What are the dangers of closed craniocerebral injury? Modern principles of classification of traumatic brain injury What is closed traumatic brain injury

Penza State University

medical school

department of technical and electrical engineering

course "Extreme and military medicine"

Traumatic brain injury

Penza 2003

Compiled by: Candidate of Medical Sciences, Associate Professor Melnikov V.L., Art. teacher Matrosov M.G.

Traumatic brain injury is one of the most common injuries and accounts for >40% of the total number; the mortality rate for severe injuries of the skull and brain reaches 70-80%. The mechanism of traumatic brain injury can be direct or indirect. An example of an indirect mechanism would be traumatic brain injury resulting from a fall from a height onto the legs or pelvis. When landing and stopping the movement of the skeleton, the skull, due to inertia, seems to be pushed onto the spine and a fracture of the base of the skull can occur. If this does not happen, the skull stops, and the brain, continuing to move, hits its base and standing bones.

Classification of traumatic brain injuryTable 1.

Syndromes: Hypertensive - cerebrospinal fluid pressure is increased. Hypotensive - cerebrospinal fluid pressure is reduced. Normotensive - cerebrospinal fluid pressure is not changed.

Diagnosis of traumatic brain injury: There are four main groups of clinical symptoms: cerebral, local, meningeal and brainstem.

General cerebral symptoms. Their formation is based on functional (reversible) changes in the substance of the brain. Appearing after injury, these signs gradually regress and, ultimately, disappear without a trace. These include:

1. Loss of consciousness. It proceeds according to the stem type and is characterized by three forms of manifestation: a) stunning - expressed by a short-term disturbance of orientation followed by mild drowsiness. Particular attention should be paid to this form of disorder of consciousness, since victims remain on their feet and do not regard the state of stupor as a loss of consciousness; b) stupor - a more severe degree of impairment of consciousness, in which the reaction to gross stimuli (pain, loud cry) in the form of coordinated defensive movements, opening of the eyes is still preserved; c) coma - prostration with a complete loss of perception of the surrounding world, deepening, characterized by adynamia, atony, areflexia, depression of vital functions.

2. Memory loss (amnesia). It may be: retrograde, when patients do not remember the events immediately preceding the injury; anterograde - loss of memory for events that occurred after the injury; anterograde - a combined form of memory loss for events before and after injury.

Headache. There can be both diffuse and local pain, bursting or squeezing the head.

Dizziness. Instability in the Romberg pose.

Nausea, vomiting. Depending on the type and nature of the injury, nausea can be short-term with one or two vomiting and long-term with frequently repeated vomiting, even indomitable.

Positive Mann-Gurevich sign. The doctor asks the patient to follow with his eyes, without turning his head, any object in his hand, and makes several (3-5) oscillatory movements of the object in the frontal plane. If the patient’s well-being has worsened, cerebral and autonomic manifestations have intensified, and tachycardia has appeared, then the symptom is considered positive.

7. Autonomic symptoms. Weakness, noise or ringing in the ears, pallor or hyperemia of the skin, increased humidity or dryness, lability of the pulse and other vegetative manifestations.

Local(they are also focal) symptoms. The reason for their appearance is organic damage to some part of the brain and loss of function in the zone of its innervation. Clinically defined local signs are nothing more than paresis, paralysis, sensitivity disorders and dysfunction of the sensory organs. For example: motor or sensory aphasia, anisokaria, smoothness of the nasolabial fold, deviation of the tongue, monoparesis of the limbs, hemiparesis, etc.

Meningeal (meningeal) symptoms. They are the result of irritation of the meninges directly by trauma (bruises, ruptures), pressure from bone fragments, foreign bodies, hematomas (the dura mater has baroreceptors), blood, infection and other ingredients. Typical severe meningeal symptoms can be identified during an external examination of the patient. He takes a forced position, lying on his side with his head thrown back and his legs bent at the knees and hip joints (the “trigger” pose). Other characteristic symptoms are photophobia. The victim tries to turn away from the light source or covers his face with a blanket. There is increased excitability, and an extreme reaction to harsh stimuli can be a convulsive seizure.

Patients complain of intense headaches that get worse when moving their heads. Localization of pain is the frontal and occipital areas with irradiation to the neck or eyeballs. Often there is pain in the eyeballs. When the meninges are irritated, nausea and vomiting are observed, the latter being repeated and debilitating.

Pathognomonic meningeal signs are nuchal rigidity and positive Kernig and Brudzinski signs. An increase in body temperature to 39-40°C is typical, especially if an infection occurs.

Stem symptoms. In their genesis they are no different from local ones, but the damage affects only the brain stem and its structures that regulate vital functions. Injury to the brain stem can be primary, or arise as a result of brain dislocation and pinching of the brain stem into the foramen of the cerebellar tentorium or in the occipito-cervical dural infundibulum.

Stem symptoms are divided into non-upper-trunk, lower-trunk and dislocation.

Upper stem(mesodiencephalic syndrome) is characterized by a disorder of consciousness in the form of stupor or stupor. Mild breathing disorders - tachypnea and “orderly breathing”, when the duration of inhalation and exhalation becomes the same. Cardiovascular disorders consist of increased heart rate up to 120 per minute. and an increase in blood pressure to 200/100 mm Hg.

Upper brainstem symptoms include a large number of oculomotor disorders. This is a symptom of “floating gaze”, divergence in the vertical and horizontal planes, convergence, gaze paresis, etc.

Muscle tone is high, reflexes are animated or increased, bilateral pathological reflexes from the feet appear (Babinsky, Gordon, Oppenheim). Swallowing is not impaired. Body temperature is high.

Nizhnestvolova(bulbar) syndrome is characterized by a more severe condition. There is no consciousness - coma. Respiratory disorder reaches an extreme degree, pathological forms of breathing occur. The pulse is weak and frequent. Blood pressure drops to 70/40 mmHg. and below. The pupils are wide, the reaction to light is subtle. Swallowing is severely impaired. Thermoregulation is reduced.

Dislocation syndrome- this is a rapid transition from the upper brainstem to the lower brainstem syndrome as a result of brain infringement.

Traumatic brain injury can occur with increased, normal or decreased cerebrospinal fluid pressure, depending on which hyper-, normo- and hypotensive syndromes are distinguished. Diagnosis of the syndrome can be carried out on the basis of clinical manifestations and using auxiliary methods.

Hypertension syndrome occurs in 65% of victims with traumatic brain injury. It occurs more often in older people. It occurs with a bursting headache, high blood pressure, and bradycardia. A positive symptom of “raised head” (pillow) is noted - patients take a forced position with the head end raised, since an elevated position reduces headaches.

Traumatic brain injury with hypotension syndrome occurs in 25% of victims. A decrease in cerebrospinal fluid pressure is more often observed in young people, occurring with a compressive headache, with normal or low blood pressure, and tachycardia. Vegetative signs are pronounced, most often manifested by pallor and sweating. Increased fatigue, lethargy, and mental exhaustion are noted. A positive symptom of “lowered head” is that giving the patient a Trandelenburg position reduces headaches.

During a lumbar puncture with the patient in a supine position, cerebrospinal fluid flows out in drops at a frequency of 60 per minute, and the pressure measured by a manometer is 120-180 mm of water column. These numbers are considered the norm. An increase in the frequency of drops and cerebrospinal fluid pressure is regarded as hypertension, and a decrease is considered as hypotension.

Lumbar puncture should be performed in all patients with concussion and more severe TBI.

Additional research methods

Craniography- the most common method. When examining patients with traumatic brain injury, two panoramic craniograms are required: straight and lateral. .

Schemes of craniograms in overview projections with explanations are presented in Fig. 1.

Rice. 1. Scheme of craniograms in direct (A) and lateral (B) projections:

(A) 1. Pyramid. 2. Lesser wing of the main bone. 3. Mastoid process. 4. Atlantooccipital

joint. 5. Atlantoaxial joint. 6. Frontal sinus. 7. Sagittal suture. 8. Lambdoid suture. 9. Coronal suture. 10. Maxillary sinus.

(B) 1. Pyramid. 2. Main bone. 3. Turkish saddle. 4. The anterior part of the large wings of the main bone. 5. Frontal sinus. 6. Coronal suture. 7. Lambdoid suture. 8, 9. Anterior and posterior branches of the meningeal artery, 10. Internal and external auditory canals. 11. Shadow of the auricle cartilage. 12. Nasal bones. 13. Cheek bones. 14. Maxillary sinus

Echoencephalography- this is the registration of the position of the midline structures of the brain (epiphysis, third ventricle, interhemispheric fissure, etc.) by receiving a reflected ultrasound signal from them (M-echo). The method is based on the ability of ultrasound to propagate in various media and give reflection at the border of structural formations with inhomogeneous acoustic resistance. The ultrasonic wave reflected from the object is recorded on the screen of the echoencephalograph in the form of a peak located along the midline. During volumetric processes in the cranial cavity (hematomas, hygromas, traumatic cysts, abscesses, tumors), the midline structures of the brain shift toward the healthy hemisphere. This is revealed on the echoencephalogram in the form of a displacement of the M-echo from the midline by 3 mm or more. With pronounced volumetric processes, for example, with epi- and subdural hematomas, the displacement of the M-echo can reach 8-15 mm (Fig. 2).

Rice.2

Normal echogram (A). Displacement of midline structures and M-echo with intracranial hematoma (B)

Carotid angiography. This research method is based on the introduction into the carotid artery of substances that have the property of absorbing X-rays, which ensures the visibility of blood vessels on an X-ray at different phases of cerebral circulation. By changes in the filling and location of the vessels, the degree of circulatory disturbance in the brain and its causes are judged.

CT scan- an X-ray method of research using a computer, which allows one to obtain images of the structures of the brain and bones of the skull both in whole form and in sections with a thickness of 3 to 13 mm. The method allows you to see changes and damage to the bones of the skull, structures of the brain, identify intracerebral and intracranial hemorrhages and much more.

Patients with traumatic brain injury should undergo ophthalmological and otorhineurological examination.

Lumbar puncture done to clarify the pressure of the cerebrospinal fluid, determine its composition and the patency of the cerebrospinal fluid pathways.

The manipulation is performed with the patient lying on his side, on a hard table with his legs bent towards the stomach. The back is bent as much as possible. The place for puncture is the space between the III and IV lumbar vertebrae. Treat the skin with iodine tincture, then with alcohol until traces of iodine disappear, the entry of which into the lumbar canal is extremely undesirable. The puncture site is anesthetized with a 1% novocaine solution in an amount of 5-10 ml. The puncture is performed with a special needle with a mandrel, directing its course strictly sagittally and at an angle to the frontal plane. The angle corresponds to the inclination of the spinous processes. The sensation of needle failure usually corresponds to the needle being in the subarachnoid space. When removed from the mandrin needle, cerebrospinal fluid begins to flow out. The pressure is measured with a manometer, and then 2 ml of cerebrospinal fluid is taken for examination. In case of high blood pressure, the cerebrospinal fluid should be slowly released by drip until the cerebrospinal fluid pressure normalizes.

Normally, cerebrospinal fluid is clear. In an adult, the subarachnoid space and ventricles contain 100-150 ml of cerebrospinal fluid, which is completely renewed up to 6 times a day. It is absorbed and in return produced mainly by the choroid plexuses of the ventricles.

Laboratory examination: colorless transparent liquid, cytosis in 1 μl - 2-3; pH - 7.35-7.80; protein - 0.15-0.33 g/l; glucose - 0.5-0.8 g/l.

CLINICAL AND DIAGNOSTICS OF INDIVIDUAL

NOSOLOGICAL FORMS OF CRANIOBRAININJURIES

Brain concussion

The cause of a concussion is a mechanical injury of direct or indirect impact, followed by the development of general cerebral symptoms. The nature of the headaches and the position in bed depend on the cerebrospinal fluid pressure, and the severity of clinical manifestations depends on the severity of the injury.

Nystagmus, slight asymmetry of the face may appear due to the smoothness of the nasolabial fold and drooping of the corner of the mouth, deviation of the tongue. These and other local “microsymptoms” usually occur within 1-2 days. Longer persistence of these signs indicates the presence of a brain contusion.

Additional research methods practically do not provide information that reliably confirms the diagnosis. An exception is lumbar puncture, which can be used to determine changes in cerebrospinal fluid pressure.

With proper treatment, the patient's condition improves by the end of the first week, and complete regression of clinical signs occurs after 2-4 weeks. The most stable are headache and the Mann-Gurevich symptom, the test of which should be used to determine the timing of bed rest. Once it disappears (becomes negative), patients are allowed to sit up in bed and then get up and walk.

Brain contusion

Brain contusion occurs due to direct and indirect mechanisms of impact. An example of an indirect mechanism of injury is a counter-impact, when a wave of “perturbed” brain matter, consisting of 80% water, reaches the opposite wall of the skull and hits its superior parts or is destroyed by tightly stretched areas of the dura mater.

A brain contusion is an organic lesion. As a result of the injury, areas of crushing and necrosis of brain tissue, severe vascular disorders with phenomena of hemorrhagic softening occur. Around the area of ​​brain contusion there is a zone of severe molecular concussion. Subsequent pathomorphological changes are expressed in encephalomalacia and lysis of a portion of the medulla, its resorption. If an infection occurs during this period, a brain abscess is formed. In an aseptic course, the brain tissue defect is replaced by a scar of neuroglia or brain cysts are formed.

The clinical picture of brain contusion is that immediately after the injury, victims experience general and local symptoms, and in severe forms, meningeal and brainstem symptoms are added.

There are three degrees of brain contusions.

/ degree (mild bruise). Loss of consciousness from several minutes to 1 hour. Upon restoration of consciousness, pronounced general cerebral symptoms and local, predominantly microfocal signs are determined. The latter are stored for 12-14 days. Violations of vital functions are not determined.

Grade I brain contusion may be accompanied by moderate subarachnoid hemorrhage and fractures of the bones of the vault and base of the skull, which are detected on craniograms.

// degree (moderate). Switching off consciousness after injury reaches 4-6 hours. During the period of coma, and sometimes in the first days of recovery of consciousness, moderately severe disorders of vital functions (upper brainstem signs) are detected in the form of bradycardia, tachypnea, increased blood pressure, nystagmus, etc. As a rule, these phenomena are transient.

Upon return of consciousness, amnesia, intense headache, and repeated vomiting are noted. In the early post-comatose period, mental disorders may be observed.

When examining the patient, distinct local symptoms are found that last from 3-5 weeks to 6 months.

In addition to the listed signs, with a second degree brain contusion, pronounced meningeal symptoms are always detected, fractures of the vault and base of the skull can be found, and in all cases significant subarachnoid hemorrhage.

Additional research methods: with lumbar puncture, increased cerebrospinal fluid pressure and a significant admixture of blood in it are determined. Craniograms show fractures of the skull bones. Echoencephalography gives a displacement of the M-echo of no more than 3-5 mm.

Illdegree. Loss of consciousness after injury is prolonged - from several hours to several weeks. The condition is extremely serious. Severe disturbances of vital functions come to the fore: changes in heart rate (bradycardia or tachycardia), arterial hypertension, disturbances in the frequency and rhythm of breathing, hyperthermia. Primary brainstem symptoms are clearly expressed: floating movements of the eyeballs, gaze paresis, tonic nystagmus, bilateral mydriasis or miosis, impaired swallowing. If the patient is in stupor or in a state of moderate coma, it is possible to identify local symptoms in the form of paresis or paralysis with impaired muscle tone and reflexes. Meningeal symptoms include stiff neck, positive Kernig and Brudzinski signs.

Grade III brain contusion is usually accompanied by fractures of the vault and base of the skull and massive subarachnoid hemorrhage.

Electroencephalography - with a brain contusion and crushing, high-amplitude delta waves appear in the destruction zone. With extensive convexital lesions, zones of electrical silence are found corresponding to the most severely affected area.

BRAIN COMPRESSION

The causes of compression of the brain can be: intracranial hematomas, bone fragments, foreign bodies, hygromas, pneumocephalus, hydrocephalus, subarachnoid hemorrhage, edema and swelling of the brain. The first four of these causes cause local compression of the brain and are the true root causes of intracranial catastrophes with a fairly typical course and frequent tragic outcome. The remaining nosological forms arise as a consequence of the listed or other severe injuries of the skull and brain, or as a natural subsequent stage of local compression of the brain. They lead to a total increase in brain volume and, as the pathology progresses, can cause dislocation and pinching of the brain in the foramen magnum.

