Psychiatry - H.T. Sonnyk 2003

Mental disorders associated with traumatic brain injury

Traumatic brain injury is merely the beginning of a complex disease in terms of its clinical manifestations, progression, and outcome. Its characteristic neurological disorders are studied by neurologists, while psychiatric complications are investigated by psychiatrists.

This pathology has always been at the focus of attention for surgeons, neurologists, and psychiatrists, as it continues to hold a significant place in peacetime trauma statistics. On average, it accounts for 36-40% of all trauma cases. In peacetime, traffic accidents are the most frequent cause of TRAUMATIC BRAIN INJURIES (accounting for about half of all cases), followed by domestic accidents, and least frequently, occupational injuries.

Injuries resulting from TBI represent a severe category of trauma, yielding a considerable mortality rate (10-12%) and leaving behind a range of consequences, among which psychiatric disorders occupy a prominent place, ultimately leading to disability (19%) or a decrease in working capacity (47%).

Historical Background.

METABOLISM/2.html">THE CONCEPT OF cerebral concussion (commotio) was introduced into medicine by the French scientist Littre in 1705. Subsequently, in 1773, another French researcher, Petit, divided traumatic brain injuries into concussions, compressions, and contusions. A major contribution to The Study of traumatology, including brain injuries, was made by N.I. Pirogov, who introduced the distinction between open and closed TBIs and paid considerable attention to the study of blast injuries when characterizing the latter.

ETIOPATHOGENESIS.

The initiating factor of all pathophysiological processes developing in traumatic brain injury is, undoubtedly, the mechanical force. General brain shaking and The impact of the Brainstem and base against the cranial bones cause disturbances in hemodynamics and CEREBROSPINAL FLUID dynamics. The force of the mechanical Shock sets the cerebrospinal fluid in motion, driving it from the Lateral ventricles into the third and fourth ventricles, thereby irritating the centers located in their walls.

Hypertension develops within the cerebral ventricles and the subarachnoid space (although hypotension is possible in 20% of cases), accompanied by severe disturbances originating from the regulatory centers of the Hypothalamus.

The Pathogenesis of disorders (including psychoses) occurring in the initial and acute periods of traumatic brain injury is primarily associated with non-inflammatory diffuse or local cerebral edema. The factors driving edema are diverse, the principal one being an increase in the permeability of cerebral capillaries. Following an initial reflex spasm of cerebral arterioles and capillaries, their subsequent dilation occurs, leading to slowed Blood flow and the leakage of plasma beyond the vascular bed. Progressing throughout the first week post-injury, the edema is complicated by phenomena of cerebral Hypoxia and acidosis.

In concussion, all of this is supplemented by petechial hemorrhages, whereas in contusion, it involves the direct destruction of brain tissue and more massive hemorrhages, which can be delayed in onset and prone to recurrence. In the remote aftermath, the Organization of previously necrotic areas is possible, resulting in The formation of cysts or scars that, by irritating adjacent regions of brain tissue, may provoke seizure activity and other paroxysms.

In light of the Pavlovian school of research, when the brain is injured, the initial diffuse reaction of the Central Nervous system in mild cases manifests as supraliminal protective inhibition of the cortical Cells (nubilation), which in severe lesions also encompasses subcortical structures with the temporary shutdown of complex unconditioned Reflexes (sopor, coma).

The Nature and frequency of traumatic psychiatric disorders depend not only on the severity of the injury itself, but also on its specific features, the circumstances under which it was sustained, and the premorbid functional state of the patient's central nervous system.

Classification.

Traumatic brain injuries are classified into closed and open.

In closed injuries, the integrity of the soft Tissues is unbroken, and the intracranial cavity remains entirely sealed.

Open injuries (wounds) of the Skull are categorized as non-penetrating and penetrating. In the former, only the integrity of the soft tissues and cranial bones is compromised, whereas the latter are accompanied by damage to the dura mater and, in some cases, the brain tissue itself.

The current classification of closed brain injuries is based on differences in The Nature of the traumatic lesion and pathogenetic mechanisms. Accordingly, the following types are distinguished:

Concussions - brain injuries characterized by diffuse, generally functional Disorders of the brainstem and base resulting from impact against the bony skull. Concussions are invariably accompanied by a loss of consciousness (knockout, knockdown).

Contusions - bruising of the brain with predominantly local organic lesions of the convexity cortex.

Compressions - compression of the brain.

Blast injuries - injuries caused by the action of a blast wave.

Birth trauma is also classified as a distinct category.

