Psychiatry - O. K. Napreyenko 2001

Clinical Psychiatry
Mental Disorders Associated with Traumatic Brain Injury

Traumatic Brain injury is a common pathology, accounting for nearly 20% of all peacetime mechanical trauma. According to casualty analyses during local conflicts, craniocerebral injuries combined with other wounds, diseases, and combat stress reactions emerge as a leading pathology. Psychiatric service data indicate that such patients comprised 10% of individuals registered for dispensary care.

Mental disorders resulting from traumatic brain injury are diverse, spanning a wide range from mild asthenic symptoms to dementia. The aftermath of a craniocerebral injury is encompassed by METABOLISM/2.html">THE CONCEPT OF "traumatic disease." Traumatic disease should be understood as traumatic brain lesions that share a common Etiology, developmental trajectory, outcome, and pathological anatomy. The Specific features of psychiatric disorders following traumatic brain injury depend on The Nature of the lesion, the intensity and extent of the trauma, its localization, temporal factors, complications, comorbidity, layered psychogenic factors, and social conditions.

Etiology, Pathogenesis, Classification

Craniocerebral injuries (CCIs) are classified into closed and open. Closed injuries include contusion (contusio), concussion (commotio), and compression (compressio). The distinction between open and closed HEAD injuries is based on the Nature of the damage (the risk of infectious complications and neuropsychological symptomatology) and management specifics (open injuries require surgical intervention).

Closed craniocerebral injuries represent a highly pressing issue. Categorizing closed head injuries and their associated mental disorders is a challenging task due to diverse injury mechanisms, localization, extent, and intensity, as well as A wide variety of clinical manifestations influenced by the time elapsed since the injury and potential complications. The classification of closed CCIs was proposed by Petit in 1773 and remains in use today. However, modern authors emphasize that compression should not be viewed as a distinct form, as it results from increased pressure associated with elevated CEREBROSPINAL FLUID volume, hematomas, and brain edema, and in some cases, brain Swelling. It has also been proposed to use the term "commotion-contusion syndrome" (Spasokukotsky). Commotion is characterized not only by a specific injury mechanism (concussion) but also by a selective, predominantly Brainstem localization.

Based on the time of onset, the stages of CCI sequelae are distinguished as follows: the initial stage, occurring immediately after trauma; the acute stage, lasting 6 weeks; the late stage; and the remote stage.

Modern psychiatry shows a trend toward classification unification to foster scientific mutual understanding and facilitate epidemiological research. Domestic psychiatry distinguishes: 1) psychoses of the initial and acute periods (twilight states, oneiroid syndrome, delirium, Korsakoff syndrome, apallic syndrome, akinetic mutism, affective psychoses, delusional psychoses) and paroxysmal states; 2) mental disorders of convalescence and remote periods (traumatic asthenia, traumatic asthenia with predominant apathy, psychopath-like disorders, cyclothymia-like disorders, paroxysmal states and altered states of consciousness, affective psychoses, hallucinatory-delusional psychoses, paranoid states and paranoid psychoses, traumatic dementia, traumatic parkinsonism). The classical psychiatric concepts applied in domestic psychiatry are continually updated and refined. According to ICD-10, mental disorders caused by craniocerebral injury are categorized under F0 "Organic, including symptomatic, mental disorders."

From DSM-IV:

293.0 Delirium due to...

294.0 Amnestic disorder due to...

294.1 Dementia due to head trauma.

The Use of the DSM-IV classification allows coding on Axis III for a general medical or neurological condition.

A distinction is made between acute and chronic mental disorders arising as a direct consequence of trauma or in the post-traumatic remote period.

Acute mental disorders occurring directly As a result of brain injuries include:

✵ transient disturbances of consciousness;

✵ transient cognitive impairments;

✵ affective and autonomic disturbances;

✵ acute traumatic psychoses;

✵ acute psychogenic reactions following CCI.