Compression of the brain by bone fragments and foreign bodies

Compression of the brain by bone fragments occurs during fractures of the skull vault with prolapse of fragments deeper than the internal bone plate. Depressed fractures of the calvarium are mainly of two types. The first is when, as a result of mechanical action, the fragments are displaced at an angle, the apex of which “looks” into the cranial cavity, and the peripheral ends of the fragments retain connection with the mother bone. Such fractures are called impression fractures. The second type of fracture (depression) occurs when the injury is inflicted with great force, and the damaging agent has a small contact area. For example, a blow with a hammer, brass knuckles or a similar object. As a result of the injury, a fenestrated fracture occurs, the size and shape of the wounding object. The bone plate that covered the resulting “window” falls into the cranial cavity and leads to compression of the brain (Fig. 3).

Foreign bodies enter the cranial cavity mainly as a result of gunshot (bullet, shrapnel) wounds. However, penetrating injuries to the skull are also possible with cold steel or household objects, parts of which, breaking off, remain in the cranial cavity.

Rice. 3. Depressed fractures of the calvarium: A - impression; B - depressed.

Preliminary data allow us to make a diagnosis of brain contusion (of varying severity), which in fact accompanies depressed fractures and foreign bodies of the skull with compression of the brain. The final diagnosis is made after craniography, computed tomography, echoencephalography, with the help of which depressed skull fractures or foreign bodies in it are identified, and clinical data and the results of additional research methods on the topography of the location of the ingredient causing pressure on the brain tissue must match.

Compression of the brain by intracranial hematomas

Intracranial hematomas occur in 2-9% of the total number of traumatic brain injuries. There are epidural, subdural, subarachnoid, intracerebral, intraventricular hematomas (Fig. 4).

Fig4. Intracranial hematomas: 1 - epidural; 2 - subdural; 3 - intracerebral; 4 - intraventricular

The clinical manifestations of various hematomas are not the same, but in their course a number of patterns can be traced that allow intracranial hematomas to be considered in one group. Schematically, it looks like this: a history of head trauma with loss of consciousness (often for a short period). Upon return of consciousness, general cerebral symptoms are identified, on the basis of which a diagnosis of “concussion” can be made. Optimally, the patient is hospitalized and appropriate treatment is prescribed: rest, sedatives, etc. In some cases, victims may not seek help, since short bed rest, as a rule, relieves general cerebral symptoms. Moderate headaches and amnesia persist. The patient's condition improves significantly. Thus, rupture of an intracranial vessel at the time of injury due to the lack of clinical evidence of brain compression remains unnoticed. As compression increases, meningeal and then local symptoms appear (anisokaria, mono- or hemiparesis, etc.). A disorder of consciousness of the cortical type occurs. Psychomotor and speech agitation occurs, which subsequently turns into depressed consciousness (stupor), often with convulsive seizures and subsequent cerebral coma. The outcome of brain compression if left untreated is usually death. Thus, intracranial hematoma is characterized by a three-phase course: injury with loss of consciousness - improvement of the condition (“bright interval”) - deterioration of the condition with a tragic outcome.

Light interval refers to the time from the return of consciousness after the initial injury to the appearance of signs of brain compression. The duration of the light interval can be from several hours to several days, weeks and even months. Depending on this, hematomas are divided into acute (light period up to 3 days), subacute (from 4 to 21 days) and chronic (more than three weeks).

What determines the duration of the light interval?

It has now been proven that hematomas are mainly formed during the first three hours, and their volume, significantly exceeding 30-50 ml, does not always interrupt the light interval. The reason is that the brain is not “squeezed” into the skull, but has certain spaces between it and the membranes with a certain intracranial pressure. A formed hematoma at an early stage does not cause pronounced compression of the brain, since it, like any living organ, sacrifices its volume to a certain extent, compensating for its functional state. Gradual vascular disorders, hypoxia, increasing edema, and then swelling of the brain lead to an increase in its volume and a sharp increase in pressure along the area of ​​contact between the hematoma and the brain. A breakdown of the compensatory capabilities of the central nervous system occurs, which is expressed in the end of the light interval. A further increase in brain volume leads to displacement of the midline structures, and then dislocation of the brain stem into the foramen of the cerebellar tentorium and the occipito-cervical dural infundibulum.

An increase in the duration of the clear interval in the acute stage may be due to the absorption of the liquid part of the blood from the hematoma and a decrease in its volume. The duration of imaginary well-being is also facilitated by dehydration carried out in a hospital for patients diagnosed with a concussion or cerebral contusion, which does not allow the development of pronounced swelling of the brain tissue.

With subacute and chronic hematomas, it is possible to increase their volume (on days 16-90) due to the influx of fluid. The decomposition of spilled blood and the increase in the content of high molecular weight proteins increase the oncotic pressure in the hematoma. This causes diffusion of the cerebrospinal fluid until an osmotic equilibrium is created between the liquid contents of the hematoma and the cerebrospinal fluid.

It is possible that the lucid interval may be interrupted by repeated hemorrhages in the epi- or subdural space when a blood clot breaks off from a damaged vessel. This can occur with a sudden sharp change in arterial and intracranial pressure - when sneezing, coughing, straining, etc.

Thus, the duration of the clear interval depends on many factors, and not just on the time and intensity of bleeding.

Epidural hematomas

Epidural hematoma - This is a limited accumulation of blood between the bones of the skull and the dura mater of the brain. Suprathecal hemorrhages occur as a result of a direct mechanism of injury when exposed to a traumatic agent with a small area of ​​application of force of varying intensity and account for 0.6-5% of all traumatic brain injuries.

The source of epidural hematoma formation most often is damage to the branches of the middle meningeal artery, the vein of the same name, or the spongy substance of a broken bone. This explains the fact that epidural hematomas in 73-75% of cases are located in the temporal region. The dura mater is tightly adjacent to the bones of the skull and is fused with them along the suture lines, therefore the area of ​​epidural hematomas is limited and most often is 6-8 cm in diameter.

Suprathecal hematomas usually have a hemispherical shape with a height in the central part of up to 4 cm. The amount of blood poured into the epidural space is often in the range of 80-120 ml, although local accumulation of blood in a volume of 30-50 ml leads to compression of the brain.

The clinical picture of acute epidural hematoma is characterized by a predominantly classical course.

The history reveals the presence of a head injury, accompanied by loss of consciousness. Upon return of consciousness, only general cerebral symptoms are found in the patient.

In the further clinical course of epidural hematoma, 4 stages can be distinguished: a light interval, a stage of excitation, inhibition and cerebral coma.

The light period is short, from several hours to 1.5-2 days, in most cases it does not exceed 24 hours. This stage begins with the return of consciousness and is characterized by the presence of the already described cerebral symptoms. During the first hours after injury, the severity of cerebral symptoms fades. At rest, dizziness and vomiting disappear, nausea and headache decrease. The victim is adequate, oriented in time and space, and critically assesses his condition.

In the next stage, the patient develops unconscious anxiety. He is overly active, strives to change the position of his limbs, sit down, stand up, and leave the room. The face is hyperemic, there is aloofness or fear in the eyes. Patients cannot stand bright light or noise. This excitement is caused by increased headaches, which are painful and bursting in nature. The victim covers his head with his hands, takes a forced position, begs or demands immediate help, agrees and insists on surgical treatment.

Persistent nausea, repeated vomiting, terrifying dizziness appear - everything floats before your eyes. The pulse rate slows down, moderate bradycardia occurs (51-59 beats/min), blood pressure increases (from 140/80 to 180/100 mm Hg). Breathing becomes moderately faster (21-30 breaths per minute). At this stage, focal microsymptoms may appear: mild anisokaria - slight dilation of the pupil on the side of the hematoma, smoothness of the nasolabial fold, moderate deviation of the tongue. Percussion of the skull can reveal areas of increased pain (usually above the hematoma), to which the patient reacts with a pained grimace.

During the inhibition stage, the patient's behavior changes radically. He no longer rages or asks for anything. A secondary disorder of consciousness occurs, beginning with stupor and progressing to stupor. The victim is indifferent to his surroundings, his gaze is pointlessly directed into the distance. Bradycardia (41-50 beats/min.) and tachypnea (31-40 breaths per minute) increase. Asymmetry in blood pressure appears. On the arm opposite to the lesion, blood pressure will be 15-20 mmHg. higher than on the arm on the side of the hematoma. Focal symptoms increase. Among them, the main diagnostic role is played by: dilation of the pupil on the side of the hematoma, smoothness of the nasolabial fold, abnormal grins, deviation of the tongue, spastic hemiparesis with a predominant lesion of the arm on the opposite half of the body. Meningeal signs are identified in the form of stiff neck and positive Kernig and Brudzinski signs.

The final stage of untreated epidural hematoma is the stage of cerebral coma. It is caused by displacement and compression of the brain. It is characterized by dislocation signs: the transition of bradycardia to tachycardia (120 beats/min. and above), tachypnea to pathological types of breathing, blood pressure begins to steadily decrease, reaching critical numbers (below 60 mm Hg), swallowing disorders, a symptom of floating gaze, gross anisocaria and dissociation of meningeal symptoms, muscle tone and reflexes along the body axis. In the final phase, bilateral mydriasis with lack of pupillary response to light, areflexia, muscle atony, and death occurs.

A favorable outcome for epidural hematoma is possible with early diagnosis and timely adequate treatment. In addition to clinical signs, craniography, computed tomography, echoencephalography and carotid angiography are of diagnostic value, with the help of which they can identify fractures of the cranial vault, most often the scales of the temporal bone, an area of ​​​​increased density of a plano-convex or biconvex shape adjacent to the skull, displacement of the median M-echo by 6-15 mm and displacement of intracerebral vascular structures.

An ophthalmological examination reveals congestion in the fundus.

Subdural hematomas

A subdural hematoma is a limited accumulation of blood between the dura and arachnoid membranes of the brain. The incidence of these hemorrhages ranges from 1 to 13% of all traumatic brain injuries. Subdural hematomas most often occur with an indirect mechanism of injury, such as a counter-strike on the side opposite to the application of force. The area of ​​contact with the traumatic agent is large, so significant destruction occurs in this place: skull fractures, brain contusions, subarachnoid hemorrhages.

The source of the formation of subdural hematomas is most often damage to the transitional veins in the area between the surface of the brain and the sagittal sinuses as a result of displacement of the brain or bone fragments. Another reason is the rupture of the delicate pial vessels during sharp rotation of the head and displacement of the hemispheres around the vertical or horizontal axes. These same vessels are damaged during brain contusions.

Subdural hematomas can reach 250-300 ml, but more often their volume is 80-150 ml. In 60% of cases, hematomas form over the convex surface of the brain in the form of a cloak 1-1.5 cm thick, covering 1-2 lobes over an area of ​​4x6 to 13x15 cm.

Clinical manifestations of subdural hematomas in the classical version are close to the course of epidural hemorrhages, but at the same time they have a large number of distinctive features and signs that allow differential diagnosis of these nosological forms of injury in the acute period. (Table 2).

Thus, there are quite a few signs that make it possible to distinguish the clinical picture of an epidural from a subdural hematoma.

Subdural hygroma

Subdural hygroma - It is a localized collection of cerebrospinal fluid in the space beneath the dura mater resulting from trauma.

Subdural hygromas are much less common than hematomas in a similar situation. The issue of pathogenesis of hygroma has not been completely resolved. The reasons for the limited accumulation of cerebrospinal fluid under the dura mater are considered to be damage to the arachnoid membrane, like a valve that allows the cerebrospinal fluid to move in only one direction - from the subarachnoid to the subdural space. Hygromas can also occur due to changes in the vessels of the dura mater, creating conditions for blood plasma to leak into the subdural space, or as a result of severe brain damage when communications arise between the intrathecal spaces and lateral ventricles.

The clinical manifestations of subdural hygromas are heterogeneous, since they can occur both in isolation and in combination with many nosological forms of traumatic brain injury, most often accompanying severe brain contusion.

If the hygroma occurs in isolation, then its clinical picture is very similar to that of a subdural hematoma, especially in its three-phase course. As a rule, after an injury with a short-term loss of consciousness, a clear interval occurs, usually lasting 1-3 days and with typical cerebral symptoms. Then the headache intensifies, stupor appears and increases, meningeal and local symptoms appear in the form of facial nerve paresis, mono- or hemiparesis, and sensory disturbances.

However, in the classic clinic of intracranial hematoma, you can notice some features typical of subdural hygroma, or signs that are most often found with it. This is a long clear period (1-10 days) - hygromas often have a subacute course. Headaches are paroxysmal, radiating to the eyeballs and cervical-occipital region. Photophobia and local pain on percussion of the skull are characteristic. The general condition of patients deteriorates slowly, as do signs of brain compression, which increase relatively more gently and gradually. Mental disorders such as frontal syndrome are often observed (decreased criticism of one’s condition, euphoria, disorientation, apathetic-abulic symptoms), proboscis and grasping reflexes appear. Psychomotor agitation often develops.

Paresis of the limbs of a spastic type with hypertonicity and revitalizationreflexes. Quite often, patients with hygromas have convulsive seizures starting from the muscles of the face or on the contralateral side. Subdural hygromas are characterized by a gradual, wave-like deepening of secondary disturbances of consciousness. So, in the early stages, after a convulsive seizure, consciousness is restored and contact can be made with the patient.

Acute hygromas are characterized by the absence of anisocaria, and if it is present, then, unlike hematomas, the reaction of the pupil to light is preserved.

Intracerebral hematomas

Intracerebral hematoma - This is a post-traumatic hemorrhage into the substance of the brain with the formation of a cavity filled with blood. The incidence of intracerebral hemorrhages is approximately 5-7% of all intracranial hematomas. The favorite localization is the frontotemporal lobe. The size of intracerebral hematomas is relatively small and is 1-3 cm in diameter, but can reach 7-8 cm. The volume of spilled blood is most often in the range of 30-50 ml, sometimes more massive hematomas are found - 120-150 ml.

The source of cerebral hemorrhages is damaged vessels of the brain substance due to its contusion or other types of traumatic brain injury

The clinical picture of isolated intracerebral hemorrhages tends to be three-phase and have acute, subacute and chronic stages of the course. The latter depend on the volume of the hematoma and the brain’s response to injury, expressed by edema and swelling.

In the acute course of a hematoma, a clear gap is observed in half of the patients, in the rest it is absent or in an erased form. After the initial loss of consciousness, which can last from several minutes to several days, a period of imaginary well-being begins, which differs from meningeal hematomas in its short duration (no more than 6 hours), the presence, in addition to general cerebral, meningeal and gross focal symptoms in the form of hemiparesis and plegia. It should be emphasized that paresis and paralysis in patients with intracerebral hematomas always develop contralaterally, while pupil dilation in 50% of victims occurs on the side of the hematoma, in the rest - on the opposite side. The light interval, as a rule, ends with a sudden entry into a coma. Vegetative-stem symptoms appear early in the form of respiratory failure, cardiovascular

activities. Hormetonia syndrome often develops, characterized by strong tonic tension in the muscles of the limbs and trunk with a predominance of extensors. Sometimes there are epileptic seizures. All symptoms tend to increase.

Computed tomography, echoEG, angiography and pneumoencephalography can facilitate diagnosis, with the help of which it is possible to respectively identify an area of ​​altered density in the brain substance, a displacement of the M-echo, a displacement of the vascular and median structures of the brain.

Intraventricular hematomas

Intraventricular hematomas - These are post-traumatic hemorrhages in the cavities of the lateral, III and IV ventricles of the brain. This type of hemorrhage occurs only against the background of a severe brain contusion and practically never occurs in isolation.

Intraventricular hematomas account for 1.5 to 4% of all intracerebral hemorrhages. They are caused by rupture of the choroid plexuses of the ventricles as a result of hydrodynamic shock at the time of injury. Most often, one of the lateral ventricles is affected. 40-60 and even 100 ml of blood can flow into it.

The clinical picture of intraventricular hematoma depends on the rate of bleeding into the ventricle and the severity of the concomitant brain contusion. Blood pressure on the walls of the ventricle and irritation of the reflexogenic zones embedded in them not only aggravate the severity of the injury, but also gives the clinical picture some originality. There is a disorder of consciousness in the form of stupor or coma. Literally following the injury, vegetative-stem disorders appear and rapidly increase. Against the background of progressive intracranial hypertension, combined with arterial hypertension, hyperthermia occurs, reaching 38-41°C. The victim's face and neck are hyperemic with symptoms of hyperhidrosis.

Severe motor agitation with the presence of hormetonia is considered characteristic of intraventricular hematomas. Extensor spasms can be provoked by external stimuli, even by neurological examination techniques. Sometimes they are combined with epileptic seizures.

