Mental disorders in brain injuries. Mental disorders in traumatic brain injuries

Brain injuries and their consequences remain one of the most difficult and unresolved problems of modern medicine and are of great importance due to their prevalence and severe medical conditions. social consequences. As a rule, a significant increase in the number of people who have suffered head injuries is observed during periods of war and the years immediately following them. However, even in conditions of peaceful life, due to the growth of the technical level of development of society, a fairly high incidence of injuries is observed. According to data carried out in the early 90s. epidemiological study of traumatic brain injury, in Russia, more than 1 million 200 thousand people receive brain damage annually (L.B. Likhterman, 1994). In the structure of disability and causes of death, traumatic brain injuries and their consequences are already long time take second place after cardiovascular pathology(A.N. Konovalov et al., 1994). These patients make up a significant proportion of people registered in psychoneurological dispensaries. Among the forensic psychiatric population, a significant proportion are people with organic brain lesions and their consequences of traumatic etiology.

Brain injury refers to mechanical damage to the brain and skull bones of various types and severity. Traumatic brain injuries are divided into open and closed. With closed head injuries, the integrity of the skull bones is not compromised; with open ones, they are damaged. Open head injuries can be penetrating or non-penetrating. With penetrating injuries, there is damage to the substance of the brain and meninges, while with non-penetrating injuries, the brain and meninges are not damaged.

With a closed head injury, concussion (commotion), bruises (concussion) and barotrauma are distinguished. Concussion occurs in 70–80% of victims and is characterized by changes only at the cellular and subcellular levels (tigrolysis, swelling, watering of brain cells). Brain contusion is characterized by focal macrostructural damage to the brain substance of varying degrees (hemorrhage, destruction), as well as subarachnoid hemorrhages, fractures of the bones of the vault and base of the skull, the severity of which depends on the severity of the contusion. Edema and swelling of the brain are usually observed, which can be local or generalized.

Traumatic brain disease. Pathological process, developing as a result mechanical damage brain and characterized by all its diversity clinical forms unity of etiology, pathogenetic and sanogenetic mechanisms of development and outcomes is called traumatic brain disease. As a result of a head injury, two oppositely directed processes are simultaneously launched, degenerative and regenerative, which occur with a constant or variable predominance of one of them. This determines the presence or absence of certain clinical manifestations, especially in long term head injuries. Plastic restructuring of the brain after a head injury can last a long time (months, years and even decades).

During traumatic brain disease there are 4 main periods: initial, acute, subacute and long-term.

The initial period is observed immediately after a head injury and is characterized by a loss of consciousness lasting from a few seconds to several hours, days and even weeks, depending on the severity of the injury. However, in approximately 10% of victims, despite severe skull damage, loss of consciousness is not observed. The depth of switching off consciousness can be different: stupor, stupor, coma. When deafened, there is a depression of consciousness with the preservation of limited verbal contact against the background of an increase in the threshold of perception of external stimuli and a decrease in one’s own mental activity. With stupor, deep depression of consciousness occurs with preservation of coordinated defensive reactions and opening of the eyes in response to painful, sound and other stimuli. The patient is usually drowsy, lies with his eyes closed, motionless, but with the movement of his hand he localizes the place of pain. Coma is a complete shutdown of consciousness without signs of mental life. There may be memory loss for a narrow period of events during, before and after the injury. Retrograde amnesia may reverse over time when the period of memory of events narrows or fragmentary memories appear. Upon restoration of consciousness, cerebrasthenic complaints, nausea, vomiting, sometimes repeated or repeated, are typical. Depending on the severity of the head injury, various neurological disorders, vital disorders important functions.

In the acute period of a traumatic illness, consciousness is restored and cerebral symptoms disappear. In case of severe head injuries, after the return of consciousness, a period of prolonged mental adynamia is observed (from 2–3 weeks to several months). In persons who have undergone closed lung or moderate head injury, within 1–2 weeks “minor contusion syndrome” is observed in the form of asthenia, dizziness, and autonomic disorders (A.V. Snezhnevsky, 1945, 1947).

Asthenia manifests itself as a feeling internal tension, a feeling of lethargy, weakness, apathy. These disorders usually worsen in the evening. When changing body position, while walking, when going up and down stairs, dizziness, darkening of the eyes, and nausea occur. Sometimes psychosensory disorders develop when patients feel as if a wall is falling on them, the corner of the room is beveled, and the shape of surrounding objects is distorted. Memory impairment, deterioration of reproduction, irritable weakness, general cerebral disorders (headaches, dizziness, vestibular disorders). The ability to work is noticeably reduced, attention is disrupted, and exhaustion increases. Characterized by a change in the meaning-forming function and a decrease in the motivating function, a weakening of socially significant motives.

The depth and severity of asthenic disorders vary significantly. Some anxiety, irritability, restlessness, even with minor intellectual and physical stress, are replaced by lethargy, weakness, a feeling of fatigue, difficulty concentrating, and autonomic disorders. Typically, these disorders are transient in nature, but they can also be more persistent and pronounced and significantly aggravate the lack of performance.

The main symptom of minor contusion syndrome is headache. It occurs periodically with mental and physical stress, bending of the torso and head. Less often, the headache lasts constantly. All patients have disturbed sleep, which becomes restless, unrefreshing, with vivid dreams and is characterized by awakening with a feeling of fear. Persistent insomnia may occur.

Autonomic-vascular disorders are manifested by hyperhidrosis, hyperemia skin, cyanosis of the hands, sudden redness and blanching of the face and neck, trophic disorders of the skin, palpitations. Depending on the severity of the head injury, various neurological disorders are possible - from paresis, paralysis and intracranial hypertension to diffuse neurological microsymptoms.

The course of a traumatic disease in the acute period is wavy, periods of improvement are replaced by deterioration of the condition. Deterioration of the condition is observed under mental stress, under the influence of psychogenic factors, and atmospheric fluctuations. At the same time, asthenic manifestations intensify, the development of convulsive seizures, disturbances of consciousness such as twilight or delirious, acute short-term psychotic episodes of hallucinatory and delusional structure is possible.

The duration of the acute period is from 3 to 8 weeks, depending on the severity of the head injury.

Under acute period traumatic illness is characterized by either a complete recovery of the victim or a partial improvement in his condition. Its duration is up to 6 months.

The long-term period of a traumatic illness lasts several years, and sometimes the entire life of the patient. First of all, it is characterized by cerebrasthenic disorders with irritability, sensitivity, vulnerability, tearfulness, increased exhaustion during physical and especially mental stress, and decreased performance. Patients complain of sleep disturbances, intolerance to heat and stuffiness, a feeling of lightheadedness when driving in public transport, and a slight decrease in memory. Hysteriform reactions may occur with demonstrative sobbing, wringing of hands, exaggerated complaints about poor health, and demands for special privileges. An objective examination reveals minor scattered neurological symptoms and vasovegetative disorders. Typically, cerebrasthenic disorders have favorable dynamics and after a few years are completely leveled out.

Affective pathology is characteristic of the late stage of a traumatic illness. It can manifest itself as mild depressive disorders in combination with more or less pronounced affective lability, when, for a minor reason, mood swings in the downward direction easily occur. Clinically more pronounced affective disorders are possible in the form of depressive states with a feeling of loss of interest in previous everyday concerns, an unreasonable interpretation of the attitude of others towards oneself in a negative way, an experience of inability to active actions. Depressive affect can acquire a tinge of dysphoria, which is expressed in angry-negative reactions and a feeling of internal tension.

Depressive disorders are usually accompanied by increased excitability, irritability, anger, or gloominess, gloominess, dissatisfaction with others, sleep disorders, and impaired ability to work. In this case, mood disorders can reach the level of severe dysthymia or even dysphoria. The duration of such dysthymic and dysphoric states is no more than one to one and a half days, and their appearance is usually associated with situational factors.

In the structure of depressive states, an apathetic component can be detected when patients complain of boredom, indifference, lack of interest in the environment, lethargy, and decreased physical tone.

Most of these individuals are characterized by a decrease in the threshold of psychogenic sensitivity. This leads to an increase in situationally determined hysterical reactions and other primitive forms of expression of protest (auto- and hetero-aggression, reactions of the opposition), an increase in the rudeness and brutality of the affective reaction. The forms of behavior of patients in such cases are determined by short-term affective-explosive reactions with increased irritability, excitability, touchiness, sensitivity, and inadequacy of response to external influences. Affective outbursts with violent motor discharge usually occur for an insignificant reason, do not correspond in strength of affect to the genetic cause, and are accompanied by a pronounced vaso-vegetative reaction. To minor, sometimes harmless, remarks (someone laughs loudly, talks) they give violent affective discharges with a reaction of indignation, indignation, and anger. Affect is usually unstable and easily exhausted. Its long-term cumulation with a tendency to long-term processing of experiences is not typical.