The clinical course of traumatic psychiatric disorders conventionally comprises three periods:

1. Initial period.

2. Acute period.

3. Period of delayed consequences.

Mental disorders in cerebral trauma.

I. Immediate manifestations of trauma: torpor, coma.

II. Acute traumatic mental disorders.

1. Non-psychotic forms:

a) asthenoneurotic syndrome:

✵ astheno-abulic,

✵ asthenodepressive,

✵ asthenohypochondriac.

b) surdomutism;

c) epileptiform (convulsive) syndrome.

2. Acute traumatic psychoses:

a) traumatic delirium;

b) twilight state of consciousness;

c) Korsakoff's (amnestic) syndrome;

III. Persistent traumatic disorders:

1. Traumatic asthenia (cererasthenia);

2. Post-traumatic psychopath-like personality development.

3. Traumatic encephalopathy;

4. Traumatic Epilepsy;

5. Traumatic parkinsonism;

6. Traumatic dementia;

IV. Late traumatic psychoses:

1. Twilight states of consciousness, delirious syndrome;

2. Depressive and manic syndromes;

3. Hallucinatory-paranoid (schizophreniform) syndrome.

CLINICAL PICTURE.

The characteristics of neuropsychiatric disorders following HEAD trauma depend on the Nature of the lesion, the intensity and localization of the injury, the time factor, and potential complications.

Due to the multitude of Factors Determining the Clinical presentation of head injuries, their symptomatology is extremely diverse, encompassing mental, motor, sensory, autonomic-vascular, and vestibular symptoms and syndromes, focal signs of injury, as well as general cerebral reactions.

Somato-neurological disorders in traumatic brain injury:

a) general cerebral symptoms — headache, nausea, vomiting, dizziness;

b) elevated intracranial pressure — optic disc congestion (papilledema), enhanced digital markings on skull radiographs, pain upon eye movement to the side or pressure on the eyeballs, cerebrospinal fluid changes (hyper- and hypotension, alterations in protein content and formed elements);

c) vestibular disorders — dizziness and nausea triggered by flickering objects before the eyes, reading, and Gurevich's oculostatic phenomenon (instability in the Romberg position during ocular convergence);

d) autonomic innervation disorders — diffuse dermographism, hyperhidrosis under psychological stress, lability of vascular reactions and pulse;

e) neurological symptoms indicating an organic lesion of the central nervous system.

Mental disorders arising after a traumatic brain injury

can be categorized according to three periods of the disease course.

In the initial and acute periods, neurological and mental disorders are quite diverse.

Despite A number of shared features between closed and open traumatic brain injuries, their clinical manifestations in the initial and acute periods must be considered separately. However, in the remote consequences period (the third period), differences attributable to The Mechanism of injury are smoothed out to such an extent that personality changes and mental disorders in patients who have suffered a traumatic brain injury should be differentiated no longer by the mechanism of onset, but According to the severity of the lesion.

I. Initial period of traumatic brain injury.

It occurs immediately after the injury and in 94-95% of cases is accompanied by an instant clouding of consciousness, the intensity of which can range from mild and brief nubes/obnubilation to deep coma.

Predominantly in patients with severe closed head and brain trauma, a severe degree of impaired consciousness (stupor/obtundation) is observed, arising either immediately or as a transitional stage from sopor or coma During the first 24 hours.

Deep loss of consciousness, protracted transition to clear consciousness with varying degrees of obtundation and prolonged persistence of its mild forms, as well as The Emergence of periodic agitation states against this background, usually indicate the severity of the trauma.

Obtundation of consciousness.

The state of mild obtundation generally lasts for 4–5 days. Thereafter, patients regain orientation in time and space. They not only answer questions posed to them but also begin to take an interest in their own condition. Facial expression ceases to be mask-like, though some hypomimia persists. The swallowing act is fully restored, appetite improves, and Sleep does not exceed 9–10 hours per day. Such patients emerge from obtundation as early as the second day of hospitalization, consider themselves healthy, and insist on discharge.

In moderate obtundation, patients are disoriented in time and space, behave apathetically, exhibit a mask-like facial expression, have impaired swallowing, and sleep from 12 to 24 hours per day. At the same time, they are capable of following simple instructions and giving monosyllabic Answers to elementary questions. These patients are characterized by a diminished reaction to external stimuli (sound, light). The recovery of effective motor Functions proceeds gradually in them. In an uncomplicated course, a noticeable improvement occurs after 4–5 days, and moderate obtundation transitions into mild.