Neurological symptoms with intraventricular hematomas are usually bilateral.

Dysregulation of breathing appears quite early in the form of tachypnea (30-70 breaths per minute), which persistently progress, reaching pathological forms (Cheyne-Stokes, Biota). Subsequently, signs of brain dislocation appear (transition of bradycardia to tachycardia, reaching 160 or more beats per minute with bilateral mydriasis, the appearance of pathological reflexes from the feet.

In patients with intraventricular hematomas, motor-tonic phenomena are often detected in the form of automated gestures, stereotypical hand movements (“scratching”, “stroking”, “pulling the blanket”), as well as oral and manual hyperkinesis of the subcortical type (sucking and smacking movements of the lips, tremor limbs), which manifest from the initial period and can persist until the agonal state.

Lumbar puncture reveals copious amounts of blood in the cerebrospinal fluid.

Subarachnoid hemorrhage.

Subarachnoid hemorrhage - This is a post-traumatic accumulation of blood in the subarachnoid space, which does not cause local compression of the brain. This intracranial hemorrhage does not occur in isolation, but is a companion to traumatic brain injuries, mainly brain contusion. Subarachnoid hemorrhages occur in 15-42% of all traumatic brain injuries, and in severe forms they reach 79%. Even higher figures are given by forensic doctors, who observed subarachnoid hemorrhages in 84-92% of cases, and some in 100% of all traumatic brain injuries.

The source of subarachnoid hemorrhages is ruptured vessels of the membranes that limit the subarachnoid space, or increased vascular permeability as a result of injury. The spilled blood spreads over large areas (from 50 to 300 cm 2 or more), taking on a lamellar character. Subsequently, most of the blood is absorbed into the subdural space and further into the blood vessels of the dura mater, the remaining red blood cells undergo decay. It has been established that blood and its toxic breakdown products (bilirubin, serotonin) irritate the meninges and cause disturbances in cerebral circulation, liquor dynamics, and sharp fluctuations in intracranial pressure with a disorder of brain functions.

What is pathognomic for subarachnoid hemorrhages is that loss of consciousness after the initial injury is replaced by a state of stupor, disorientation, and often psychomotor agitation. The restoration of consciousness is accompanied by retro- and anterograde amnesia, memory impairment of the asthenic type and Korsakoff traumatic amnestic syndrome.

In victims with subarachnoid hemorrhage, by the end of the first day, meningeal syndrome develops as a response to irritation of the membranes with blood. It is characterized by intense headache in the occipital and frontal regions, pain in the eyeballs and neck, photophobia, nausea and repeated vomiting, stiff neck and positive Kernig syndrome. The syndrome increases, reaching a peak on days 7-8, and then declines and disappears by days 14-18.

As a result of irritation by blood of the recurrent branch of the trigeminal nerve (1st branch), tentorium cerebellum syndrome occurs, manifested by photophobia, injected conjunctival vessels, lacrimation, and rapid blinking. As the flow of fresh blood into the cerebrospinal fluid decreases, the syndrome fades and completely disappears by 6-7 days.

The breakdown products of blood and brain detritus inhibit the cortical section of the motor analyzer. Because of this, from 2-3 days there is a weakening of the tendon and periosteal reflexes (especially the knee), which disappear completely by 5-6 days. By 8-9, sometimes by 12-14 days, and even later, reflexes are restored and return to normal.

For 7-14 days after the injury, an increase in body temperature remains 1.5-2 degrees above normal.

A reliable sign of subarachnoid hemorrhage is the presence of blood in the cerebrospinal fluid.

SKULL FRACTURES

Fractures of the skull bones account for up to 10% of fractures of all skeletal bones and are classified as severe injuries, because they are unthinkable without damage to the underlying structures - the membranes and substance of the brain. 18-20% of all severe traumatic brain injuries are accompanied by skull fractures. There are fractures of the facial and cerebral skull, and fractures of the vault and base are distinguished among injuries of the cerebral skull.

Fractures of the base of the skull

Fractures of the base of the skull arise predominantly from an indirect mechanism of injury when falling from a height onto the head, pelvis, lower limbs due to impact through the spine, and also as a continuation of fractures of the vault. If the fracture is single, then the fracture line can pass through one of the cranial fossae of the base: the anterior, middle or posterior, which will subsequently determine the clinical picture of the injury. The latter has characteristic manifestations also because a fracture of the base of the skull is accompanied by a rupture of the dura mater, which is intimately fused to it and often forms a connection between the cranial cavity and the external environment. Thus, the picture of a fracture of the base of the skull consists of clinical manifestations of concomitant brain injury (contusion of varying severity) and symptoms that are pathognomonic for a violation of the integrity of the anterior, middle or posterior cranial fossa.

In the first case, hemorrhages occur in the paraorbital tissue (symptom of “glasses”) and leakage of cerebrospinal fluid mixed with blood from the nasal passages. It should be noted that with traumatic brain injuries, multiple bruises of the soft tissues of the head are possible with the formation of a large number of different sizes and localizations of bruises and bleeding from the nose, ear canals, etc. It is necessary to be able to differentiate bruises and bleeding as a result of the direct mechanism of injury from the symptom of “glasses” and liquorrhea.

Traumatic “spectacles” appear 12-24 hours or more after the injury, often symmetrical. The color of the bruise is homogeneous and does not extend beyond the orbit. Palpation is painless. There are no signs of mechanical impact - wounds, abrasions, eye injuries. A fracture of the base of the skull may be accompanied by exophthalmos (hemorrhage into the retrobulbar tissue) and subcutaneous emphysema when the air cavities are damaged.

With direct trauma, bruising appears immediately after the blow. They are not symmetrical and often extend beyond the orbit and are painful on palpation. There are signs of direct mechanical impact: skin abrasions, wounds, hemorrhages in the sclera, bruises of uneven color, etc.

Blood mixed with cerebrospinal fluid on white cotton fabric produces a stain in the form of two rings of different colors. In the center, the color is more intense due to the formed elements of blood, but in the periphery it has a sterile color, formed by an excess of the liquid part.

In case of a fracture of the middle cranial fossa, characteristic signs should be considered a bruise in the posterior wall of the pharynx and liquorrhea from the ear canals.

A fracture of the posterior cranial fossa is accompanied by severe bulbar disorders (damage to the brain stem) and bruising into the subcutaneous tissue of the mastoid region. It should be noted that all bruises from a fracture of the base of the skull appear, as well as the symptom of “glasses”, no earlier than 12-24 hours from the moment of injury. The clinic is the leader in diagnosing fractures of the base of the skull, since primary radiographs in standard settings can detect bone damage in only 8-9% of victims. This is due to the complexity of the anatomical structure of the bones that form the bottom of the skull, and the no less complex course of the fracture line, which selects holes in the weakest places of the base of the skull. For reliable diagnosis, special techniques are required, which cannot always be used due to the severity of the patient’s condition.

Cranial vault fractures

Cranial vault fractures result from a direct mechanism of injury, where the point of application of force and the site of injury coincide. An indirect mechanism is also possible when the skull, which has a spherical shape, is compressed; the fracture occurs at the point of intersection of the force lines with an extreme load, and not in the pressure zone.

Fractures of the calvarium are divided into linear (cracks), depressed (impression and depression) and comminuted.

Clinical diagnosis of closed calvarial fractures, which account for about 2/3 of all fractures, is extremely difficult. Subperiosteal and subgaleal hematomas and severe pain complicate palpation, which should already be extremely gentle to avoid

displacement of the comminuted fracture and injury to the underlying formations. The idea of ​​a possible fracture may be suggested by the history of the severity of the mechanical injury and the symptom of axial load - compression of the head in the sagittal and frontal planes. In this case, the pain radiates to the fracture site. To clarify the diagnosis, it is necessary to perform craniography in standard settings, but also according to forensic data In medical autopsies, about 20% of fractures remain unrecognized.

The greatest difficulty in diagnosis is presented by linear fractures, which are often mistaken for a vascular pattern. The latter differs from a linear fracture in that it has a tree-like shape with a wider base and thin apex. In addition, twisted branches extend from the trunk, which in turn have the same branches, but thinner.

Rice. 5. X-ray signs of a calvarial fracture:

A - normal vascular pattern; B - symptom of enlightenment and zigzag;

B - symptom of line doubling (symptom of “ice flake”)

Linear fractures have a number of distinctive features:

1. Symptom of transparency (linear clearing) - is associated with a break in the bone and is often distinct, but sometimes it may be due to the vascular pattern or the contour of the cranial sutures.

Symptom of bifurcation - Along the course of the cracks, in some areas the line bifurcates, and then again goes single. Bifurcation occurs with through cracks, when a beam coming at an angle to the fracture line can separately reflect the edges of the outer and inner vault plates. An illusion is created that islands of bone are gouged out along the fracture line, which is why this sign is called the “ice flake” symptom. The symptom of bifurcation absolutely confirms the diagnosis of a fracture.

Zigzag symptom(lightning) - expressed by a zigzag line of enlightenment. Refers to reliable signs of a fracture that have absolute diagnostic value (Fig. 5).

Sometimes, along with cracks, seams come apart.

Treatment of patients with traumatic brain injury

Treatment of patients with traumatic brain injury is a complex and extensive range of medical measures, the choice of which in each specific case depends on the type, severity and progression of the injury, the stage at which therapy was started, age, concomitant diseases and much more.

Assistance to victims with traumatic brain injury can be divided into three periods: assistance at the pre-hospital stage, treatment in a hospital (hospital stage) and “follow-up treatment” in a polyclinic setting (outpatient stage) or under the supervision of a family doctor.

Providing assistance at the prehospital stage is as follows:

Place the patient in a horizontal position. Create peace of mind with the means at hand: pillow, bolsters, clothes.

Check and, if necessary, clear the airways from vomit, tongue retraction, etc.

Stop external bleeding by pressing the edges of the wound with your fingers or a pressure bandage.

Cold to the head.

Give oxygen inhalation.

According to indications, the following are used: analeptics (cordiamin, cititon, lobeline), cardiac glycosides (strophanthin K, korglykon).

Transport the patient urgently (necessarily in a supine position) to a medical facility.

All patients with traumatic brain injury must be hospitalized! Treatment in a hospital can be conservative or surgical. Bloodless treatment methods are used much more often, while surgical interventions are performed according to strict indications.

Patients with concussion, brain contusion, closed calvarial fractures, fractures of the base of the skull, and subarachnoid hemorrhages are treated conservatively.

All patients, regardless of the type of injury, are prescribed:

Strict bed rest. Its duration depends on the severity of the injury. So, with a grade I concussion, strict bed rest lasts 5-7 days, grade II - 7-10 days. For grade I brain contusion - 10-14 days, grade II - 2-3 weeks and grade III - at least 3-4 weeks. To determine the termination of strict bed rest, in addition to the specified periods, the Mann-Gurevich symptom is used. If it is negative, the patient can sit up in bed, and after adaptation, stand up and walk under the supervision of staff.

Cold to the head. Use ice packs wrapped in a towel to prevent frostbite. To cool the head, helmets of various designs were offered (with a system of constantly circulating cold water, with a system of thermoelements, etc.). Unfortunately, our industry does not produce these necessary devices for treating patients. Exposure to head hypothermia depends on the severity of the injury. For mild injuries (concussion and cerebral contusion of the first degree), its exposure is limited to 2-3 hours, and for severe injuries, exposure lasts 7-8 hours or more, up to 1-2 days. But it should be remembered that when using cold for a long time, take a break of 1 hour every 2-3 hours.

The purpose of using cold is to normalize vascular disorders, reduce the production of cerebrospinal fluid, prevent cerebral edema, reduce the need for oxygen in brain tissue, and reduce headaches.

3. Sedatives(sodium bromide, bromocamphor, corvalol), etc. tranquilizers(Elenium, Seduxen, Tazepam).

4. Sleeping pills(phenobarbital, barbamyl, etaminal sodium). Strict bed rest, the prescription of tranquilizers, sedatives and hypnotics are a set of measures aimed at creating rest for the damaged organ, i.e. brain. Medicines weaken external stimuli, prolong physiological sleep, which has a beneficial effect on the functions of the central nervous system.

5. Antihistamines(diphenhydramine, fenkarol, diazolin).

As a result of vascular disorders and hypoxia of the brain, destruction and resorption of intracranial hemorrhages, and disintegration of the destroyed brain matter, a mass of histamine-like substances (serotonin, etc.) is formed, therefore the prescription of antihistamines is mandatory.

The further choice of treatment prescriptions depends on the height of the patient’s cerebrospinal fluid pressure. With increased cerebrospinal fluid pressure (hypertension syndrome), treatment should be as follows: position in bed according to Fowler - with the head end elevated, diet No. 7 with limited salt and liquid.

To reduce cerebral edema, dehydration is used. Concentrated hypertonic solutions are administered intravenously to increase the osmotic pressure in the vascular bed and cause the outflow of fluid from the interstitial spaces of the brain. For osmotherapy, use 40% glucose solution, 40% sodium chloride solution, 25% magnesium sulfate solution, 15% mannitol solution at the rate of -1-1.5 per 1 kg of body weight. The last two drugs have pronounced diuretic properties. Of the diuretics, furosemide (Lasix) is most often used for tissue dehydration. Cleansing enemas help remove fluid from the body.

Unloading lumbar punctures directly reduce cerebrospinal fluid pressure, when, following a lumbar puncture, 8-12 ml of cerebrospinal fluid are slowly released.

For hypotensive syndrome, the following is prescribed: diet No. 15, position in bed according to Trandelenburg - with the leg end raised. Solutions with low salt concentrations (isotonic Ringer-Locke, 5% glucose solution) are administered intravenously. Subcutaneous injections of caffeine-sodium benzonate 1 ml of 10% solution and vagosympathetic novocaine blockades have a good therapeutic effect.

In some cases, it becomes necessary to prescribe certain groups of drugs and medications. So, for open injuries, when there is a threat of developing infectious complications, antiseptics, antibiotics and sulfonamides are used.

In case of violation of vital functions, analeptic drugs are administered that stimulate the respiratory center and vascular tone (cordiamin, lobeline hydrochloride, cititon); to normalize blood pressure in the entire vascular bed, adrenomimetic substances are used (adrenaline hydrochloride, norepinephrine hydrotartrate, mesatone). Weakness of the heart muscle is treated with cardiac glycosides (strophanthin K, corglycon).

Traumatic brain injury is often part of a polytrauma accompanied by shock and blood loss. In the complex of anti-shock therapy, blood and plasma-substituting solutions (reopolyglucin, gelatinol, Acesol) are transfused, analgesics (morphine hydrochloride, promedol, analgin), hormones (hydrocortisone) and other drugs are administered.

Surgical treatment patients with acute traumatic brain injury is inevitable with open injuries and in the presence of signs of brain compression. For open injuries, primary surgical treatment is performed. The wound is closed with sterile material. The hair around it is shaved off. The skin is washed with soapy water, wiped with napkins and treated twice with a solution of 5% iodine tincture. Local infiltration anesthesia is performed with a 0.25% solution of novocaine with the addition of antibiotics. After anesthesia, the wound is thoroughly washed with an antiseptic solution (furacilin, hydrogen peroxide, rivanol) and examined. If only soft tissue is damaged, nonviable tissue is excised. For compressed wounds with crushed edges, it is better to excise them to a width of 0.3-0.5 cm to the bone. The bleeding is stopped and the wound is sutured.

If a fracture is detected during inspection of the wound, then it is necessary to carefully remove all small loose fragments with tweezers and examine the dura mater. If there is no damage, normal color, or preserved pulsation, the shell is not opened. The edges of the bone wound are resected with pliers to a width of 0.5 cm. Hemostasis is performed and sutures are placed on the wound.

If the dura mater is damaged, i.e. If there is a penetrating wound to the skull, then primary surgical treatment is performed as described above, but with economical excision of the edges of the shell. For better inspection of the subdural space, the wound of the dura mater is expanded. Loose bone fragments, brain detritus, and blood are washed out with hydrogen peroxide and warm isotonic sodium chloride solution. After stopping the bleeding, the dura mater is sutured, if possible, and layer-by-layer sutures are applied to the soft tissues of the skull.

Compression of the brain, regardless of the reasons that caused it, must be eliminated immediately after diagnosis.