Chronic mental disorders include:

✵ mild cognitive impairment;

✵ organic emotionally labile (asthenic) disorder;

✵ organic anxiety disorder;

✵ organic affective disorder;

✵ organic delusional disorder;

✵ organic hallucinatory disorder;

✵ prolonged post-traumatic cognitive impairment;

✵ organic amnesic syndrome;

✵ delirium;

✵ dementia;

✵ organic personality disorder;

✵ post-concussion syndrome;

✵ traumatic Epilepsy;

✵ focal neuropsychiatric disorders.

Clinical Picture

Typically, psychopathological complications caused by TBI have a regredient course. Depending on the severity, various consciousness disturbances are observed. In mild TBI, consciousness is impaired in the form of obtundation. Patients are lethargic, sluggish, and drowsy. They give monosyllabic Answers TO QUESTIONS. General cerebral symptoms appear: headache, dizziness, nausea, and vomiting. In more severe injuries, consciousness disorders are deeper—soporous or comatose states. During recovery from such a state, several stages described by Penfield are observed: I — restoration of pulse and Respiration after a brief cessation; the patient does not move and does not respond to stimuli; II — reaction to stimuli with protective movements; restoration of the pupillary reflex; III — more complex verbal reactions, notably in the absence of orientation. Euphoria or irritability is common during the transitional period. Typical symptoms include severe weakness, adynamia, headache, and dizziness. As general cerebral symptoms recede, focal symptoms are often distinguished: paralysis, paresis, sensory organ impairment, cranial nerve disorders, etc. The period during which the patient was unconscious is erased from memory. Following recovery of consciousness, mnestic impairments are observed. Post-traumatic (anterograde) amnesia is a predictor of the severity of post-traumatic cognitive disorders. Sometimes retrograde amnesia occurs, covering the time span prior to the injury. Retrograde amnesia may undergo reverse development. Clinically, this manifests as fragmentary memories. In A number of cases, transient or persistent Korsakoff's syndrome is observed.

In the acute period of cerebrotraumatic disorders, transient focal manifestations with agnosic, aphasic, and apraxic symptoms may develop. Their pathogenesis involves mechanisms such as local edema and circulatory disturbances.

Acute cerebrotraumatic psychoses are a type of symptomatic (exogenous) reactions described by Bonhoeffer. These include delirium, epileptic excitement, twilight state, amnesia, hallucinosis, manic-expansive, and paranoid psychoses.

Acute traumatic psychoses differ psychopathologically from chronic ones. According to K. Schneider, in chronic organic psychoses, cognitive impairment is predominant, whereas the core symptom of acute psychoses is impaired consciousness.

In some cases of acute traumatic psychosis, consciousness impairment is less distinct. Reversible Changes in the intellectual and personal spheres ("transitional syndromes") come to the forefront.

The duration of acute traumatic psychosis does not exceed 6 weeks. It develops after the initial period of unconsciousness ends. The Organism's response to mechanical damage, decreased brain oxygen saturation, and Circulatory Disorders are significant for pathogenesis. Vegetative-endocrine, vascular, and cerebral-metabolic manifestations reinforce one another. At the same time, diffuse brain edema is decisive in the course of traumatic illness. Since such patients are usually treated by surgeons rather than psychiatrists, the initial psychopathological symptomatology—such as mild euphoria, importunacy, anxiety, depression, or mania—is regarded by physicians as "psychologically motivated" manifestations. It is not even mentioned in the medical history.

The patient's age also plays a role in the pathoplastics of acute traumatic psychoses. The younger the person, the more frequent the psychomotor and epileptiform disorders. In mature age, affective, anxious, hypochondriacal, hallucinatory, and delusional disorders predominate.