Severe obtundation lasts for 5–8 days, and sometimes longer. During the first 4–5 days after the injury, the clinical picture shows no tendency toward improvement, and the patients' condition remains largely stable. Such patients are difficult to contact, hardly react to external stimuli, do not answer questions addressed to them, but upon persistent demand—for example, "raise your hand!", "open your Mouth!"—they are able to perform elementary actions. The swallowing act is preserved but slowed down, and sleep lasts at least 18–20 hours per day. Patients are mostly inactive, apathetic, with poor facial expression, but psychomotor agitation is observed in many cases. This state manifests as an urge to continuously change position in bed, performing numerous unnecessary and meaningless movements, actively resisting attempts to put them to bed, while constantly murmuring incomprehensible words and phrases.

Comatose and soporose states.

In sopor, consciousness is completely switched off, yet the patient is capable of swallowing with difficulty and responds to painful stimuli while remaining unresponsive to words. When the angle of the lower jaw is advanced forward, an expression of dissatisfaction appears on the patient's face.

In a state of coma, the casualty lies motionless, the facial complexion is pale or cyanotic, muscular hypotonia is observed, and there is no reaction to any stimuli. Severe autonomic disorders are pronounced: the pulse is weakened and slowed, pupils are dilated and unresponsive to light, and breathing is shallow. In some cases of coma, breathing becomes frequent (35 or more per minute), rattling, and non-rhythmic. The disappearance of the swallowing reflex, even with a satisfactory pulse, is a symptom of a poor prognosis and requires the urgent application of active and consistent measures, such as lumbar puncture, decompressive craniectomy, etc.

Patients cannot remain in a comatose state for more than a day: either they succumb, or this condition transitions into a severe clouded state of consciousness lasting 5-6 days or longer. In 5% of cases, patients with severe, life-threatening injuries who were in a coma do not survive.

II. The acute period of traumatic brain injury.

Against the background of returning consciousness, various neuropsychiatric disorders appear in terms of symptoms and severity, including asthenia, focal symptoms of organic damage, paroxysmal states, and transient psychoses.

Non-psychotic forms.

Post-traumatic asthenia—an astheno-neurotic (astheno-abulic, astheno-depressive, astheno-hypochondriac) syndrome is an essential manifestation of the acute period. It features a distinct, and in severe cases pronounced, adynamic component. In milder courses, the general condition is characterized by irritability, dissatisfaction, outbursts of anger combined with increased fatigability, lability of mood (crying spells), and various somatic Complaints. Characteristically, the more severe the asthenia, the fewer complaints are expressed.

The Structure of such asthenia also includes transient intellectual decline, memory impairment, and high fatigability of active attention. Hyperesthesia is a rather constant disorder, accompanied in some cases by hyperpathia. Falling asleep in such patients is impaired and may be accompanied by surges of vivid imagery and memories. Sleep is shallow, often with nightmares.

Concussions are characterized by vestibular disorders, especially spontaneous dizziness upon changing body position, which may be accompanied by nausea and vomiting. Vasomotor and vegetative disorders are equally constant, including pulse lability with a predominance of bradycardia, blood pressure fluctuations, sweating and acrocyanosis, thermoregulation disorders with a feeling of chilliness, dermographism, and facial hyperemia that intensifies with minor physical exertion. Hypersalivation or, conversely, dryness in the mouth is frequently observed.

In a number of cases, craniocerebral injuries are accompanied by asthenic-type memory disorders. Patients forget the content of a conversation with the physician, memory capacity is reduced, and the recall of current events, including subjectively important ones, is incomplete. Sometimes they cannot recall which events of the current day preceded one another. Complaints arise regarding difficulty concentrating, lethargy, headaches, and irritability. At the same

Often, low mood and melancholy in post-traumatic asthenia reach such a degree of severity that one can speak of an astheno-depressive syndrome, which at a certain stage is frequently encountered in the clinic of traumatic encephalopathy. In patients with traumatic brain injuries, the course of the disease may worsen under The Influence of life difficulties, and depressive disorders accompanied by suicidal tendencies may arise.

Traumatic surdomutism, or deaf-mutism, is predominantly observed after blast injuries resulting from the detonations of aerial bombs, artillery shells, and landmines. In this case, the powerful influx of impulses acting on The Nervous System under such intense acoustic stimulation leads to hearing impairment and the suppression of other Sense Organs, as well as a general disruption of Higher Nervous Activity.

