NEUROLOGY AND NEUROSURGERY - Y. V. ALEKSEENKO - 2014

CRANIOCEREBRAL TRAUMA

Introduction

Craniocerebral trauma (CCT) is the leading cause of death and disability among adults under the age of 45. The prevalence of neurotrauma is so high that the examination and Treatment of this patient population, particularly at the initial stages, involves a broad range of specialists: neurologists, neurosurgeons, general surgeons, traumatologists, intensive care specialists, otolaryngologists, ophthalmologists, dentists, internists, and even pediatricians. Later on, patients with the long-term consequences of CCT require ongoing care from neurologists, psychiatrists, internists, rehabilitation specialists, and physical therapists.

The steady increase in traffic accidents and domestic injuries entails enormous economic losses. Providing highly informative diagnostic Methods (CT and MRI) and effective treatment significantly increases the cost of specialized care, demands high qualifications from neurologists and neurosurgeons, and requires continuous improvement in healthcare Organization. Finally, the accumulation of individuals with post-traumatic neurotrauma sequelae within the working-age population leads to negative socio-psychological trends in many spheres of modern society. Legal, forensic, and expert issues frequently arise in this branch of practical medicine. Therefore, both in patient care and medical documentation, it is essential not only to have a general grasp of the problem but also to adhere to the unified CCT Classification and the guidelines regulating the provision of neurotrauma care in healthcare facilities of the Republic of Belarus.

Prevalence of Craniocerebral Injuries

Across various countries, approximately 2,000–3,000 individuals per million population are hospitalized annually due to CCT. For every hospitalized patient, another 3–4 victims are evaluated by emergency medical services, hospital emergency departments, and general practitioners before receiving outpatient treatment. Overall, According to the U.S. National Center for Health Statistics, the prevalence of acute CCT in the population ranges from 2.0 to 6.1 per 1,000 individuals.

Of all hospital admissions, approximately 5% are brought in comatose with severe CCT. Another 5–10% sustain moderate injuries. Meanwhile, the remaining 85–90% consist of patients with mild CCT. A large-scale epidemiological study conducted across the USSR between 1985 and 1990 established that the number of victims with acute CCT of varying severity is at least 1.2 million per year, of whom at least 100,000 suffer from severe CCT. Furthermore, approximately 1.5 to 3 million people seek medical attention annually for isolated soft tissue INJURIES OF THE HEAD; thus, over 4.2 million victims require specialized neurosurgical care each year. Among the urban population, the incidence of acute injuries to The Skull and Brain ranges from 2.1 to 7.2 new cases per 1,000 individuals annually (2.7–9.7 for men and 1.6–5.2 for women), while in children, this figure reaches up to 11.2 in certain regions.

In The Structure of CCT, the mildest form—concussion—accounts for 81–90%. Contusions of the brain constitute 5–13%, and various types of compression make up 1–9%. Males and the 20–39 age group remain consistently predominant among the victims. A distinctive feature of CIS countries is the dominance of domestic and intentional (crimes-related) injuries, whereas in Western European countries and America, traffic accidents constitute the primary group. Road traffic accidents account for 10–20% of brain injuries, of which only 50% involve automobiles. Alcohol intoxication is documented in approximately 10–15% of CCT cases. Mortality among hospitalized patients with severe traumatic brain injuries reaches 15–30%. Furthermore, 25–50% of patients with severe trauma die at the scene or en route to the hospital.

A significant proportion of CCT patients end up in non-specialized hospital units where the capabilities for comprehensive evaluation and treatment are severely limited. All of this highlights the scale of organizational, economic, and purely clinical challenges faced by specialists involved in providing neurotrauma care.

Classification of Craniocerebral Trauma

In 1774, the French surgeon J. Petit described three forms of brain injury: concussion, contusion, and compression, which formed The basis of the modern CCT classification. Currently, the following main Clinical forms of craniocerebral injury are distinguished:

   ■ Cerebral concussion

   ■ Focal cerebral contusions of mild, moderate, and severe grades

   ■ Diffuse axonal brain injury

   ■ Brain compression

   ■ Head compression

All possible variants of craniocerebral injury are grouped according to their severity.

   Mild CCT    ■ Cerebral concussion

   ■ Mild cerebral contusion

   Moderate CCT    ■ Moderate cerebral contusion

   ■ Subacute and chronic brain compression

   Severe CCT    ■ Severe cerebral contusion

   ■ Diffuse axonal brain injury

   ■ Acute brain compression

Closed traumatic brain injury (TBI) refers to injuries where the integrity of the scalp remains intact or soft tissue wounds occur without aponeurosis damage. Fractures of the cranial vault bones that are not accompanied by injury to the overlying soft Tissues and aponeurosis are also classified as closed.

Open TBI is diagnosed when there are scalp wounds with damage to the aponeurosis, cranial vault fractures with injury to adjacent tissues, or basilar skull fractures accompanied by bleeding or CEREBROSPINAL FLUID leakage (otorrhea or rhinorrhea). If the dura mater remains intact, open TBIs are classified as non-penetrating; if compromised, they are considered penetrating.

A TBI occurring without any extracranial injuries is termed isolated. If the mechanical force causes simultaneous extracranial injuries, the trauma is classified as Polytrauma (or combined-associated injury). Typically, such injuries result from motor vehicle accidents or falls from a height. Combined Trauma involves mechanical impact alongside other damaging factors, such as thermal, radiation, or chemical agents. These most frequently occur during industrial accidents, natural disasters, or military operations.

A primary TBI occurs independently of any predisposing medical condition that could have caused the patient to fall and strike their head. Secondary TBIs result from impaired consciousness, balance, or orientation caused by various cerebral or somatic disorders (e.g., stroke, syncope, epileptic seizures, hypoglycemia, or vertigo).

Naturally, the same individual may experience both initial and recurrent TBIs. Each of these characteristics plays a crucial role in developing diagnostic and treatment strategies, selecting preventive measures, and determining patient prognosis.

The clinical course of traumatic brain injury progresses through several distinct periods.

Acute period: spans from the moment of impact until the stabilization of impaired Functions at various levels.

Intermediate period: extends from the stabilization of functions to their complete or partial recovery, or stable compensation.

Remote period: encompasses Clinical Recovery, the maximum possible rehabilitation of impaired functions, or the onset and/or progression of new trauma-induced pathological conditions. In cases of progressive injury, this period is indefinite.

Following a concussion, the acute period lasts approximately 2 weeks, and the intermediate period about 2 months. In moderate cerebral contusion, the acute period spans 4–5 weeks, with the intermediate period lasting about 4 months. For severe traumatic brain injury involving major contusion, the acute period lasts 6–8 weeks and the intermediate period approximately 6 months.

Pathogenesis of Traumatic Brain Injuries

Over the past 20 years, the findings of pathomorphological and experimental studies, coupled with the introduction of advanced in vivo neuroimaging techniques (CT and MRI) into neurotraumatology, have significantly transformed our understanding of the Pathophysiology of traumatic brain injuries.

The cornerstone of TBI pathogenesis is the delivery of mechanical energy, which triggers a cascade of diverse pathological and compensatory processes varying in nature, depth, and duration. The subsequent clinical course is largely dictated by The Mechanism of injury. All brain injuries are conventionally divided into Primary and secondary categories. Primary injuries refer to structural alterations at the tissue, cellular, and subcellular levels that occur at the moment of impact and are predominantly irreversible. These include diffuse and focal brain injuries. Diffuse injuries result from intense linear or angular acceleration-deceleration forces applied to the head, typically seen in falls from a height or motor vehicle accidents. The instantaneous application of significant mechanical energy leads to subtle—sometimes exclusively microscopic—yet widespread damage to axons, glial Cells, and synaptic structures throughout the cerebral hemispheres.

The mildest form of diffuse injury is a concussion, in which light Cell/15.html">Microscopy reveals no macroscopic or microscopic abnormalities in the brain tissue. The transient loss of consciousness and rapidly resolving autonomic dysfunction characteristic of this form of TBI are attributed to a sudden disruption of interneuronal connectivity. Conversely, severe diffuse axonal injury (DAI) involves widespread axonal tearing and degeneration within the Brainstem and the White matter OF the hemispheres, accompanied by petechial hemorrhages and necrosis. This results in the persistent disconnection of cortical, brainstem, and spinal pathways, clinically manifested by coma, profound sensorimotor deficits, and a prolonged vegetative state.

Focal injuries represent another category of primary damage. They are caused by the Displacement of the brain within the cranial vault during impact, typically resulting in contusions or lacerations of the basal Regions of the frontal and temporal lobes. Another variant of focal damage is superficial cortical contusions, which develop at the site of impact (coup) and the opposite side (contrecoup). These are particularly pronounced underlying a depressed skull fracture when the contact area with the offending object is small. Certain types of intracranial hemorrhages and head compression injuries are also classified as primary damage.

As demonstrated in experimental studies, primary diffuse and focal brain injuries do not cease at the moment of impact. This implies that for a certain period post-injury, a specific volume of axonal damage and the transition of a contusion zone into necrosis remain reversible. The cytotoxic processes driving neuronal tissue death are complex and unfold over several hours; they include the release of free radicals, the opening of calcium Ion Channels, and The conversion of Fatty acids into vasoactive substances that trigger vasospasm and neural ischemia. Interdependent disruptions in METABOLISM/26.html">Energy Metabolism and cerebral Blood flow constitute the core mechanism of traumatic brain injury pathogenesis. The administration of antioxidants, calcium channel blockers, and other mechanism-specific agents during this phase can limit destructive processes to some degree and represents the most promising therapeutic direction of the past decade.

Secondary brain injuries manifest at varying intervals following trauma of any severity, and their mechanisms are often pathogenetically interrelated. Secondary intracranial mechanisms of brain damage include: 1) brain compression by epidural, subdural, and intracerebral hematomas; 2) cerebral edema and Swelling; 3) intracranial Hypertension; 4) cerebral vasospasm; and 5) intracranial infections (meningitis, encephalitis, abscess, etc.). The detrimental effects of these factors are frequently compounded by extracranial (systemic) mechanisms, which are particularly common in multi-system trauma involving soft tissues, the chest and abdominal cavities, the spine, Ribs, and extremity bones. These systemic factors encompass hypoxemia, arterial hypotension, anemia, disseminated intravascular coagulation (DIC), and others. Clinical experience shows that 92% of patients with combined TBI exhibit various secondary brain injury factors, predominantly of an ischemic nature. These effects can persist for minutes or even longer despite meticulous intensive care monitoring and treatment.

Cerebral blood supply, metabolism, and functional activity are largely governed by the stability of a key physiological parameter: cerebral blood flow (CBF). This stability is maintained by a dynamic equilibrium among intracranial pressure, cerebral perfusion pressure, systemic arterial pressure, cerebrovascular tone, The rate of cerebrospinal fluid (CSF) secretion and resorption, and numerous other regulatory mechanisms. Reduced cerebral blood flow and ischemic brain damage in severe TBI are frequently driven by cerebral edema-swelling and intracranial hypertension. Edema refers to an excess of Water within the brain tissue. Cytotoxic edema is characterized by intracellular fluid accumulation resulting from hypoxic disturbances in osmoregulation. Vasogenic edema arises from increased vascular permeability, leading to the leakage of plasma and its components into the extracellular space. Typically, a combination of vasogenic and cytotoxic components is observed. Brain edema generally develops concurrently with swelling—an increase in brain tissue volume driven by increased blood content (hyperemia) caused by cerebral vasodilation. This process involves not so much an overall increase in cerebral blood flow as its redistribution from the cortical and leptomeningeal Arteries into the white matter of the hemispheres.

The Emergence of an additional space-occupying lesion (hematoma) within the cranial vault, alongside The Development of cerebral edema and swelling—particularly in severe TBI—leads to escalating intracranial hypertension and the compression of the ventricular system and basal cisterns. As pressure gradients across the craniovertebral junction equalize, brain herniation occurs, leading to the compression of brainstem structures. Most frequently, this involves the compression of the Midbrain by the medial temporal structures (uncus) against the tentorial notch, and the compression of the Medulla Oblongata at the foramen magnum by the cerebellar Tonsils. The resulting clinical signs of mesencephalic and bulbar dysfunction signal a critical progression of the traumatic process and the urgent need for medical intervention. If left unchecked, progressive brainstem herniation can lead to respiratory and cardiac arrest.

In light of modern insights into TBI pathogenesis, patient evaluation and management must focus on timely limitation of primary brain damage and the Prevention of secondary insults through the earliest possible detection and correction of conditions that destabilize metabolic and circulatory processes in the Central Nervous system. From the outset of treatment, optimal conditions must be established to facilitate sanogenetic, compensatory, and regenerative mechanisms.