Psychopathological phenomenology in TBI depends on the lesion focus (characteristic of open injuries). According to modern concepts, the left hemisphere of the cerebrum is responsible for formal-logical Functions, whereas the right provides sensory-perceptual imagery of the world. Signs of right hemisphere damage include right-sided hemiplegia, speech impairment, disinhibition, or depressed mood. Left hemisphere damage is clinically characterized by left-sided hemiplegia, impairment of orientation in space and time, body schema, constructive praxis, and visuospatial thinking. When the frontal lobe is injured, apato-abulic disorders, pseudoparalytic syndrome, isolated agraphia, and frontal apraxia are observed. Temporal lobe lesion symptomatology may be represented by sensory aphasia, auditory agnosia, acalculia, auditory hallucinations, and psychosensory disorders. Parietal lobe damage is characterized by apraxia, alexia, and agnosia of cutaneous and deep sensation, and occasionally an ecstatic state with a feeling of "the end of the world." Occipital lobe lesion symptomatology consists of visual agnosia, visualization of mental images, and visual hallucinations. It is not specific to traumatic illness and is characteristic of organic brain pathology as a whole.

Apathy or euphoria with futile activity, isolated impoverished fantasies, and confabulations are the most frequent symptoms during the acute period of traumatic illness. Confabulations are usually revealed when questioning the patient about the circumstances of the injury, especially in cases where objective information is lacking. The undulating state of consciousness and the regredient course of traumatic illness may arouse suspicion of malingering, particularly in legal proceedings. Euphoric mood, lack of insight, and carelessness in such patients often veil the clinical picture and lead to an underestimation of the patient's severity. Confabulatory experiences can serve as the plot for developing delusional ideas. Most commonly, these are expansive, depressive, or hypochondriacal delusions. Unlike endogenous Affective Disorders, in expansion, the illness has a monotonous course. The main symptom is asthenia.

With an unfavorable dynamic of traumatic illness, most commonly in patients with a history of alcohol abuse, delirium or clouded consciousness develops.

In traumatic delirium, productive psychopathological experiences are incomplete and fragmentary. The affect of anxiety or fear predominates. Lucid intervals may occur.

Twilight clouding of consciousness indicates paroxysmal tendencies in the course of the disease. The clinical picture of these disorders consists of transient, brief disturbances of consciousness with a sudden onset, accompanied by affects of fear, anguish, rage, and disorientation with vivid hallucinations or delusions. Patient behavior can be brutal, aggressive, and unpredictable. After the attack subsides, Sleep ensues with amnesia of everything that occurred. Twilight consciousness disorder has significant forensic-psychiatric importance, as such patients become dangerous to themselves and others, committing severe socially dangerous acts with typical criminalistic features. Special cruelty, suddenness, and motivelessness of the committed act are characteristic. The damage done does not correspond to the individual's personality, and upon emerging from the pathological state, the patient does not attempt to conceal the traces of the crime.

Delusional and hallucinatory disorders in the acute period of traumatic illness are the most difficult for nosological classification. Y. Elsaesser (cited by H. Gruhle et al.) divided post-traumatic psychoses into three groups: 1) overtly "exogenous psychoses" with a schizophrenic coloring; 2) typical endogenous psychoses indistinguishable from Schizophrenia; 3) all psychotic states having partly organic and partly endogenous manifestations.

It should be emphasized that schizophreniform oneiric states with daydreams can have a purely traumatic origin, especially with damage to the parietal lobe of the brain. These states resemble epileptic aura and are distinguished by their short duration.

Differential diagnostic criteria for distinguishing schizophreniform and epileptiform traumatic psychoses can include clinical manifestations (paroxysmality, saturation, polarity of experiences, and EEG changes typical of epileptiform psychoses).

Hallucinosis (both visual and auditory) may also manifest as a symptom of traumatic brain disease. Its pathogenesis is closely linked to localized cerebral impairments.

Affective traumatic psychoses typically present as periodic depressions and manias. Depression arises against a backdrop of asthenia accompanied by explosive, dysphoric, or hypochondriacal features. In manic states—which are observed more frequently than depression—patients tend to be callous, irritable, and prone to litigious behavior. The onset of affective traumatic psychoses is usually preceded by some exogenous noxious factor that exacerbates psycho-organic symptoms.