Along with the loss of hearing and speech, such patients exhibit motor retardation and hypomimia, known as pseudoparkinsonism. At the same time, orientation and understanding of surrounding events are not impaired.

The phenomena of surdomutism disappear gradually. Initially, if the hearing organ itself was not damaged, hearing improves. Speech is restored, as a rule, suddenly, often under the Influence of External factors—waking up from a nightmare, a joyful event, alcohol intoxication, etc. Mutism may be replaced by stuttering or aphonia.

Epileptiform (convulsive) syndrome—among paroxysmal states, various epileptiform seizures predominate in duration (seconds, minutes) and symptomatology, often partial and abortive. In addition to tonic and clonic seizures, the motor component may manifest as polymorphic hyperkinesias (choreiform, athetoid, torsional) or states of transient immobility. The frequency of seizures varies widely; sometimes they occur in series, and status epilepticus may develop.

Psychosensory paroxysms (metamorphopsias, body schema disorders), as well as phenomena close to "déjà vu" or, conversely, " jamais vu", are combined with a depressed-anxious affect. Phenomena resembling prolonged absences may be observed—complete loss of consciousness for 1–2 minutes, accompanied by immobility and amnesia. Short-term states of ecstasy lasting several seconds or minutes, accompanied by a sensation of flying, rapid movement in space, and external detachment from the surroundings, can be attributed either to an aura of consciousness or to special states.

Paroxysmal disorders in the acute period of traumatic brain injury do not indicate a poor prognosis, as they are caused by hypertension-Hydrocephalus syndrome and disappear once liquor-dynamics are restored.

Traumatic psychoses of the acute period.

Traumatic delirium predominantly occurs immediately after the patient emerges from a coma, but sometimes it may appear a few weeks after the restoration of consciousness. The onset is acute, against the background of asthenia, under the influence of provoking factors. The total duration is usually from several hours to several days.

The plots of visual hallucinations become groups or crowds of people, transport, less often large animals. Affects of anxiety and fear, along with fragmentary delusional ideas, dominate. Activity is aimed at defense; attempts to escape or attack are characteristic. Sometimes lucid intervals occur, which can be so prolonged that they give the physician a false impression that the psychosis has resolved. Emergence from the delirious state occurs, as a rule, through critical sleep into severe post-traumatic asthenia. Memories of the morbid period remain fragmentary.

Twilight states of consciousness under the influence of provoking factors can occur quite frequently, predominantly in the evening hours. Manifestation forms:

1) various ambulatory automatisms;

2) psychomotor agitation dominated by:

a) incoherence of thinking, vivid affectively charged hallucinations, fragmentary delusions, and a tendency to brutal aggression; b) pseudodemented-puerile features;

3) drowsiness with immobility approaching stupor.

Twilight states are always accompanied by a pathological narrowing of consciousness and tend to recur throughout the acute period.

Korsakoff's (amnestic) syndrome.

The most prolonged form of acute traumatic psychosis, the duration of which can reach up to three months, and occasionally even longer. It predominantly arises as a consequence of severe injuries accompanied by cranial bone fractures and massive intracranial hemorrhages.

Korsakoff's syndrome appears either immediately after the subsiding of stupor symptoms or a few days later, succeeding delirium or twilight states of altered consciousness.

At its onset, Korsakoff's syndrome may exhibit a tendency toward clinical complication with the emergence of altered consciousness symptoms. This is evidenced by nocturnal states of confusion, particularly delirious ones, numerous vivid scene-like dreams, and, during the day, symptoms of nubilation that are especially conspicuous against the background of an elevated mood.

Such patients retain The ability to understand their interlocutor and maintain verbal contact, yet they remain incapable of retaining current events in memory (names, conversation topics, etc.), which renders them exceptionally passive and bewildered. Amnesia (fixation, retrograde, and, to a lesser extent, anterograde) is combined with confabulations and pseudoreminiscences of varying intensity that fill in the memory gaps. The content of the confabulations largely depends on the dominant affective state—expansive or hypochondriacal. A characteristic feature is The connection between the content of confabulations and the event that necessitated hospitalization. Occasionally, numerous confabulations appear without noticeable memory impairments, which serves as a sign of developing confabulosis.

Pronounced retrograde amnesia invariably serves as a prognostically reliable indicator of persistent impairment. Korsakoff's syndrome, much like other acute psychoses, culminates in the reduction of symptoms leading to profound asthenia, provided it does not transition into the corresponding form of traumatic dementia.