Many patients develop psychopathic-like disorders in the late period of traumatic illness. However, it is often difficult to talk about a clinically defined psychopath-like syndrome. Emotional-volitional disorders in these cases, with all their typological uniformity, are not constant, arise under the influence of additional exogenous influences and are more reminiscent of psychopathic reactions of the explosive, hysterical or asthenic types.

Behind the façade of cerebrasthenic and emotional-volitional disorders, most patients exhibit more or less pronounced intellectual-mnestic changes. Mental and physical exhaustion, increased distractibility, weakened ability to concentrate lead to decreased performance, narrowed interests, and decreased academic performance. Intellectual weakness is accompanied by slowness of associative processes, difficulties in memorization and reproduction. It is usually not possible to unambiguously interpret these disorders due to a psychoorganic defect, as well as to assess its depth and quality due to the severity of asthenic manifestations, which, on the one hand, potentiate these disorders, and on the other, are one of the factors in their development.

A distinctive feature of all patients in the long-term period of head injury is the tendency to periodic exacerbations of the condition with aggravation of all components of the psychoorganic syndrome - cerebrasthenic, affective-volitional, intellectual-mnestic - and the appearance of new optional symptoms. Such exacerbations of psychopathological symptoms are always associated with external influences (intercurrent diseases, psychogenic disorders). Patients experience increased headaches, psychophysical fatigue, general hyperesthesia, sleep disturbances, and a sharp increase in vaso-vegetative disorders. At the same time it is increasing emotional stress, irritability and short temper sharply increase. Poorly corrected affective explosiveness takes on an extremely rude, brutal character and finds outlet in aggressive acts and destructive actions. Hysterical manifestations lose situational mobility and expressiveness, become sharp, monotonous with a pronounced component of excitability and a tendency to self-inflation. Personal disharmony is intensified due to the appearance of senesto-hypochondriacal and hysteroform (feeling of a lump in the throat, feeling of lack of air, interruptions in the heart) disorders, unstable ideas of self-deprecation, low value, attitude.

In the forensic investigative situation, the reactive lability characteristic of these individuals with the slight occurrence of psychogenic layers is also revealed. This manifests itself in a decrease in mood, increased affective excitability and lability, and in some cases in the appearance of hysteroform and puerile-pseudodementia disorders.

IN in rare cases After severe head injuries, traumatic dementia develops. The psychopathological structure of personality in these cases is determined by a gross psychoorganic syndrome with a pronounced decrease in all indicators of attention, thinking, memory, ability to predict, and the collapse of mechanisms for regulating cognitive activity. As a result, the integral structure of intellectual processes is disrupted, the combined functioning of acts of perception, processing and recording of new information, comparing it with previous experience is disrupted. Intellectual activity loses the property of a purposeful adaptive process, and a mismatch occurs in the relationship between the results of cognitive activity and emotional-volitional activity. Against the background of the collapse of the integrity of intellectual processes, a sharp depletion of the stock of knowledge, a narrowing of the range of interests and their limitation to the satisfaction of basic biological needs, a disorder of complex stereotypes of motor activity and labor skills are revealed. Marked more or less pronounced violation critical abilities.

The formation of a psychoorganic syndrome in these cases follows the path of becoming an apathetic version of a psychoorganic personality defect and consists of paired symptoms such as torpidity of thinking and at the same time increased distractibility, decreased vital tone, apathy and adynamia in combination with affective lability, dysmnestic disorders with increased exhaustion . Pathopsychological research reveals in these cases increased exhaustion, fluctuations in performance, decreased intellectual productivity, impaired memory both direct and through indirect connections, weakened focus and inconsistency of judgments, and a tendency to perseveration.

During a traumatic illness, paroxysmal disorders and states of altered consciousness (traumatic epilepsy) may appear. Paroxysmal disorders occur both during the first year after the injury and in its long-term period after 10–20 or more years. Paroxysmal disorders of the acute and subacute period of a traumatic illness have a more favorable course and over time remain only in the anamnesis of the disease. Epileptiform disorders in the late period of traumatic brain injury have a less favorable prognosis. They are characterized by high polymorphism. These can be grand mal seizures, minor and abortive seizures, absence seizures, convulsive states without impairment of consciousness, non-convulsive seizures with a minimal convulsive component, vegetative seizures, attacks of psychosensory disorders.

Sometimes episodes of twilight stupefaction are observed. They manifest themselves as an acute and sudden onset without warning, a relatively short duration of the course, an affect of fear, rage with disorientation in the environment, the presence of vivid hallucinatory images of a frightening nature, and acute delirium. Patients in this state are motorically excited, aggressive, and at the end of the psychosis they experience terminal sleep and amnesia.

Illegal acts in such states are always directed against the life and health of others, do not have adequate motivation, are characterized by cruelty, failure to take measures to conceal the crime, and the experience of the alienness of the act. In forensic psychiatric practice they are often assessed as short-term painful disorders mental activity in the form of a twilight state.

In the long-term period of a traumatic illness, traumatic psychoses may occur. They usually occur 10–15 years after a head injury. Their development is projected by repeated head injuries, infectious diseases, and psychogenic influences. They occur in the form of affective or hallucinatory-delusional disorders.

Affective psychoses are manifested by periodic states of depression or mania. Depressive syndrome is characterized by decreased mood, melancholy affect, and hypochondriacal feelings. With mania, the background mood is elevated, anger and irritability predominate. At the height of affective psychoses, twilight stupefaction may develop. The psychotic state occurs in combination with a psychoorganic syndrome of varying severity. The course of psychosis is 3–4 months with subsequent reverse development of affective and psychotic symptoms.

Hallucinatory-delusional psychoses also occur without warning. At the initial stage of their development, clouding of consciousness is possible like twilight or delirium with the inclusion of hallucinatory phenomena. Subsequently, the clinical picture is dominated by polymorphic hallucinatory-delusional disorders with the inclusion of elements of the Kandinsky-Clerambault syndrome. In a milder version of the course of psychosis, the patients’ experiences are in the nature of overvalued ideas of hypochondriacal or litigious content. Late traumatic psychoses differ from schizophrenia in the presence of a pronounced psychoorganic syndrome, the appearance at the height of their development of a state of impaired consciousness, and upon recovery from psychosis - signs of asthenia and intellectual-mnestic disorders.

Forensic psychiatric assessment of persons who have suffered head injuries is ambiguous and depends on the stage of the disease and the clinical manifestations of the disease. The most difficult expert assessment is the acute period of a traumatic illness, since experts do not observe it personally. To assess the mental state, carried out retrospectively, they use medical documentation from surgical hospitals, where the patient is usually admitted immediately after receiving a head injury, materials from criminal cases, and the patient’s description of his condition relative to that period. Taking into account retro- and anterograde amnesia, the information provided by patients is usually extremely scarce. At the same time, practice shows that in the acute period of a traumatic illness, serious illegal actions directed against the individual and transport offenses are often committed. The expert assessment of victims is of particular importance.

In relation to persons who have committed unlawful acts, mild and moderate traumatic brain injuries are of greatest importance, since consciousness in these cases is not deeply clouded and is of a undulating nature. In persons in this condition, gait is not impaired and individual purposeful actions are possible. Nevertheless, a confused facial expression, lack of adequate speech contact, disorientation in the environment, further retro- and anterograde amnesia indicate a violation of consciousness in the form of deafness. These conditions fall under the concept of temporary mental disorder and indicate the insanity of these persons in relation to the act charged with them.

Medical measures that can be recommended for such patients are determined by the severity of the residual effects of the head injury. At full reverse development Patients with mental disorders require treatment in general psychiatric hospitals.

If the examination reveals pronounced post-traumatic disorders in the subject (epileptiform seizures, periodic psychoses, pronounced intellectual and mental decline), compulsory medical measures may be applied to the patients in specialized psychiatric hospitals.

When experts commit transport offenses, the mental state of the driver is assessed from two positions. First, the driver may have had a history of traumatic brain injury, and at the time of the accident it is important to assess whether he or she had an abortive epileptiform disorder such as petit mal seizure, absence seizure, or full-blown seizure. The second position is that at the time of the accident the driver often receives a second traumatic brain injury. The presence of the latter masks the previous post-traumatic state. If the subject has previously suffered from a traumatic illness, this must be confirmed by appropriate medical documentation.