For depressed closed fractures of the calvarium, an incision is made into the soft tissue down to the bone with the expectation of exposing the fracture site. A milling hole is placed next to it, through which they try to lift the depressed fragment using a levator. If the fragments were able to be lifted, which happens very rarely, and they do not move, then the operation can be completed, having first made sure that there are no indications for extended surgery. If the fragments cannot be lifted, then the depressed portion of the bone is resected from the side of the burr hole. The further course of the intervention is the same as during primary surgical treatment, but without excision in the dura mater.

If the brain is compressed by hematomas or hygroma, resection or osteoplastic surgery can be performed. The first option of the operation is that a search burr hole is placed in the projection of the suspected hematoma. If a hematoma is detected, the hole is expanded by gradual resection of the bone to the desired size (6x6, 7x7 cm). Through the created window, intervention is performed on the brain and membranes. The operation is completed by suturing the soft tissue, leaving a large defect in the skull bones. This operation creates good decompression of the brain, especially when compression of the brain is combined with severe contusion. But resection trepanation also has negative sides. After this, another intervention is necessary to close the skull defect with synthetic material (steractyl) or autologous bone taken from the rib. If this is not done, post-trepanation syndrome will develop. Changes in intracranial pressure caused by physical stress (straining, coughing, sneezing, etc.) lead to frequent movements of the brain matter into the “window” of the skull defect. Trauma to the brain from the edges of the burr hole causes the development of a fibrotic process in this area. Adhesions are formed between the brain and the membranes, bones and integument of the skull, which cause local pain and headaches, and subsequently epileptic seizures. Osteoplastic trepanation does not leave skull defects requiring subsequent plastic surgery. A semi-oval incision is made from the base downwards in the soft tissue down to the bone. Along the incision line, without separating the soft tissue flap, five milling holes are drilled - two at the base of the flap and three along the arc. Using a guide, a Gigli saw is passed through two milling holes and the bone bridge is sawed off. All holes are gradually connected into a single one, and the bone-soft tissue the flap on the feeding pedicle is turned downwards. The further course of the operation depends on the type of injury. After completion of the intervention in the cranial cavity, the bone flap is put in place and the soft tissue is sutured in layers.

Test task for self-study on the topic"Traumatic brain injury"

Mechanisms of traumatic brain injury.

Classification of traumatic brain injury.

Name the general cerebral symptoms.

Name local symptoms.

Name meningeal symptoms.

Name the stem symptoms.

What is hyper-, hypo- and normotensive syndrome and how to define it?

How is a concussion diagnosed?

On what basis is the diagnosis of “brain contusion” made?

Gradation of injury severity, clinical differences in degrees of severity.

Causes of compression of the brain.

Clinic of compression of the brain by bone fragments and foreign bodies, as distinguished from brain contusion.

Clinic of brain compression by intracerebral and intraventricular hematomas.

Clinic of brain compression by epi- and subdural hematomas, as distinguished from brain contusion.

What is a subdural hygroma?

Difference between the clinic of concussion, bruise and compression by epi- and subdural hematomas.

Clinic of subarachnoid hemorrhage.

Fracture of the base of the skull, diagnosis.

Traumatic glasses and liquorrhea, their diagnosis. Signs of damage to the anterior, middle and posterior cranial fossae.

Fractures of the cranial vault, diagnosis, tactics.

First aid for traumatic brain injuries.

Conservative treatment of acute traumatic brain injury, give a pathogenetic rationale.

Conservative treatment of brain damage during the recovery period.

Surgical treatment of traumatic brain injury (TBI): puncture, trephination, trepanation.

Techniques of various types of trepanations, necessary instruments.

What is post-trepanation syndrome, its treatment.

Outcomes and long-term consequences of TBI.

Traumatic brain injury (TBI), among other injuries to various parts of the body, accounts for up to 50% of all traumatic injuries. Often, TBI is combined with other injuries: the chest, abdomen, bones of the shoulder girdle, pelvis and lower extremities. In most cases, head injuries are sustained by young people (usually males) who are in a certain stage of alcoholic intoxication, which significantly worsens the condition, and by unintelligent children who do not sense danger well and cannot calculate their strength in some amusements. A large share of TBI occurs in road traffic accidents, the number of which is only increasing every year, because many (especially young people) get behind the wheel without sufficient driving experience and internal discipline.

Every department can be at risk

Traumatic brain injury can affect any structure (or several simultaneously) of the central nervous system (CNS):

• The most vulnerable and susceptible to injury main component of the central nervous system is gray matter of the cerebral cortex, concentrated not only in the cerebral cortex, but also in many other parts of the brain (GM);
• White matter, located mainly deep in the brain;
• Nerves piercing the bones of the skull (cranial or cranial) - sensitive, transmitting impulses from the senses to the center, motor, responsible for normal muscle activity, and mixed, having a dual function;
• Each of them blood vessels, nourishing the brain;
• Ventricular walls GM;
• Pathways ensuring the movement of cerebrospinal fluid.

Simultaneous injury to different regions of the central nervous system significantly complicates the situation. Severe traumatic brain injury changes the strict structure of the central nervous system, creates conditions for edema and swelling of the brain, which leads to disruption of the functional capabilities of the brain at all levels. Such changes, causing serious disorders of important brain functions, affect the functioning of other organs and systems that ensure the normal functioning of the body, for example, systems such as the respiratory and cardiovascular systems often experience suffering. In this situation there is always a danger of complications in the first minutes and hours after receiving damage, as well as the development of serious consequences remote in time.

With TBI, you should always keep in mind that the brain can be injured not only at the site of the impact itself. No less dangerous is the impact of counter-impact, which can cause even more harm than the force of the impact. In addition, the central nervous system may experience suffering caused by hydrodynamic fluctuations (CSF push) and a negative effect on the processes of the dura mater.

Open and closed TBI - the most popular classification

Probably all of us have heard more than once that when it comes to brain injuries, there is often a clarification: it is open or closed. What's the difference?

Invisible to the eye

Closed head injury(with it the skin and underlying tissues remain intact) includes:

1. The most favorable option is;
2. A more complex option than just a concussion is a brain contusion;
3. A very serious form of TBI is compression resulting from: epidural when blood fills the area between the bone and the most accessible one - the outer (dura) meninges, subdural(blood accumulation occurs under the dura mater), intracerebral, intraventricular.

If cracks in the cranial vault or fracture of its base are not accompanied by bleeding wounds and abrasions that damage the skin and tissue, then such TBIs are also classified as closed craniocerebral injuries, although conditionally.

What's inside if it's already scary outside?

An open craniocerebral injury, which has its main signs of a violation of the integrity of the soft tissues of the head, skull bones and dura mater, is considered to be:

• Fracture of the vault and base of the skull with soft tissue damage;
• Fracture of the base of the skull with damage to local blood vessels, which entails the flow of blood during a blow from the nostrils or from the auricle.

Open TBIs are usually divided into gunshot and non-gunshot, and, in addition, into:

1. Non-penetrating lesions of soft tissues (meaning muscles, periosteum, aponeurosis), leaving the outer (dura) meninges intact;
2. Penetrating wounds with disruption of the integrity of the dura mater.

Video: about the consequences of closed TBI – “Live Healthy” program

The division is based on other parameters

In addition to dividing brain injuries into open and closed, penetrating and non-penetrating, they are also classified according to other criteria, for example, TBI is classified according to severity:

• ABOUT easy brain injury is referred to as concussion and bruises of the brain;
• Average the degree of damage is diagnosed in cases of brain contusions that, taking into account all the violations, can no longer be classified as mild, and they do not yet reach a severe traumatic brain injury;
• TO severe degrees include severe contusion with diffuse axonal damage and compression of the brain, accompanied by profound neurological disorders and numerous disruptions in the functioning of other vital systems.

Or according to the characteristics of lesions of the central nervous system structures, which allows us to distinguish 3 types:

1. Focal damage that mainly occurs against the background of a concussion (impact-counter-impact);
2. Diffuse(acceleration-deceleration injury);
3. Combined lesions (multiple injuries to the brain, blood vessels, liquor pathways, etc.).

Considering the cause-and-effect relationships of head trauma, TBI is described as follows:

• Traumatic brain injuries that occur against the background of complete health of the central nervous system, that is, a blow to the head is not preceded by brain pathology, are called primary;
• ABOUT secondary TBI is discussed when they become a consequence of other cerebral disorders (for example, the patient fell during an epileptic attack and hit his head).

In addition, when describing brain injury, experts emphasize such points as, for example:

1. Only the central nervous system, namely the brain, was damaged: then the injury is called isolated;
2. TBI is considered combined when, along with damage to the brain, other parts of the body (internal organs, skeletal bones) were damaged;
3. Injuries caused by the simultaneous damaging influence of various unfavorable factors: mechanical stress, high temperatures, chemicals, etc., as a rule, are the cause combined option.

And finally: there is always a first time for something. So it is with a TBI - it can be the first and the last, or it can become almost habitual if it is followed by a second, third, fourth, and so on. Is it worth reminding that the head does not like blows and even with a mild concussion from a head injury one can expect complications and consequences that are distant in time, not to mention a severe traumatic brain injury?

More favorable options

The mildest type of head injury is a concussion. the symptoms of which even non-medics can recognize:

• As a rule, having hit his head (or received an external blow), the patient immediately loses consciousness;
• More often, loss of consciousness is followed by a state of stupefaction, less often psychomotor agitation can be observed;
• Headache, nausea, and vomiting are commonly perceived as characteristic symptoms of a cervical concussion;
• After an injury, signs of ill health such as pale skin, heart rhythm disturbances (tachy- or bradycardia) cannot be ignored;
• In other cases, there is a memory impairment of the retrograde amnesia type - the person is unable to remember the circumstances that preceded the injury.

A more severe TBI is considered to be a bruise of the brain, or, as doctors call it, a concussion. With a bruise, general cerebral disorders (repeated vomiting, severe headache, impaired consciousness) and local lesions (paresis) are combined. How pronounced the clinical picture is, which manifestations occupy a leading position - all this depends on the region in which the lesions are located and the scale of the damage.

As evidenced by the trickle of blood flowing from the ear...

Signs of fractures of the base of the skull also appear depending on the area in which the integrity of the cranial bones is compromised:

1. A stream of blood flowing from the ears and nose indicates a fracture of the anterior cranial fossa (AC);
2. When not only the anterior but also the middle CN is damaged, cerebrospinal fluid leaks from the nostrils and ear, the person does not react to odors, and ceases to hear;
3. Bleeding in the periorbital region gives such a clear manifestation that does not raise doubts about the diagnosis as a “symptom of glasses”.

As for the formation of hematomas, they occur due to injury to arteries, veins or sinuses and lead to compression of the brain. These are always severe traumatic brain injuries that require emergency neurosurgical surgery, otherwise the rapid deterioration of the victim’s condition may leave him no chance of life.

Epidural hematoma is formed as a result of injury to one of the branches (or several) of the middle meningeal artery, which supplies the dura mater. In this case, the blood mass accumulates between the skull bone and the dura mater.

Symptoms of the formation of an epidural hematoma develop quite rapidly and manifest themselves:

• Unbearable pain in the head;
• Constant nausea and repeated vomiting.
• The patient's lethargy, sometimes turning into excitement, and then into a coma.

This pathology is also characterized by the appearance of meningeal symptoms and signs of focal disorders (paresis - mono- and hemi-, loss of sensitivity on one side of the body, partial blindness of the homonymous hemianopia type with loss of certain halves of the visual fields).

Subdural hematoma is formed against the background of injury to the venous vessels and the time of its development is significantly longer than that of an epidural hematoma: at first it clinically resembles a concussion and lasts up to 72 hours, then the patient’s condition seems to improve and within about 2.5 weeks he believes that he is going to amendment. After this period, against the background of general (imaginary) well-being, the patient’s condition sharply worsens, and pronounced symptoms of general cerebral and local disorders appear.

Intracerebral hematoma- a rather rare phenomenon that occurs mainly in elderly patients; their favorite place of localization is the basin of the middle cerebral artery. Symptoms tend to progress (general cerebral disorders appear first, then local disorders increase).

Post-traumatic refers to serious complications of severe traumatic brain injury. It can be recognized by complaints of intense headache (until consciousness leaves the person), rapid loss of consciousness and the onset of a coma, when the victim no longer complains. These symptoms are also quickly joined by signs of dislocation (displacement of structures) of the brain stem and cardiovascular pathology. If at this moment a lumbar puncture is performed, then in the cerebrospinal fluid you can see a huge amount of fresh red blood cells - erythrocytes. By the way, this can also be detected visually - the cerebrospinal fluid will contain blood impurities, and therefore will acquire a reddish tint.

How to help in the first minutes

First aid is often provided by people who, by chance, find themselves close to the victim. And they are not always health workers. With TBI, however, it should be understood that loss of consciousness can last a very short time and therefore not be recorded. However, in any case, a concussion, as a complication of any (even seemingly mild) head injury, should always be kept in mind and, taking this into account, help the patient.

If a person who has received a TBI does not come to his senses for a long time, he needs to be turned over on his stomach and his head tilted down. This must be done in order to prevent vomit or blood (in case of injuries to the oral cavity) from entering the respiratory tract, which often happens in an unconscious state (absence of cough and swallowing reflexes).

If the patient has signs of impaired respiratory function (there is no breathing), measures should be taken to restore the patency of the airways and, before the ambulance arrives, provide simple artificial ventilation (mouth-to-mouth, mouth-to-nose).

If the victim has bleeding, it is stopped with the help of an elastic bandage (a soft lining on the wound and a tight bandage), and when the victim is taken to the hospital, the surgeon will suture the wound. It’s worse when there is a suspicion of intracranial bleeding, because its complication is most likely hemorrhage and hematoma, and this is already a surgical treatment.

Due to the fact that a traumatic brain injury can occur in any place that is not necessarily within walking distance of a hospital, I would like to introduce the reader to other methods of primary diagnosis and first aid. In addition, among the witnesses trying to help the patient, there may be people with certain knowledge in medicine (nurse, paramedic, midwife). AND here's what they should do:

1. The first step is to assess the level of consciousness in order to determine, based on the degree of response, the patient’s further condition (improvement or deterioration), and at the same time – psychomotor status, the severity of pain in the head (not excluding other parts of the body), the presence of speech and swallowing disorders;
2. If blood or cerebrospinal fluid leaks from the nostrils or ears, assume a fracture of the base of the skull;
3. It is very important to pay attention to the victim’s pupils (dilated? different sizes? how do they react to light? strabismus?) and report the results of your observations to the doctor to the arriving ambulance team;
4. You should not ignore such routine activities as determining the color of the skin, measuring pulse, respiratory rate, body temperature and blood pressure (if possible).

With TBI, any part of the brain can suffer, and the severity of one or another neurological symptoms depends on the location of the lesion, for example:

• A damaged area of ​​the cerebral cortex will make any movement impossible;
• If the sensitive cortex is damaged, sensitivity will be lost (all types);
• Damage to the frontal lobe cortex will lead to a disorder of higher mental activity;
• The occipital lobes will no longer control vision if their cortex is damaged;
• Injuries to the cortex of the parietal lobes will create problems with speech, hearing and memory.

In addition, we should not forget that cranial nerves can also be injured and give symptoms depending on which area is affected. And also keep in mind fractures and dislocations of the lower jaw, which, in the absence of consciousness, press the tongue against the back wall of the pharynx, thereby creating a barrier to the air flowing into the trachea and then into the lungs. To restore the passage of air, it is necessary to push the lower jaw forward, placing your fingers behind its corners. In addition, the injury can also be combined, that is, with a TBI, other organs can be damaged at the same time, so a person who has received a head injury and is in an unconscious state must be treated with extreme care and caution.

And one more important point when providing first aid: you need to remember about the complications of TBI, even if at first glance it seemed mild. Bleeding into the cranial cavity or increasing cerebral edema increases intracranial pressure and can lead to compression of the GM(loss of consciousness, tachycardia, increased body temperature) and brain irritation(loss of consciousness, psychomotor agitation, inappropriate behavior, obscene language). However, let's hope that by that time the ambulance will have already arrived at the scene and quickly taken the victim to the hospital, where he will receive proper treatment.

Video: first aid for TBI

Treatment is exclusively in a hospital setting!

Treatment of TBI of any severity is carried out only in a hospital setting, because loss of consciousness immediately after receiving a TBI, although it reaches a certain depth, does not in any way indicate the real condition of the patient. The patient can prove that he feels fine and can be treated at home, however, given the risk of complications, he is provided with strict bed rest (from one week to a month). It should be noted that even a concussion of the brain, having a favorable prognosis, in the case of large-scale damage to parts of the brain can leave neurological symptoms for life and limit the patient’s ability to choose a profession and further ability to work.