Concussion

Concussion (commotio cerebri) is currently regarded as the mildest form of diffuse traumatic brain injury, unaccompanied by structural abnormalities of the brain tissue detectable macroscopically or even via light microscopy. This type of injury results from a brief mechanical impact that imparts intense linear and/or angular acceleration to the head. Typical scenarios include falls from standing height, blows to an unfixed head in boxing, or head impacts during motor vehicle collisions. The pathomorphological substrate of a concussion consists of ultrastructural and cytochemical disruptions of the synaptic and axonal apparatus located in the upper brainstem and cerebral hemispheres. Its pathogenesis is rooted in the reversible dysfunction of non-specific brain systems, clinically manifested by transient alteration of consciousness and autonomic dystonia syndrome.

The hallmark of a concussion is a brief alteration of consciousness—ranging from complete loss to Other forms of impairment lasting from several seconds to a few minutes. Approximately 20–30% of patients experience a short period of post-traumatic retrograde or anterograde amnesia. Anterograde amnesia refers to memory loss for events immediately following the recovery of consciousness. Congrade amnesia involves memory impairment for the duration of altered consciousness itself. Retrograde amnesia is the loss of memory for the period immediately preceding the traumatic impact. As a rule, patients can only approximate the duration of impaired consciousness based on circumstantial evidence and often struggle to accurately recount the event.

Vomiting may occur, typically shortly after the injury. Complaints are dominated by headache, dizziness, nausea, fatigue, tinnitus, and pain upon eye movement. Patients frequently report visual discomfort when fixing their gaze on nearby objects, alongside vestibular hyperesthesia.

Signs of autonomic dysfunction form the core clinical profile of a concussion. Subjective symptoms predominate, including hypersalivation or dry Mouth, flushing of the face, sensations of heat or chills, diaphoresis, blood pressure and pulse lability, Skin pallor, palpitations and other chest discomfort, fatigue, orthostatic reactions, and tobacco intolerance. Sleep disturbances are also characteristic. Following a concussion, the majority of patients report absent-mindedness, memory deficits, slowed thinking, impaired concentration, and an overall decline in intellectual productivity. Neuropsychological testing can confirm impairments in complex mental processes for several weeks post-injury.

Focal neurological signs are absent. A number of microsigns are occasionally detected, such as fine horizontal nystagmus, weak convergence of the eyeballs, and unsteady performance of coordination tests. However, their diagnostic significance is low due to the lack of data on premorbid status, potential consequences of previous injuries, and other diseases in cases of delayed patient admission.

There is no pronounced meningeal syndrome. Some patients exhibit symptoms of mild meningeal irritation rather than true syndrome—pain upon eye movement, borderline nuchal rigidity, and Kernig's signs, which disappear within the first few days following the injury.

There are no cranial bone injuries. Cerebrospinal fluid pressure and composition show no significant deviations. Fractures of the cranial vault bones or a minor admixture of blood in the cerebrospinal fluid, even in the absence of focal and meningeal signs, are always accompanied by damage to the Meninges and brain tissue, indicating a more severe injury—a brain contusion. Computed tomography (CT) reveals no Changes in the density of the brain tissue and cerebrospinal fluid-containing spaces. Therefore, The Use of advanced Instrumental Diagnostic Methods (CT, MRI, craniography, echoencephaloscopy) as well as cerebrospinal fluid analysis in concussion is aimed at ruling out more severe craniocerebral injuries, but cannot be used to confirm the Diagnosis.

Thus, diagnosing a concussion is based primarily on medical history, subjective clinical manifestations, and non-specific objective neurological symptoms, among which the key ones are:

   ■ a history of head injury;

   ■ characteristic biomechanics of concussive injury;

   ■ brief loss of consciousness lasting from a few seconds to a few minutes, post-traumatic amnesia;

   ■ cephalic syndrome (headache), dizziness, nausea;

   ■ vomiting;

   ■ AUTONOMIC DYSFUNCTION SYNDROME.

In a sense, this diagnosis is retrospective, since the absence of more severe brain damage can only be confirmed after dynamic observation over several days and a comprehensive examination. The overall condition of patients improves significantly During the first, or less commonly the second, week after the injury.

Brain contusions

Cerebral contusion differs from concussion in that it presents macroscopically detectable areas of brain tissue damage. Mild contusions are typically characterized by localized edema, moderately severe ones by extensive zones of hemorrhagic imbibition, and severe contusions by brain tissue maceration and detritus formation. Brain contusions are frequently accompanied by subarachnoid hemorrhages, as well as fractures of the cranial vault and skull base. Local, lobar, hemispheric, or generalized cerebral edema is commonly observed.

The Clinical presentation of brain contusions of any severity comprises both general cerebral and focal neurological manifestations. The former include impaired consciousness, headache, dizziness, nausea, and various other symptoms common to all types of traumatic brain injury, which vary significantly in severity and duration. Focal neurological signs invariably indicate localized brain damage. This may manifest as functional deficits (paresis, paralysis, hypesthesia) or be accompanied by irritation phenomena (focal seizures). It is important to note that damage to various levels of the brainstem can be primary (resulting from basal-brainstem contusion) or secondary, arising from hemispheric edema, intracranial hypertension, brainstem compression, and ischemia. This poses a severe threat to the patient's life and is frequently the direct cause of death.

Mild cerebral contusion

Mild cerebral contusion is characterized by a loss of consciousness at the moment of trauma lasting from a few minutes up to an hour. Post-traumatic amnesia is frequently observed. Patients typically complain of headache, dizziness, nausea, and other subjective disorders shared with concussion. Vomiting may recur. A crucial factor in diagnosing a brain contusion is the emergence of local neurological deficit signs—most commonly mild pyramidal insufficiency and cranial nerve dysfunction—which resolve within 2 to 3 weeks post-injury. Meningeal syndrome is detectable. Vital functions remain unimpaired; tachycardia or bradycardia may occur, occasionally accompanied by arterial hypertension. Respiration and body Temperature show no significant deviations. Unlike concussions, mild brain contusions may involve fractures of the cranial vault and skull base, along with a minor admixture of blood in the cerebrospinal fluid. The cerebrospinal fluid is most often unchanged or contains traces of blood. Its pressure is elevated in many patients, and less frequently normal or reduced.

In approximately half of mild contusion cases, computed tomography (CT) reveals areas of decreased density corresponding to localized cerebral edema. This edema may lead to a slight narrowing of the cerebrospinal fluid spaces. These alterations appear within the first hours following injury, typically peak on the third day, and resolve within two weeks without leaving residual traces. Modern X-ray CT resolution is insufficient for detecting punctate diapedetic hemorrhages within the brain parenchyma, which are characteristic of the pathomorphology of mild contusions.

Mild cerebral contusions represent a heterogeneous group of head and brain injuries that differ significantly in biomechanics and the interplay between the local and diffuse Components of the traumatic process. Mild contusions accompanied by prominent general cerebral symptoms and meningeal signs are frequently observed and may initially be misdiagnosed as a "severe concussion." An impact by a heavy object on a fixed head results in an injury where signs of localized brain damage predominate, corresponding to the Location OF THE cranial vault fracture. A distinct group comprises so-called "pauci-symptomatic" mild brain contusions, where patients feel well from the very first hours post-injury, and focal symptoms are either absent or rapidly resolve. Nevertheless, CT or skull radiography incidentally reveals limited fractures of the cranial vault or damage to the brain parenchyma, indicating that the injury is more severe than a concussion. Traumatic brain injuries involving cranial vault fractures are invariably associated with localized damage to the brain tissue, meninges, and Blood Vessels, and must be classified as contusions. Overall, mild brain contusions have a favorable prognosis with clinical manifestations fully reversible within 3 weeks.

Moderately severe cerebral contusion

The duration of unconsciousness in moderately severe brain contusions ranges from several tens of minutes to 4–6 hours. Distinct retrograde and anterograde amnesia is evident. General cerebral symptoms—severe headache, dizziness, nausea, and repeated vomiting—persist for an extended period. Meningeal signs are identifiable. Focal neurology is well-defined and depends on the contusion site, manifesting as extraocular motility disorders, limb paresis, sensory disturbances, ataxia, and aphasia. These symptoms gradually subside over 3 to 5 weeks. Signs of brainstem involvement (nystagmus, dissociation of meningeal signs, Muscle tone, and deep tendon Reflexes along the body axis, bilateral pathological reflexes) do not exhibit a progressively threatening character. Blood is typically present in the cerebrospinal fluid, and cranial vault and skull base fractures are detected. Bradycardia or tachycardia, elevated blood pressure, tachypnea, and a mild elevation in body temperature are also noted.

CT scans reveal hypodense zones within the brain parenchyma containing dense micro-inclusions, as well as areas of homogeneous density increase. This indicates the presence of edema, petechial hemorrhages, and hemorrhagic imbibition of the brain tissue within the contusion zone, devoid of gross structural destruction.

Severe cerebral contusion

Severe cerebral contusion is characterized by profound general cerebral disturbances. Unconsciousness lasts from several hours to several weeks, periodically accompanied by motor agitation. Subsequently, in cases with a favorable outcome, retro- and anterograde amnesia is revealed. Against the backdrop of profound depressed consciousness, life-threatening respiratory and cardiac dysfunctions frequently develop, along with impaired gag reflex and compromised airway patency, necessitating urgent interventions in an intensive care unit or critical care Setting.

The neurological profile is frequently dominated by brainstem signs: ocular bobbing, gaze paresis, coarse nystagmus, bilateral mydriasis or miosis, and horizontal or vertical ocular divergence. Variable muscle tone, bilateral pathological reflexes, and decerebrate rigidity (or hypertonic fits) are also observed. During the first hours or days post-injury, these brainstem disturbances may mask signs of localized hemispheric damage. Focal hemispheric symptoms are typically severe and resolve slowly. Limb paresis, aphasia, extrapyramidal muscle tone disorders, frontal lobe psychiatric syndromes, and other conditions manifest in accordance with the lesion localization. Generalized or focal epileptic seizures are occasionally noted. Severe contusions are characterized by pronounced autonomic, metabolic, and trophic disorders (hyperthermia, hyperglycemia, hypoalbuminemia, acid-base and electrolyte imbalances, and dystrophic changes in the skin and Internal Organs). Fractures of the cranial vault and skull base, alongside massive Subarachnoid Hemorrhage, are invariably present.

CT typically reveals extensive areas of heterogeneous brain tissue density caused by tissue maceration (brain detritus), accumulations of liquid blood and blood clots, and edema. The ventricular System of the brain is frequently grossly distorted. By 30 to 40 days post-injury, these alterations transform into areas of atrophy and cyst formation.

In some cases of severe primary brainstem injury (or even traumatic brainstem rupture), patients die immediately after the trauma. Later on, fatal outcomes may be driven by escalating metabolic and ischemic disorders, cerebral edema, and secondary brainstem dislocation. Overall, the mortality rate across all forms of severe TBI ranges from 15% to 30%, with 25% to 50% of victims dying at the scene or on the way to a medical facility.

Diffuse Axonal Injury of the Brain

Diffuse axonal injury (DAI) primarily occurs in children and young adults. This type of brain injury is typically caused by intense angular or rotational acceleration-deceleration forces, such as those sustained in motor vehicle accidents, falls from significant heights, or barotrauma. As a result, stretching and numerous tears of axons occur within the white matter of the cerebral hemispheres and the brainstem.

Gross morphological changes On the surface of the hemispheres and the Base of the brain are typically absent. However, petechial hemorrhages are occasionally detected in the corpus callosum, centrum semiovale, and rostral brainstem. The most significant changes are revealed through microscopic examination. Within the damaged areas of the white matter, multiple "axonal bulbs" (thickened ends of severed neural processes) become apparent in the first few days. This is followed by axonal degeneration and fragmentation, myelin breakdown along the nerve tracts, and macrophage proliferation. If patients survive the early post-injury phase, demyelination, atrophy, and ventricular enlargement progressively develop in the white matter. The impairment of central nervous system integrative functions, clinical severity, and adverse outcomes are driven by the extent of structural damage, brain swelling, and dislocation.

Diffuse axonal injury is typically characterized by the onset of a prolonged comatose state immediately following trauma. Phenomena of decerebration and decortication are frequently observed. Muscle tone ranges from diffuse hypotonia to normotonia/hormetonia—reflex episodes of tonic Muscle contraction with a predominance in the extensors and pronators of the extremities. Gross brainstem signs are evident, including diminished corneal reflexes, upward gaze paresis, suppression of the oculocephalic reflex, and others. Persistent meningeal syndrome is consistently observed. Motor deficits generally present as tetrapareses of a pyramidal-extrapyramidal type. Pronounced autonomic dysfunctions are noted, such as hyperthermia, hyperhidrosis, and hypersalivation. Disruptions of vital functions, such as respiratory disorders requiring prolonged mechanical ventilation and other intensive care measures, are common.