The most important thing for an expert opinion is the analysis of the traffic pattern, the testimony of those in the car with the driver at the time of the accident, the statement or denial alcohol intoxication, the person responsible for the accident’s description of his mental state. If at the time of the offense the expert’s consciousness is impaired, the person is declared insane. In cases where a traumatic brain injury was received at the time of the accident, regardless of its severity, the person is considered sane. The driver's further condition is assessed according to the severity of the traumatic brain injury. In case of complete reverse development of the post-traumatic state or mild residual effects, the person is sent for investigation and trial. If the expert commission ascertains the presence of pronounced post-traumatic disorders, then the person should be sent for treatment to a psychiatric hospital with routine supervision, both on a general basis and for compulsory treatment. The further fate of the patient is determined by the characteristics of the course of the traumatic disease.

Forensic psychiatric examination of victims who received a head injury in a criminal situation has its own characteristics. At the same time, a complex of issues is resolved, such as the ability of a person to correctly perceive the circumstances of the case and testify about them, the ability of him to correctly understand the nature of the unlawful acts committed against him, as well as his ability, due to his mental state, to participate in judicial investigative actions and exercise his right to protection (procedural capacity). In relation to such persons, a comprehensive commission with a representative forensic medical examination the issue of the severity of bodily injuries as a result of a head injury received in a criminal situation is resolved. If a person, as a result of illegal actions committed against him, received minor injury, it can correctly perceive the circumstances of what happened and testify about them, as well as understand the nature and significance of what happened and exercise its right to defense.

If a person is diagnosed with signs of retro- and anterograde amnesia, he cannot correctly perceive the circumstances of the case and give correct testimony about them. It should be taken into account that such persons often replace memory disorders related to the period of the offense with fictions and fantasies (confabulation). This indicates the victim’s inability to correctly perceive the circumstances of the case. In this case, the examination is obliged to establish the time boundaries of memory disorders, taking into account the reverse dynamics of retrograde amnesia at the time of the examination. If post-traumatic disorders are not severe, then such a person can subsequently independently exercise his right to defense and participate in a court hearing. In case of severe head injuries and severe post-traumatic disorders, the person cannot perceive the circumstances of the case and give correct testimony about them.

When determining the severity of bodily injuries received by a victim in a criminal situation, a comprehensive forensic and forensic psychiatric examination is based on the severity of the traumatic brain injury, the duration of the initial and acute periods and the severity of mental disorders in the late period of the traumatic illness.

Forensic psychiatric examination of the long-term consequences of head trauma mainly concerns resolving the issue of the sanity of these individuals. By the time the crime is committed and the examination is carried out, they usually have minor post-traumatic disorders in the form of psychopathic-like, neurosis-like, affective and asthenic disorders, which does not exclude their sanity. In the presence of pronounced intellectual-mnestic disorders, up to traumatic dementia, patients should be declared insane.

Long-term consequences of brain injury include traumatic cerebrovascular disease, traumatic encephalopathy, traumatic dementia and late traumatic psychoses.

Traumatic cerebrovascular disease.

Traumatic cerebrasthenia is observed most often in persons who have suffered a concussion, and is characterized by a clinical picture that is largely reminiscent of neurasthenia. The development of traumatic cerebrastia is sometimes very far removed in time from the moment of traumatic injury. There are cases where traumatic cerebrovascular disease developed 10 years or even more after the injury. However, more often this disease occurs after the end of the acute post-traumatic period. In cases where this syndrome gradually develops in the period long after the injury, the pathogenetic involvement of a number of other factors that disrupt compensatory capabilities cannot be excluded.

The leading symptoms in the symptomatology are complaints of rapid exhaustion and fatigue, intolerance to any additional stress, and difficulties if necessary to adapt to new living and working conditions. In addition, patients experience constant or intermittent headaches. It should be recognized as typical that headaches arise or intensify during work, during a tiring conversation, when the weather changes, or while riding in a tram or car. Finally, important symptom Traumatic cerebrasthenia is the high sensitivity of patients to temperature, knocking, noise and other external stimuli. Neurological examination usually does not show pronounced organic symptoms; As a rule, attention is drawn to signs indicating lability and even perversity of the autonomic innervation. Patients easily blush, turn pale, have sweating or dry skin, hypersalivation or dry mouth. In this case, sometimes there is a lack of adequate autonomic reactions to external stimuli. For example, sweating occurs in the cold, and dry skin occurs in hot weather.

Symptoms of traumatic cerebrastia, if the patient is given timely rest and the necessary therapy is carried out, weaken or even disappear completely. However, they can just as easily reappear under unfavorable circumstances. Liquorodynamic disorders, in all likelihood, play a significant role in the formation of the clinical picture, therefore dehydration therapy, drugs that reduce the production of cerebrospinal fluid and reduce spinal pressure, have a therapeutic effect.

Against the background of the main cerebrasthenic syndrome, a number of other functional abnormalities may occur: hypochondriacal thoughts, obsessive fears appear, a state of increased irritability is observed, and in some cases, on the contrary, lethargy and apathy. Sometimes, during the period of exacerbation of cerebrospinal gravis, vestibular disorders, sleep disorders, etc. come to the fore. In the origin of these variants of traumatic cerebrasthenia, of course, not only the individual characteristics of the person and the nature of the previous injury, but also the living conditions of the patient play a role.

Everyday clinical practice shows that in the anamnesis of persons suffering from various types psychopathy, including asthenic and hysterical, there are traumas received in childhood. It is quite clear that the reactivity of the central nervous system, altered under the influence of a traumatic factor, in particular its increased vulnerability and intolerance to all kinds of stress, predisposes to the formation of psychopathic character traits. It is known that children suffering from traumatic cerebrastia do not succeed in school and lag behind their peers in development. Thoughts about one’s own inferiority in some cases harden oneself and lead to loose behavior, while in others they increase self-doubt and contribute to excessive shyness. Under unfavorable conditions of upbringing, children with traumatic cerebrovascular disease are the main reserve from which the ranks of psychopathic personalities are replenished.

Traumatic encephalopathy (cerebropathy).

The clinical picture of encephalopathy is very similar to that of traumatic cerebrovascular disease. In these cases, signs of weakness of internal inhibition also come to the fore, only with greater intensity: incontinence, hot temper, irritability, fatigue and exhaustion of the nervous system. As a rule, traumatic encephalopathy occurs as a result of previous contusions and brain injuries, which explains the presence focal symptoms from the central nervous system. Of these symptoms, the most consistently observed are disturbances of oculomotor innervation, in particular convergence paresis, anisocoria, facial asymmetry, and deviation of the tongue away from the midline. Along with severe neurological symptoms, weakness may be noted vestibular apparatus, detected during a calorimetric test or rotation on a Barany chair, asymmetry of autonomic innervation, etc.

One of the common types of traumatic encephalopathy is the so-called traumatic epilepsy. Epileptiform seizures arise as a result of focal brain damage in the motor and premotor areas of the frontal lobe. Unlike epilepsy, with traumatic epilepsy, as a rule, there are no personality changes of the epileptic type. The nature of epileptiform seizures varies widely. Along with convulsive paroxysms such as major and minor seizures, attacks of dysphoria and episodes of a twilight state of consciousness are possible. Periodic psychoses of the organic type described by a number of authors in children and adults are most often caused by traumatic brain damage.

Another equally common type of traumatic encephalopathy is its psychosensory form. This includes those cases where vestibular disorders easily occur. Such patients constantly complain of dizziness that occurs when driving fast, in movies, or when changing body position. In addition to dizziness, many patients experience metamorphopsia and sensations of body diagram disorder. There are known cases of traumatic parkinsonism, which in its manifestations resembles the chronic stage of epidemic encephalitis. In the clinical picture of this form, along with amyostatic disorders, symptoms such as attachment, violent crying, and laughter are observed.

Traumatic encephalopathy is an even more favorable soil for the development of a psychopathic personality type. Under unfavorable environmental conditions, a well-known psychopathic-like state arises, the leading signs of which are irritability, anger, limited interests, excessively expressed egocentrism, malice and aggressiveness. This kind of psychopathic development is observed mainly in cases of trauma received in childhood.

The tendency of persons who have suffered trauma to abuse alcoholic beverages has long been noted. This is explained mainly by the weakening of the mechanisms of internal inhibition and, therefore, increased suggestibility and subordination. Once among people suffering from alcoholism, these patients are more easily accustomed to systematically drinking alcohol than completely. healthy people. It should be taken into account their increased sensitivity to the effects of alcohol, which is expressed in the fact that intoxication occurs from relatively small doses. At the same time, the features of alcoholic degradation deepen the symptoms of traumatic cerebral gravis, encephalopathy and often make patients disabled.