Treatment of TBI is mainly conservative, unless other measures are provided (surgery if there are signs of brain compression and hematoma formation), and symptomatic:

The Hard Way – Brain Injuries in Newborns

It is not so rare for newborns to be injured when passing through the birth canal or in the case of the use of obstetric instruments and certain obstetric techniques. Unfortunately, such injuries do not always cost the baby “a little bloodshed” and the parents “a little fright”; sometimes they leave consequences that become a big problem for the rest of their lives.

At the very first examination of the baby, the doctor pays attention to the following points that can help determine the general condition of the newborn:

• Is the baby capable of sucking and swallowing?
• Is his tone and tendon reflexes reduced?
• Is there any damage to the soft tissues of the head;
• What condition is the large fontanel in?

In newborns who received injuries during passage through the birth canal (or various obstetric injuries), complications such as:

1. Hemorrhages (in the brain, its ventricles, under the membranes of the brain - in connection with which subarachnoid, subdural, epidural hemorrhage is distinguished);
2. Hematomas;
3. Hemorrhagic permeation of the brain substance;
4. CNS lesions caused by contusion.

Symptoms of birth injury to the brain mainly come from the functional immaturity of the brain and reflex activity of the nervous system, where consciousness is considered a very important criterion for determining disorders. However, it should be borne in mind that there are significant differences between changes in consciousness in adults and babies who have just seen the light, therefore, in newborns, for a similar purpose, it is customary to study the behavioral states characteristic of children in the first hours and days of life. How does a neonatologist find out about problems in the brain of such a young child? Pathological signs of impaired consciousness in newborns include:

• Constant sleep (lethargy), when the baby can only be awakened by severe pain caused to him;
• Stunned state – the child does not wake up when exposed to pain, but reacts by changing his facial expressions:
• Stupor, which is characterized by a minimum of the baby’s reactions to stimuli;
• A comatose state where there are no reactions to pain.

It should be noted that to determine the condition of a newborn who was injured at birth, there is a list of various syndromes that the doctor focuses on:

1. Hyperexcitability syndrome (the child does not sleep, constantly writhes, grunts and screams);
2. Convulsive syndrome (convulsions themselves or other manifestations that may correspond to this syndrome - apnea attacks, for example);
3. Meningeal syndrome (increased sensitivity to irritants, reaction to percussion of the head);
4. (anxiety, large head, increased venous pattern, bulging fontanelle, constant regurgitation).

Obviously, diagnosing pathological conditions of the brain caused by birth trauma is quite difficult, which is explained by the immaturity of brain structures in children in the first hours and days of life.

Medicine can’t do everything...

Treatment of birth brain injuries and care of a newborn require maximum attention and responsibility. A severe traumatic brain injury in a child received during childbirth requires the baby to stay in a specialized clinic or department (with the baby placed in an incubator).

Unfortunately, birth injuries to the brain are not always without complications and consequences. In other cases, the intensive measures taken save the child’s life, but cannot ensure his full health. Leading to irreversible changes, such injuries leave a mark that can significantly negatively affect the functioning of the brain and the entire nervous system as a whole, posing a threat not only to the child’s health, but also to his life. Among the most severe consequences of birth trauma, the following should be noted:

• Dropsy of the brain or, as doctors call it -;
• Cerebral palsy (CP);
• Mental and physical retardation;
• Hyperactivity (increased excitability, restlessness, nervousness);
• Convulsive syndrome;
• Speech impairment;
• Diseases of internal organs, allergic diseases.

Of course, the list of consequences can be continued... But whether the treatment of birth injury to the brain will cost with conservative measures or will have to resort to neurosurgical operation depends on the nature of the injury received and the depth of the disorders that followed it.

Video: head injuries in children of different ages, Dr. Komarovsky

Complications and consequences of TBI

Although there has already been mention of complications in various sections, there is still a need to touch upon this topic again (in order to understand the seriousness of the situation created by TBI).

Thus, During the acute period, the patient may experience the following troubles:

1. External and internal bleeding, creating conditions for the formation of hematomas;
2. Leakage of cerebrospinal fluid (cerebrospinal fluid rhinorrhea) – external and internal, which threatens the development of an infectious and inflammatory process;
3. Penetration and accumulation of air in the skull (pneumocephalus);
4. Hypertensive (hydrocephalic) syndrome or - increased intracranial pressure, as a result of which the development of impaired consciousness, convulsive syndrome, etc.;
5. Suppuration of wound sites, formation of purulent fistulas;
6. Osteomyelitis;
7. Meningitis and meningoencephalitis;
8. GM abscesses;
9. Bulging (prolapse, prolapse) of the GM.

The main cause of death of the patient in the first week of illness is considered to be cerebral edema and displacement of brain structures.

TBI does not allow either doctors or the patient to calm down for a long time, since even in the later stages it can present a “surprise” in the form of:

• Formation of scars, adhesions and, development of hydrops GM and;
• Convulsive syndrome with subsequent transformation into, as well as astheno-neurotic or psychoorganic syndrome.

The main cause of death of the patient in the late period is complications caused by purulent infection (pneumonia, meningoencephalitis, etc.).

Among the consequences of TBI, which are quite diverse and numerous, I would like to note the following:

1. Movement disorders (paralysis) and persistent sensory impairment;
2. Impaired balance, coordination of movements, changes in gait;
3. Epilepsy;
4. Pathology of ENT organs (sinusitis, sinusitis).

Recovery and rehabilitation

If a person who has received a mild concussion in most cases is safely discharged from the hospital and soon remembers his injury only when asked about it, then people who have experienced severe traumatic brain injury face a long and difficult path of rehabilitation in order to restore lost basic skills . Sometimes a person needs to learn to walk, talk, communicate with other people, and take care of himself independently. Here, any means are good: physical therapy, massage, all kinds of physiotherapeutic procedures, manual therapy, and classes with a speech therapist.

Meanwhile, to restore cognitive abilities after a head injury, sessions with a psychotherapist are very useful, who will help you remember everything or most of it, teach you to perceive, remember and reproduce information, and adapt the patient in everyday life and society. Unfortunately, sometimes lost skills never return... Then all that remains is to teach a person to serve himself and contact people close to him to the maximum (as far as intellectual, motor and sensory abilities allow). Of course, such patients receive a disability group and need outside help.

In addition to the listed activities during the rehabilitation period, people with a similar history are prescribed medications. As a rule, these are vitamins.

TO traumatic brain injury(TBI) include traumatic (mechanical) damage to the skull and intracranial formations (brain matter, membranes, blood vessels), manifested by temporary or permanent neurological and psychosocial disorders.

The main clinical and morphological types of traumatic brain injury are:

• A concussion in which there are no obvious morphological changes in the brain substance and minimal clinical symptoms.
• Brain contusion (contusion), characterized by the formation of traumatic foci of damage to the brain substance.
• Compression of the brain by intracranial hematoma, bone fragments of the cranial vault, massive contusion lesions, accumulation of air in the cranial cavity (so-called pneumocephalus).
• Severe diffuse axonal damage to the brain, characterized by massive rupture of axons (long processes) of nerve cells and the patient’s serious condition with the development of a long coma (lack of consciousness).

Common, but not mandatory, clinical manifestations of traumatic brain injury are:

• Memory impairment (amnestic syndrome).
• Signs of vegetative lability (pallor, hyperhidrosis (sweating), change in pupil size, pulse lability, etc.).
• Focal symptoms such as pupillary disorders (inequality of pupil sizes - anisocoria, dilation or constriction of the pupils), asymmetry of tendon reflexes, paresis (decreased strength) in the arms and legs, paresis of the facial nerve, sensory disturbances and others.
• Meningeal symptoms in the form of symptoms such as:
  • Stiffness of the neck and neck muscles.
  • Kernig's sign (difficulty or impossibility of straightening the leg (preliminarily raised upward in a supine position) in the knee joint).
  • General hyperesthesia (increased sensitivity to light, sounds, tactile).
• Leakage of cerebrospinal fluid from the ear (otoliquorrhea) or nasal passages (nasal liquorrhea).

The main diagnostic methods for head trauma are cranial radiography, computed tomography (CT) and, to a lesser extent, magnetic resonance imaging (MRI). When diagnosing, it is necessary to take into account that the severity of the patient’s condition (for example, satisfactory condition), especially in the first hours and days after the injury, may not correspond to the severity of the traumatic brain injury (for example, severe injury). In this regard, careful and thorough examination and observation of patients, even with minimal symptoms, is necessary.

Treatment for mild to moderate trauma consists of bed rest and symptomatic therapy. If indicated, the fight against cerebral edema, anticonvulsant treatment, nootropic, and antioxidant therapy are carried out. In case of severe contusion, diffuse axonal damage and compression of the brain, intensive therapy is carried out and, in the presence of critical impairment of vital functions, resuscitation measures are carried out. Compression of the brain by an intracranial hematoma is an indication for emergency surgery to remove the hemorrhage and, if necessary, in the case of severe cerebral edema, for surgical decompression of the brain by forming a sufficiently large trepanation window of the cranial vault (so-called infratemporal decompression).

The prognosis for traumatic brain injury depends on many factors. Factors that worsen the prognosis are the severity of the injury, the duration of brain compression, and the length of stay in a comatose state.

• Epidemiology

  In terms of prevalence, traumatic brain injury ranks first among all brain diseases. The incidence of traumatic brain injury ranges from 180 to 220 cases per 100,000 population per year, with 75–80% of patients receiving a mild traumatic brain injury (concussion), and the remaining 25–30% approximately divided in half between moderate and severe TBI. Mortality among all patients with TBI is 7–12%, and in patients with severe TBI, postoperative mortality is 28–32%. The average age of most victims is 20–30 years, with 2.5–3 times more men than women. Up to 70% of TBI victims have positive blood alcohol levels. Post-traumatic epileptic seizures are observed in approximately 2% of patients with traumatic brain injury, in 12% of patients with severe traumatic brain injury, and in more than 50% of cases of penetrating traumatic brain injury.

• Classification
  • Based on the nature and severity of damage to the brain substances, they are divided into:
    • Brain concussion.
    • Brain contusion.
    • Compression of the brain (with cerebral edema, intracranial hematoma, bone fragments of the cranial vault, subdural hydroma (accumulation of fluid under the hard shell of the brain), extensive contusion lesions, air with pneumocephalus (accumulation of air in the cranial cavity)).
    • Severe diffuse axonal brain damage.
  • Based on the degree of integrity of the head tissue, the susceptibility of the intracranial contents to infection from the outside, or the possibility of developing pneumocephalus (accumulation of air in the cranial cavity), closed and open traumatic brain injury are distinguished.
    • A closed traumatic brain injury is characterized by the preservation of the integrity of the soft tissues of the head or the presence of a soft tissue wound that does not affect the cranial aponeurosis. In this case, the risk of developing meningitis is extremely low, and the development of pneumocephalus is not possible.
    • An open traumatic brain injury is characterized by the presence of injury to the soft tissues of the head, including, at a minimum, damage to the aponeurosis of the skull, and also possibly involving deeper formations (vault and base of the skull (fracture), membranes (rupture), brain tissue). In this case, there is a risk of developing purulent-septic complications, pneumocephalus, and compression of the brain by skull fragments. Open traumatic brain injury is divided into two types:
      • Penetrating traumatic brain injury, in which there is damage to the dura mater (both in the presence of a head wound and in its absence, as well as in the detection of cerebrospinal fluid leakage from the ear or nose). In this case, the risk of infection and purulent-septic complications is extremely high.
      • Non-penetrating traumatic brain injury in which the dura mater remains intact.
  • Based on the severity of traumatic brain injury, there are:
    • Mild TBI (this includes a concussion and mild brain contusion, a linear fracture of the cranial vault is possible).
    • Moderate (this includes moderate brain contusion; possible: fracture of the vault and base of the skull, traumatic subarachnoid hemorrhage (SAH), epileptic seizures).
    • Severe degree (this includes severe brain contusion, brain compression, severe axonal damage to the brain; possible fracture of the vault and base of the skull, traumatic SAH, epileptic seizures, severe brainstem and diencephalic disorders).
  • Based on the combination of traumatic brain injury with other traumatic injuries and the impact of several traumatic factors, the following are distinguished:
    • Isolated TBI.
    • Combined TBI, when combined with damage to other organs (chest, abdomen, limbs, etc.).
    • Combined TBI, when exposed to several traumatic factors (mechanical, thermal, radiation, chemical).
  • Three periods of the course of traumatic brain injury
    • An acute period, which is based on the processes of interaction of the injured substrate, reactions of damage and protection. Approximate dates:
      • For a concussion – up to 1-2 weeks.
      • For mild bruises – up to 2-3 weeks.
      • For moderate injuries – up to 4-5 weeks.
      • For severe injury – up to 6-8 weeks.
      • For diffuse axonal damage – up to 8-19 weeks.
      • For compression of the brain - from 3 to 10 weeks.
    • An intermediate period, which is based on the resorption and organization of damaged areas and the development of compensatory and adaptive processes in the central nervous system. Its duration is:
      • For mild TBI – up to 2 months.
      • For moderate cases – up to 4 months.
      • For severe cases – up to 6 months.
    • A long-term period, which is based on the completion of processes or the coexistence of local and distant destructive-regenerative processes. With a favorable course, complete or almost complete clinical balancing of pathological changes occurs; with an unfavorable course, cicatricial, atrophic, adhesive, vegetative-visceral, and autoimmune processes occur. The duration of the period with a favorable course is up to 2 years, with a progressive course it is not limited.

Etiology and pathogenesis

• Main causes of traumatic brain injury
  • Domestic trauma.
  • Road injury.
  • A fall.
  • Sports injury.
  • Work injury.
  • Secondary injury due to a patient fainting, with epilepsy, with a stroke.

Traumatic brain injuries are divided into primary, associated with the direct impact of traumatic forces and occurring at the time of injury, and secondary, which is a complication of the primary brain injury.

Primary damage includes: damage to neurons and glial cells, synaptic breaks, disruption of the integrity or thrombosis of cerebral vessels. Primary brain damage can be local, leading to the formation of foci of contusion and crushing of the brain, and diffuse, associated with axonal damage to the brain due to rupture of axons during the movement of the brain inside the cranial cavity.

• Pathogenesis of brain contusion

  Foci of contusion (traumatic crushing of brain tissue) arise from direct local exposure to a traumatic agent. Often accompanied by fractures of the vault or base of the skull, as well as intracranial hemorrhage. Clinical and morphological comparisons have shown that in the presence of a skull fracture, the patient always has a focus of contusion or crush of the brain, which in practical work plays a role in making a diagnosis.

  Contusion foci are formed directly at the site of application of force, or according to the principle of counter-impact (counter-impact), when the brain is damaged on the wall of the skull opposite to the site of application of force. Especially often, foci of bruises form in the basal parts of the frontal and anterior parts of the temporal lobe of the brain. The development of local vasospasm, ischemic changes and perifocal edema, necrosis of brain tissue play a role in the pathogenesis of the formation of a contusion focus. The development of diapedetic hemorrhages with the formation of a focus of brain contusion with hemorrhagic impregnation is possible.

  With concomitant cerebral contusion, a rupture (mainly of the branches of the middle meningeal artery) results in the formation of an epidural hematoma (between the dura mater (above it) and the skull). The sources of subdural hematomas (under the dura mater of the brain) are ruptures of the pial veins at the site of brain contusion, parasinus veins and venous sinuses of the brain.

• Pathogenesis of diffuse axonal brain damage

  Diffuse axonal damage to the brain is manifested by damage (rupture) of the axons (long processes) of the nerve cells of the cerebral cortex during direct exposure to a damaging factor, due to the movement of the more mobile hemispheres of the brain relative to the fixed trunk, which leads to tension and twisting of the axons of the white matter of the hemispheres, corpus callosum and brain stem. Diffuse axonal injury is most often caused by acceleration-deceleration trauma, especially with a rotational component. Pathomorphologically, it manifests itself in the form of such pathomorphological processes as: retraction and rupture of axons with the release of axoplasm (1st day, hours), reactive formation of microglial processes of astrocytes (days, weeks), demyelination of white matter pathways (weeks, months). Clinically, axonal damage corresponds to a wide range of disorders from concussion to severe brain contusion.