A characteristic feature of the clinical course in diffuse axonal injury is the transition from a coma into a vegetative state lasting anywhere from several days to many months. During this period, patients open their eyes spontaneously or in response to stimuli. The eyeballs are either immobile or exhibit roving Eye Movements. Tracking, visual fixation, and compliance with commands are impossible. Brief periods of wakefulness alternate with longer intervals of sleep. Respiration, systemic Circulation, and Cardiac Activity stabilize. The striking contrast between the loss of mental functions and the preservation of vegetative functions is definitive for this clinical phenomenon. It is characterized by a specific state of functional or anatomical disconnection between the cerebral hemispheres and the subcortical-brainstem structures. With the suppression of cortical function, disinhibition of subcortical, brainstem, and spinal automatisms occurs. Postural-tonic and uncoordinated protective motor reactions develop spontaneously or in response to stimulation.

As patients emerge from this state, the extrapyramidal syndrome begins to dominate, manifested by muscular rigidity, bradykinesia, oligophasia, and impaired motor coordination. Psychological disturbances occupy a significant place. Altered states of consciousness give way to asthenia, accompanied by profound physical and mental exhaustion.

Computed tomography (CT) in such injuries reveals an increase in brain volume and compression of the cerebrospinal fluid spaces, although the tomographic picture may sometimes remain within age-related norms. A diffuse atrophy process develops at a later stage.

Diffuse axonal injury is a severe brain trauma. However, its outcomes depend not only on the severity and extent of axonal damage, but largely on secondary pathological changes (such as edema and impaired cerebral metabolism), as well as extracranial complications. The more severe and prolonged the coma, the worse the prognosis. Nevertheless, with appropriate therapy and well-structured rehabilitation, regression of neurological deficits is possible, alongside partial or (significantly less often) complete recovery of mental functions, even after a prolonged vegetative state.

Traumatic Brain Compression

Brain compression (compressio cerebri) is a multi-factorial pathological process. It is fundamentally driven by The formation of an additional intracranial mass lesion resulting from trauma. Once intracranial reserve spaces are exhausted, this mass causes compression of the brain tissue, distortion of the ventricular system, intracranial hypertension, and brainstem dislocation and herniation. In the development of life-threatening impairments of cerebral functions, alongside mechanical factors, disturbances in blood and cerebrospinal fluid circulation, edema, and ischemia play a critical role. Intracranial hematomas are the most frequent cause of brain compression. This localized blood accumulation can occur at the site of impact or in the contre-coup zone. Primary hematomas form immediately after the trauma, whereas delayed hematomas develop 24 hours or later. A distinction should be made between the time of hematoma formation and the onset of its clinical manifestations. Specifically, patient deterioration and the emergence of neurological symptoms are associated with the gradual exhaustion of cerebral functional compensation reserves, typically manifesting after a lucid interval. While the classification of intracranial hematomas into acute, subacute, and chronic based on their clinical progression rate is somewhat conventional, it is essential to bear in mind that chronic hematomas possess an important qualitative distinguishing feature—a capsule.

Variants of traumatic brain compression (L. B. Lichterman, 1994).

   • Intracranial hematomas (frequency ratio 4:8:3:1:5)

   epidural

   subdural             acute (1–3 days)

   intracerebral             subacute (4–14 days)

   intraventricular             chronic (> 2 weeks)

   multiple

   • Depressed skull fractures

   • Contusion foci with perifocal edema

   • Subdural hygromas

   • Pneumocephalus

   • Other causes of compression

Clinically, brain compression, regardless of the specific Etiology, is characterized by the progressive development—after a certain time interval following the injury—of generalized cerebral symptoms (impaired consciousness, headache, repeated vomiting, etc.), focal signs (hemiparesis, unilateral mydriasis, partial seizure attacks, etc.), and brainstem symptoms (bradycardia, elevated blood pressure, respiratory rhythm disturbances, upward gaze limitation, bilateral pathological signs, etc.). The so-called lucid interval in the patient's condition, spanning from the moment of trauma to the exacerbation of the aforementioned neurological deficits, may be

masked or, in some cases, absent entirely. The Nature of the clinical manifestations, their dynamics, and the potential outcomes of brain compression significantly depend on the presence or absence of a concomitant brain contusion.

Subdural Hematoma

Subdural hematomas, located between the dura mater and the arachnoid mater, are among the most common causes of brain compression. They develop following traumatic brain injury (TBI) of varying severity and frequently occur not only on the side of mechanical impact, but on the contralateral side as well. The hemorrhage results from a focal brain contusion and rupture of pial or cortical vessels. Less commonly, indirect head trauma (such as sudden vehicular deceleration or a fall from a height onto the feet or buttocks) can cause displacement of the cerebral hemispheres and rupture of the Veins draining into the superior sagittal sinus. Subdural hematomas have an average volume of 80-150 ml. The extravasated blood typically spreads freely through the subdural space, covering a significant portion of the cerebral hemisphere, though it may also extend basally into the anterior and middle cranial fossae.

The clinical presentation of a subdural hematoma is characterized by a triphasic alteration of consciousness. Initial loss of consciousness at the moment of trauma is followed by a brief period of lucidity. Following this lucid interval—which in acute hematomas may last for minutes, hours, or even days—drowsiness intensifies, accompanied by psychomotor agitation, behavioral abnormalities, disorientation, stupor, and ultimately coma. Headache worsens and recurrent vomiting occurs. Signs of focal brain damage become more pronounced, including mydriasis on the side of the hematoma, hemiparesis and hemihypesthesia of the contralateral limbs, focal seizure activity, aphasia, and others. Concurrently with the depression of consciousness, a secondary brainstem syndrome develops, characterized by bradycardia, elevated blood pressure, respiratory rhythm disturbances, vestibuloculomotor deficits, and tonic convulsions.

The clinical course of a subdural hematoma depends significantly on the severity of the primary brain injury. The classic presentation with a well-defined lucid interval is rare and typically observed against the Background of a mild or moderate brain contusion. It is much more common to observe the formation of a subdural hematoma without a distinct lucid interval, which corresponds to multiple severe cranial and cerebral injuries. In such cases, from the moment of trauma, stupor or coma exhibits progressive deterioration. Acute subdural hematomas are most characteristic of severe TBI accompanied by skull fractures, whereas subacute and chronic hematomas are associated with moderate and mild injuries.

In subacute subdural hematomas, the lucid interval regarding the patient's well-being may last up to 2 weeks. Secondary disturbances of consciousness sometimes acquire a "frontal lobe" psychiatric profile. Patients exhibit reduced insight into their condition, disorientation in time and place, euphoria, behavioral inappropriateness, and decreased activity. They complain of persistent headaches. By the time subacute hematomas are present, papilledema has usually developed. After 2 weeks, a Connective Tissue capsule forms around the hematoma, and the extravasated blood undergoes structural changes. The blood clots lyse, and the Contents of the hematoma transform into a turbid, dark brown fluid.

Chronic subdural hematomas are distinguished by the presence of a capsule and a lucid interval that can last for weeks, months, or even years. Chronic subdural hematomas occur more frequently in elderly and senile patients due to the presence of reserve intracranial spaces. In adults, this is primarily driven by atrophy (alcoholic encephalopathy), whereas in children, it is associated with Developmental anomalies of the skull and brain. The size of a chronic subdural hematoma often increases as a result of recurrent hemorrhages from the capsular vessels, driven by hyperfibrinolysis within the hematoma contents caused by fibrin degradation products.

The diagnosis of subdural hematomas is based on a triphasic change in consciousness and the Progressive development of generalized and focal neurological manifestations. A midline shift on echoencephaloscopy is characteristic. Cerebral angiography reveals a sickle-shaped avascular zone formed by cortical vessels displaced away from the cranial vault by the hematoma. X-ray and magnetic Resonance CT scans are the most informative diagnostic tools, as they allow evaluation of the location, size, and density of the hematoma, as well as the extent of edema and brain shift. The limited capabilities of instrumental examinations sometimes necessitate the creation of exploratory burr holes. In cases of suspected traumatic hematoma, lumbar puncture is contraindicated due to the risk of exacerbating brain herniation.

Epidural Hematoma

An epidural hematoma is a localized hemorrhage situated between the inner table of the skull and the dura mater. Most commonly, it results from mechanical impact to the temporal and parietal regions, which at the moment of impact causes local cranial deformation, bone fracture, and laceration of the dural vessels. The source of bleeding is typically the Branches of the middle meningeal artery, meningeal veins, or, less frequently, dural sinuses or diploic vessels. An epidural hematoma is lentiform (lens-shaped) in shape, measures 7-8 cm in diameter, and usually has a volume of 80-120 ml.

Immediately following trauma—which is characterized by signs of mild to moderate brain contusion—patients remain in stable condition for several minutes or hours. Subsequently, headaches intensify, followed by recurrent vomiting, facial flushing, and occasionally psychomotor agitation. Disturbances of consciousness progressively worsen, with lethargy giving way to stupor and then coma. The prominence of focal neurological deficits increases, most frequently manifesting as a deepening contralateral hemiparesis. Anisocoria is detected. An initially sluggish pupillary response on the side of the hematoma eventually progresses to fixed mydriasis with absent light reflexes. Bradycardia and a tendency toward elevated blood pressure are characteristic. In the comatose state, vital function impairments reach critical, life-threatening levels.

Against the backdrop of severe TBI, acute epidural hematomas may present with an obscured lucid interval or lack one entirely. In subacute epidural hematomas, the lucid interval may last for several days. Chronic epidural hematomas are rare.

Key factors in identifying epidural hematomas include a lucid interval, progressive ipsilateral mydriasis, and contralateral hemiparesis, frequently accompanied by bradycardia and arterial hypertension. Localized tenderness upon cranial Percussion may be present. Suspicion is raised by skull vault fractures crossing the grooves of meningeal vessels on craniograms and a midline shift on echoencephaloscopy. A characteristic avascular zone on angiograms helps indirectly confirm and localize the epidural blood collection. Comprehensive information regarding the location and size of the hematoma is provided by CT or MRI. In the absence of instrumental methods, diagnostic burr holes are placed at sites typical for epidural hematomas.

Intracerebral Hematoma

This occurs infrequently and represents an accumulation of liquid blood or clots within the brain parenchyma. It is most often located in the white matter or coincides with the zone of a contusion focus. The bleeding source is primarily The Vascular System of the middle cerebral artery. In severe TBI, it is commonly associated with epi- and subdural hematomas. CT scans reveal a rounded or elongated area of homogeneous, high-density signal within the brain tissue with clearly defined margins.

Subdural Hygroma

This condition represents a TBI-induced localized accumulation of cerebrospinal fluid in the subdural space, leading to brain compression. Hygromas form as a result of damage to the subarachnoid cisterns at the base of the brain. The fluid content of a hygroma is bloody, xanthochromic, or clear, closely resembling cerebrospinal fluid in biochemical composition. The clinical presentation of a subdural hygroma is virtually indistinguishable from that of a subdural hematoma. Among the primary features, meningeal signs are more prominent. CT imaging reveals not only the hypodense zone of the hygroma but also its source, featuring a characteristic pathway of basal cistern rupture and a direct communication between the convexity fluid collection and the skull base via the lateral fissure.

Depressed Skull Fractures

These are fractures in which bone fragments are displaced below the level of the adjacent cranial vault, causing compression of the brain. They are classified into impression fractures, where the fragments remain attached to the vault bones, and depression fractures, where the bone fragments are detached from intact vault bones and lie beneath their surface. Neurologically, signs of focal brain damage generally correspond to the site of the bone defect. The presence of a depressed skull fracture is an indication for surgical intervention, as the encroaching fragments cause irritation and compression of the Cerebral Cortex, damage dural sinuses, and pose a severe threat of pyogenic-septic complications.

Pneumocephalus

Pneumocephalus refers to the ingress of air into the cranial cavity—subdurally, subarachnoidally, into the brain parenchyma, or within the cerebral ventricles. Most frequently, it results from a skull base fracture involving damage to the ethmoid labyrinth and is accompanied by cerebrospinal fluid leak (otorrhea/rhinorrhea). Intracranial air accumulation leading to brain compression can occur during sneezing, coughing, or straining due to a valvelike mechanism. Pneumocephalus is accompanied by headache and a sensation of fluid sloshing when the head is turned. Air is readily visible on standard skull radiographs. The potential for infection to enter the cranial cavity creates a high risk for the development of purulent meningoencephalitis.