III. The Period of Long-Term Sequelae.

The primary Clinical symptoms of the acute and initial periods typically either completely resolve within 2 to 6 weeks post-injury with a full restoration of health, or merely diminish in intensity and scope. The latter trajectory indicates that the third period transitions into the phase of long-term sequelae and The Development of traumatic disease, the core manifestation of which is psychoorganic syndrome of varying severity.

Long-Term Traumatic Mental Disorders.

Traumatic cerebasthenic syndrome (pseudoneurasthenic state) is the most prevalent mental disorder in the long-term period following a traumatic brain injury (TBI). It is characterized by a triad of pathological disorders: asthenia, dyssomnia, and autonomic dysfunctions.

Asthenia proper, as a consequence of TBI, is a persistent, overarching symptom that merely transforms across various Stages of the disease's progression. While adynamia often predominates in the acute phase, the long-term sequelae are dominated by heightened irritability against a backdrop of fatigue, exhaustion, a certain decline in immediate memory, and impaired attention (stability, concentration, and shifting capacity). These impairments are typically accompanied by lability of affective reactions, which are largely disproportionate to the stimulus. Mood rises disproportionately with minor successes and plummets just as sharply at the slightest adversity. Exhibiting emotional lability and low frustration tolerance, patients frequently resort to shouting and insults. However, such outbursts of irritation rapidly subside, giving way to mental and physical exhaustion. Furthermore, these patients exhibit heightened sensitivity to proprioceptive, interoceptive, and external stimuli alike (noise, bright light, sharp odors, etc.), manifesting as various unpleasant sensations in the Skin, mucous membranes, Muscles, and Internal Organs.

Autonomic disorders may manifest as pulse and blood pressure lability, tachycardia, dizziness, headaches, persistent spontaneous dermographic reactions, general and distal hyperhidrosis. The condition can deteriorate sharply under the influence of weather factors. Vestibular disorders frequently occur, with patients poorly tolerating travel in vehicles. The onset of dyssomnias, predominantly involving sleep-onset difficulties, is characteristic.

Against the background of cerebasthenic disorders, various neurosis-like symptoms, elementary phobias, anxiety, and subdepressive states are occasionally observed. Externally, such asthenia may resemble a neurosis, but its organic nature is evidenced by micro-neurological signs (exaggerated tendon reflexes, tremor) and elevated cerebrospinal fluid pressure.

Post-traumatic psychopathic personality development involves the emergence of large-scale personality changes (psychopathic-like states) several years after the resolution of the acute phase.

It manifests primarily through explosiveness and histrionic traits, occasionally dominated by sensitive or paranoid radicals. Emotional reactions become intensified and poorly differentiated.

Psychopathic-like disorders can be persistent and dominate the clinical picture. Their external manifestations, severity, and correlation with the asthenic background largely depend on the age at the time of injury, its severity, premorbid personality traits, and microsocial conditions. Alcohol abuse can play a critically significant role.

In cases of mild to moderate trauma during adolescence or youth, pre-existing psychopathic character traits may undergo a rapid exacerbation.

The differentiation of such psychopathic-like states from true psychopathies is based primarily on their more complex, essentially polymorphic psychopathological structure. Indeed, they consistently feature coexisting heterogeneous psychopathic radicals that never combine in true psychopathies.

Traumatic encephalopathy is a pathological brain condition resulting from a concussion and characterized by psychopathological and focal neurological symptoms—dependent on the localization and extent of the lesion—along with a general decline in mental activity and impairments in intellectual-mnestic functions.

Autonomic-vascular and vestibular disorders are also observed; however, they are less pronounced and less stable than those seen in traumatic cerebasthenic syndrome.

Thus, traumatic encephalopathy is dominated by cortical lesion syndromes (frontal, parietal, temporal, etc.), leading to the formation of persistent mental impairment that may assume the following clinical forms:

Explosive type: characterized by sharp irritability, explosiveness, loss of self-control, brutality, and aggressiveness. Owing to these traits, patients are in constant conflict with others, display egocentrism, an unbridled drive to satisfy their own desires, and may exhibit litigious tendencies.

Euphoric type: distinguished by an inappropriately elevated baseline mood accompanied by a lack of insight into one's actions, lightheartedness, and uninhibited drives.

Apathetic type: characterized by lethargy, aspontaneity, and sluggishness.

Both traumatic asthenia and traumatic encephalopathy are organic disorders that differ in the depth of brain involvement.

