mnestic disorders. During sessions with a psychologist, patients are taught methods and techniques of autogenic training and relaxation. [8]

Prevention

Prevention of the root causes of retrograde amnesia is to take measures to maximize the health of the nervous, endocrine and cardiovascular systems. And first of all - it is the observance of a healthy lifestyle: reasonable physical activity, walks, parting with bad habits, good nutrition, compliance with the optimal regime of workload and rest.

It is advisable to avoid the obvious risks of head injury, infection (good handling of raw foods; dress appropriately when going to the forest, etc.), and traumatic mental influences. The appearance of symptoms such as various kinds of headaches, dizziness, blood pressure spikes and other signs of vascular disorders should not be ignored.

Forecast

Retrograde amnesia of traumatic, iatrogenic, infectious, toxic and psychogenic genesis can even go away on its own. This directly depends on the severity of the neurological impairment resulting from the underlying cause.

In the presence of serious organic disorders of brain activity, the prognosis is less favorable, however, much depends on the age and general state of health of the patient, the localization of trauma or ischemia area, their extensiveness.

The least favorable prognosis for memory recovery is in patients with extensive degeneration of cerebral cortical structures.