In addition to mechanical factors, psychogenic factors accompanying traumatic brain injury (TBI) are of great significance. Psychic asthenia, one of the leading symptoms in traumatic illness, serves as a "breeding ground" that facilitates The Development of Psychogenic Disorders. The clinical Diagnosis of psychogenic disorders in cases of trauma is based on the dissociation between the severity of physical injury and the manifestation of psychiatric disturbances. According to I. A. Kudryavtsev's classification (1988), acute psychogenic disorders comorbid with TBI include: 1) hysterical reactive psychoses (hysterical depression, pseudodementia, puerile syndromes, hysterical stupor, delusional fantasies, hysterical hallucinosis); 2) endoform reactive psychoses (paranoid reactive state, hallucinatory-paranoid reactive state, hallucinatory-paranoid stuporous reactive state, depressive-asthenic reactive state, depressive-stuporous reactive state, and depression).

The development of a specific form of reactive psychosis depends on the severity of the traumatic pathology. For instance, more pronounced organic cognitive disorders tend to lead to pseudodemented disturbances in patients, whereas milder traumatic injuries give rise to depressive disorders.

Residual Sequelae of TBI

Following the resolution of the acute stage of traumatic illness, psychiatric disorders tend to subside, albeit without a full recovery of mental health. The Nature and manifestations of residual (chronic) psychological impairments depend on the severity and localization of the brain injury, the patient's pre-morbid mental health status, social environment, and adaptive capacity.

Functional brain weakness (asthenia) is the hallmark feature of long-term TBI sequelae. ICD-10 uses the term "post-concussional syndrome," whereas the older designation for this disorder is "traumatic encephalopathy." The clinical description of traumatic encephalopathy distinguishes between vegetative and psychopathological components. The vegetative component includes symptoms such as vascular lability, fluctuations in overall metabolism, hypersensitivity to weather changes, sleep disturbances, hyperhidrosis, positional headaches, dizziness, and poor tolerance to psychoactive substances. Psychopathological disorders encompass mental exhaustion, impaired concentration, anxiety, affective instability with a propensity for irritability, and disturbances of drives.

Functional brain weakness may be compensated for with timely Treatment or can follow a progressive course driven by the accumulation of pathogenic factors of exogenous-organic or psychogenic origin.

Sex differences should also be taken into account. In women, vegetative-vasomotor and affective lability are more pronounced, and they frequently require prolonged treatment even following mild concussions. The lability and sensitivity observed in patients who have suffered a TBI are associated with damage to the regulatory centers of the Diencephalon.

Stertz described the psychopathological syndrome of diencephalic damage: a loss of psychic energy and depression accompanied by a subjective sense of "fading mental faculties." In the clinical management of long-term TBI sequelae, depressive disorders must be differentiated from axial asthenic syndromes, which do not require antidepressant therapy. The feelings of guilt characteristic of depression can sometimes lead to suicide.

According to ICD-10, post-traumatic depression falls under the category of "Organic affective disorder" (F06.3). If symptoms of anxiety predominate in the clinical picture, the condition is classified under "Organic anxiety disorder" (F06.4).

TBI can also trigger the development of "organic hallucinosis" (F06.0) and "organic delusional [schizophrenia-like] disorder" (F06.2).

The most Typical symptoms of organic hallucinosis are auditory and visual hallucinations occurring against a Background of clear consciousness, with only minimal cognitive impairment.

Organic delusional disorder is most frequently observed in lesions of the parietal and temporal lobes of the right cerebral hemisphere. Delusional ideas can range from rudimentary to fully elaborated and systematized, with ideas of persecution being the most common. When delusions develop, consciousness remains intact and significant cognitive deficits are absent. Unlike schizophrenia, organic delusional disorder preserves affective appropriateness, and formal Thought Disorders are not detected.