Crushing Head Injuries

Head crushing is a specific type of neurotrauma frequently encountered in earthquakes, structural collapses, transportation accidents and catastrophes, as well as in the coal and mining industries. Such injuries can occur on a mass scale.

The mechanism of this specific injury typically comprises two components: an initial impact from falling heavy objects or the patient falling, followed by sustained compression of the head. An essential element of a head-crushing injury is soft-tissue trauma accompanied by progressive edema developing 2-3 days after release, along with trophic disturbances that can progress to extensive tissue necrosis. The resorption of tissue breakdown products is accompanied by high fever, pronounced weakness, nausea, repeated vomiting, dyspeptic symptoms, and others. Due to soft-tissue necrosis and infection, the injury soon assumes an open character. The exclusion of a significant portion of the diploic and emissary veins from the cranial venous network leads to diminished outflow of intracranial venous blood via the external jugular Venous system and impaired cerebral hemodynamics. Patients with multiple depressed fractures exhibit head deformation. The clinical picture of prolonged head compression is determined by The ratio of intra- to extracranial injuries, as well as the direction of the compressive force—frontal or lateral.

CT is the primary diagnostic modality. It allows for the assessment of soft tissues (the location and extent of edema and subaponeurotic hematomas), skull bones, and the Nature of the brain injury. Traditional craniography is also valuable in identifying cranial bone injuries.

If patients present with soft-tissue head wounds, primary surgical debridement should be deferred during the Initial Stages of medical evacuation, with delayed debridement performed in specialized hospitals. Severe, prolonged head compression limits surgical options for depressed skull fractures and frequently necessitates a conservative management strategy. Extensive defects of the scalp require plastic reconstruction.

Scalp Soft Tissue Injuries

Isolated soft tissue injuries account for 60-70% of all head traumas. At the same time, they accompany the majority of concussions, cerebral contusions, and intracranial compressions. Among superficial skin injuries, abrasions and contusions are the most common. Abrasions do not extend deeper than the papillary layer, whereas contusions result from blood infiltration into the subcutaneous adipose tissue. Deeper injuries include puncture, contused, lacerated, chop, incised, bite, scalp, and gunshot wounds, as well as subcutaneous hemorrhages. Wounds may be cutaneous (with edges that readily adhere and bleeding that typically stops spontaneously), skin-aponeurotic (with gaping, bleeding edges), and occasionally penetrate to the bone. Scalp avulsions present as a complete detachment of the skin and subcutaneous tissue from the underlying structures. Extensive avulsion injuries are hazardous due to significant blood loss, the potential for Shock, and subsequent flap necrosis. Subcutaneous hemorrhages form between the aponeurosis and subcutaneous tissue and are prone to suppuration. Most wounds bleed profusely and are heavily contaminated, thus requiring emergency surgical debridement, tetanus prophylaxis, and prevention of purulent complications. It is essential to keep in mind the diagnostic and forensic significance of soft tissue head injuries: they confirm the occurrence of trauma, help deduce its mechanism and time of infliction, and indicate the location and extent of concomitant intracranial damage.

Traumatic Injuries to the Skull Bones

Traumatic injuries to the BONES OF THE cranial vault and base are not classified as an independent form of TBI. Their presence invariably indicates a cerebral contusion and, less frequently, accompanies brain compression. Various types of fractures are distinguished: linear (the most common, approximately 80%), comminuted, depressed, and fenestrated. Based on THE POSITION OF the bone fragments relative to the plane of the vault, they are categorized as impression fractures (where fragments retain their connection to the skull) and depression fractures (where this connection is lost). In some cases, linear fractures of the vault extend to the skull base. Vault fractures and fissures can be complicated by the development of epidural hematomas. Here, a crucial radiological sign is a fissure crossing a vascular groove. Depressed fractures may also serve as an independent cause of brain compression. Traumas involving skull bone fractures consistently carry a high risk of infectious complications, such as meningitis, encephalitis, and brain abscess.

The clinical presentation of basilar skull fractures, apart from signs of cerebral contusion and cranial nerve palsies, comprises several specific symptoms: nasal and aural bleeding, cerebrospinal fluid leakage from the Nose and ears (rhinorrhea, otorrhea), and occasionally pneumocephalus. Fractures in the anterior cranial fossa manifest with periorbital ecchymosis, epistaxis, nasal CSF leakage, sometimes subcutaneous emphysema, and damage to the olfactory, optic, or oculomotor nerves. Fractures of the middle cranial fossa most frequently cross the petrous part of the Temporal bone, potentially injuring Cranial Nerves III through VIII. This is accompanied by otorrhea, CSF leakage, and characteristic ecchymosis over the mastoid process and the temporalis muscle. Injuries to the posterior cranial fossa extend toward the foramen magnum or jugular foramina and are accompanied by pronounced general cerebral symptoms (headache, dizziness, nausea, repeated vomiting) and occasionally bulbar signs.

Skull radiography in two standard projections enables the diagnosis of the majority of bone injuries. However, conventional radiographs relatively rarely reveal basilar skull fractures, for which indirect signs are usually sufficient for recognition. To determine the precise nature of intracranial lesions, CT scanning is indicated for all patients with fractures of the cranial vault and base.

Traumatic Subarachnoid Hemorrhage

This is the most frequent type of intracranial traumatic hemorrhage. Unlike a hematoma, it is characterized by a more or less uniform distribution of blood within the subarachnoid space. Subarachnoid hemorrhage accompanies the majority of cerebral contusions; therefore, the presence of blood in the cerebrospinal fluid following TBI is considered a key indicator of brain tissue damage. Blood—specifically Hemoglobin breakdown products and other active substances (oxyhemoglobin, bilirubin, serotonin, kinins)—irritates the meninges and, in combination with other factors, induces vasospasm and cerebral Circulatory Disorders. The formation of clots and the blockage of arachnoid granulations by Blood Cells lead to impaired CSF circulation and resorption. The ultimate outcome of the hemorrhage by days 8–10 is leptomeningeal fibrosis.

The clinical picture of a subarachnoid hemorrhage features meningeal syndrome. Many patients exhibit elevated BODY TEMPERATURE AND inflammatory changes in peripheral blood. In favorable clinical courses, the regression of meningeal symptoms typically lags behind the normalization of the CSF, usually occurring by days 14–21.

Subarachnoid hemorrhage is diagnosed through CSF analysis (taking care to rule out a traumatic tap). It should be noted that by days 5–7, concurrently with the clearance of erythrocytes, xanthochromia develops in the cerebrospinal fluid and typically resolves during the third week post-injury.

Class="center">Severity of Subarachnoid Hemorrhage

CT scans frequently reveal indirect signs of subarachnoid hemorrhage, such as increased density within the basal cisterns, pontine cisterns, Sylvian fissure, and subarachnoid spaces.

Features of Traumatic Brain Injury in the Context of Alcohol Intoxication

Alcohol is a confounding factor that alters the course of traumatic illness, masks its clinical manifestations, and complicates both Anamnesis taking and the diagnostic process.

It is well known that alcohol possesses analgesic properties and dampens stress responses. Some specialists suggest that alcohol exerts a certain protective effect in TBI by mitigating the degree of brain damage and the severity of clinical symptoms. Conversely, alcohol intoxication undoubtedly exacerbates traumatic pathology because it targets the very same neural structures and regulatory mechanisms that are most vulnerable during trauma. For instance, alcohol deepens impairments of consciousness and amnesia, complicating their structure. Even small doses of alcohol predictably lower the "commotional" threshold, making it easier for mechanical energy to induce consciousness disorders. The Adverse effects of alcohol become particularly evident in alterations of cerebral blood flow and metabolic processes as its blood concentration rises. Beyond The Nervous System, the Toxic effects of alcohol impact the cardiovascular, respiratory, urinary, and other bodily systems. The risk of respiratory complications increases due to glossoptosis and the aspiration of vomitus.

Due to the overlapping symptoms of trauma and alcohol intoxication, certain manifestations are difficult to interpret unambiguously, including altered states of consciousness, nystagmus, convergence weakness, vestibular dysfunction, muscular hypotonia, hyporeflexia, ataxia, autonomic disorders, nausea, and vomiting. Account must also be taken of the frequency of CSF hypotension and impaired venous outflow following alcohol intoxication, and how these overlap with post-traumatic manifestations. The degree of alcohol intoxication is of critical significance: differentiating severe TBI with mild intoxication from mild TBI with severe intoxication can be extremely challenging. In some cases, high doses of alcohol may obscure focal neurological signs or, conversely, induce reflex asymmetries and other pathological reflexes.

Mild TBI in The Setting of mild to moderate alcohol intoxication is chiefly characterized by deeper disturbances of consciousness at the moment of impact compared to other cases. Post-traumatic amnesia is detected much more frequently, leading over half of patients to be uncertain about whether they lost consciousness during the injury. These patients exhibit a shorter-lived migrainous/cephalgic syndrome and a more rapid recovery of general well-being. In cerebral contusions, an early elevation of intracranial pressure is characteristic, alongside a sluggish development and muted presentation of meningeal signs. Intracranial compression combined with alcohol intoxication presents with an obscured lucid interval, a rapid rise in intracranial pressure, and early brain shift (dislocation) phenomena.

The patient's condition and TBI diagnosis acquire distinct features in chronic alcoholism and during withdrawal. Such patients frequently develop psychopathological disorders and seizure activity. Psychotic states are particularly hazardous, where psychomotor agitation, aggression, and inappropriate behavior pose a direct threat to the patients themselves and those around them.

Thus, concurrent alcohol intoxication significantly complicates the identification of any TBI and increases the likelihood of diagnostic errors. Obviously, alcohol consumption severely hinders early—and therefore most effective—brain injury Diagnostics. In this light, confirming not only the presence of alcohol intoxication but also its exact degree, through rapid blood and urine alcohol assays, is critically important. Treatment for such patients must include effective detoxification.

Complications of Traumatic Brain Injuries

Intracranial suppurative-inflammatory complications are the most prevalent in open and penetrating TBIs. Approximately 20% of penetrating skull and brain injuries are complicated by post-traumatic meningitis. Its onset is characterized by escalating general cerebral and meningeal symptoms, as well as the appearance of systemic signs of infection. Reliable diagnosis of this dangerous complication is only possible through cerebrospinal fluid analysis, which reveals inflammatory changes. The lymphocyte and neutrophil counts per 1 µL of CSF can reach hundreds or thousands. Post-traumatic encephalitides are equally perilous; in these cases, purulent, necrotic, or hemorrhagic changes extend beyond the meninges into the brain parenchyma. In addition to the symptoms listed above, they are accompanied by focal neurological deficits. Management of meningitis and encephalitis involves maximum daily doses of antibiotic therapy, supplemented by detoxification, dehydration therapy, and metabolic and vasoactive agents.

Brain abscesses following TBI most commonly result from circumscribed encephalitis and can also form around retained bone fragments and foreign bodies. They may develop either during the acute phase of trauma or at later stages. Diagnosing a post-traumatic abscess is invariably extremely complex; it can be suspected based on signs of a mass effect and, occasionally, infectious-inflammatory symptoms. CT or MRI greatly AIDS in identifying a brain abscess, typically revealing a rounded hypodense lesion with a hyperdense capsule and perifocal brain edema. Treatment is generally surgical—total excision with the capsule, needle aspiration, or drainage—combined with intensive antibiotic therapy. In selected cases, cure may be achieved through conservative antibiotic therapy under serial CT monitoring. Less frequently observed complications include cranial Osteomyelitis and other purulent-inflammatory conditions.

Fat embolism of cerebral vessels occurs in polytrauma involving TBI, most commonly associated with fractures of long tubular bones. Ischemic damage to brain tissue ensues when un emulsified droplets of free fat exceeding 6 µm in diameter enter the microvasculature and capillary bed after bypassing the pulmonary filter into the systemic circulation. Consequently, the clinical presentation of cerebral fat embolism unfolds against the backdrop of simultaneous damage to multiple internal organs, primarily the Lungs. Symptoms of this complication often mimic those of traumatic brain compression. A few days post-injury, the patient may experience lethargy, disorientation, delirium, agitation, or even coma. Fluctuating levels of consciousness, multi-focal neurological signs, and seizure episodes are possible. Characteristic features include tachycardia, blood pressure instability, pronounced dyspnea, cough, and hyperthermia. Several pathognomonic signs exist: petechiae on the skin, oral mucosa, and conjunctiva, fat emboli in retinal vessels, and fat globules in urine and sputum. Prevention of fat embolism entails reliable limb immobilization and minimizing patient transfers during transit in polytrauma cases. Treatment comprises dehydrating agents, microcirculatory and fat-droplet dispersion enhancers (such as Trental or Lipostabil), and nootropics.