Traumatic dementia.

The most severe form of long-term consequences of traumatic brain injury is dementia. Its development is not always associated with the severity of previous injuries, although in most cases it certainly depends on extensive damage to the brain. The clinical picture of traumatic dementia includes symptoms of lethargy, lack of initiative, apathy, or, conversely, irritability, impulsiveness, and explosiveness. In this case, quite often pronounced memory disorders are observed, sometimes like Korsakov's syndrome. As the process deepens, the ability to correct one’s own mistakes, correctly navigate the situation, and make meaningful decisions is impaired. Traumatic dementia, as a rule, is a progressive disease. However, stationary forms of traumatic dementia are also observed.

Late traumatic psychoses.

In persons suffering from traumatic cerebrovascular disease and encephalopathy, so-called late traumatic psychoses occur, mainly episodically. They occur most often in the form of episodes of disturbance of consciousness such as delirious syndrome. However, there are manic and depressive symptom complexes that resemble circular psychosis in clinical picture. Distinctive features of episodic psychoses are their short duration (from 1-2 days to 2-3 weeks) and the presence of signs of organic brain damage.

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Classification of mental pathology of traumatic origin

Psychopathological characteristics of the initial and acute periods of traumatic illness

Nonpsychotic syndromes of the acute period of traumatic illness

Traumatic psychoses of the acute period

Mental disorders of late and long-term periods

Non-psychotic mental disorders

GENERAL INFORMATION

Mental disorders caused by traumatic brain injury occupy an important place among mental illnesses in children.

All traumatic brain injuries are usually divided into three groups: intrauterine, birth and postpartum. By localization, injuries of the central and peripheral nervous system, i.e., the brain and spinal cord, are distinguished. For psychopathology, brain injuries are most important.

Based on the nature of the traumatic effect on the brain, there are: open And closed skull injuries. The first are characterized by a violation of the integrity of the skull bones, which, in turn, are divided into penetrating injuries with damage to the meninges and brain substance and non-penetrating injuries. With a closed injury, the skull bones are not damaged. It occurs much more often than open. Therefore, below we consider mental disorders in closed brain injury in children and adolescents.

Traumatic brain injury can occur both in utero and during childbirth. In the future, children may experience household, play, street, transport and other types of it.

Observations show that head injuries in children are more common at the age of five, then their curve falls, rising again by the age of ten.

Intrauterine trauma associated with various bruises of a pregnant woman from falling, lifting heavy objects, jumping and other factors leads to disruption of intrauterine development of the fetus.

Birth trauma (long, rapid labor, obstetric surgery) can lead to intracranial hemorrhage. It has been established that hemorrhages can occur as a result of asphyxia, which is observed during pathological childbirth, and when the placental circulation of the mother is disrupted. Often a consequence of birth trauma is Little's disease, manifested by cranial nerve paresis, spastic tetraparesis, various subcortical symptoms and a slight decrease in intelligence.

Closed brain injury is differentiated into concussion (commotion) and bruise (contusion). When a concussion occurs, the brain stem is predominantly affected (the medulla oblongata, the pons, and sometimes the midbrain). When a bruise occurs, it is mainly the cerebral hemispheres that are affected. The presence of these two types of injuries is justified not only by clinical, but also by anatomical data. A combination of concussion and brain contusion may occur.

At concussion Brain function is grossly impaired, but at the same time no pronounced anatomical changes are observed. At the same time, the person instantly loses consciousness and falls: his face turns pale, his gaze is motionless, his pupils are dilated and do not react to light, his breathing is shallow, his pulse is rare, tendon reflexes are not evoked. Vomiting and convulsions are sometimes observed. IN severe cases Death may occur as a result of damage to the medulla oblongata. With a mild concussion, consciousness returns within a few minutes, sometimes psychomotor agitation and retrograde amnesia appear immediately after the injury. In the first days, headaches are observed, aggravated by sudden movements, dizziness, noise and ringing in the ears, nausea, pulse lability, etc. The basis of these phenomena is a violation cerebral circulation and functions of the vestibular apparatus.

For a long period after the injury, headache, dizziness, increased emotional excitability, and hypomnesia may occur. In the late period of trauma, acute mental disorders with motor agitation, confusion and subsequent amnesia sometimes come to the fore, which subsequently lead to significant changes in the core of the personality.

Contusion a mild degree is clinically manifested only by a state of stupor, sometimes the disturbance of consciousness is completely absent. In general, focal and cerebral symptoms in concussion are more pronounced than in concussion. They depend primarily on the location of the lesion and are caused by the resulting destruction of the brain matter as a result of its soaking in spilled blood, as well as bruise of brain tissue due to a counter-impact. The more severe course of a contusion compared to a concussion is caused by the fact that with a concussion, in addition to the brain stem The cerebral hemispheres are also affected.The symptoms of mental disorders depend on the intensity and location of the damage.

PATHOGENESIS OF CLOSED SKULL INJURY

In the clinical picture of a closed skull injury, three stages of pathophysiological changes in the brain that have been injured can be distinguished. Each stage is characterized by specific psychopathological, neurological and somatic manifestations.

First, acute stage occurs immediately after brain injury. At the same time, diffuse protective inhibition develops in patches of the cerebral cortex, the prevalence and duration of which is directly proportional to the severity of the injury. Objectively, this is expressed by loss of consciousness, disruption of the heart and breathing. Gradually, certain areas of the cerebral cortex, the cells of which were not damaged, as well as subcortical formations are freed from inhibition. Consciousness is restored, cerebral symptoms disappear and signs of focal brain damage appear. Since hearing and speech, especially in early optogenesis, are closely interrelated, in the first stage of closed brain injury, deafness is combined with muteness.

In the case when protective inhibition in the cerebral cortex does not weaken for a long time, but disappears in the subcortex, the clinical picture of traumatic psychosis develops with or without delirium. Outside of the delirious state, mental disorders are manifested by increased motor skills, euphoria, decreased criticality and absurd behavior such as puerilism. Motor retardation with apathy, lethargy, reaching stupor may also be observed.

In more severe cases, amnesia and focal disorders such as aphasia and paresis occur. In children, a delirious state with traumatic psychosis is observed less frequently than with infectious psychosis. However, they more often experience a state of deafness and confusion, insufficient understanding of the environment, a disorder in the analysis and synthesis of environmental phenomena: children complain that the objects around them have changed. IN acute stage closed brain injury, mental disorders of varying severity can be observed; in the most severe situations, death occurs in the very first days after the injury. In most cases, after the end of the acute stage, which lasts on average from 3 to 7 weeks, gradual restoration of functions and a decrease in acute phenomena begin.

Second, late stage pathophysiological changes develop 3-7 weeks after injury. It is characterized mainly by weakening of active inhibition, inertia and weakness of excitation processes. Clinically, this is manifested by various asthenic and encephalopathic conditions, a predominance of subcortical function, a sharp decrease in performance, emotional instability in the form of increased efficiency and lability of emotions. At the slightest provocation the patient cries, and the tears disappear as quickly as they appear. Severe autonomic disorders are observed: tachycardia at the slightest excitement, red dermographism, hyperemia of the skin of the face, neck, chest, increased sweating, etc. Neurological symptoms include trembling of the eyelids, tongue, fingers of outstretched arms, increased tendon reflexes. Unfavorable biological microsocial environmental factors intensify these symptoms, up to seizures of certain groups of mice, transforming into epileptiform seizures or mental equivalents.

Third, distant stage pathophysiological changes caused by closed injury skull, observed 2-3 years after the injury. It is especially important for speech pathologists and medical staff of auxiliary schools to know the psychopathological symptoms characteristic of this distant stage, called the period of residual phenomena. It is marked by the formation of persistent focal or general cerebral disorders, the severity of which can be very different, and is determined by the degree of injury and therapeutic and pedagogical measures in the first, acute stage. In this case, two opposing trends operate: on the one hand, the plasticity of a growing organism contributes to the compensation of impaired functions, and on the other, ontogenetically younger structures of the nervous system are subject to scarring processes and anatomical and destructive changes.

CHRONIC MENTAL DISORDERS

WHAT ARE THE CONSEQUENCES OF BRAIN INJURIES?

The consequences of brain injuries can be both minor organic changes in the form of cerebrovascular disease, and gross organic disorders, up to traumatic dementia. The severity of persistent mental disorders is largely determined by the location of the injury, its nature, the effectiveness of treatment measures carried out at the time of injury, in the acute and late stages, as well as the environmental conditions in which the patient lived in the period of time between the injury and the development of long-term consequences. Even minor repeated trauma to the skull, infections, intoxication and other adverse environmental influences significantly aggravate the long-term consequences of injuries. In most children and adolescents who have suffered a traumatic brain injury, impaired functions are compensated. A defectologist has to encounter the following types of irreversible residual mental disorders.