Post-Traumatic Personality and Behavioral Changes (F07)

Post-traumatic personality and behavioral changes are diverse. In domestic literature, these disorders have been described as "psychopath-like syndrome." They most commonly occur following damage to the frontal and temporal lobes of the brain. Characteristic features include the exacerbation of pre-morbid personality traits or The Emergence of entirely new qualities. Von Bayer distinguishes between hyper- and hypotypic post-traumatic personality disorders. In the former case, There is a "unmasking" of the individual's negative traits, whereas in the latter, characteristic personality attributes disappear, manifesting as devaluation and leveling. Personality disorders frequently lead to the degradation and antisocial behavior of the TBI survivor.

Behavioral disorders in the remote period of TBI present a serious challenge. If the TBI occurred during childhood or adolescence, alterations in gender-role behavior may ensue. Egoism, capiousness, intolerance, cognitive deficits, and a tendency toward dysphoria can foster aggressive behavior in society. Post-traumatic mental rigidity prevents patients from adopting adaptive behavioral patterns. Such individuals are often callous and uncompromising in the pursuit of their instinctive needs, which frequently leads to cruel and aberrant sexual behaviors.

Lesions of the frontal lobes result in distinct psychiatric disorders, notably "a loss of spontaneous activity while retained capacity for action via external initiation" (Beringer). According to Kleist's observations, patients with frontal lobe damage experience a specific weakening of pragmatic thought. Semantic processes become "simplified," leaving patients incapable of predicting the consequences of their actions or fully appreciating the urgency of a problem.

The diagnosis of "organic personality disorder" (F07.0) must meet the following ICD-10 criteria (at least 3 features must persist for 6 months or longer):

1) a consistently reduced ability to sustain goal-directed activity, particularly activities that are prolonged and not immediately rewarding;

2) the presence of at least one affective symptom (emotional lability; euphoria with a tendency toward "shallow," situationally inappropriate jokes; irritability and/or outbursts of anger and aggression; apathy);

3) poor control over emotional expression or drives, accompanied by a failure to anticipate the consequences of such behavior;

4) habitual cognitive disturbances manifested as excessive mistrust and paranoid suspiciousness, or an over-preoccupation with a single theme (e.g., religion) or a rigid division of others' behavior into "correct" and "incorrect";

5) marked alterations in speech output characterized by circumstantiality, vagueness of concepts, viscosity, or a tendency toward hypergraphia;

6) altered Sexual Behavior (reduced or increased drive, or A change in sexual preference).

Traumatic dementia (F02) develops following severe TBI. Alongside intellectual and mnemonic impairments, traumatic dementia presents with neurological and autonomic changes characteristic of traumatic disease, as well as distinct psychopathological features: lethargy, apathy, emotional lability, and euphoria punctuated by irritability. The course of traumatic dementia may be stationary, regressive, or progressive. Compensatory capacity depends on the patient's age, administered treatment, comorbid conditions, exposure to harmful factors, and the psychosocial environment. The clinical course of traumatic disease may also be complicated by paroxysmal states. Paroxysmal disorders are diverse and may include polymorphic seizure states and altered states of consciousness. Patients experiencing twilight states of consciousness pose a particular danger to society; these episodes are accompanied by aggressive, sudden, and inappropriate (unmotivated) actions.

Clinical Features and Pathogenesis of Blast Injuries

Blast-induced brain injuries account for 86.8% of all combat-related Nervous system trauma. This is a complex, specific type of Polytrauma characterized by the simultaneous impact of multiple factors on the victim's body. I. A. Yerokhin and co-authors (1987) identify the following factors:

✵ massive receptor stimulation;

✵ massive Blood loss and tissue Hemorrhage;

✵ pronounced Metabolic Disorders;

✵ early secondary toxemia;

✵ secondary immunodeficiency;

✵ mutual aggravation syndrome.