Extracranial complications of TBI are even more diverse. They are driven by a complex interplay of factors encompassed by THE CONCEPT OF traumatic illness, predominantly manifesting as circulatory, ischemic, and metabolic-dystrophic disorders:

   • Hypoxia;

   • hypovolemic shock in severe polytrauma involving TBI;

   • disseminated intravascular coagulation;

   • Pneumonia;

   • myocardial infarction, Cardiac Arrhythmias, acute Heart Failure;

   • erosions and ulcers of the Esophagus, Stomach, duodenum, gastrointestinal bleeding;

   • dystrophic changes in the skin, Liver, Kidneys, and other internal organs.

In some cases, it is precisely TBI complications that determine the severity of the patient's condition, while their successful treatment dictates the prognosis for recovery. A clear distinction should be made between complications and sequelae of TBI.

Sequelae of Traumatic Brain Injury

There is currently no universally accepted classification of TBI sequelae. Below is a list of the most common post-traumatic syndromes.

   • Post-traumatic cranial defects

   • Post-traumatic cranial deformity

   • Post-traumatic cerebrospinal fluid fistula

   • Post-traumatic cranial nerve injury

   • Intracranial foreign bodies

   • Post-traumatic meningo-cerebral scars

   • Post-traumatic arachnoiditis

   • Post-traumatic brain atrophy: a) diffuse, b) local

   • Post-traumatic cyst: a) subarachnoid, b) intracerebral

   • Post-traumatic chronic hematoma: a) subdural, b) epidural, c) intracerebral

   • Post-traumatic chronic subdural hygroma

   • Post-traumatic chronic pneumocephalus

   • Post-traumatic porencephaly

• Post-traumatic Hydrocephalus

   • Post-traumatic ischemic brain injury

   ■ Post-traumatic carotid-cavernous fistula

   ■ Post-traumatic arterial aneurysm

   ■ Post-traumatic thrombosis of intracranial sinuses

   ■ Post-traumatic pachymeningitis

   ■ Growing skull fractures

   ■ Post-traumatic Epilepsy

   ■ Post-traumatic parkinsonism

   ■ Post-traumatic cerebrovascular disorders

   ■ Post-traumatic psychiatric dysfunctions

   ■ Post-traumatic autonomic dysfunctions

   ■ Other rare forms of traumatic brain injury sequelae

TBI sequelae can be divided into 3 groups (L. S. Gitkina, F. V. Oleshkevich, A. M. Klimovich et al., 1993). The first group comprises deficit syndromes, characterized by the impairment of motor, sensory, and intellectual-mnestic functions. These are observed only in severe or moderate injuries and are most pronounced in the acute phase. The second group includes neurosis-like syndromes (asthenic, hypochondriacal, depressive, etc.) and autonomic dystonia. They are equally prevalent in the intermediate and late recovery periods of TBI regardless of severity. Under The Influence of additional factors

of a medical and social nature, these disorders may take a protracted course and lead to patient disability. The third group encompasses other, rather heterogeneous disorders (hypertensive, epileptic, and vestibular syndromes, etc.); their clinical specifics require an individualized approach for detection and management.

Diagnosis of Traumatic Brain Injuries

The protocol for examining patients with TBI includes several main stages. Their Implementation depends on the patient's condition, the specialists' training, and the medical facility's resources.

   1. Verification of the injury and preliminary Assessment of the patient's severity status.

   1.1. Establishing the fact of TBI. This can be done through accounts from the patient or accompanying persons, medical documentation, or based on direct signs such as soft tissue head injuries.

   1.2. Assessment of consciousness impairment. This includes identifying clear consciousness and appropriate behavior, obtundation, stupor, coma, psychomotor agitation, etc., evaluated using the Glasgow Coma Scale. A Conclusion is drawn regarding the feasibility of obtaining reliable anamnestic data.

   1.3. Evaluation of the vital Functions of the cardiovascular and respiratory systems. Pulse and blood pressure are measured, and the rate and efficacy of breathing are assessed.

   1.4. Determination of the localization and nature of external head injuries. Special attention is paid to potential heavy bleeding and major skull defects that require emergency care and precautions when moving the patients.

   2. Clarification of the localization and extent of skull and brain damage.

   2.1. Determining the biomechanics of the traumatic brain injury. This is established through the anamnesis or inferred from the nature of head injuries and other indirect signs. The acceleration-deceleration mechanism accounts for the predominance of diffuse brain injury, whereas the coup-contrecoup mechanism is typical of localized focal brain contusions.

   2.2. Identification of symptoms of focal brain damage. This may include cranial nerve dysfunction, limb paresis, anisoreflexia, aphasia, ataxia, and less commonly, sensory disturbances.

2.3. Detection of meningeal syndrome.

2.4. Identification of the occurrence and nature of epileptic seizures.

    2.5. Identification of other important indirect signs of skull and brain injury. In basilar skull fractures of various locations, delayed perioribital ecchymosis ("raccoon eyes sign"), subcutaneous emphysema, cerebrospinal fluid leakage or bleeding from the ear or nose, retroauricular hematoma, etc., may be detected.

    3. Exclusion of brain compression. To this end, historical data and serial monitoring are used to rule out any delayed progression of generalized, focal, and brainstem symptoms following the trauma. Special attention is paid to the worsening of impaired consciousness and the appearance of brainstem dislocation signs.

    4. Instrumental diagnostics of traumatic brain injuries.

4.1. Skull radiography in two projections.

4.2. Echoencephaloscopy.

4.3. Computed tomography.

4.4. Cerebral angiography.

4.5. Cerebrospinal fluid examination.

4.6. Diagnostic burr hole trepanation of the skull.

    5. Detection of associated traumatic injuries to the Skeleton and internal organs, as well as comorbid conditions. The most critical task is to determine the weight of each component of the trauma in the overall assessment of the patient's severity and to identify the dominant pathology.

    6. Formulation of a detailed diagnosis indicating the form and severity of the TBI, as well as the severity of the patient's condition.

Diagnostics, much like the treatment of neurotrauma, consists of several stages. It begins at the accident scene, continues in the hospital emergency department, and proceeds to the neurotraumatology or neurosurgery departments. The objectives of the examination at any of these stages remain unchanged: 1) determining the severity of the TBI; 2) assessing the severity of the patients' condition; 3) predicting changes in their condition. As for the completeness of the diagnostic program and The sequence of Procedures, they depend on many, often unpredictable, circumstances. Therefore, the general framework for examining patients with TBI outlined above requires specification and additional clarification.

When assessing patients at the scene, primary focus is placed on cardiovascular parameters (blood pressure, pulse), respiration (airway patency, respiratory rate and efficiency), and the level of consciousness evaluated using the Glasgow Coma Scale. The main challenge during transportation is to prevent Traumatic shock and hypoxia.

Respiratory and circulatory functions require priority monitoring in the hospital emergency department before deciding on further diagnostic plans. The neurological examination in TBI is relatively straightforward, encompassing the assessment of altered consciousness, motor asymmetries (ranging from anisoreflexia to limb paralysis), and responses to painful stimuli. It is essential to rule out upper and lower limb motor deficits caused by cervical spine and Spinal Cord injuries. A crucial element of the neurological examination is assessing the Symmetry and pupillary light reflexes. Bilateral absence of pupillary light reflexes indicates brainstem damage. Unilateral impairment of pupillary responses is sometimes caused by optic or Oculomotor nerve injury and can be determined by comparing direct and consensual responses. Anisocoria accompanies brain contusion or compression only in a fraction of cases. Although intracranial hypertension is observed in many TBI patients, papilledema is rarely detected during the initial examination. It should be noted that traditional neurological findings reliably reflect the extent of brain damage only under conditions of normal ventilation, stable hemodynamics, and the absence of toxic influences. Otherwise, distinguishing between traumatic, ischemic, and toxic impairments of the nervous system is extremely difficult. Naturally, the characteristics of consciousness and other elements of the neurological status must be determined prior to administering tranquilizers, muscle relaxants, and other specific neurotropic agents.

A critical aspect of the examination is the earliest possible detection of all extracranial components of the injury. These include not only skeletal trauma but also pneumothorax, hemothorax, intra-abdominal bleeding, and internal organ damage. Approximately 35% of all TBIs are polytraumas, and in severe forms of neurotrauma, multiple extracranial injuries are identified in 50% of cases. Ruling out intra-abdominal bleeding is particularly challenging in comatose patients. It is generally considered that arterial hypotension (systolic pressure below 90 mm Hg) is much more frequently caused by extracranial injuries than by brain trauma.

Upon admission to the hospital emergency department, all TBI patients must undergo skull radiography in anteroposterior and lateral projections. The minimum indications for craniography include impaired consciousness, even the mildest and briefest amnesia, and soft tissue injuries of the scalp. In many cases, especially when a detailed history is lacking or the patient is comatose, lateral radiographs of the cervical spine are necessary. A simple and widely available ultrasound method—echoencephaloscopy—is also employed.

The presence of vault or skull base fractures, as well as a midline shift on echo, significantly increases the risk of intracranial hematomas, regardless of the neurological findings. Therefore, CT is recommended for this category of patients. Furthermore, CT is indicated for patients who do not fully regain consciousness within 24 hours, as well as for those experiencing seizures or distinct focal neurological deficits. Early CT scanning is especially crucial in the presence of coma, as it reveals intracranial hematomas in approximately 40% of such patients. Clearly, no clinical symptoms allow specialists to promptly and definitively differentiate between brain compression and diffuse axonal injury with progressive edema. It is also evident that reliably predicting the development of intracranial hematomas over the next few days based solely on clinical signs is currently impossible. Consequently, over the past decade, CT has become the most informative and essential diagnostic tool for acute TBI. Undeniably, this investigation is warranted at the slightest suspicion of an injury more severe than a concussion. MRI is a more sensitive method than X-ray CT for detecting subtle parenchymal lesions and more frequently uncovers structural changes in mild TBI. Nevertheless, for addressing the primary tactical concerns of the acute injury period, the capabilities of modern CT generations are entirely adequate, and its use is even considered preferable in diagnosing acute hematomas.

In many cases, carotid angiography reveals a characteristic avascular zone and a shift of the anterior cerebral artery in the presence of intracranial hematomas; therefore, in the absence of CT equipment, this method is considered the primary diagnostic tool. Contrast-enhanced imaging of cerebral vessels is undeniably necessary when a TBI can be presumptively attributed to an ischemic stroke or spontaneous subarachnoid hemorrhage. In certain circumstances, diagnostic burr hole trepanation remains the only viable option.

Subsequently, cerebrospinal fluid analysis is performed to diagnose subarachnoid hemorrhage or meningitis as complications of the acute post-traumatic period. The indication for this Procedure is meningeal syndrome. However, in the presence of severe intracranial hypertension and suspected intracranial hematoma, lumbar puncture should be avoided due to the risk of herniation syndromes.

An ophthalmological examination in the emergency department is necessary upon admission for patients with ocular globe and orbital trauma. In other cases, it can be performed electively. The presence and severity of retinal angiopathy (arterial narrowing, venous dilation, tortuosity, and congestion) directly correlate with TBI severity. Papilledema typically develops on days 2 to 4 following severe trauma and reflects the degree of elevated intracranial pressure.

With the advancement of CT, The Role of Electroencephalography in detecting local brain lesions has diminished. At the same time, this method remains indispensable for assessing changes in the brain's functional state across various periods of the traumatic illness. Electroencephalography is of particular importance when examining comatose patients, as other objective monitoring modalities for brain function dynamics are severely limited. Changes in electrical brain activity indirectly characterize the efficacy of pharmacological agents. In recent years, computerized methods of quantitative bioelectrical signal analysis—such as EEG frequency spectrum analysis and brain electrical activity mapping—have been applied for these purposes. The level and extent of brainstem injuries are quite thoroughly characterized by changes in short-latency auditory and somatosensory evoked potentials. Electroencephalography is widely utilized to detect epileptiform activity in the acute and remote periods of brain injury.

Assessment of impaired consciousness in traumatic brain injuries

The depth and duration of impaired consciousness in TBI are regarded as the most critical criteria for assessing injury severity and the patient's condition. Therefore, precise evaluation of these impairments is given special emphasis in the diagnostics of any trauma. As with other neurological and neurosurgical disorders, both quantitative and qualitative disturbances of consciousness can be observed in TBI.