Traumatic cerebrovascular disease observed in children and adolescents who have suffered primarily from a concussion, and clinically resembles neurasthenia or asthenia. The clinical picture of traumatic brain injury includes emotional disorders. For a long time, sometimes V For many years, these patients complain of headaches and dizziness that occur spontaneously or under certain conditions - school activities, noise, turning the head. Such patients experience irritability, mood instability, and a tendency to sudden affective outbursts; They are characterized by weakening of memory, slow type of thinking, and decreased attention. Character changes are possible with more pronounced antisocial and hysterical reactions than in adults.

Children with this mental disorder are disobedient at school and at home, aggressive, and prone to running away and wandering. Some of them exaggerate their painful condition, demonstrate unnatural stuttering, trembling, accompanied by crying, screaming, and threats. This pathological condition leads to the child’s separation from school life and causes a kind of intellectual and social decline, which should not be identified with true dementia, despite some intellectual impairment. Teaching such children presents certain difficulties and complicates the work of teachers and educators.

Children (adolescents) suffering from traumatic cerebrastia, especially at the beginning of school, more often than others become repeaters, display hypochondriacal ideas with a tendentious interpretation of the environment: they claim that they are treated poorly, hostile actions are carried out against them and therefore they refuse to attend school. Thanks to the attentive attitude of parents and teachers, timely treatment, the correct regimen, and the social orientation of the development of interests, improvement occurs, the patient begins to be more critical of his surroundings.

The prognosis for such mental disorders depends on the severity of the injury and the further living conditions of the child after it. Since this pathology is determined not so much by an intellectual defect such as dementia, but by a defect in the emotional-volitional sphere, appropriate therapeutic and pedagogical measures undoubtedly contribute to significant compensation for the defect.

Traumatic encephalopathy occurs predominantly as a result of brain contusion and is characterized by more pronounced neurological and psychopathological symptoms of organic brain damage. In these cases, focal (paresis of cranial nerves, aphasia, alexia, agraphia, apraxia) and general (irreversible impairment of memory, thinking, affective instability, etc.) neurological symptoms are pronounced. The prognosis for patients with traumatic encephalopathy is more unfavorable than for patients with traumatic cerebrovascular disease, due to atrophy of certain areas of brain tissue, scar degeneration, internal dropsy and other organic changes. Vestibular disorders are also observed, but they are less pronounced than with traumatic cerebrastia.

In some cases of traumatic encephalopathy, due to a sharp weakening of the regulatory influence of the cerebral cortex on subcortical formations, affective disorders and the predominance of primitive drives and instincts come to the fore. Patients with this variant of traumatic encephalopathy are characterized by impulsive actions, outbursts of anger, and a tendency to conflicts with others, quarrels, and fights. Their critical attitude towards their behavior is reduced, they are disinhibited and fussy, persistent in achieving their egoistic desires, ignore social norms of behavior, do not get along well in a team, show rudeness, cruelty, and a tendency to vagrancy. Such hyperdynamism with impaired intellectual activity (without pronounced dementia), manifested either by irritability with outbursts of anger, or euphoria, clowning and foolish behavior, entails failure at school, inability to master educational material, and loss of interest in educational activities. Hypompesia, defective mental operations, the pathological aspect of characterological characteristics, a tendency to develop, when life situations become more complicated, reactive psychoses, pseudodementia, stupor and other pathological phenomena lead to a sharp decrease in the performance of such children. Family and school must take into account that the correction of such post-traumatic mental disorders is very difficult. Children with these manifestations need systematic treatment and training using special methods.

In another variant of traumatic encephalopathy, neurological symptoms in combination with apathy, lethargy, slowness, a sharp decrease in activity and motor retardation come to the fore in the clinical picture. In this case, signs of damage to the cerebral cortex and persistent mental disorders predominate in the form of memory loss, severe exhaustion, loss of previous knowledge and skills, difficulty concentrating, and a significant decrease or loss of performance. Thus, this apathetic-adynamic variant of encephalopathy is characterized by a significant decrease in intellectual level.

Traumatic epilepsy, arising in the long-term period of traumatic brain injury, is characterized by a polymorphism of pathological manifestations - convulsive seizures with a subcortical component, autonomic disorders, mental equivalents in the form of dysphoria, a twilight state of consciousness. Hysterical attacks with expressive movements are also observed. Seizures are caused by scarring of brain tissue in the motor and premotor areas of the frontal lobe of the hemisphere. Convulsive seizures of the Jacksonian type with preservation of consciousness are possible. Convulsions first cover a limited group of muscles, and then become generalized and are combined with loss of consciousness (the same as with true epilepsy).

Unlike true epilepsy, in traumatic epilepsy seizures occur, firstly, under the influence of external pathogenic factors, and secondly, they are not accompanied by a rapid increase in personality changes of the epileptic type. The duration of the disease, the frequency of convulsive seizures, and mental equivalents, which are also observed in traumatic epilepsy, cause a decrease in intelligence, the predominance of sadness and malice. But still, in most cases, traumatic epilepsy does not entail such pronounced changes in the psyche that are characteristic of true epilepsy, which is an independent disease. The organic nature of brain damage in traumatic epilepsy gives grounds for the use of pathogenetic treatment, under the influence of which convulsive seizures disappear in many patients.

Traumatic parkinsonism is predominantly a consequence of traumatic damage to the base of the brain (brain stem). Against the background of vestibular and autonomic disorders, especially in early childhood, disorders similar to parkinsonism due to encephalitis develop, while sleep disorders and importunity are not as pronounced as with epidemic encephalitis. On the mental side, along with amyia and stiffness, lethargy, apathy, lack of initiative, and indifference to the environment are observed. Unfavorable environmental conditions contribute to the development of a psychopathic-like state, the leading signs of which are limited interests and anger.

Traumatic dementia is the most difficult I love it form of long-term consequences of traumatic brain injury, mainly contusion, especially with simultaneous damage to the frontal and parietal lobes of the cerebral hemispheres. Sometimes the same kind of dementia is a consequence of a severe concussion without damage to the brain substance. The clinical picture of this dementia reveals significant personality changes and persistent declines in intelligence in the form of various variants of mental retardation. Regardless of the child’s age, the difficulty of forming new temporary connections and the impossibility of reproducing past experience are noted, which, in fact, determines car the mud of dementia.

Characterized by a sharp weakening of memory, especially the ability to remember current events, weakness of judgment, and decreased intelligence. Patients lack purposeful interests

sy, criticality is reduced, amnestic aphasia and other forms of disorders of speech, writing, counting, etc. are often observed. As the pathological process deepens, comprehension is disrupted, confusion and hallucinatory experiences are sometimes noted.

Late traumatic psychosis can occur many years after a traumatic brain injury, most often manifesting itself in the form of an episodic disorder of consciousness such as a delirious state. The appearance of a hysterical reaction, short-term depressive, manic and hebephrenic syndromes is possible. However, they are observed relatively rarely in children. These acute, episodic mental disorders develop V in cases where a patient with residual effects of brain injury is exposed to unfavorable microsocial or biological factors(excessive mental trauma, complicated life situation, acute infection).

Mental disorders can occur when the human body (including the brain) is damaged by lightning, electric current, or prolonged or intense exposure to solar and thermal (infrared) radiation.

The passage of a strong electric current through the body causes stupor or loss of consciousness, accompanied by agitation and affects of fear, followed by amnesia. Sometimes, as a result of electric shock, residual phenomena are observed in the form of cerebrospinal fluid, epileptiform seizures, hypomnesia and dizziness.

Sunstroke is caused by prolonged or intense exposure to direct sunlight on the body, heatstroke is caused by a violation of the body's thermoregulation as a result of prolonged exposure to high air temperatures or thermal radiation. Harbingers of sunstroke and heatstroke are dizziness, tinnitus, vomiting, and unsteady gait. Then delirium or coma sets in, body temperature rises to 40 °C or more. The prognosis is quite serious; in severe cases, death is possible. Persistent consequences: a long-term condition of cerebrospinal fluid, sometimes aphasia.

Treatment consists of artificial respiration, the use of tonics (camphor, caffeine, ether), the introduction of an isotonic sodium chloride solution, and bloodletting; in sunny or heatstroke In addition, cooling is necessary (pouring cold water, cold compress, etc.).

TREATMENT AND PEDAGOGICAL EVENTS

The prognosis of a closed skull injury depends primarily on its severity, the nature of the biological “soil” that is injured, the age of the victim, the volume and nature of treatment and pedagogical measures in the acute and late stages, as well as on additional pathogenic factors affecting the body.