Direct brain injury, cerebral dyscirculation, and vital function impairments drive the development of cerebral Hypoxia. An elevation of cytoplasmic, mitochondrial, and membrane enzyme levels in the cerebrospinal fluid serves as a marker of structural and metabolic Central Nervous System damage. Extracranial injuries that alter the ionic COMPOSITION OF THE blood influence the clinical manifestation and dynamics of the traumatic disease. The resulting hypo-osmolality exacerbates consciousness disturbances, Muscle rigidity, seizure states, supranuclear ophthalmoplegia, and Brain Edema and Swelling. The leading neurological syndromes clinically associated with blast injuries include cortico-focal, hypertensive-hydrocephalic, extrapyramidal, epileptiform, psycho-organic, and asthenic syndromes. In the remote period of blast injury, persistent organic personality changes are formed. Affective disorders are more pronounced in blast injuries, with apathy and dysphoria being nearly constant phenomena, and dysphoria occasionally alternating with euphoria. Mood swings may be associated with states of motor agitation, restlessness, or adynamia. Signs of organic psychosyndrome (impaired memory, attention, and thinking) are constant. The most frequent forms of psychoses include stupor, delirium, and twilight states of consciousness. As evidenced by experience in providing care to the wounded and injured in local wars, surdomutism in the wounded tends to be severe and atypical in character.

Diagnosis

Traumatic psychoses must be differentiated from psychoses of other etiologies that coincide temporally with the trauma, such as fat embolism or hemorrhage. In cases of subdural and epidural hematomas, the diagnosis can be established based on unilateral neurological changes or instrumental diagnostic findings.

The precursor to acute traumatic psychoses resulting from fat embolism is a fracture of long tubular bones. To verify the diagnosis, five pathognomonic signs of cerebral fat embolism should be considered: 1) fundoscopic changes; 2) cutaneous petechiae; 3) fat content in the cerebrospinal fluid; 4) bronchopneumonic changes in the Lungs; and 5) decreased Hemoglobin levels. Psychopathological features include a prolonged period of impaired consciousness, a minimal number of subjective Complaints after regaining consciousness, localized and vivid symptomatology, and a clinical course characterized by abrupt, stepwise deteriorations.

Establishing a nosological diagnosis in the remote post-TBI period can be challenging, primarily due to discrepancies between objective (neurological) signs and psychiatric disorders. Clinical examination should be supplemented with instrumental Methods, such as EEG, REG, EchoEG, CT, MRI, and others.

According to the DSM-IV classification, the following diagnostic criteria are proposed for traumatic disease:

1) a wide spectrum of acute and chronic clinical manifestations;

2) the duration of the disorientation period can be considered a prognostic factor determining the outcome of the disease;

3) classic contrecoup brain lesions and acute edema are observed;

4) acute manifestations (amnesia, agitation, autism, and other psychiatric disturbances, i.e., acute post-traumatic psychosis, delirium);

5) chronic manifestations (amnesia, mood disorders, personality changes, and occasionally dementia);

6) Factors influencing the disease course, including premorbid personality traits, epilepsy (decreased working capacity), litigation, emotional stress resulting from the trauma, psychological reaction to cognitive decline, and the localization and severity of brain damage;

7) regardless of the severity of brain injury, the patient's adaptive capacity can influence the disease course (Kaplan, Sadock, 1998).

Treatment

A targeted therapeutic strategy must be developed for the injured patient, as timely treatment can prevent many of the negative consequences of TBI. The formulation of a treatment plan should take into account the following factors:

1) the neurological aspect (severity and localization of the injury);

2) mental state during the acute period (consciousness disturbances and amnesia);

3) comorbidity (somatic condition, substance abuse, mental illness, personality traits);

4) microsocial conditions.

During the acute period, rest and bed rest are recommended for 3 weeks. It is important to assess the mental status even if the patient has no complaints. Medical treatment involves prescribing decongestants and vascular agents. Nootropics should be used to restore brain functions, and anticonvulsants to prevent paroxysmal disorders. The drugs of choice are tranquilizers (seduxen, rudotel, etc.) with a vegetative-stabilizing effect. The administration of neuroleptics is also promising. Hyperbaric Oxygenation yields good results in TBI.