• Secondary brain damage

  Secondary brain damage plays an important role in the pathogenesis of acute traumatic brain injury, i.e. the action of damaging factors during the subsequent hours and days after injury, which lead to damage to the brain substance predominantly of the hypoxic-ischemic type. Secondary brain damage may result from intracranial factors (impaired cerebral vascular reactivity, autoregulation disorders, cerebral vasospasm, cerebral ischemia, cerebral reperfusion, cerebrospinal fluid circulation disorders, cerebral edema, changes in intracranial pressure, cerebral compression and dislocation syndrome, seizures, intracranial infection), and extracranial causes (arterial hypotension (systolic blood pressure 45 mm Hg), severe hypocapnia (PaCO2

Clinic and complications

• Characteristic symptoms
  • Characteristic, but not obligatory, clinical manifestations of head injury are:
    • Traces of trauma on the skin of the head, such as abrasions, bruises, wounds.
    • Impaired consciousness (stunning, stupor, coma).
    • Memory impairments (amnestic syndrome), such as retrograde amnesia (impaired memory for events that followed the trauma) or anteroretrograde amnesia (impaired memory for events that preceded and followed the trauma).
    • General cerebral symptoms such as headache, nausea, vomiting, sudden depression or loss of consciousness.
    • Psychomotor agitation, disorientation of the patient in place and time.
    • Signs of vegetative lability, such as pale skin, hyperhidrosis (sweating), changes in pupil size, pulse lability, etc.).
    • Nystagmus is an involuntary, rhythmic oscillatory movement of the eyeballs, involving slow eye movement in one direction (slow phase of nystagmus), followed by rapid eye movement in the opposite direction (fast phase). The direction of nystagmus is determined by the direction of the fast phase. Nystagmus can be observed both with a concussion and with severe brainstem lesions.
    • Focal symptoms such as:
      • Pupillary disorders, which can manifest as:
        • Inequalities in pupil sizes – anisocoria, which can be observed with the development of temporotentorial herniation, in particular with intracerebral hemorrhages. As a rule, in this case, anisocoria is combined with increasing depression of consciousness. Moderate, transient, unstable anisocoria can be observed with mild trauma, as a manifestation of autonomic lability.
        • Dilation or constriction of the pupils. Persistent pronounced bilateral dilation of the pupils (bilateral mydriasis) without reaction to light is observed with bilateral temporotentorial herniation of the brain and is accompanied by depression of consciousness to the level of stupor or coma. Bilateral constriction of the pupils (bilateral miosis) in the form of pinpoint pupils is observed with gross stem lesions. Changes in the diameter of the pupils are possible, having an unstable, transient nature, with a mild injury.
      • Asymmetry of tendon reflexes. Paresis (decreased strength) or paralysis of the central type, usually on one side, separately in the arm, in the leg, or in the arm and leg at the same time (hemiparesis or hemiplegia). In severe forms of contusion or compression of the brain, paresis may be detected in both legs (lower spastic paraparesis (paraplegia)) or in the legs and arms (tetraparesis (tetraplegia)). With central paresis in the leg (legs), pathological foot signs are often detected: Babinsky's, Rossolimo's, Bekhterev's, Zhukovsky's, Oppenheim's, Gordon's, Schaeffer's, Hirschberg's, Poussep's symptoms and some others. As a rule, the symptoms of Babinsky, Oppenheim, Rossolimo, and Bekhterev are most often determined in the clinic, which is done as follows:
        • Babinsky's symptom: with line irritation of the sole, a reflex extension of the thumb is observed, sometimes isolated, sometimes with simultaneous spreading of the remaining fingers (“fan sign”).
        • Oppenheim's sign is obtained as a result of pressing the flesh of the thumb along the anterior surface of the tibia from top to bottom. The symptom is the same extension of the thumb as with Babinski's phenomenon.
        • Rossolimo's symptom: reflex flexion of the II – V toes as a result of a short blow to the tips of the named toes with the fingers of the examiner or with a hammer.
        • Bekhterev's symptom: the same flexion of the fingers as in Rossolimo's symptom, but when tapping with a hammer on the anterior outer surface of the dorsum of the foot.
      • With fractures of the temporal bone, peripheral paresis of the facial nerve may develop, and with hemispheric lesions of the contusion, central paresis may occur.
      • Sensitivity disorders are usually of the conduction type. Not seen often. Decreased sensitivity can be in the form of hypoesthesia in the arm, leg, or hemihypesthesia (in the arm and leg of one side of the body), on one half of the face.
    • In case of a fracture of the temporal bone with a rupture of the dura mater and eardrum, there may be a leakage of cerebrospinal fluid (CSF) from the ear (external auditory canal) - the so-called. otoliquorhea. When the bottom of the anterior cranial fossa is fractured with a rupture of the dura mater, cerebrospinal fluid may leak from the nose through the damaged frontal sinus or ethmoid bone - the so-called. nasal liquorrhea.
    • Meningeal syndrome, as a sign of irritation of the meninges with subarachnoid hemorrhage, severe brain contusion, intracranial hematoma. The syndrome can be manifested by one symptom or a combination of symptoms such as:
      • Stiffness of the neck and neck muscles, i.e. an increase in the tone of these muscles, due to which the adduction of the head to the chest is limited, and with a passive tilt of the head, the examiner feels noticeable resistance to the tilt.
      • Kernig's sign, which is detected as follows. The leg of the patient lying on his back is passively bent at the hip and knee joints, after which an attempt is made to straighten it at the knee joint. In this case, extension of the leg becomes impossible or difficult due to tonic tension of the muscles that flex the lower leg.
      • Brudzinski's sign. There are several types of symptoms:
        • The upper Brudzinski symptom is expressed in bending the legs at the knee joints in response to an attempt to bring the head to the chest.
        • Brudzinski's pubic symptom is flexion of the legs at the knee and hip joints with pressure on the area of ​​the pubic symphysis of the patient lying on his back.
        • The lower Brudzinski sign can be of two types.
        • The contralateral identical Brudzinski symptom is involuntary flexion of the leg at the hip and knee joints while passively flexing the other leg at the same joints.
        • Contralateral reciprocal Brudzinski's symptom is the involuntary extension of a leg bent at the hip and knee joints, with passive flexion of the other leg in the same joints.
      • General hyperesthesia, i.e. increased sensitivity to light, sounds, tactile sensations.
      • Pain on palpation of the exit points of the branches of the trigeminal nerve.

• Clinical forms of traumatic brain injury
  • Brain contusion (contusio cerebri)

    Foci of contusion can occur both at the site of application of force and as a counter-impact on the side of the brain opposite to the blow or at the base of the skull. Often, brain contusion is accompanied by traumatic subarachnoid hemorrhage, but there is no relationship between the presence of subarachnoid hemorrhage and the severity of TBI. The exception is common basal subarachnoid hemorrhage, which has a significant adverse effect on the course and prognosis of traumatic brain injury.

    Often, with a brain contusion, a fracture of the vault or base of the skull is observed. Leakage of cerebrospinal fluid from the ear (otoliquorrhea) or nose (nasal liquorrhea) are signs of a basal skull fracture.

  • Compression of the brain (compressio cerebri) Brain compression is one of the most dangerous forms of traumatic brain injury due to the possibility of rapid development of brain herniation and a life-threatening condition at any time. The most common cause of compression of the brain with the development of herniation is intracranial hematoma. More rare causes: Compression by bone fragments of the cranial vault. Subdural hydroma (fluid accumulation in the subdural space). Extensive contusion lesions with pronounced perifocal cerebral edema. For pneumocephalus (accumulation of air in the cranial cavity). With diffuse cerebral edema.
    • • In relation to the hard shell and brain tissue, the following types of intracranial hemorrhages are distinguished:
        • Epidural hematoma is an accumulation of blood between the skull and the dura mater, i.e. above the dura mater of the brain. The sources of bleeding in epidural hematomas are the branches of the middle cerebral artery, i.e. arterial bleeding is observed - quite intense and under high pressure. A factor limiting the spread of the hematoma is the fairly tight fixation of the dura mater to the periosteum of the skull and in the area of ​​the cranial sutures, i.e. a hematoma, as it were, peels off the membrane of the brain from the cranial vault. In connection with these circumstances, the epidural hematoma has a characteristic shape: even with large sizes (100-150 ml or more), it is not located over the entire hemisphere, but has a limited area, but at the same time has a relatively large thickness, due to which a pronounced compression effect is achieved brain
        • Subdural hematoma is an accumulation of blood between the dura mater of the brain and the cerebral hemisphere, i.e. under the dura mater. The source of bleeding in subdural hematomas is pial (pia mater - soft shell), parasagittal and other veins, while venous bleeding is low-intensity and under relatively low blood pressure. In addition, there is no obstacle to the subdural spread of the hematoma, and therefore the hemorrhage, as a rule, has a large area of ​​distribution over the hemisphere and a relatively small thickness.
        • An intracerebral hematoma is an accumulation of blood in the brain. Morphologically, the spreading of brain tissue by the shed blood can be observed with the formation of a hemorrhage cavity, as a rule, with arterial intracerebral bleeding or venous bleeding from a large vein. Otherwise, when bleeding from small vessels of the brain, a hemorrhage is formed as a hemorrhagic soaking of the brain, without the formation of a cavity. As a rule, swelling of the brain tissue of varying severity forms around a cerebral hemorrhage - perifocal edema.
      • Intracranial hematomas are divided into:
        • Acute hematomas (manifest in the first 3 days).
        • Subacute hematomas (manifest from 4 days to 3 weeks) and.
        • Chronic hematomas - appear after 3 weeks and up to several years.
        • Acute subdural hematomas occur in approximately 40%, chronic in 6%, acute epidural in 20%, intracerebral in 30% of cases. It is necessary to distinguish between the time of hematoma formation (it has been shown that most hematomas are formed in the first hours after injury) and the time of clinical manifestation of the latter.
      • Based on the volume of hematomas, they are divided into:
        • Small hematomas (up to 50 ml), a significant part of which can be treated conservatively.
        • Medium-sized hematomas (50 – 100 ml), etc.
        • Large hematomas (more than 100 ml), which pose a significant danger regarding herniation and the development of a serious condition for the patient.
      • The classic clinical picture of intracranial hematomas (occurs only in 15–20% of cases) is characterized by symptoms such as:
        • The light interval is the time of clear consciousness from the moment of restoration of consciousness at the time of injury until the onset of pronounced clinical manifestations of the hematoma. The light period can be several hours. It is known that traumatic intracranial hematomas form either at the time of injury or reach a critical volume within several hours after injury due to ongoing bleeding. Delayed development of hematoma symptoms can be observed both in the first case (due to the formation of perifocal cerebral edema) and in the second case, due to an increase in the size of the hematoma.
        • Increasing depression of consciousness. The severity of depression of consciousness directly correlates with the size of the hemorrhage and the severity of cerebral edema.
        • Anisocoria is an inequality in the size of the pupils, with a wider pupil, as a rule, observed on the side of the hematoma. Dilation of the pupil on the affected side is a consequence of paresis of the oculomotor nerve and serves as an initial sign of the development of lateral tentorial herniation.
        • Bradycardia (40 – 60 beats/min), usually increasing as consciousness is depressed.
        • Hemiparesis, i.e. decreased strength in the arm and leg on one side of the body, or hemiplegia (paralysis in the arm and leg on one side of the body), usually on the side opposite the hematoma (i.e., heterolateral). For example, if the hematoma is located above the left hemisphere, then, with a typical clinical picture, paresis will be in the right arm and leg.
      • In other cases (i.e., most often), the clinical picture of intracranial hematomas is blurred, any components of the clinical picture are absent or not characteristically manifested (for example, immediately after the injury, a coma develops without a clear interval, bilateral mydriasis (dilated pupils) is detected), and not always it is possible to diagnose the nature, location and size of the hematoma without additional research methods (CT tomography). The clinical picture of a hematoma largely depends on its volume, the degree of concomitant brain contusion and the severity and rate of increase of cerebral edema. The effect of compression in intracerebral hematomas can be observed already with a volume of 50–75 ml, and with concomitant brain contusion even with a volume of 30 ml.
      • It is known that most intracranial hematomas form in the first hours after injury, but hematomas can manifest themselves clinically at different times.
      • In 8–10% of cases, multiple intracranial hematomas occur (two, less often three), for example, a combination of epidural and subdural hematomas, subdural and intracerebral hematomas, hematomas over different hemispheres of the brain. As a rule, this combination is observed in severe trauma.

• Complications of traumatic brain injury
  • Most common craniocerebral complications

Diagnostics

• Basic provisions
  • Diagnosis of traumatic brain injury is based on analysis of the clinical picture, establishing a connection between the fact of head injury and the clinical and morphological picture, which is confirmed and clarified using radiography of the skull, computed tomography of the head and some other diagnostic methods.
  • If, based on the clinical picture, there is reason to think that the patient has a concussion, he, as a rule, undergoes an X-ray of the skull (to exclude a fracture of the vault or base) and echoencephaloscopy (as a screening method to exclude a space-occupying formation (primarily hematoma)) . Signs that may indicate a mild traumatic brain injury include:
    • Satisfactory condition, no respiratory or circulatory disorders.
    • Clear (or temporarily slightly stunned) consciousness of the patient.
    • Absence of focal neurological symptoms (paresis in the limbs, speech disorders, anisocoria (persistent or increasing inequality of pupil sizes)).
    • Absence of meningeal symptoms.
  • It is necessary to distinguish between the severity of the patient's condition and the severity of the traumatic brain injury, which, especially in the early stages after injury, may not correspond to each other.
  • For example, a clinical picture of a concussion during the initial examination of a patient may, after a few tens of minutes or a few hours, be replaced by a picture of the rapid development of compression by an intracranial hematoma and herniation of the brain, which will correspond to an increase in the volume of hemorrhage and cerebral edema after injury. And, for example, auricular liquorrhea (leakage of cerebrospinal fluid from the ear), accompanying a fracture of the base of the skull and penetrating traumatic brain injury, can be practically the only clinical manifestation of severe injury if the patient’s condition is satisfactory.
  • A patient with a concussion requires qualified observation for the next at least 5 to 7 days after the injury. If signs of an intracranial hematoma appear and increase, an emergency additional examination and a decision on surgery is required. The following symptoms are signs of intracranial hemorrhage and decompensation of intracranial hypertension with the development of herniation:
    • Increasing headache.
    • Increasing depression of consciousness, up to coma. The development of psychomotor agitation is possible.
    • The development of persistent anisocoria (differences in pupil sizes), as a rule, parallels depression of consciousness. In the future, persistent dilation of both pupils (i.e., mydriasis) may develop.
    • Development of hemiparesis (hemiplegia), i.e. weakness (or paralysis) in an arm and leg on one side, usually on the side opposite the dilated pupil (i.e., contralateral).
    • The development of a convulsive seizure in a patient - focal or generalized.
  • If clinical signs of an intracranial hematoma (increasing compression of the brain) are detected in a patient, further examination is carried out. The most informative method is computed tomography of the brain (CT), which allows to identify the presence, location and size of hemorrhage, the presence of a fracture of the vault or base of the skull, determine the severity of cerebral edema and the degree of dislocation of intracerebral structures.
  • In the absence of computed tomography (or MRI tomography), diagnosis of intracranial hematoma is carried out on the basis of indirect data - data from echoencephaloscopy (EchoES). If a displacement of the midline structures of the brain by more than 3 mm and a characteristic clinical picture of brain compression is detected, there is a high probability of intracranial hematoma.
  • If echoencephaloscopy data does not give a clear displacement of 4 – 7 mm or more (but is in the region of 2.5 – 3 mm), but there is a clinical picture of increasing compression of the brain, the rule “if in doubt, trepanate” has not lost its relevance. Diagnostic burr holes (from 1 to 3) are placed at the site of the suspected hematoma, and if hemorrhage is directly visually detected in the epidural or subdural space, extended surgical intervention is performed.
  • In the case of a clinical picture of a concussion and the presence of displacement of the midline structures of the brain during EchoES, or with a fracture of the calvarium crossing the vascular groove, an emergency CT scan is indicated to exclude intracranial hematoma, and in the absence of a CT, dynamic observation with an assessment of the level of consciousness and the results of EchoES over time.
  • It must be remembered that the clinical picture of a concussion or brain contusion does not exclude the possibility of the formation of an intracranial hematoma, which may appear later. The main method for verifying intracranial hematomas is CT (MRI) of the brain. Difficulties may arise in cases where an intracranial hematoma is absent on a CT scan immediately after an injury, but then forms several hours (days) later and is detected on a repeat CT scan.
  • Diagnosis of brain contusion is based on clinical picture data (general cerebral, focal, meningeal symptoms), confirmed by CT scan of the brain, or echoencephaloscopy data for the absence of displacement of brain structures and/or spinal puncture data for subarachnoid hemorrhage (presence of blood in the cerebrospinal fluid). In some cases, it is impossible to clinically distinguish between compression of the brain by a hematoma or a focus of brain contusion with perifocal edema. In this case, a CT scan is performed, and in its absence, diagnostic burr holes are applied.
  • An open craniocerebral injury, as a rule, is detected already at the stage of primary surgical treatment of a head wound, as well as in the case of nasal liquorrhea (leakage of cerebrospinal fluid from the nose) or auricular liquorrhea (leakage of cerebrospinal fluid from the ear). Confirmation of the diagnosis is carried out on the basis of skull radiography and/or CT.
  • Severe diffuse axonal brain injury is diagnosed based on the clinical picture and is confirmed by the exclusion of intracranial hematoma or areas of brain contusion according to CT or MRI.
  • Traumatic hemorrhages in the posterior cranial fossa are difficult to diagnose and dangerous. If the patient is operated on in a comatose state, the prognosis is usually unfavorable. A hematoma of the posterior cranial fossa can be suspected in a patient with a fracture of the occipital bone (according to skull radiography), which is combined with such signs as: repeated vomiting, bradycardia, cerebellar symptoms (ataxia, coordination disorders, asynergia, large-scale spontaneous nystagmus), meningeal syndrome. Reliable diagnosis is possible using CT or MRI data. If it is not possible to perform them urgently, the application of a diagnostic milling hole is indicated. EchoES in this case is not informative.
  • The presence of wounds, abrasions, and bruises on the victim’s head may or may not be combined with a traumatic brain injury. The latter option is possible if, for example, a patient develops a stroke, falls and injures the soft tissues of the head. In this case, differentiation between stroke and traumatic brain injury is necessary, which is possible based on CT or MRI data.
  • Upon admission of a patient with a traumatic brain injury, it is necessary to perform a general examination to identify combined injuries of the spine, chest, limbs, and abdomen, which can determine the severity of the condition. In a coma state, diagnosis is extremely difficult and usually requires the involvement of specialists in related fields.
  • In many cases, more traumatic brain injury is combined with alcohol intoxication. The latter usually complicates diagnosis, both in the direction of exaggerating the severity of the injury and in the direction of underestimating it. The patient's serious condition, depression of consciousness, and convulsions may be caused by alcohol intoxication. These cases require special attention from the doctor and, if necessary, exclusion of intracranial hematoma according to CT or echoencephaloscopy.
  • Tension pneumocephalus can be suspected if the patient has liquorrhea and clinical signs of increasing compression of the brain. The diagnosis is confirmed by evidence of air accumulation in the cranial cavity with compression of the brain on radiography or CT.