Adverse consequences are observed in cases where a brain that is already somewhat defective as a result of residual effects of past diseases or an ontogenetically still completely unformed brain is injured. In this case, the injury delays the child's development and leads to severe intellectual impairment. If an injury occurs in an older child, its consequences are more favorable. The activity of therapeutic intervention and the elimination of additional harmful factors also have prognostic significance.

Treatment of patients with traumatic brain injury in the acute stage primarily consists of complete rest and strict bed rest, the duration of which depends on the severity of the injury: for mild injury, absence of loss of consciousness, vomiting and nausea - up to 15 days, for severe injury - up to 2 months . If the patient is unconscious, he should lie on his side. To enhance the function of the respiratory and circulatory organs, stimulating drugs are used - camphor, caffeine, lobelia, etc. During this period, it is advisable to prescribe sleeping pills, restorative and tonic drugs.

Patients who have suffered a traumatic brain injury are given intravenous hypertonic solutions and prescribed insulin. For encephalopathy, accompanied by hyperdynamism and disinhibition, medications are used that enhance the process of inhibition in the cerebral cortex and reduce irritability. Drugs that stimulate the central nervous system (corazol, cordiamin, caffeine, etc.) are also prescribed. To reduce intracranial pressure, a spinal puncture is used, but not immediately after the injury, but after some time.

Therapeutic and pedagogical measures in the long-term period after injury are determined by the nature of residual phenomena, individual and age characteristics sick. Those suffering from traumatic cerebrovascular disease are prescribed hypertonic solutions, physiotherapeutic procedures, hydrotherapy, and small doses of sleeping pills.

For encephalopathy, good results are obtained by treatment with bioquinol, iodine preparations, the use of diathermy, ultraviolet irradiation: with increased intracranial pressure - x-ray irradiation, spinal puncture, moderate doses of narcotic analgesics; for speech disorders - administration of glucose, magnesium sulfate, hexamethylenetetramine, sodium iodide.

For traumatic epilepsy accompanied by persistent headache, intravenous administration of hypertonic solutions is effective. Along with the use of anticonvulsants, good results are achieved by introducing air into the ventricles of the brain (pneumoencephalography), which helps eliminate adhesions formed after injury and restore normal circulation of cerebrospinal fluid. If necessary, neurosurgical intervention is performed. The use of therapeutic exercises is recommended.

Prevention of exacerbation of the consequences of traumatic brain injury involves eliminating various factors that can intensify painful symptoms. It is necessary to protect children who have suffered a brain injury from cooling and overheating, infections and intoxications, overwork and idle pastime. One of the most important preventive, therapeutic and pedagogical measures is a properly organized regimen.

Children and adolescents who have suffered severe brain injury should be monitored at a dispensary for a long time and periodically receive preventive treatment.

Of great importance are pedagogical measures aimed at training the ability for intellectual tension, developing skills for concentrating attention, as well as the gradual inclusion of such a student in the team, working according to an individual plan. Equally important is the elimination of mental trauma. The educational load should be monitored by a teacher and a doctor in order to timely provide short-term rest or switch to another type of activity that does not require stress.

Students who have suffered a brain injury are characterized by a polymorphism of mental disorders: memory loss, inferiority of mental operations, speech disorders, dyslexia, etc. A student’s persistence in achieving a goal does not always produce the necessary results; he begins to feel and understand his inadequacy, his pride is infringed, and resentment arises against those who are not very attentive or very demanding of him. It is in these cases that psychotherapeutic conversations between the teacher and the student play an important role, directing his emotions in the right direction, mobilizing his willpower to develop compensatory and adaptive mechanisms that increase the possibility of inclusion in educational and work activities. Significant intellectual disability is a diagnostic criterion for transferring such a student from a general education school to a auxiliary school.

One of the therapeutic and pedagogical activities is the choice of a future profession. In this case, one should take into account the nature of the brain injury, the severity of persistent residual consequences, the compensatory and adaptive capabilities of the body or, conversely, the tendency to relapse, further aggravation of psychopathological symptoms, as well as the period of time that has passed since the injury, which in the absence of gross destructive changes in the tissue brain is a positive factor.

MENTAL DISORDERS IN CRANIO BRAIN TRAUMA

Traumatic brain injuries (TBI) are one of the most common causes of death and permanent disability. The number of patients with traumatic brain injuries increases by 2% annually. The structure of peacetime injuries is dominated by domestic, transport, industrial, and sports injuries. Complications of traumatic brain injuries are of great medical importance, such as the development of traumatic cerebrastia, encephalopathy, epileptiform syndrome, pathocharacterological disorders, dementia, as well as their impact on the social adaptation of patients. Skull injuries in more than 20% of cases are the cause of disability due to neuropsychiatric diseases.

There are 5 clinical forms of TBI:

concussion - characterized by loss of consciousness lasting from several seconds to several minutes;

mild brain contusion - characterized by loss of consciousness after injury lasting from several minutes to 1 hour;

moderate brain contusion - characterized by loss of consciousness after injury lasting from several tens of minutes to 4-6 hours;

severe brain contusion - characterized by loss of consciousness after injury lasting from several hours to several weeks;

compression of the brain - characterized by life-threatening general cerebral, focal and brain stem symptoms that occur some time after the injury and are of an increasing nature.

The severity of the victim’s condition is determined, first of all, by dysfunction of the brain stem and the body’s life support systems (breathing, blood circulation). One of the leading signs of damage to the brain stem and parts of the brain located directly above it is impaired consciousness.

There are 5 gradations of the state of consciousness in TBI.

clear consciousness - complete preservation of consciousness with adequate reactions to surrounding events;

deafening - a violation of perception while maintaining limited verbal contact against the background of an increase in the threshold of perception of external stimuli and a decrease in one’s own activity;

stupor - switching off consciousness while maintaining coordinating defensive reactions and closing the eyes in response to painful, sound and other stimuli;

coma - switching off consciousness with a complete loss of perception of the surrounding world and oneself.

Vital function impairment, which is often associated with brainstem damage, should also be assessed. These violations are assessed according to the following criteria:

1) moderate violations:

moderate bradycardia (51-59 per minute) or tachycardia (81-100 per minute);

moderate arterial hypertension (140/80-180/100 mm Hg) or hypotension (below 110/60-90/50 mm Hg);

2) pronounced violations:

bradycardia (41-50 per minute) or tachycardia (101 - 120 per minute);

tachypnea (31-40 per minute) or bradypnea (8-10 per minute);

Arterial hypertension (180/100-220/120 mm Hg) or hypotension (less than 90/50-70/40 mm Hg);

3) gross violations:

bradycardia (less than 40 per minute) or tachycardia (over 120 per minute);

tachypnea (over 40 per minute) or bradypnea (less than 8 per minute);

arterial hypertension (over 220/180 mm Hg) or hypotension (maximum pressure less than 70 mm Hg);

4) critical violations:

periodic breathing or apnea;

maximum blood pressure less than 60 mm Hg. Art.;

One of the main and immediate causes The death of victims with severe TBI is the process of acute intracranial dislocation. Its danger is due to the development of axial deformation of the brain stem with its subsequent destruction as a result of irreversible dyscirculatory disorders. An additional, but very important criterion for assessing TBI and its severity is the condition of the scalp. Their damage in conditions of brain damage and its barrier functions increases the risk of purulent-septic complications. In this regard, the following are highlighted:

Closed TBI, in which there is no violation of the integrity of the scalp or there are wounds that do not penetrate the aponeurosis, fractures of the bones of the base of the skull, not accompanied by injury to the nearby area of ​​the scalp;

Open TBI when there are head wounds with damage to the aponeurosis, fractures of the bones of the calvarium with injury to nearby soft tissues, fractures of the base of the skull, accompanied by bleeding or liquorrhea (auricular, nasal):

a) non-penetrating injury - the dura mater remains intact;

b) penetrating trauma - the integrity of the dura mater is disrupted.

CLASSIFICATION OF MENTAL DISORDERS RESULTING FROM TRANO BRAIN TRAUMA

The most acute initial period. Stunning, stupor, coma, impaired cardiovascular activity and breathing.

Acute period. Non-psychotic syndromes: asthenic, apaticoabulic, epileptiform seizures, anterograde and retrograde amnesia, surdomutism. Psychotic syndromes: twilight state of consciousness, traumatic delirium, dysphoria, Korsakov's syndrome.