Traumatic epilepsy is a variant of traumatic encephalopathy characterized by epileptiform phenomena, the manifestations of which depend on the localization and Specifics of the injury. Convulsive seizures may also occur in the acute period As a result of the irritative action of, for example, bone fragments. However, the development of traumatic epilepsy is indicated by seizures caused by the consequences of the TBI itself, which emerge many months or even years after the trauma.

Paroxysmal disorders exhibit a characteristic polymorphism, with generalized, Jacksonian, and minor seizures being the most common. Direct involvement of the motor cortex may result in Jacksonian-type seizures while consciousness remains intact. In other instances, paroxysms may begin as Jacksonian seizures and subsequently generalize, accompanied by a loss of consciousness. Unlike genuine epileptic seizures, these episodes are of longer duration and occasionally feature hysterical components. Typically, such cases are clearly linked to a psychotraumatological situation; the seizure is triggered by a burst of anger or sobbing before transitioning into the patient's habitual epileptic paroxysm stereotype.

Persistent symptoms of traumatic epilepsy include autonomic-vasomotor and vestibular disturbances, increased fatigue, and a moderately pronounced overall decline in intellectual-mnestic functions—signs characteristic of any traumatic encephalopathy.

In addition to seizures, patients may experience twilight states, altered states of consciousness, mood fluctuations (dysphoria), and personality changes (irritability, impulsivity); however, these are notably devoid of mental rigidity (viscosity) and psychomotor slowing.

The emergence of twilight states indicates an unfavorable clinical prognosis.

Traumatic parkinsonism is the result of massive brainstem lesions involving the extrapyramidal system. Against a backdrop of prominent brainstem symptoms (vasomotor, autonomic, and vestibular) in the acute stage, patients develop symptoms identical to those of encephalitic parkinsonism: rigidity, amimia, muscular hypertonia, slow and monotonous speech, oculomotor disorders, convergence insufficiency, and occasionally gaze palsy.

Psychological symptoms include lethargy, apathy, lack of initiative, and fatigue. Hypersensitivity to stimuli is occasionally observed. Patients are passively cooperative and abulic, and display a lack of insight into their condition. The clinical course is uniform and non-progressive, with a tendency toward symptom reduction.

Traumatic dementia is an irreversible pathological condition resulting from severe diffuse brain tissue damage. Fundamentally, it represents a form of traumatic encephalopathy characterized by neurological deficits, apathy or euphoria, alongside significant intellectual degradation, loss of insight into one's actions, and profound memory impairment. It is marked by the presence of focal symptoms and a non-progressive course. Paroxysms and twilight states of consciousness are observed occasionally.

IV. Late Traumatic Psychoses.

Late traumatic psychoses manifest between one and fifteen years following the sustained injury. As a rule, they occur under the combined influence of pathogenic factors and pre-existing asthenia resulting from the unfavorable progression of traumatic brain disease. The Initial Stages of the illness are often so vividly colored by psychological trauma, infection, or alcohol abuse that Differential Diagnosis with a corresponding exogenous psychosis becomes quite problematic for the clinician.

Twilight states of consciousness, delirium syndrome.

States of clouded consciousness are predominantly observed in patients with convulsive seizures and present a polymorphic structure. Occasionally, they occur immediately following convulsive episodes, or, less frequently, after minor seizures.

Such "twilight states" begin abruptly, accompanied by motor disturbances—primarily agitation—and an inability to engage in productive verbal communication. These episodes are typically brief (lasting minutes to hours), and resolution is often lytic, followed by complete amnesia.

When occurring independently of a paroxysm—usually precipitated by somatic insults, such as alcohol binges—they are heralded by prodromal symptoms including dyssomnia, cerebral-organic signs (headaches, tinnitus, asthenic manifestations, etc.), and a depressed-anxious mood. Only thereafter does the clouding of consciousness develop, accompanied by diverse productive disorders, primarily delusional, hallucinatory, and affective, and less commonly psychosensory.

The clinical picture of the psychosis incorporates both delirious and oneiroid components, all accompanied by marked vegetative-vascular symptoms. The duration of these states ranges from several hours to 3–5 days. Lucid intervals are characteristic. Resolution is critical, typically following prolonged sleep, and is accompanied by partial amnesia, which is not invariably present.

Depressive and manic syndromes (affective psychoses).

The clinical course is typically characterized by periodic manias, depressions, or a bipolar pattern. The manic form is more prevalent than the depressive, and in its bipolar variant, it invariably follows a more severe course than depression. Female patients predominate.