It is necessary to distinguish between the severity of a traumatic brain injury, which primarily characterizes the nature of the anatomical damage to the brain and may not correspond to the clinical picture, and the severity of the condition of a patient with a traumatic brain injury.

• • Degree of impairment of consciousness. In Russia, the qualitative classification of oppression of consciousness is widespread:
    • Clear consciousness. Characterized by complete preservation of consciousness and orientation.
    • Stunning (stunned consciousness). Moderate stunning is characterized by depression of consciousness with limited verbal contact, decreased activity, partial disorientation, and moderate drowsiness. With deep stupor, disorientation, deep drowsiness, and only simple commands are observed.
    • Sopor. It is characterized by switching off consciousness with preservation of coordinated defensive reactions (localization of pain) and opening of the eyes in response to painful and sound stimuli.
    • Coma. It is characterized by a complete shutdown of consciousness, lack of localization of painful stimuli, and failure to open the eyes to pain and sound.
      • In moderate coma, uncoordinated defensive movements in response to pain are possible.
      • In deep coma, there are no defensive movements.
      • In extreme coma, muscle atony, areflexia, bilateral mydriasis (dilation of the pupils) or miosis (constriction of the pupils), and severe disturbances in vital functions are detected.
    doesn't open 1 Motor
    reaction
    (D)follows instructions 6 localizes pain 5 withdraws a limb in response to pain 4 pathological flexion movements (triple flexion of arms and extension of legs)
    decortication rigidity 3 limb extension
    (arm extension and pronation and leg extension)
    decerebrate rigidity 2 absent 1 Speech reaction
    (R)meaningful answer 5 confused speech 4 individual words 3 sounds 2 absent 1 The general condition is assessed in points G+D+R= from 3 to 15 points.

    Table of correspondence between gradations of state of consciousness and the Glasgow Coma Scale.

    Computed tomography is the most accurate and reliable research method for traumatic brain injury. The lack of CT scanners everywhere and the relative high cost of the study limit its widespread use. CT is a more informative method for head trauma than MRI. CT allows:

    • Verify fractures of the vault and base of the skull
    • Presence of intracranial hematoma (its nature, location, size).
    • The presence of a focus of brain contusion (its location, size, nature, presence of a hemorrhagic component).
    • Determine the degree of compression of the brain by the volumetric process.
    • Determine the presence of diffuse or perifocal edema and its degree.
    • Identify subarachnoid hemorrhage.
    • Identify intraventricular hematoma.
    • Determine the presence of pneumocephalus.
    Indications for CT tomography are:

    • Suspicion of traumatic intracranial hematoma.
    • Traumatic brain injury, especially severe or moderate, or suspicion of it (if there are traces of trauma on the head).
    • Comatose state of the patient, signs of increasing herniation of the brain.
    • The appearance of signs of intracranial hematoma several hours, days, weeks after the diagnosis of a concussion.

    CT scan showing a linear fracture in the right posterior frontal region (arrow).

    
    Axial CT tomogram of a depressed comminuted fracture of the right frontotemporal region.

    
    Axial CT image in bone mode, showing a transverse fracture of the petrous temporal bone (arrow).

    
    Axial CT tomogram. A large focus of contusion of the right frontal lobe with a hemorrhagic component and pronounced perifocal cerebral edema is identified; a small subcortical contusion in the right temporal lobe with perifocal edema (short arrow); small frontal subdural hematoma (long arrow).

    
    MRI tomography. The focus of a bruise with hemorrhagic impregnation in the left temporal lobe. Arrows indicate subdural blood collections.
    CT scan of the brain in a patient with TBI, showing multiple small focal hemorrhages (arrows), consistent with diffuse axonal damage to the brain.

    
    MRI showing swelling of the corpus callosum (arrow) in a patient with diffuse axonal brain damage.

    Level consciousness	Glasgow Coma Scale Scores
    clear consciousness	15 points
    moderate stun	13-14 points
    deep stun	13-14 points
    sopor	9-12 points

Classification is a necessary basis for both scientific generalization and quantitative study of any phenomenon. In relation to traumatic brain injury - a multidisciplinary problem at the intersection of neurosurgery, neurology, psychiatry, traumatology, surgery, pediatrics, geriatrics, resuscitation, social hygiene and a number of other specialties - the need to create a single, comprehensive classification is especially obvious.

Without it, it is impossible to conduct epidemiological studies, i.e. find out the frequency and structure of TBI, its relationship with social, geographic, economic and other factors, have its real statistics. Without classification, it is impossible to create a data bank on TBI. Without it, it is impossible to compare the quality of work of different neurosurgical institutions.

Classification of TBI is necessary:

• to unify clinical and forensic diagnosis,
• for triage of victims at the stages of medical evacuation,
• to develop adequate tactics and standards of medical and surgical treatment for TBI,
• for targeted therapy,
• for comparison of treatment results,
• to create predictive algorithms.

The classification of TBI organizes our knowledge of the problem as a whole. It is this that ensures the uniformity of diagnosis formulations and the use of modern terminology by attending physicians. The classification of TBI in concentrated form should reflect:

• the level of our knowledge on TBI, its patho- and sanogenesis,
• the level of development of fundamental sciences basic to the problem: anatomy, physiology of the central nervous system, blood and liquor circulation, cerebral metabolism, etc.,
• level of development of modern diagnostic and treatment technologies,
• level of development of society: its civilization, culture, economy, etc.,
• modern traumatic factors: socio-economic, environmental, climatic, criminal, etc.,
• the level of rehabilitation capabilities of medicine and society as a whole.

History of TBI classification

The prevalence of TBI even in the early stages of human history and the accumulation of treatment experience inevitably led to the appearance of the first signs of classification constructs.

In an Egyptian papyrus discovered by Edwin Smith, dating from 3000-2500. BC, 27 cases of head trauma are described, and in 13 of them there were fractures of the skull bones. Thus, for the first time, head trauma is divided into two types: 1) without a skull fracture and 2) with a skull fracture.

Several thousand years before the use of X-rays, the core principle of classification of TBI was used to verify bone fractures, on which the modern ICD 10 revision is still based. It is interesting that the division of TBI into trauma with and without skull fractures immediately acquires direct practical significance, indicating different severity of injury, different prognosis and different treatment tactics (according to the level of knowledge of the time).

Noteworthy are certain excerpts from the “methodological recommendations” given in the Egyptian papyrus: “If you examine a person with a head injury that reaches the bones of the cranial vault, then you need to palpate the wound. If damage to the bones of the arch is not detected, one must say: “There is a wound to the head, which, although it reaches the bone, does not cause damage to it. A suffering that I will heal." The wounds should be bandaged by applying a bandage of raw meat on the first day, and then treated with daily bandages with honey and copra until recovery.”

Skull fractures with dural irritation were also treated: “If you examine a person with a gaping head wound with damage to the skull bones, it must be palpated. He often cannot turn his head to the sides and tilt it across due to neck stiffness. It should be said: “There is an open head injury with damage to the skull bones and stiff neck. Suffering to be cured." After suturing the edges of the wound, raw meat should be applied on the first day. The bandage is contraindicated. Leave the patient alone until the acute period of the injury is over. Then treat him with honey bandages until he recovers.”

In case of penetrating head wounds with damage to the dura mater, the case was considered more severe: “If you examine a person with a gaping head wound that penetrates to the bone, deforms the skull and exposes the brain, this wound should be palpated. If the skull is crushed into small pieces and if you feel a fluctuation under your fingers, if blood flows from both nostrils of the patient and if the muscles of his neck are rigid, then you should say: “Suffering that cannot be cured.”

Analyzing the above excerpts from the papyrus, it can also be argued that here for the first time such important concepts in modern neurotraumatology as closed and open, non-penetrating and penetrating TBI are introduced. At the same time, differentiated tactics for their treatment are proposed, based, of course, on the available capabilities.

1000 years later, the “Hippocratic Collection” included the work “On Head Wounds,” which identifies and describes in detail various forms of open TBI. According to Hippocrates, an untreated skull fracture leads to fever after 7 days in summer and after 14 days in winter, wound suppuration, convulsions and death.

The next important step was taken in constructing a classification of TBI - for the first time, a classification of skull fractures was proposed. Among them, Hippocrates identified: 1) simple, 2) bruised, 3) depressed, 4) notched (hedra), 5) shockproof.

Based on this classification, the following treatment tactics were proposed: simple and contused fractures required trepanation; depressed fractures (as strange as it may seem to us) were not considered indicated for surgery. During trephination, it was recommended to leave the inner bone plate intact. Therefore, it is acceptable to believe that it was carried out not for the removal of intracranial hemorrhages (Hippocrates does not even mention hematomas), but for prophylactic purposes - for external drainage of pus.

The direct manifestation of TBI was known to Hippocrates. He postulated that the inevitable consequence of a concussion is an immediate loss of speech, the victim is deprived of all functions, lies without feelings and movements, as in the case of apoplexy. And it is even more strange that, having accurately described the clinic of brain damage, Hippocrates pays almost no attention to closed TBI. But this is not surprising. Knowledge about the functional significance of the brain was practically absent.

The great Hippocrates considered the brain to be only a gland that produced mucus that cooled the heart. Hence the interest and development of the obvious: wounds of the soft coverings of the head, skull fractures and ignoring the main thing in the problem - damage to the brain itself. And this despite the amazing powers of observation of Hippocrates, who so convincingly described the external signs of brain injury.

Aulus Cornelius Celsus, an outstanding Roman scientist and physician, in his book “On Medicine,” devotes a special chapter to TBI, calling it “On Fractures of the Roof of the Skull.” Outlining in detail the clinical picture, diagnosis and treatment of injuries to the bones of the skull, he, following Hippocrates, also distinguishes impact and anti-impact fractures - i.e. on the side of application of the traumatic agent and on the opposite side of the head.

Perhaps Celsus was the first to introduce the concept of “traumatic intracranial hematoma,” pointing out, which is very important, its formation even in the absence of bone damage. “If an insensible state sets in and the person loses consciousness, if paralysis or convulsions follow, then it is very likely that the meninges are also damaged and therefore there is even less hope for a successful outcome.” And further: “It’s rare, but it still sometimes happens that the entire bone remains undamaged, but inside the braincase some vessel ruptures from a blow, internal hemorrhage occurs, and the blood coagulated in a given place causes severe pain”...

In the work of Celsus, the external manifestations of acute traumatic edema-swelling of the brain are quite clearly outlined: “the swelling reaches the point that the membrane begins to rise even above the bone cover (after removal of bone fragments) ...”

The research of Galen of Pergamon in medicine and physiology dominated the minds of the 15th century. Autopsy was prohibited in Rome, so Galen conducted his research on animals, transferring the data obtained to humans. Hence many of the inadequacies of his brain anatomy and physiology. His ideas were based on the humoral theory of Hippocrates. He strictly followed the Hippocratic classification of skull fractures. However, in its practical application he went further, proposing to remove bone fragments in depressed fractures using multiple perforations.

The largest figure of the Middle Ages in the field of surgery, including surgery for head injuries, appears to be Guy de Chauliac. His book "Grand Surgery" was written in Latin. Since its first printed edition (1478, France), it has gone through more than 100 editions in Latin, French, Italian, Dutch, English, German and Spanish. For many centuries, surgeons in Europe treated Guy de Chauliac's manual as they did the Bible (although a number of provisions, such as the healing role of pus, were erroneous and set surgery back).

Guy de Chauliac made a significant contribution to the classification by first dividing head wounds into two categories: 1) with tissue loss and 2) without tissue loss. At the same time, the loss of part of the tissues of the head extended not only to the soft tissues and bones of the skull, but also to the substance of the brain. Guy de Chauliac was the first to note that the leakage of damaged brain matter into a wound is not always fatal.

Berengario de Carpi wrote a Treatise on Traumatic Brain Injury, which gained great popularity in Europe. He divided TBI into three categories: 1) incision - wounds of the scalp, 2) contusion caused by stone impacts, blunt trauma, 3) perforation caused by darts or arrows. All of them can be associated with skull fractures. Carpi divided TBI into: 1) primary - a blow to the head - with a stick, stone, etc., and 2) secondary - a blow to the head due to a fall - contralateral injury. Carpi described not only an epidural, but also a subdural hematoma.

The translation of Hippocrates' works in the 16th century, first into Latin and then into French, made them accessible to surgeons of the time. Among them, Ambroise Pare stands out for his contribution to neurotraumatology. He described a traumatic subdural hematoma formed by the counter-impact mechanism in King Henry II (who was injured at a knightly tournament and died from it on the 12th day). A. Paré published a fundamental illustrated monograph (1585, Paris), in which he presented in detail head injuries, including skull fractures, accompanied by concussion.

Johannes Skultetus divided head wounds into various categories, from simple injuries to the scalp to damage to the meninges. He described cerebral edema 6 months after injury; Apparently it was a chronic subdural hematoma.

In the 17th-18th centuries, knowledge about the localization of brain functions became quite deep and widespread. And this could not but affect the emergence of fundamentally new classification structures for traumatic brain injury, based not only and not so much on damage to the bones of the skull, but also on damage to the brain itself, its membranes, blood vessels and substance. In neurotraumatology, the period of “cranial osteology” is being replaced by the period of “cranial neurology”.

Beauville, and after him Jean Louis Petit in the second half of the 17th - first half of the 18th century, began to clearly distinguish “commotio cerebri” from “contusio” and “compressio”. J. Petit believed that the mechanism of concussion is based on vibration. He was the first to describe the increase in intracranial pressure with epidural hematomas, based on his experience of trephination for the purpose of their evacuation. J. Petit distinguished between immediate loss of consciousness due to concussion and delayed loss of consciousness due to compression by extravasates.

Percival Pott described the classic signs of concussion, as well as the lucid interval of meningeal hematomas.

In fact, the beginning of a three-century reign of the classical classification of traumatic brain injury was laid, dividing it into three main forms: concussion, bruise and compression of the brain. Of course, attempts to modernize TBI classifications continued, but they usually did not stand the test of time and practice. After all, it is in classification that the merging of the theoretical aspects of the problem and pressing daily applied tasks occurs, or here they irreconcilably collide.