Late period. Non-psychotic disorders: asthenic, asthenoneurotic, epileptiform, psychopathic (affective instability) syndromes. Late traumatic psychoses: hallucinatory-paranoid, manic-paranoid, depressive-paranoid syndromes.

Long-term consequences of TBI. Cerebroasthenia, encephalopathy, dementia, traumatic epilepsy, post-traumatic personality development.

Mental disorders of the acute period are represented mainly by states of loss of consciousness of varying degrees: coma, stupor, stupor. The depth of impairment of consciousness depends on the mechanism, location and severity of the injury. With the development of coma, consciousness is completely absent, patients are motionless, their breathing and cardiac activity are impaired, blood pressure decreases, pathological reflexes arise, and there is no reaction of the pupils to light. The majority of patients after mild or moderate traumatic brain injuries develop stupor, characterized by slowed thinking and incomplete orientation. Patients are drowsy and react only to strong stimuli. After emerging from the stupor, fragmentary memories of this period are possible.

In the acute period of skull injury, asthenic, asthenoneurotic states develop, less often - surdomutism, antero- and retrograde amnesia, some patients develop psychoses that occur in the form of states of altered consciousness: delirium, epileptiform disorder, twilight disorder of consciousness, occurring immediately after leaving an unconscious state . With asthenic syndrome in the acute period of traumatic brain injury, a decrease in mental productivity, increased fatigue, a feeling of tiredness, hyperesthesia, autonomic disorders, and decreased motor activity are observed. Patients often complain of headaches and confusion.

Delirium most often develops in patients who abuse alcohol or with the development of toxic-infectious complications. Such patients are mobile, jump up, try to run somewhere, and experience frightening visual hallucinations. Traumatic delirium is characterized by the presence of vestibular disorders. The transition from delirious syndrome to amentive syndrome is prognostically unfavorable. The twilight state of consciousness develops most often in the evening, manifesting itself in complete disorientation, abrupt delusional ideas, isolated hallucinations, fear, and motor disturbances. The exit from the twilight state occurs through sleep with further amnesia of painful experiences. A twilight state of consciousness can occur with attacks of motor agitation, a stuporous state, motor automatisms, and puerile-pseudo-dementia behavior.

In the acute period, patients may develop individual or serial epileptiform seizures, hallucinosis, most often auditory, as well as visual and tactile. In cases of severe traumatic brain injury, after the patient recovers from a coma, the development of Korsakov's syndrome with fixation, retro- or anterograde amnesia, confabulations and pseudo-reminiscences is possible. Sometimes patients lose the ability to critically assess the severity of their condition. Korsakoff's syndrome can be transient and disappear after a few days or last a long time and lead to the formation of organic dementia.

The duration of the acute period of traumatic brain injury ranges from 2-3 weeks to several months. During this period, the development of traumatic affective and affective-delusional psychoses is also possible, in which exogenous factors play a significant role: physical activity, fatigue, intoxication, infectious diseases, etc. The clinical picture of these disorders is represented by manic, depressive and affective-delusional disorders, which are combined with confabulations. Depressive states are accompanied by hypochondriacal delirium. The most common are manic states with euphoria, delusions of grandeur, anosognosia, moderate motor activity with rapid development of exhaustion, headache, lethargy, and drowsiness, which disappear after rest. Mania of anger is often observed.

During the period of convalescence or in the late period of acute traumatic disorders, subacute and prolonged traumatic psychoses are observed, which may have a tendency to repeated attacks and a periodic course.

Mental disorders of the long-term period are characterized by different variants of psychoorganic syndrome within the framework of traumatic encephalopathy. The severity of the formed defect is determined by the severity of the traumatic brain injury, the extent of brain damage, the age of the victim, the quality of the treatment provided, hereditary and personal characteristics, personality attitudes, additional exogenous harm, somatic condition, etc. The most common consequence of TBI is traumatic cerebral gravis, which develops at 60 -75% of cases. The clinical picture of the disease is dominated by weakness, decreased mental and physical performance, combined with irritability and fatigue. There are short-term outbreaks of irritability, after which patients, as a rule, regret their incontinence. Autonomic disorders are manifested by fluctuations in blood pressure, tachycardia, confusion, headache, sweating, vestibular disorders, sleep-wake rhythm disorder. Patients do not tolerate traveling in public transport well, cannot swing on swings, or look at the TV screen or moving objects. They often complain of deterioration in health when the weather changes and stays in a stuffy room.

Torpidity and rigidity of nervous processes are characteristic. The ability to quickly switch types of activities decreases, and the forced need to perform such work leads to decompensation of the condition and an increase in pronounced cerebrasthenic symptoms.

Traumatic cerebrastia is often combined with various neurosis-like symptoms, phobias, hysterical reactions, autonomic and somatic disorders, anxiety and subdepressive symptoms, and autonomic paroxysms.

Traumatic encephalopathy develops as a result of residual effects of organic brain damage, the localization and severity of which determine the features of the clinical picture - psychopathic syndromes, traumatic psychoses or defective organic conditions. Most often, affective disorders occur against the background of psychopathic disorders of the excitable and hysterical types. Patients with the apathetic variant of encephalopathy are characterized by severe asthenic disorders, mainly exhaustion and fatigue, they are lethargic, inactive, there is a decrease in their range of interests, memory impairment, and difficulty in intellectual activity.

In traumatic encephalopathy, emotional agitation often prevails rather than inhibition. Such patients are rude, quick-tempered, and prone to aggressive actions. They experience mood swings and easily occurring outbursts of anger that are not adequate to the cause that caused them. Productive activities may be hampered by affective disturbances, further causing self-dissatisfaction and irritation reactions. The thinking of patients is characterized by inertia, a tendency to get stuck on unpleasant emotional experiences. Dysphoria may develop in the form of attacks of melancholy, angry or anxious mood lasting several days, during which patients can commit aggressive and auto-aggressive acts and exhibit a tendency toward vagrancy (dromomania).

In addition to traumatic encephalopathy, in the long-term period of traumatic brain injury, the development of cyclothyme-like disorders is possible, which are usually combined with asthenic or psychopathic syndromes and are accompanied by a dysphoric component. The most common are subdepressive states, characterized by suspiciousness, tearfulness, senestopathies, vegetative-vascular disorders, a hypochondriacal mood regarding one’s health, sometimes reaching the level of overvalued ideas with the desire to receive exactly the treatment that, in the patient’s opinion, he needs.

The symptoms of hypomanic states are characterized by an enthusiastic attitude of patients towards their environment, emotional lability, and weakness. It is also possible that overvalued ideas about one’s health may appear, litigious behavior, increased irritability, and a tendency to conflict. The duration of these states varies. Unipolar seizures are common. Often in the background affective disorders alcohol abuse occurs.

Epileptiform paroxysmal disorders (traumatic epilepsy) can develop at different times after a traumatic brain injury, most often after several years. They are distinguished by polymorphism - there are generalized, Jacksonian seizures, non-convulsive paroxysms: absence seizures, attacks of catalepsy, so-called epileptic dreams, psychosensory disorders (metamorphopsia and body diagram disorders). The appearance of vegetative paroxysms with severe anxiety, fear, hyperpathy and general hyperesthesia is possible. Often, after convulsive seizures, twilight states of consciousness occur, which usually indicates an unfavorable course of the disease. They are often caused by additional exogenous factors, primarily alcohol intoxication, as well as mental trauma. The duration of twilight states is insignificant, but sometimes reaches several hours.

In the long-term period of traumatic brain injury, so-called endoform psychoses can be observed: affective and hallucinatory-delusional, paranoid.

Affective psychoses occur in the form of monopolar manic or (less often) depressive states and are characterized by an acute onset, alternating euphoria and anger, and Mori-like senseless behavior. In most cases, a manic state occurs against the background of exogenous factors (intoxication, repeated injuries, surgery, somatic illness).

Depressive states can be triggered by mental trauma. In addition to melancholy, anxiety and hypochondriacal experiences with a dysphoric assessment of one’s condition and environment appear.

Hallucinatory-delusional psychoses, as a rule, occur acutely against the background of symptoms of traumatic encephalopathy with a predominance of apathetic disorders. The risk of the disease increases in patients with somatic disorders, as well as after surgery. Unsystematic concrete delusions, real hallucinations, alternation of psychomotor agitation and retardation are observed, affective experiences are caused by delusions and hallucinations.

Paranoid psychoses develop most often in men 10 or more years after a traumatic brain injury. The clinical picture is characterized by the presence of overvalued and delusional ideas of jealousy with litigious and querulant tendencies. Paranoid ideas of jealousy can be combined with ideas of damage, poisoning, persecution. Psychosis occurs chronically and is accompanied by the formation of a psychoorganic syndrome.