During initial manic episodes, states of clouded consciousness are frequent; these disappear in subsequent depressive episodes (in a bipolar course), but recur during repeated manic states.

Depressions are accompanied by tearfulness or dysphoria, vasovegetative disorders, and hypochondriasis that fluctuates between overvalued ideas and full-blown delusions. Progression of the condition is indicated by mounting anxiety and agitation or, less commonly, depressive-paranoid disorders.

Seizures last from 1 to 3 months, with varying frequency. Each subsequent paroxysm follows a stereotyped ("cliché") pattern, with a gradual simplification of symptoms.

Manic episodes generally have an acute onset. Within an elevated affective state, cheerfulness, anger, and irritability alternate. In severe cases, moria-like foolishness and puerile-pseudodemented traits emerge. Motor activity is unproductive and fidgety. When the clinical picture of the psychosis is complicated, twilight or amentiform clouding of consciousness develops, accompanied by fragmented delusions, hallucinations, and incoherent motor agitation dominated by stereotyped elementary motor reactions. Verbal agitation is similarly disjointed.

The duration of mild manic episodes is 1–3 months, extending up to half a year when complicated by disturbances of consciousness. Periodic manias generally follow a stereotyped ("cliché") course with gradual progression. Only in a minority of patients, primarily those over 50 years of age, are the attacks complicated by mild delusional confabulations. Organic changes in manic and bipolar psychoses may reach the degree of pronounced dysmnestic dementia.

Hallucinatory-delusional syndrome.

Hallucinatory-delusional psychoses account for approximately 33% of all late traumatic psychoses. As a rule, they manifest after the age of 40 under the influence of triggering factors.

In the remote post-traumatic period, asthenic manifestations with a distinct apathetic component or psychopathy-like states with dysphoria and explosiveness are predominantly observed. Paroxysms, including convulsive seizures, may occur. The onset of hallucinatory-delusional psychosis is preceded by episodes of twilight, delirious, or oneiroid clouding of consciousness featuring intense verbal hallucinations and delusions. Less frequently, initial attacks present as acute sensory delusions combined with verbal hallucinations. During subsequent paroxysms, verbal hallucinosis and hallucinatory delusions dominate the clinical picture.

In the majority of cases, the psychoses follow a paroxysmal course, characterized by a progressive shortening of exacerbations and a smoothing out of the clinical presentation due to the reduction of delusional and affective components, as well as a decrease in the intensity of hallucinosis. Occasionally, paranoid disorders—such as pathological jealousy or litigious tendencies—come to the fore within the structure of reduced paroxysms. Transition to a chronic course is rarely observed; in such instances, the psychosis either "freezes" at the stage of hallucinosis or gradually becomes complicated by the symptoms of a sparse hallucinatory paraphrenia. In these patients, organic changes are most prominent, reaching the level of dementia.

Treatment.

Patients who have suffered a traumatic brain injury (TBI) must be treated in neurological or surgical inpatient units, and in the event of psychiatric disorders, in psychiatric facilities. For mild injuries, strict bed rest is required for at least ten days, whereas for moderate and severe cases, it must be maintained for at least three weeks.

Acute period: immediately following the injury, primary medical efforts are directed at alleviating cerebral edema (the core pathogenetic link in the development of psychiatric disorders). Patients with contusion and concussion should have cold applied to the head. Dehydration therapy is recommended in all cases, administered via IV infusion of 40% glucose (40–60 ml) and subcutaneous injection of 500 ml of isotonic sodium chloride solution. Simultaneously, measures are taken to reduce vascular permeability: 10 ml of 10% calcium chloride solution, and 5% pentamine (1 ml twice daily). To combat intracranial hypertension, repeated lumbar punctures are performed with the slow drainage of up to 40 ml of cerebrospinal fluid, along with the intramuscular injection of 10 ml of 25% magnesium sulfate and 2 ml of 1% Lasix.

To treat seizure activity and psychomotor agitation in the acute period, 0.5% seduxen (3–4 ml IV) is used. To manage psychomotor agitation within clouded states of consciousness (delirious or twilight states), the parenteral administration of 2 ml of 2.5% chlorpromazine (aminazine) and 3 ml of 2% diphenhydramine (dimedrol) is indicated.

To prevent the onset of comatose states and other complications, the intravenous administration of piracetam (70–140 mg/kg of body weight daily) and hyperbaric Oxygen therapy are indicated.