Quantitative disturbances involve the depression of consciousness down to its complete loss and are assessed using the widely adopted Glasgow Coma Scale. It allows for the evaluation of a patient's condition based on three parameters: eye opening, verbal response, and motor response to external stimuli.

The total score ranges from 3 to 15. Severe trauma corresponds to 3-7 points, moderate to 8-12, and mild to 13-15. The patient's condition is assessed upon admission and, depending on its severity, at regular intervals until full recovery.

Glasgow Coma Scale

In domestic practice, the following grades of states of consciousness are more frequently used (T. A. Dobrokhotova, L. B. Likhterman, 1994).

In addition to quantitative disorders, neurological and neurosurgical diseases present a wide range of qualitative or disintegrative disturbances—various types of clouding and alteration of consciousness. They are differentiated by the ratio of so-called productive symptoms (hallucinatory, dreamlike states, phenomena of derealization and depersonalization, etc.) to deficit manifestations (impoverishment and loss of various mental processes).

Instrumental diagnostic methods in traumatic brain injury

Skull radiography

All TBI patients admitted to the hospital emergency department should undergo skull radiography in anteroposterior and lateral projections. Subsequently, if necessary, targeted views of the orbits, temporal bones, Occipital bone, Paranasal Sinuses, and others are performed.

Vault and skull base fractures are diagnosed most frequently. Complete fractures of the skull vault involve all bone layers. Linear, comminuted, and depressed (hole) fractures are distinguished. Incomplete injuries affect only the outer or inner table. Such fractures are visible only when the fracture plane coincides with the beam direction; therefore, they are typically not detected on standard radiographs. The length of a linear fracture on X-rays is always less than its anatomical extent. Attention should be paid to intersections of the fracture line with the grooves of meningeal arteries, which are accompanied by thin-walled veins. Injury to these vessels can lead to the formation of epidural hematomas. Diagnosing fractures along sutures is difficult. The main sign of such a defect is the absence of the serrated suture pattern in some areas. Healing of linear fractures in childhood takes from 6 months to 1.5–2 years. In adults, the fracture line remains visible on images for a long time, sometimes for life.

Skull base fractures are in most cases a continuation of vault fractures and are rarely isolated. They are usually accompanied by a tear of the dura mater and the formation of a communication between the cranial cavity and the external environment via the ear and oral cavities, the Orbit, ethmoid air cells, or paranasal sinuses. The appearance of nasal or otic liquorrhea (CSF leakage) and post-traumatic pneumocephalus are considered characteristic signs of such injury. Opacification of the paranasal sinuses most often indicates the presence of blood within them. In some cases, determining the exact fracture site fails even with special projections and tomography.

In the long-term period following TBI, calcifications may appear at the sites of hemorrhages, contusion foci, abscess capsules, cyst walls, and scar areas. Patchy radiolucency and irregular widening of diploic veins are regarded as radiological signs of osteomyelitis. Metal foreign bodies are easily detected on skull radiographs. Pieces of Glass, wood, and other Materials are recognized with greater difficulty. Their precise localization is possible only by comparing radiographs in different projections.

Echoencephaloscopy

Echoencephaloscopy is the simplest and most accessible method, based on the reflection of ultrasound from the boundary between intracranial structures and media with different acoustic densities. One of the most important parameters in echoencephaloscopy is the distance to the midline brain structures, which is determined by the position of the reflected signal (M-echo) on the oscilloscope screen. Normally, the shift of the midline brain structures (and accordingly the M-echo) should not exceed 2 mm. In concussion, echoencephaloscopy reveals no significant deviations. In focal contusions of the cerebral hemispheres, due to brain tissue edema, an M-echo shift towards the healthy side is detected. Supratentorial hematomas cause a particularly significant shift of midline structures, which can reach 8–16 mm. The informativeness of the method is low in basal, frontopolar, and bilateral hemispheric hematomas due to the insignificant change in the position of midline structures. Echoencephaloscopy makes it possible to monitor the width of the Third ventricle and indirectly assess the presence of intracranial hypertension.

Computed tomography

This is an X-ray imaging method based on computer mathematical reconstruction of the spatial distribution of X-ray absorption values by Tissues of the head, torso, or limbs. Calculation of absorption coefficients for each point of the matrix allows obtaining a series of axial slices of the head or another body part on a computer monitor across a wide range of halftone values, characterizing differences in brain tissue density of less than 0.5%. Gray and white matter, ventricles and subarachnoid spaces, skull bones, blood, edematous tissues, etc., are clearly identified on tomograms. The density scale ranges over 1000 relative Hounsfield units (with the absorption capacity of water taken as 0).

Currently, X-ray CT has become the leading diagnostic method for TBI and has no contraindications. Acute subdural or epidural hematomas are characterized by a biconvex or crescent-shaped zone of homogenous high density adjacent to the skull bones. In some cases, hematomas are bilateral, multiple, or have an atypical shape. The density of an acute epidural hematoma is higher than that of a subdural one due to the mixing of the latter with cerebrospinal fluid and brain detritus. Gradually, as a result of content liquefaction and blood pigment breakdown, the hematoma density decreases. After 1–6 weeks, it becomes isodense, i.e., close in absorption characteristics to brain tissue, which significantly complicates diagnostics. Detection becomes possible with contrast enhancement and consideration of secondary signs, which include compression or medial displacement of hemispheric subarachnoid sulci, narrowing of the ipsilateral lateral ventricle, and dislocation of midline structures. Following the isodense phase, a low-density phase ensues, in which the absorption coefficients of the extravasated blood and cerebrospinal fluid level out.

Brain contusions on CT can appear variously. A mild brain contusion presents as a localized area of decreased density. According to densitometric indices, it corresponds to brain tissue edema. Punctate hemorrhages are not detectable by X-ray CT. In deeper contusional brain injuries, small high-density foci are revealed against a background of homogenous decreased or increased density. Morphologically, the picture corresponds to microfocal hemorrhages in the contusion zone or moderate hemorrhagic imbibition of tissues. Severe brain trauma appears on tomograms as heterogeneous increased density (fresh blood clots) alternating with low-density areas of edematous and lacerated tissue. Massive round or oval foci of intense homogenous increased density may represent intracerebral hematomas. Diffuse axonal injury is characterized by increased brain volume due to swelling or generalized edema, as well as frequently petechial hemorrhages in the corpus callosum, brainstem, and periventricular regions. CT provides a unique opportunity to observe the dynamics of mass-effect formation, deformation of CSF spaces, and the development of dislocative complications.

Tomographic techniques also reveal extracranial injuries. Soft tissue injuries of the scalp are detected as local thickening with areas of moderate density increase, indicating blood infiltration. The direction and depth of the wound tract can be established, along with its projection relations to skull bone fractures. Differences in absorption coefficients facilitate the differentiation of subaponeurotic hematomas, scalp soft tissue contusions, subcutaneous accumulations of CSF, and pus. In depressed fractures or penetrating head wounds, it is possible to simultaneously examine the entire complex of injuries: soft tissue wounds, bone defects, brain destruction, air, blood pools, and even foreign bodies.

The diagnostic value of CT remains very high even beyond the acute phase of trauma. The method reveals the structural and morphological basis of long-term TBI consequences. Glial and connective tissue scars, cystic cavities, areas of brain atrophy, hydrocephalus, and other changes are clearly distinguishable on tomograms.

Magnetic resonance imaging

This is a non-invasive imaging method for the BRAIN AND SPINAL cord, based on the physical phenomenon of nuclear magnetic resonance, which occurs in a magnetic field when its frequency matches the natural precession frequency of protons in water molecules, Lipids, and Proteins. MRI uses principles of computer reconstruction of head slice images similar to X-ray tomography. Here, the distribution of density and Energy Levels of nuclei of certain chemical elements (hydrogen, phosphorus, carbon, etc.) is calculated. Therefore, along with the gross structure of brain tissues, the method partly allows assessing their histological features and the state of certain metabolic processes.

An advantage of magnetic resonance technology is the acquisition of tomograms in any arbitrarily chosen plane without changing the patient's position within the magnet bore or PARTS OF THE tomograph. At the same time, the image of brain structures features high contrast. A contraindication for MRI is the presence of metallic Foreign bodies in the cranial cavity, as There is a risk of their displacement under the Influence of the magnetic field and consequent brain tissue damage during the scan. Examination is impossible when a mechanical ventilator or cardiac pacemaker is connected. Intracranial clips are a relative contraindication unless made of non-magnetic materials. Dental prostheses and other metal dental structures can cause artifacts, but do not pose a serious danger during the examination.

In the acute stage of intracranial hematomas, MRI is less informative than X-ray CT due to the biochemical transformations of oxyhemoglobin and deoxyhemoglobin within the hematoma. Over time, the image contrast of intracranial hemorrhages on MRI increases significantly due to the formation of methemoglobin. Chronic hematomas are easily differentiated from other space-occupying lesions, such as tumors. Compared to X-ray CT, MRI has a distinct advantage in recognizing planar, parasagittal, and isodense hematomas. In brain contusions, the method makes it possible to detect contusion foci and perifocal edema of much smaller sizes than achievable with X-ray techniques, owing to its higher sensitivity to changes in tissue Hydration.

MRI is uninformative in detecting skull bone fractures. At the same time, sagittal tomograms are essential in diagnosing polytrauma, as they allow examination of the craniovertebral junction area, reveal spinal cord injuries, traumatic intervertebral disc herniations, epidural hematomas in the spinal canal, compression and comminuted vertebral body fractures, and spondylolisthesis. Subarachnoid and intracerebral hemorrhages are much better visualized on X-ray CT.

Cerebral angiography

This method of cerebral vessel contrast study is currently widely used in neurology and neurosurgery. To visualize the vessels, 50–60% solutions of triiodinated compounds are used. The main stage of the procedure is puncture of the common carotid artery with a thin-walled needle equipped with a stylet. Less commonly, a catheter is introduced via the femoral artery using the Seldinger technique. Fifteen to twenty minutes prior to angiography, the patient is administered 2 ml of papaverine, 2 ml of diphenhydramine, and 0.5 ml of atropine. Local anesthesia with a 2% novocaine solution is mandatory. In children under 7 years of age and in adults with psychomotor agitation, epileptic seizures, or altered consciousness, local anesthesia is supplemented with intravenous general anesthesia. To fill the common carotid artery basin, 8–10 ml of the contrast agent is injected over 1–1.5 seconds, and at the end of the injection, skull radiographs are taken in anteroposterior or lateral projections.

In the absence of CT, cerebral angiography remains the primary diagnostic method for intracranial hematomas. When located typically (in the temporal and parietal regions), direct radiographs reveal sufficiently convincing signs. These include a shift of the anterior cerebral artery toward the unaffected side and the displacement of hemispheric vessels—branches of the middle cerebral artery—away from the cranial vault bones. Lateral angiograms are less informative in these cases. Other patterns of vascular displacement may be observed with polar or basal hematomas. When intracerebral hematomas form deep within the frontal and temporal lobes, an increased distance between the anterior and middle cerebral arteries is detected. The extravasation of contrast medium from the vascular bed can serve as a universal sign of all intracranial hematomas, particularly when major vessels are displaced. However, this phenomenon is present only during the first few hours post-injury in the setting of ongoing hemorrhage.

Angiography also helps identify other pathological conditions, such as vascular spasm and thrombosis, shunting, and compensatory blood flow redistribution. In cases of pronounced intracranial hypertension and edema, the cerebral blood flow velocity decreases, which manifests on angiograms as a prolongation of the arterial phase. It should be borne in mind that vascular displacement may be caused by extensive perifocal edema surrounding a contusion focus.

The main indications for cerebral angiography in TBI include suspected intracranial hematoma, the need to rule out other space-occupying processes (such as tumors or abscesses), or underlying cerebrovascular diseases. A contraindication to angiographic examination is intolerance to iodine-containing contrast agents. Severe central respiratory disorders and a drop in blood pressure below 60 mmHg are also considered contraindications. The latter does not inherently pose a direct danger, but it increases the likelihood of contrast stasis in major vessels and the false appearance of carotid thrombosis. Arterial hypertension and a comatose state are not contraindications for angiography per se. In rare cases, seizures or transient paresis of the contralateral limbs may occur during the procedure. Paravascular hematomas in the neck may develop following the procedure and typically resolve without specific treatment. The advent of non-invasive neuroimaging modalities—such as X-ray and magnetic resonance computed tomography—has significantly streamlined patient evaluation and reduced the clinical reliance on cerebral angiography in neurotrauma cases.