Traumatic dementia after traumatic brain injury develops in 3-5% of cases. It can be a consequence of traumatic psychoses or the progressive course of a traumatic illness with repeated injuries, and also arise as a result of developing cerebral atherosclerosis. With traumatic dementia in patients, memory impairment, a decrease in the range of interests, lethargy, faint-heartedness, sometimes importunity, euphoria, disinhibition of drives, overestimation of one’s capabilities, and lack of criticism predominate.

Rare types of injuries in peacetime include injury from a blast wave, which is a complex injury in the form of a concussion, brain contusion, trauma to the sound analyzer, and cerebrovascular accidents due to sharp fluctuations in atmospheric pressure. When injured by a blast wave, a person feels like a blow from an elastic body to the back of the head, he experiences a short-term loss of consciousness, during which he is motionless, blood flows from the ears, nose, and mouth. After clearing consciousness, severe adynamia may develop: patients are sedentary, lethargic, indifferent to their surroundings, want to lie even in uncomfortable positions. Retro- and anterograde amnesia is rare, constant complaints are headache, heaviness, noise in the head.

The development of adynamic asthenia, a feeling of physical or mental discomfort, irritability, a feeling of weakness and powerlessness are possible. Autonomic and vestibular disorders are often observed in the form of headache, confusion, sudden feeling of heat, difficulty breathing, pressure in the head or heart area. Patients present with various hypochondriacal complaints, and there is hyperesthesia to sounds, light, and smells. They often get worse in the evenings. The process of falling asleep, as a rule, is disrupted; sleep consists of unpleasant, vivid, often frightening dreams of military themes.

The most characteristic sign of traumatic injury from a blast wave is surdomutism. Hearing, as a rule, is restored before speech; patients begin to hear, but cannot speak. Speech restoration occurs spontaneously under the influence of emotional significant situations. An objective examination reveals mild diffuse neurological symptoms: anisocoria, impaired eye movements, tongue deviation.

The acute period of these disorders ranges from 4 to 6 weeks, then other mental disorders appear. During this period, mood swings are possible, and young people may experience a state of euphoria with increased irritability and a tendency to attacks of anger or hysterical fits. In adulthood, depressed mood with a dysphoric tint or apathy predominates; complaints of poor physical well-being and hyperesthesia in relation to all stimuli are often noted.

AGE FEATURES OF TRAUMATIC DISEASE

The development of mental disorders of traumatic origin in children has its own characteristics. Head injuries are quite common, especially in children aged 6 to 14 years. Mental disorders in the acute period in children occur against the background of increased intracranial pressure: general cerebral and meningeal disorders, pronounced autonomic and vestibular symptoms, as well as signs of local brain damage are observed. The most severe symptoms in children develop a few days after a traumatic brain injury. The most common of them are paroxysmal disorders, which are observed both in the acute period and during the period of convalescence.

The course of traumatic illness in children is usually benign; even severe local disorders undergo reverse development. Asthenia in the long-term period is weakly expressed, motor disinhibition, emotional lability, and excitability predominate. Sometimes, after severe traumatic brain injuries suffered in early childhood, an intellectual defect resembling mental retardation appears.

In young children (up to 3 years of age), a complete loss of consciousness, as a rule, is not observed; general cerebral disorders are erased. Clear signs of traumatic brain injury are vomiting, often repeated, and vegetative symptoms: increased body temperature, hyperhidrosis, tachycardia, confusion, etc. Characteristic disturbances in the rhythm of sleep and wakefulness. The child does not sleep at night and is sleepy during the day.

Traumatic cerebrastia in children is often manifested by headaches that occur suddenly or under certain conditions (in a stuffy room, while running, in noisy places); confusion and vestibular disorders are less common. Asthenia itself can be mild, motor disinhibition, lability of emotions, excitability, vegetative-vascular disorders (increased vasomotor reactions, pronounced dermographism, tachycardia, hyperhidrosis) predominate.

Apathetic-adynamic syndrome in children is characterized by lethargy, apathy, slowness, decreased activity and desire for activity, limited contact with people around them due to rapid exhaustion and lack of interests. Such children cannot cope with the school curriculum, but do not disturb others and do not cause criticism from teachers.

In children with hyperdynamic syndrome, motor disinhibition, fussiness, and sometimes elevated mood with a hint of euphoria predominate. Children are restless, run around, make noise, often jump up, grab some things, but immediately throw them away. The mood is characterized by instability and carelessness. Patients are good-natured, sometimes foolish. There is a decrease in criticism and difficulties in learning new material. Further development of these disorders often leads to more differentiated psychopathic behavior. Children behave poorly in groups, do not learn educational material, violate discipline, disturb others, and terrorize teachers. Since such patients do not complain about their health, their inappropriate behavior for a long time is not regarded as painful and disciplinary requirements are imposed on them.

Mental disorders due to traumatic brain injury in the elderly are usually accompanied by loss of consciousness. In the acute period, autonomic and vascular disorders, confusion, fluctuations in blood pressure predominate, and nausea and vomiting are relatively rare. Due to the inferiority of the vascular system, intracranial hemorrhages are often observed, which can develop after some time and manifest themselves with a clinical picture resembling a tumor or epileptiform seizures.

In the long-term period, more permanent persistent asthenic disorders, lethargy, adynamia and various psychopathological symptoms are observed.

Pathogenesis of mental disorders. The occurrence of mental disorders in the acute period of traumatic brain injury is caused by mechanical damage and swelling of brain tissue, hemodynamic disturbances and brain hypoxia. The conduction of impulses in synapses is disrupted, disorders occur in neurotransmitter metabolism and dysfunction of the reticular formation, brain stem and hypothalamus.

Mild traumatic brain injuries are accompanied by minor disturbances in the structure of nerve cells with subsequent restoration of their functions, while with severe injuries the death of neurons occurs with the formation of glial or cystic formations. There may be a disruption of synaptic connections between nerve cells- traumatic asynapsia.

Treatment of mental disorders in traumatic brain injuries is determined by the stage of the disease, its severity and severity of clinical manifestations. All persons, even after a mild head injury, require hospitalization and bed rest for 7-10 days, and children and the elderly must stay in the hospital for a longer time.

Therapeutic measures for TBI have several directions.

Support of vital functions: a) correction of breathing disorders: restoration of airway patency, tracheostomy, mechanical ventilation; 10 ml of 2.4% aminophylline solution intravenously; b) correction of systemic hemodynamic disorders: fight against arterial hypertension (clonidine, dibazole, chlorpromazine); use of intramuscular lytic mixtures containing neurotropic, antihistamine and vasoplegic drugs (pipolfen 2 ml + tizercin 2 ml + analgin 2 ml + droperidol 4-6 ml or pipolfen 2 ml + aminazine 2 ml + pentamin 20-40 mg + analgin 2 ml ) 4-6 times a day; combating arterial hypotension (infusion therapy - rheopolyglucin or 5% albumin solution) + 0.5-1 ml of 0.6% corglicon solution and 10 ml of 10% calcium chloride solution for every 500 ml of injected fluid.

Specific treatment: a) concussion: adherence to bed rest for 1-2 days; analgesics; tranquilizers; b) contusion of the brain, lung and middle degrees severity: improvement of cerebral circulation (intravenous drip of reopolyglucin or 5% albumin solution + intravenous Cavinton); improvement of energy supply to the brain (intravenous drip of 5-20% glucose solution + insulin); restoration of the function of the blood-brain barrier (aminophylline, papaverine, 5% ascorbic acid solution); elimination of pathological changes in the water sectors of the brain (combined use of saluretics - Lasix, furosemide, urex, hypothiazide - and osmodiuretics - mannitol, glycerin); in the presence of subarachnoid hemorrhage (5% solution of aminocaproic acid, contrical, trasylol, gordox intravenously 25,000-50,000 units 2-3 times a day); anti-inflammatory therapy (a combination of penicillin and long-acting sulfonamide); metabolic therapy (nootropil, cerebrolysin); c) severe brain contusion and acute traumatic compression: emergency surgical intervention aimed at eliminating the causes of compression and its consequences; energy supply to the brain (glucose solution + insulin + 10% calcium chloride solution for every 500 ml of solution); improvement of cerebral circulation (reopolyglucin, albumin); elimination of brain hypoxia (sodium thiopental 2-3 mg per 1 kg of body weight per hour for 8-10 days after injury or gammahydroxybutyric acid (GHB) 25-50 mg per 1 kg of body weight per hour for 8-10 days + hyperbaric oxygenation, oxygen mask); correction of intracranial hypertension (dehydration, corticosteroids, aldosterone antagonists).