Psychotropic medications are used across all periods based on clinical indications. For dysphoric manifestations, neuleptil is prescribed at 20 mg twice daily. For depressive states, amitriptyline (triptizol) at 50 mg twice daily, thioridazine (tisercin) 50 mg at night, chlordiazepoxide (elenium) at 10 mg twice daily, or seduxen at 10 mg three times daily are recommended. The latter is particularly effective in cases of pronounced vasomotor-autonomic disorders. For twilight states of consciousness and delirium, the intramuscular administration of 2.5% chlorpromazine (2 ml) is advisable.

Once acute symptoms subside, reabsorption therapy is also employed: FIBS (1 ml, 30 ampoules), aloe extract (1 ml, 30 ampoules subcutaneously), hyaluronidase (lidase), vitreous body extract, etc.

In the long-term period, the treatment of asthenic and psychopath-like states is largely similar. First and foremost, this involves lighter working conditions for the first few years following the injury. General strengthening, sedative, and dehydration therapies are recommended: 40% glucose solution (20 ml) with 5 ml of Vitamin C, injections of vitamin B₁ (5%, 1 ml) and vitamin B₆ (5%, 1 ml), as well as non-barbiturate sleep-normalizing medications such as radedorm tablets (5 mg) at bedtime, adalin, and bromural.

For hyperexcitability and explosiveness, chlordiazepoxide (elenium) at 10–20 mg twice daily, neuleptil at 20 mg twice daily, and chlorpromazine at 25–75 mg are indicated.

In cases where lethargy, apathy, and fatigue predominate—following a course of general strengthening therapy—tonic and stimulating agents can be prescribed for an extended period of several months: tinctures of schisandra, ginseng, or eleutherococcus (30–40 drops three times daily). For shorter durations (2–3 weeks), phenatin (0.005 three times daily), centedrin (5 mg twice daily), as well as subcutaneous injections of strychnine (0.1%, 1 ml) and arsenic (sodium arsenate, 1%, 1 ml) are prescribed. Seduxen exerts a vegetative-stabilizing effect.

Therapy for epileptiform manifestations is conducted similarly to the treatment of epilepsy. In the treatment of endomorphic psychoses, psychotropic medications comparable to those used in the treatment of Schizophrenia and bipolar affective disorder (neuroleptics, tranquilizers, antidepressants) are indicated.

Virtually all cases of inpatient treatment for long-term TBI sequelae warrant a lumbar puncture and the application of reabsorption therapy.

Psychotherapy and the maintenance of social activity in such patients are of paramount importance. Reasonable employment placement must take into account their heightened sensitivity to high temperatures, stuffiness, atmospheric pressure fluctuations, and other factors. Sometimes this requires vocational retraining.

EXAMINATION.

Medical-labor evaluation: the occupational prognosis in TBI depends on the clinical prognosis. Patients with persistent neurosis- and psychopath-like disorders or favorably progressing traumatic epilepsy are recognized as having limited capacity for work and are assigned a Group III disability status.

Individuals with a progressive course of paroxysmal disorders and escalating personality changes—predominantly of an epileptoid type, along with endomorphic psychoses and dementia—are deemed incapacitated and assigned a Group II or even Group I disability. In some cases, individuals with asthenia dominated by an adynamic component may also be declared incapacitated.

Military-medical evaluation: individuals with pronounced, persistent sequelae of traumatic brain injury—which include traumatic dementia, paroxysmal states with progressive mental decline and intensified epileptoid personality traits, and late traumatic psychoses with a relapsing course—are deemed unfit for military service and are deregistered from military records. In the presence of persistent, yet mildly expressed residual phenomena (neurosis- and psychopath-like states), patients are deemed fit for non-combat service in wartime.

Forensic-psychiatric evaluation: severe dysphorias incorporating productive psychotic symptoms in their structure (illusions, hallucinations, affect-laden sensory delusions, etc.), as well as periods of even short-term clouded consciousness, serve as the basis for a Conclusion of legal insanity (non-accountability) should the patients commit a criminal act.

Review Questions.

1. General characteristics of traumatic brain injuries.

2. Etiopathogenesis of traumatic disease.

3. Classification of traumatic brain injuries.

4. Classification of psychiatric disorders resulting from TBI.

5. Somato-neurological disorders in TBI.

6. Immediate manifestations of injury (obtundation, stupor, coma).

7. Non-psychotic forms of acute traumatic mental disorders.

8. Acute traumatic psychoses.

9. Long-term traumatic mental disorders.

10. Late traumatic psychoses.

11. Treatment of patients with a history of TBI.

12. Expert evaluation of patients with a history of TBI.