Management of Patients with Traumatic Brain Injury

Patients with acute TBI of any severity are hospitalized in neurotrauma or neurosurgery departments. If such facilities are unavailable, casualties are admitted to a general surgical inpatient unit. Treatment must be differentiated and tailored to the individual. This entails determining the optimal combination of medications and their administration schedule, along with other therapeutic and rehabilitative measures tailored to the severity of the injury and the patient's clinical status. Another key prerequisite for effective treatment is accounting for the phased clinical course of the traumatic disease and the prevailing pathogenetic mechanisms at each specific stage. Undoubtedly, therapeutic success is ensured by continuous monitoring of neurological symptoms and the function of the body's vital systems. The primary goals and therapeutic targets of complex management in mild versus severe TBI differ significantly.

Management of Mild Traumatic Brain Injuries

Following a concussion, bed rest is recommended for several days (typically 3–5 days). Hospital stay generally ranges from 7 to 14 days, and an additional few days may be required for outpatient readaptation. The duration of bed rest, the pace of mobilization, and the timeline for returning to work are determined by the patient's subjective well-being, neurological status, age, occupational nature, and concomitant pathology. Prolonged bed rest following a concussion, regardless of the patient's actual condition, should be considered unjustified. Patients typically increase their physical activity on their own as soon as they feel able. Extended bed rest and prolonged hospitalization can induce iatrogenic effects and delay recovery. In some cases, the administration of certain medications or physical therapy may be continued after returning to work or studies. Nonetheless, concussion is an injury whose clinical manifestations are reversible in the majority of cases within 12 weeks.

Symptoms tend to be more protracted in mild cerebral contusions. In such cases, inpatient treatment may last 2 to 3 weeks. At the same time, certain forms of this more severe injury present with a relatively favorable condition of the patients from the very first days. It should be noted that many patients with mild TBI, for various reasons, either do not consult specialists, refuse hospitalization, or are managed as outpatients by a neurologist.

Virtually all cases warrant the administration of simple or combined analgesics, such as metamizole, paracetamol, pentalgin, sedalgin, spazgan, etc. During the first days post-injury, these are taken 3–4 times a day, though episodic intake as headaches intensify soon becomes sufficient. Intramuscular administration of these drugs is generally unnecessary. Traditionally, analgesics are combined with antihistamines.

Moderate dehydration is indicated only in mild cerebral contusions accompanied by increased cerebrospinal fluid pressure. The optimal approach is the administration of diakarb (0.25 g) or furosemide (0.04 g) 1–2 times daily for 1–2 weeks. Anxiety, agitation, internal tension, and sleep disturbances immediately following trauma are regarded as indications for mild tranquilizers, which also offer beneficial vegetostabilizing effects. Small doses in the afternoon or strictly at bedtime are usually sufficient. However, it should be kept in mind that even in these cases, certain patients may experience slight clinical deterioration while taking tranquilizers, manifested as increased dizziness or ataxia. Therefore, mild herbal sedatives such as valerian or motherwort are sometimes preferable. Neuroleptics in mild TBI patients are reserved for exceptional cases, such as managing acute psychotic states.

Vasoactive agents represent one of the components of drug therapy in patients with mild TBI. Their use requires careful consideration of individual vascular tone responses, as well as changes in cerebral and systemic hemodynamics as a whole. The most commonly prescribed medications are aminophylline (0.15 g three times daily), cinnarizine, and vinpocetine. Nevertheless, prolonged administration of these drugs to all patient categories—particularly those with concussions—without additional clinical justification is impractical. Conversely, in middle-aged or elderly individuals with concomitant cerebrovascular pathology, longer courses of treatment (1–3 months) and parenteral administration are often required. This is justified by the need to treat not so much the acute injury itself, but rather decompensated cerebrovascular diseases, such as dyscirculatory atherosclerotic or hypertensive encephalopathy, or vertebrogenic vascular disorders.

There is no compelling evidence that antiepileptic therapy in the acute phase of TBI can substantially reduce the risk of developing post-traumatic epilepsy. Therefore, the prophylactic administration of antiepileptic drugs to all patients with mild TBI in the absence of specific additional indications should be deemed unwarranted.

Once the period of decompensation—characterized by pronounced cephalgia, nausea, and dizziness—has subsided, the therapeutic regimen should shift toward interventions aimed at correcting metabolic and regulatory disorders within the central nervous system, thereby ensuring early rehabilitation and effective prevention of maladaptation disorders and neurosis-like conditions.

It is advisable to incorporate neurometabolic agents into the therapeutic program for the acute phase of mild TBI. Among the most popular is piracetam, which should be taken for 4–6 weeks post-injury (typically 0.4 g three times daily). Other prescribed agents include emoxypine, cerebrolysin, pantogam, bemithyl, actovegin, thiocetam, meldonium, etc. To improve metabolic processes in the CNS, multivitamin complexes containing pyridoxine, thiamine, and ascorbic acid are indicated. Toward the end of the acute phase of injury, in the presence of asthenia, courses of tonic preparations (adaptogens) such as eleutherococcus, pan

tokrine, and ginseng are employed. Electropharmacological methods may also be recommended for this purpose.

Management of Severe Traumatic Brain Injuries

During the first hours post-injury, the primary objective is the organization of intensive care aimed at restoring the functions of vital organs and systems. The efficacy of Pathogenetic Therapy in such settings is largely determined by adequate gas exchange, stable systemic hemodynamics, and preserved cerebral blood flow.

Controlling intracranial pressure is one of the core tasks of intensive care in severe TBI. Timely and appropriate management of intracranial hypertension reduces mortality in severe trauma from 85% to 35%. Moderate hypertension can be triggered by excessive neck flexion or turning the head to the side, which impairs venous outflow. Consequently, the patient's head should be kept in a neutral position and may be slightly elevated, though by no more than 30 degrees. Other common causes include airway obstruction, resistance to ventilation due to patient respiratory effort despite muscle relaxants, elevated arterial PCO2, hyperthermia, and epileptic seizures. In patients receiving neuromuscular blockers, the recognition of epileptic paroxysms is difficult; indicators include periodic pupil dilation, rising blood pressure, and specific changes in electrical brain activity. Another cause of intracranial hypertension is hyperhydration combined with hyponatremia. Nonetheless, the primary driver is the mass effect of intracranial hemorrhages and brain edema-swelling. In most cases, this requires surgical intervention, as therapeutic measures must primarily target the elimination of the underlying cause of hypertension. Intracranial pressure exceeding 25–30 mmHg poses a serious hazard and requires specific intervention. A simple initial measure is moderate hyperventilation to maintain arterial PCO₂ at 27–30 mmHg, which eliminates vasodilation and cerebral hyperemia. In cases of cerebral edema, intravenous administration of mannitol starting at a dose of 0.5 g/kg, furosemide, or albumin is most effective. Meanwhile, to ensure stable cerebral perfusion, systolic blood pressure should be maintained within 100–160 mmHg. L-Lysine aescinate exhibits good anti-edematous effects. A frequent cause of blood pressure drop in severe head injury patients is unrecognized hypovolemia resulting from uncompensated fluid loss under the influence of barbiturates. Since hyperglycemia can exacerbate ischemic brain damage in severe TBI patients, the administration of large quantities of glucose should be avoided; instead, iso-osmolar crystalloids are used at a volume of 50–60 ml/kg per day. Infusion of hypertonic NaCl solution (7.5%), especially when combined with dextrans, restores circulating blood volume more rapidly without increasing ICP (4–6 ml/kg over 5 minutes). Monitoring of plasma osmolarity and sodium concentration is essential. Hypo-osmolar solutions (5% glucose solution, 20% albumin solution) are not recommended in the management of TBI patients. To correct vascular and Metabolic Disorders, vasoactive agents (aminophylline, vinpocetine, pentoxifylline, etc.) as well as neuroprotective drugs (emoxypine, actovegin, citicoline, cytoflavin, thiocetam, meldonium, etc.) are utilized.

To control psychomotor agitation and seizures, physicians frequently employ diazepam, sodium oxybate, barbiturates (hexenal, sodium thiopental), and neuroleptics. Sodium oxybate also exerts a protective antihypoxic effect. Improper use of these medications—particularly neuroleptics and barbiturates—can in certain circumstances lead to a loss of clinical control over the patient and a worsening of consciousness, respiratory, and cardiac disorders.

During the period of cerebral edema regression (days 10–15), primary attention is directed toward normalizing neurotransmitter metabolism and stimulating reparative processes. To this end, neuroprotective agents (emoxypine, actovegin, citicoline, cortexin, cytoflavin, thiocetam, meldonium, Glycine, etc.) and neurotransmitter precursors are prescribed; these are especially crucial for patients exhibiting signs of central sympathoadrenal depression, delayed emergence from coma, or extrapyramidal disorders.

Prevention of purulent-inflammatory complications starting from the first hours post-injury is carried out using broad-spectrum Antibiotics. When selecting antibacterial agents, their ability to cross the blood-brain barrier is of decisive importance. Concurrently, analgesics, immunomodulators, and a broad range of medications are used to correct the functions of internal organs.

Proper nursing care is one of the most critical components of successful treatment in severe TBI. Severe head injuries are complicated by impaired skin trophic function and the formation of pressure ulcers. Abrasions on the face, torso, and limbs are cleansed with a 3% hydrogen peroxide solution. The skin is wiped with a 3% camphor alcohol solution or a special formulation (250 g of 96% alcohol, 250 g of distilled water, 5 ml of shampoo). The patient's position must be changed every 2–3 hours. Special rubber rings are placed beneath bony prominences, and the use of anti-decubitus mattresses is recommended. To prevent joint contractures, the limbs are fixed in physiological positions. When pressure ulcers develop, they are treated with ultraviolet or laser irradiation. Macerated areas are managed with a 5% potassium permanganate solution, and Solcoseryl ointment and other topical agents are applied. Nutrient formulas are administered 4–5 times daily via a nasogastric tube; the total volume of nutritional mixtures for adults should be at least 2.5–3 liters. Regular Oral Cavity care is required, along with instilling 20% sodium sulfacetamide and sterile petrolatum into the eyes to prevent corneal dryness. Bowel function is closely monitored, and Urinary Bladder dysfunction is managed via catheterization. In patients with a tracheostomy, regular suctioning of the Oral Cavity and Trachea is mandatory. To prevent pulmonary complications, chest percussion and vibration massage, as well as active and passive breathing exercises, are performed, along with Oxygen therapy.

As the patient's condition stabilizes—typically after 3–4 weeks—treatment is modified to address the dominant clinical syndrome. Over the subsequent weeks and months, a combination of neurometabolic and vasoactive drugs, Vitamins, resorption-promoting agents, tranquilizers, and adaptogens is utilized. Gradual expansion of the motor regimen, physical therapy, targeted and focal massage, physiotherapy, and psychotherapy are recommended.

Principles of Surgical Management in Patients with Traumatic Brain Injury

Soft tissue wounds of the scalp, excluding minor superficial skin abrasions, require primary surgical debridement. The optimal timeframe for this procedure is within the first 6 hours following the injury. However, severe Impairment of Vital functions, delayed presentation of patients, and other factors may preclude timely intervention.

Debridement of scalp wounds is performed after shaving the Hair 3–4 cm outward from the wound edges. The skin is prepared with 70% ethanol and a 5% iodine solution. Local anesthesia is achieved using 0.25% to 1% procaine (novocaine). After the removal of foreign bodies and non-viable tissue, hemostasis is secured, and sutures are applied. Arterial bleeding can be controlled by suturing the vessel through the aponeurosis. In cases of avulsion wounds, the debrided flap is sutured back into position or alternative plastic surgery techniques are employed. Subcutaneous hematomas are treated by aspirating the blood through a large-bore needle. If signs of suppuration develop, wound management should be switched to an open method using antibiotics, antiseptics, and bactericidal agents.

Brain compression resulting from a localized depressed skull fracture typically does not pose an immediate threat to life. A more serious concern is the irritation of the cerebral cortex by bone fragments, the potential formation of an epileptogenic focus, and the risk of purulent intracranial complications. Therefore, a depressed fracture with bone displacement equal to or exceeding the thickness of the skull bone requires surgical elevation, even in the absence of neurological symptoms. The surgery should be performed as early as possible. It involves removing small bone fragments (up to 2–3 cm) and repositioning larger pieces. If repositioning fails to ensure stability, the fragments are secured with sutures. Simultaneous exploration of the injury site may reveal an intracranial hematoma, injury to a venous sinus or the dura mater, or parenchymal brain damage, which would necessitate expanding The Scope of the procedure. If bone fragments injure a venous sinus, they are carefully removed and the defect is temporarily controlled by digital pressure. Subsequently, sinus repair is performed, or a muscle graft or the dura mater is sutured to the wound. In extreme cases, packing or suturing of the sinus may be required.