To arrest psychomotor agitation during the acute period of TBI, GABA preparations are recommended. Neuroleptics should be prescribed with caution due to the potential for a paradoxical effect.

For Mental disorders in the remote period of TBI, the choice of medication is determined by the psychopathological syndrome. However, preference should be given to drugs with minimal side effects, combined with vascular, vegetative-stabilizing, and nootropic agents.

In the remote period of TBI, patients should be monitored on an outpatient basis.

Repeated courses of therapy should be administered.

To prevent mental disorders in the remote period of TBI, it is recommended to organize the patients' daily routine. They should avoid stress and refrain from straining their adaptive mechanisms.

Prognosis

The prognosis in TBI depends on its severity, timeliness of treatment, patient living conditions, and The impact of additional pathogenic factors. A favorable prognosis is possible if general cerebral manifestations are resolved in the acute period, in the absence of pronounced cognitive, concomitant somatic, and neurological disorders, provided the individual has positive social attitudes. Prognostically unfavorable signs include advanced age, comorbid somatic and neurological diseases, substance abuse, personality disorders, and antisocial behavior.

Expert Evaluation

Medical and social expertise. Patients with progressive paroxysmal disorders, hallucinatory and delusional psychoses, progressive personality changes, and traumatic dementia are recognized as unfit for work. Patients with persistent asthenic disorders and curable paroxysmal conditions have limited capacity for work.

Military-psychiatric expertise. The consequences of TBI are assessed in accordance with Article 14 of the "Regulation on Military Medical Expertise and Medical Examinations in the Armed Forces of Ukraine".

Subsection "a" includes sharply pronounced, prolonged mental disorders, as well as mental impairments characterized by distinct intellectual-mnestic or personality changes. These disorders correspond to the following ICD-10 clinical descriptions: dementia, organic amnestic syndrome, organic hallucinosis, catatonic disorder of organic origin, organic delusional disorder, and pronounced organic personality disorder. Patients with such manifestations are declared unfit for military service.

Subsection "b" of Article 14 includes: moderately pronounced psychotic states with a favorable course; mental disorders manifested by emotional-volitional, endocrine, and autonomic disorders; persistent asthenic state; neurosis-like and psychopathy-like disorders. Subsection "b" should include ICD-10 diagnostic categories such as delirium, organic (affective) mood disorders, anxiety disorders of organic origin, organic dissociative disorder, organic emotionally labile (asthenic) disorder, organic personality disorder, and post-concussion syndrome with persistent symptoms. Expert Conclusions under subsection "b" depend on the patient's military category and may vary.

Subsection "c" designates transient, mild, and short-term psychotic and non-psychotic disorders that ended in recovery or mildly pronounced asthenia. Subsection "c" of Article 14 specifies the following ICD-10 disorder categories: short-term delirious episodes, mild organic (affective) mood disorders, mildly pronounced asthenic disorders, mild cognitive disorder, reversible post-encephalitic syndrome, and mild post-concussion syndrome. Patients in this category are deemed fit for military service with restrictions.

Subsection "d" indicates fully compensated conditions in which patients are recognized as fit for military service.

Forensic psychiatric expertise. Individuals who have suffered TBI frequently break the law and undergo forensic psychiatric evaluation. Those who committed an offense in a psychotic state, a state of altered consciousness, or with dementia are declared not guilty by reason of insanity (insane). Individuals recognized as insane are subject to compulsory treatment. In civil proceedings, individuals with traumatic dementia are declared legally incompetent.

CONTROL QUESTIONS

1. Classification of TBI, dynamics of traumatic injuries.

2. Etiology, pathogenesis, and prevalence of mental disorders in TBI.

3. Mental disorders in the initial and acute periods.

4. Mental disorders in the periods of convalescence and remote recovery.

5. Traumatic cerebropatia (cerebrasthenia).

6. Traumatic encephalopathy.

7. Traumatic dementia.

8. Treatment, rehabilitation, and prognosis of cerebrotraumatic disease.

9. Expert evaluation of TBI sequelae.