The detection of an intracranial hematoma is an indication for urgent surgical intervention. Depending on its location, either osteoplastic or decompressive craniectomy is performed. In cases of subdural hematomas, the dura mater visible through the Craniotomy defect appears bluish, tense, and non-pulsatile. It is incised, and blood and blood clots are evacuated from the subdural space. Thorough hemostasis is then achieved, the dura mater is closed, the bone flap is replaced, and the scalp layers are reapproximated. A drainage tube is left in the wound for 24 hours to allow for the outflow of blood and wound secretions. Recently, the removal of subdural hematomas using endoscopic techniques through a small (approximately 25 mm in diameter) trephine burr hole in the skull has become feasible.

For small volumes of epidural or subdural hematomas (up to 30 mL) in the absence of dislocation symptoms, conservative management under CT monitoring is acceptable, which typically leads to blood resorption within 3 to 4 weeks. Occasionally, spontaneous drainage of epidural hematomas occurs through skull fractures into the subaponeurotic space. In such cases, aspiration of the blood accumulated beneath the aponeurosis via needle puncture is sufficient.

The treatment of choice for intracerebral hematomas is craniotomy, incision of the brain tissue (encephalotomy), and evacuation of the hematoma. Alternatively, one may resort to placing a burr hole and performing needle aspiration of the hematoma, provided that more than 75% of its volume can be aspirated and enhanced cerebral pulsation is achieved. In cases of multiple bilateral intracerebral hematomas, only the larger and more superficially located hematoma should be removed. In certain instances, conservative management is viable under serial CT observation. This approach is permissible provided three conditions are met: 1) the patient's level of consciousness is no worse than deep obtundation; 2) the hematoma diameter does not exceed 3 cm; and 3) there are no signs of brainstem compression.

When isolated subdural and epidural hematomas are removed promptly, before severe generalized cerebral and brainstem dysfunction develops, mortality is low, and favorable functional outcomes predominate. The prognosis worsens when intracranial hematomas are accompanied by cerebral contusion foci, in older age groups, in the presence of internal organ diseases, with delayed surgical intervention, and when complicated by coma and brainstem dislocation syndromes. In such cases, mortality rates reach 50–60% for acute subdural hematomas and 30–40% for epidural hematomas. Among survivors, persistent disabling neurological deficits are common.

Recently, Surgical treatment has also occasionally been utilized for brain contusions. The removal of a contusional focus, particularly in the base of the temporal and frontal lobes, is undertaken to prevent progressive brain compression caused by extensive perifocal edema. Thus, the majority of brain compression factors are eliminated operatively.

Clinical Problems

Option 1

A 12-year-old child slipped while playing on ice, fell, and struck the back of their head. Following a brief loss of consciousness (lasting a few seconds), the child experienced nausea, repeated vomiting, diffuse headache, and chills. Over the next two hours, during examinations in the emergency department and the neurosurgery ward, the child appeared sluggish and drowsy, yet answered questions appropriately and was fully oriented. Physical examination revealed skin pallor, fine inconstant horizontal nystagmus, and convergence weakness. Kernig's sign and nuchal rigidity were equivocal. A tender soft-tissue swelling was noted in the occipital region. Blood pressure was 110/70 mm Hg, and pulse was 66 beats per minute and regular. Skull radiographs in anteroposterior and lateral projections showed no fractures. Echoencephaloscopy and head CT revealed no abnormalities. The following day, the patient complained of moderate headaches, nausea and dizziness upon changing body position, fatigue, and reading discomfort. The child had no memory of the accident or subsequent events spanning a 1.5-hour period. General well-being returned to normal by the fifth day.

   • How would you assess the child's condition upon admission?

   • Name the main neurological impairments.

   • Describe the biomechanics of the injury.

   • How can the disturbances of consciousness and memory that developed following the injury be classified?

   • List the types of post-traumatic amnesia.

   • Formulate a clinical diagnosis.

   • State the diagnostic criteria for this type of traumatic brain injury.

   • Formulate a topographic diagnosis.

   • Outline the main directions for Differential diagnosis.

   • Present the instrumental examination plan for patients with suspected mild TBI.

   • What are the indications for craniography in head injuries?

   • What is the clinical utility of performing CT and MRI in mild TBI?

   • Outline the management protocol for patients with mild TBI.

   • Describe the pharmacotherapy for concussion.

   • State the potential complications of mild TBI.

   • Name the most frequent consequences of mild TBI.

   • Formulate recommendations for the patient and their family.

Option 2

A 34-year-old man hit his head after falling from a height of 2 meters at a construction site. He experienced a brief loss of consciousness for a few minutes. He complains of a moderate diffuse headache, nausea, and Hearing loss in the left ear. Several abrasions are visible in the frontal and left temporal regions. There is extensive bruising in the parotid area. Blood-tinged fluid is observed leaking from the left ear, alongside hyperactive tendon reflexes on the right, moderate bilateral Kernig's signs, and neck stiffness. Lateral skull radiographs reveal a linear fracture of the left temporal bone extending to the skull base. Echoencephaloscopy shows a 3-mshift of the M-echo from left to right. Somatic status is unremarkable.

   • How would you assess the patient's condition?

   • Identify the primary neurological disorders.

   • Assess the biomechanics of the injury.

   • How can the hearing impairment and otorrhea be interpreted in conjunction with other examination findings and medical history?

   • Explain the Origin of the anisoreflexia.

   • Explain the results of the echoencephaloscopy.

   • Formulate a topical diagnosis.

   • Formulate and justify a clinical diagnosis.

   • Outline the main directions for differential diagnosis.

   • Propose a neurological examination plan.

   • What changes might a head CT scan reveal in this case?

   • Outline the patient management plan, estimated treatment duration, and periods of disability.

   • Name the Key Components of drug therapy.

   • What types of traumatic brain injury are classified as open?

   • List the potential complications during the acute phase of the injury.

   • Enumerate the most frequent sequelae of the remote post-traumatic period.

Option 3

A 26-year-old intoxicated man sustained a blow to the head with a metal object during a fight. He did not lose consciousness. Minor bleeding from a laceration in the left parietal region stopped on its own. He did not seek medical attention. During the night, at the insistence of his relatives, he was examined by an ambulance doctor and referred to the hospital. He complained of precordial pain. A slight elevation in blood pressure was noted (150/90 mmHg, pulse 70, regular). Upon admission, skull radiographs revealed a depressed fracture of the left parietal cranial vault measuring 2.5 by 3 cm, with bone fragments displaced 1.5 cm into the cranial cavity. Neurological examination revealed anisoreflexia (D > S). Meningeal signs were absent. Echoencephaloscopy showed no abnormalities. He adamantly refused surgical debridement of the wound and discharged himself home the following day.

   • Determine the biomechanics of the injury.

   • How would you evaluate the patient's condition?

   • State the main neurological deficits.

   • How can the elevated blood pressure and cardialgic symptoms be explained?

   • Explain THE ORIGIN OF anisoreflexia.

   • Formulate the topical diagnosis.

   • Formulate and justify the clinical diagnosis.

   • Outline the main directions for differential diagnosis.

   • Describe the neurological examination protocol.

   • What is the rationale for performing a head CT or MRI?

   • State the management tactics for the patient upon initial presentation.

   • List the Main Components of drug therapy.

   • Determine the indications for surgical treatment.

   • Indicate potential complications of the acute phase of trauma in this case.

   • Identify the most characteristic long-term sequelae of the injury for this clinical case.

   • What types of injuries are classified as open traumatic brain injuries?

   • What types of injuries are classified as penetrating traumatic brain injuries?

Case 4

A 22-year-old male, heavily intoxicated with alcohol, fell out of a moving car and struck his head against the concrete road surface. Half an hour later, he was brought to the hospital in an unconscious state. Examination of the right frontoparietal region revealed an extensive laceration measuring 4 x 9 cm without aponeurosis damage, multiple abrasions of the scalp, as well as abrasions on the torso and knee joints. During the examination, deep somnolence alternated with agitation; he was disoriented and resisted the examination. Anisoreflexia S>D was detected, along with moderate nuchal rigidity and bilateral Kernig's signs. Pathological Babinski plantar reflexes were present. Skull radiographs revealed no traumatic bone lesions. Echoencephaloscopy showed a 2-D shift of the M-echo from right to left. Blood pressure was 140/85 mm Hg. Pulse was 80 bpm, regular. Over the next few hours, a series of seizures occurred. They began with sudden muscle relaxation and respiratory arrest, followed by tonic and subsequently clonic convulsions with foaming at the mouth. In the intervals between seizures, deep somnolence persisted. Elevated blood pressure up to 160/95 mm Hg and a pulse of 94 bpm were noted. On the morning of the following day, he became agitated, completely disoriented in time and surroundings, failed to recognize relatives, and tried to hide from imaginary pursuers. The cerebrospinal fluid was bloody, revealing partially disintegrated erythrocytes. CSF pressure was 280 mm H₂O. Following complex pharmacotherapy, orientation in surroundings and time gradually recovered after two days, and his behavior became adequate. He began complaining of intense headaches and weakness. He has no recollection of the circumstances of the injury or the events of the subsequent two days. He has a history of systematic alcohol abuse for five years. Convulsive seizures had occurred twice following bouts of heavy drinking.

   • How can the patient's condition upon admission be assessed?

   • List the main neurological disorders.

   • How can the consciousness disturbances be characterized: a) immediately after the injury; b) in the intervals between seizures; c) one day after the injury?

   • Explain the echoencephaloscopy findings.

   • Explain the cerebrospinal fluid alterations.

   • How should the memory impairments that became apparent after the restoration of consciousness be characterized?

   • How should the post-traumatic series of seizures be interpreted?

   • Formulate the topical diagnosis.

   • Formulate the clinical diagnosis.

   • Outline the main directions for differential diagnosis.

   • Describe the evaluation protocol for the injured patient.

   • What is the rationale for performing a head CT or MRI?

   • What is the optimal management strategy for the patient from the time of admission?

   • What might the development of meningeal syndrome following trauma indicate?

   • What is The Significance of concurrent alcohol intoxication in the development of neurological disorders and the assessment of severity?

   • Explain the significance of remote medical history findings.

   • Name the main components of medical therapy.

   • Indicate potential complications during the acute phase of the trauma in this case.

   • Identify the most characteristic long-term sequelae of the trauma for this clinical case.

Case 5

A 59-year-old man struck his head against a log while loading firewood. He did not lose consciousness, felt no significant change in well-being, and continued working. The next day, he experienced a feeling of heaviness in his head. Over the course of a week, he suffered from moderate headaches on several occasions. Some time later, following physical exertion, he began to complain of persistent frontal and temporal pain that persisted even at night. According to his relatives, his behavior gradually changed over the month: he became lethargic, uncommunicative, and indifferent to his surroundings. Difficulties emerged in finding words and pronouncing them correctly. Upon examination, he is somnolent and somewhat disoriented in time and space. He complains of a headache. He is unable to provide any further information regarding his condition or medical history. Bilateral oral release signs, mild anisoreflexia D>S, and equivocal Kernig's signs are detected. Blood pressure is 140/90 mmHg, pulse is 60 bpm and regular. There are no abnormalities in the internal organs. Skull radiographs reveal no bone-destructive lesions. Fundoscopic examination reveals venous dilation. Echoencephaloscopy demonstrates an M-echo shift of 8 mm from left to right.

   • How would you assess the patient's condition?

   • List the main neurological disorders.

   • Which of the listed impairments determine the patient's condition at the time of examination?

   • How can the severity of the trauma sustained a month ago be assessed?

   • Assess the patient's level of consciousness during the examination.

   • Characterize the speech impairments.

   • Explain the echoencephaloscopy results.

   • Formulate the topographical diagnosis.

   • Formulate a preliminary clinical diagnosis.

   • Outline the main directions for differential diagnosis.

   • What is the optimal management strategy for the patient from the time of presentation?

   • Describe the protocol for instrumental neurological examination.

  • Outline the diagnostic workup plan.

  • Describe the likely head CT findings for this case.

  • Describe the characteristic cerebral angiography findings for this case.

  • List the symptoms of intracranial hypertension.

  • What symptoms, in addition to those listed, may be observed in chronic traumatic intracranial hematomas?

  • Indicate the pathomorphological and pathophysiological differences between acute and chronic traumatic intracranial hematomas.

  • Describe the approaches and principles of surgical management for chronic traumatic intracranial hematomas.

  • State the possible and most characteristic long-term sequelae of the injury for this case.