In the 17th-20th centuries, the classification of TBI, while maintaining the core division into concussion, bruise and compression of the brain, absorbs both clinical and organizational experience, as well as new scientific knowledge and is further developed in the works of scientists. However, all the numerous modifications and additions to the classification of TBI occurred within its recognized and stable division into concussion, contusion and compression of the brain.

Meanwhile, the structure of the causes of traumatic brain injury is changing significantly with an increase in the proportion of impulse injuries (mainly due to the acceleration-deceleration mechanism in road accidents), as well as gunshot and blast wounds. This leads to the spread of previously unknown or little known forms of TBI.

With the advent of CT and MRI in the 70-80s of the 20th century, the possibilities for recognizing and tracking the dynamics of intracranial traumatic substrates became fundamentally different. Methods of non-invasive direct visualization of the brain and serious experimental research raise the question of revising a number of basic principles of the classification of TBI. In this case, the verification basis becomes damage to the brain, and not to the bones of the skull, as was previously the case in the pre-computer era.

In recent years, many countries have developed their own classifications of TBI. For all their value, they often do not cover this problem entirely, are built on different principles, are sometimes fragmentary, and are based on the use of individual, although extremely important, signs (state of consciousness, CT data, etc.). Often, classifications of TBI do not disclose such essential concepts as closed or open TBI, primary or secondary, isolated or combined TBI, etc., which certainly reduces their effectiveness.

It is undeniable that any classification of TBI, no matter how perfect it may seem, reflects only the current level of knowledge and technology; the constant and natural process of their development will inevitably make adjustments.

Modern principles of classification of traumatic brain injury

Long-term developments at the Institute of Neurosurgery named after. N.N. Burdenko show that the classification of TBI should be based on a comprehensive account of its biomechanics, type, type, nature, form, severity of injury, clinical phase, period of progression, and outcome of the injury. We propose the following classification structure of traumatic brain injury.

According to biomechanics TBI is distinguished:

• shock-anti-shock (a shock wave propagating from the place of application of the traumatic agent to the head through the brain to the opposite pole with rapid pressure drops at the places of impact and counter-shock);
• acceleration-deceleration (movement and rotation of the massive cerebral hemispheres relative to the more fixed brain stem);
• combined (when both mechanisms act simultaneously).

By type of damage highlight:

• focal, caused predominantly by impact-shock trauma (characterized by local macrostructural damage to the brain matter of varying degrees, including areas of destruction with the formation of detritus, hemorrhagic impregnation of brain tissue, pinpoint, small- and large-focal hemorrhages - at the site of impact-counterimpact, along the shock wave);
• diffuse, predominantly caused by trauma and acceleration-deceleration (characterized by transient asynapsia, tension and widespread primary and secondary axonal breaks in the centrum semiovale, subcortical formations, corpus callosum, brain stem, as well as pinpoint and small focal hemorrhages in the same structures);
• combined, when there are simultaneously focal and diffuse brain damage.

According to the genesis of the lesion brain is differentiated for TBI:

• primary lesions - focal bruises and crushes of the brain, diffuse axonal damage, primary intracranial hematomas, brainstem ruptures, multiple intracerebral hemorrhages;
• secondary lesions:

1. due to secondary intracranial factors: delayed hematomas (epidural, subdural, intracerebral), hemo- and liquor circulation disorders as a result of subarachnoid or intraventricular hemorrhage, an increase in brain volume or swelling due to edema, hyperemia or venous congestion, intracranial infection, etc.;
2. due to secondary extracranial factors: arterial hypotension, hypoxemia, hypercapnia, anemia and others.

Among the types of TBI distinguish:

• isolated (if there are no extracranial injuries),
• combined (if mechanical energy simultaneously causes extracranial damage) and
• combined (if different types of energy are simultaneously exposed - mechanical and thermal or radiation, or chemical) injuries.

The nature Taking into account the risk of infection of intracranial contents, TBI is divided into closed and open. Closed TBI includes injuries in which there are no violations of the integrity of the scalp or there are superficial soft tissue wounds without damage to the aponeurosis. Fractures of the bones of the vault, not accompanied by injury to the adjacent soft tissues and aponeurosis, are included in closed injuries of the skull.

Open TBI includes injuries in which there are wounds to the soft tissues of the head with damage to the aponeurosis, or a fracture of the bones of the vault with damage to adjacent soft tissues, or a fracture of the base of the skull, accompanied by bleeding or liquorrhea (from the nose or ear). If the dura mater is intact, open TBI is classified as non-penetrating, and if its integrity is damaged, it is classified as penetrating.

By severity TBI is divided into three grades: mild, moderate and severe. When correlating this rubric with the Glasgow Coma Scale, mild TBI is assessed at 13-15 points, moderate TBI at 9-12, severe TBI at 3-8 points. Mild TBI includes concussion and mild brain contusion, moderate TBI includes moderate brain contusion, subacute and chronic compression of the brain, severe TBI includes severe brain contusion, diffuse axonal damage and acute compression of the brain.

Naturally, only the general spectrum of assessing the severity of TBI is considered here. In practice, this problem is solved individually, taking into account the age of the victim, his premorbidity, the presence of various components of the injury (when, for example, the extent of damage to the scalp and/or skull bones, even with a mild or moderate brain contusion, forces the classification of TBI as severe) and other factors.

By mechanism TBI can occur in:

• primary (when the effect of traumatic mechanical energy on the brain is not caused by any previous cerebral or extracerebral catastrophe) and
• secondary (when the effect of traumatic mechanical energy on the brain occurs as a result of a previous cerebral catastrophe that caused a fall, for example, during a stroke or an epileptic seizure; or an extracerebral catastrophe, for example, a fall due to extensive myocardial infarction, acute hypoxia, collapse).

TBI in the same subject can be observed for the first time and repeatedly (twice, three times).

The following are distinguished: clinical forms of TBI:

• concussion,
• mild brain contusion;
• moderate brain contusion;
• severe brain contusion;
• diffuse axonal damage;
• compression of the brain;
• compression of the head.

Let us note that brain compression is a concept that reflects a process, and therefore must always have a specific interpretation based on the substrate that causes the compression (intracranial hematomas - epidural, subdural, intracerebral, depressed fractures, subdural hygroma, crush area, pneumocephalus).

According to the rate of brain compression distinguish:

• acute - threatening clinical manifestation within 24 hours after TBI;
• subacute - threatening clinical manifestation for 2-14 days. after TBI;
• chronic - threatening clinical manifestation 15 or more days after TBI.

Based on the fact that clinical compensation is the ability of the brain and the body as a whole to restore on its own or with the help of various external factors and influences (surgical, medicinal) certain functions, the deficiency of which is caused by injury, then clinical decompensation is the partial or complete loss of this abilities due to destruction or exhaustion of compensatory mechanisms under the influence of injury.

Clinical phase of TBI

The clinical phase of TBI is determined based on a combination of general cerebral, focal and brainstem parameters. The following clinical phases are distinguished in the condition of a victim with TBI:

• Clinical compensation phase. Social and labor adaptation has been restored. There are no general cerebral symptoms. Focal symptoms are either absent or residual. Despite the functional well-being of the patient, clinically or instrumentally changes can be detected that indicate a TBI.

• Clinical subcompensation phase. The general condition of the patient is usually satisfactory. Consciousness is clear or there are elements of stunning. Various focal neurological symptoms, often mild, may be detected. There are no dislocation symptoms. Vital functions are not impaired.

• Phase of moderate clinical decompensation. The general condition of the patient is moderate or severe. Stun, usually moderate. When the brain is compressed, signs of intracranial hypertension are clearly expressed. New focal symptoms of both loss and irritation increase or appear. Secondary stem signs are detected for the first time. There is a tendency to disrupt vital functions.

• Phase of severe clinical decompensation. The general condition of the patient is serious or extremely serious. Consciousness is impaired: from deep stupor to coma. When the brain is compressed, trunk entrapment syndromes are clearly expressed, more often at the tentorial level. Violations of vital functions become threatening.

• Terminal phase. Usually an irreversible coma with severe disturbances of vital functions, areflexia, atony, bilateral fixed mydriasis.

Base periods of TBI

There are three basic periods during TBI:

• acute (interaction of traumatic substrate, damaging reactions and defense reactions)
• intermediate (resorption and organization of damage and further development of compensatory and adaptive processes)
• distant (completion or coexistence of local and distant degenerative-destructive and regenerative-reparative processes).

With a favorable course, complete or almost complete clinical balancing of pathological changes caused by TBI occurs; in case of an unfavorable course - clinical manifestation of adhesive, cicatricial, atrophic, hemo-cerebrospinal fluid circulatory, vegetative-visceral, autoimmune and other processes triggered by trauma.

The duration of the periods of TBI varies mainly depending on the clinical form of TBI: acute - from 2 to 10 weeks, intermediate - from 2 to 6 months, long-term - with clinical recovery - up to 2 years, with a progressive course - unlimited.

In each period of the course of TBI, mainly in the intermediate and long-term, its various consequences and complications may appear. Meanwhile, these two widely used concepts, which certainly must be distinguished, are usually confused. Their detailed definitions are absent in the literature, including the special monograph “Complications and Sequelae of Head Injury”, published in 1993 by the American Association of Neurological Surgeons.

Categorization of TBI outcomes

An important part of the classification of TBI is the classification of outcomes. According to the Glasgow Outcome Scale, the following outcomes of TBI are distinguished:

• good recovery;
• moderate disability;
• severe disability;
• vegetative state;
• death.

At the Institute of Neurosurgery named after. N. N. Burdenko developed on its basis differentiated TBI outcome scale highlighting the following combinations of the patient’s condition and his ability to work:

• Recovery. Full restoration of ability to work, the patient works in the same place. Has no complaints, feels good, social behavior, work and school are the same as before the injury;
• Mild asthenia. Fatigue is increased, but there is no loss of memory or difficulty concentrating; works at full load in the same place; children exhibit pre-traumatic levels of learning and academic performance.
• Moderate asthenia with memory loss; works at the same job, but is less productive than before the TBI; Children may experience a slight decline in academic performance.
• Severe asthenia: gets tired quickly physically and mentally, memory is reduced, attention is depleted; headaches and other manifestations of discomfort often occur; works in a less skilled job; III disability group; in children there is a noticeable decline in academic performance.
• Expressed disorders mental and/or motor functions. Able to take care of himself. Disability group II; in children there is a pronounced decrease in learning ability; only a special school program is available.
• Gross violations psyche, motor functions or vision. Requires personal care. I disability group; Children are only capable of acquiring basic knowledge.
• Vegetative state.
• Death.

The first four rubrics of the INC outcome scale expand and specify the “Good recovery” rubric of the Glasgow outcome scale. The INC outcome scale gives a more complete and accurate picture of the level of social and labor readaptation of victims.

Each of the given characteristics in the classification of TBI is very significant for statistics, diagnosis, treatment tactics, prognosis, as well as organizational and preventive measures for neutrotrauma.

Clinical classification of acute traumatic brain injury

The classification of the acute period of TBI is based on the nature and degree of brain damage, since in the vast majority of observations this determines the clinical course, treatment tactics and outcomes.

Clinical forms of traumatic brain injury

The generalized description of the clinical forms of TBI proposed below, reflecting the general patterns of their manifestation, is aimed mainly at young and middle-aged victims.

Brain concussion

It is observed in 70-80% of victims with TBI. Characterized by loss of consciousness after injury from several seconds to several minutes. Retro-, con-, anterograde amnesia for a short period of time. Vomiting may occur. Upon restoration of consciousness, typical complaints are headache, dizziness, weakness, tinnitus, flushing of the face, sweating, other vegetative phenomena and sleep disturbances. There is pain when moving the eyes; divergence of the eyeballs when trying to read, vestibular hyperesthesia, paleness or redness of the face, “play” of vasomotors.

The status may reveal labile, mild asymmetry of tendon and skin reflexes, small-scale nystagmus, and mild membrane symptoms that disappear during the first 3-7 days. There are no injuries to the skull bones. Cerebrospinal fluid pressure and its composition without significant changes. The general condition of patients usually improves significantly during the first and less often the second week after injury.

Concussion is considered to be the mildest form of diffuse brain damage, in which there are no macrostructural changes. Computed tomography (CT) in patients with concussion does not reveal traumatic abnormalities in the state of the brain substance and cerebrospinal fluid-containing intracranial spaces. Pathomorphologically, there is no macrostructural pathology in concussion.

Light microscopy reveals changes at the subcellular and cellular levels in the form of perinuclear titrolysis, watering, eccentric position of neuronal nuclei, elements of chromatolysis, swelling of neurofibrils. Electron microscopy detects damage to cell membranes, mitochondria and other organelles.

Brain contusion differs from concussion by macrostructural damage to the brain substance of varying degrees.

Mild brain contusion

It is observed in 10-15% of victims with TBI. Characterized by loss of consciousness after injury for up to several tens of minutes. Upon its recovery, typical complaints are headache, dizziness, nausea, etc. Retro-, con-, and anterograde amnesia is observed. Vomiting, sometimes repeated. Vital functions are usually without significant impairment. Moderate bradycardia or tachycardia may occur, and sometimes arterial hypertension. Breathing, as well as body temperature, without significant deviations.

Neurological symptoms are usually mild (clonic nystagmus, mild anisocoria, signs of pyramidal insufficiency, meningeal symptoms); regresses within 2-3 weeks. With a mild brain contusion, fractures of the calvarial bones and subarachnoid hemorrhage are possible.

In cases of mild brain contusion, CT scan in half of the cases reveals a limited zone of reduced density in the medulla, close in tomodensitometric indicators to cerebral edema (from 18 to 28 N). In this case, as pathological studies have shown, pinpoint diapedetic hemorrhages are possible, for the visualization of which the resolution of CT is insufficient. In the other half of the cases, mild brain contusion was not accompanied by obvious changes in the CT picture, which was due to the limitations of the method.

Cerebral edema with a mild injury can be not only local, but also more widespread. It manifests itself as a moderate volumetric effect in the form of narrowing of the liquor spaces. These changes are detected already in the first hours after injury, usually reach a maximum on the third day and disappear after 2 weeks, leaving no traces. Local edema in mild contusions can also be isodense, and then the diagnosis is based on the volumetric effect, as well as the results of a dynamic CT study.

Pathomorphologically, mild brain contusion is characterized by areas of local swelling of the brain substance, pinpoint diapedetic hemorrhages, and limited ruptures of small pial vessels.

Moderate brain contusion

It is observed in 8-10% of victims with TBI. It is characterized by a loss of consciousness after injury for up to several tens of minutes to several hours. Retro-, con- and anterograde amnesia are expressed. The headache is often severe. Repeated vomiting may occur. Mental disorders occur.

Transient disorders of vital functions are possible: bradycardia or tachycardia, increased blood pressure; tachypnea without disturbance of the respiratory rhythm and patency of the tracheobronchial tree; low-grade fever. Shell signs are often pronounced. Brainstem symptoms are detected: nystagmus, dissociation of meningeal symptoms along the body axis, bilateral pyramidal signs, etc.

Focal symptoms (determined by the localization of the brain contusion) are clearly manifested: pupillary and oculomotor disorders, paresis of the limbs, sensitivity disorders, speech, etc. These nesting signs gradually (within 3-5 weeks) smooth out, but can persist for a long time. Cerebrospinal fluid pressure is often elevated. With moderate brain contusion, fractures of the bones of the vault and base of the skull, as well as significant subarachnoid hemorrhage, are often observed.

In cases of moderate brain contusion, CT in most cases reveals focal changes in the form of high-density inclusions that are not compactly located in a zone of reduced density, or a moderate homogeneous increase in density in a small area. As data from operations and autopsies show, these CT findings correspond to small hemorrhages in the bruise area or moderate hemorrhagic penetration of brain tissue without gross destruction.

Dynamic CT reveals that these changes are reversed during treatment. In some clinical observations of moderate brain contusion, CT reveals foci of low density (local edema), or the traumatic substrate is not convincingly visualized.

Pathomorphologically, a moderate brain contusion is characterized by small focal hemorrhages, areas of hemorrhagic impregnation of brain tissue with small areas of softening while maintaining the configuration of the gyral grooves and connections with the pia mater.

Severe brain contusion

It is observed in 5-7% of victims with TBI. Characterized by loss of consciousness after injury lasting from several hours to several weeks. Motor agitation is often pronounced. Severe threatening disturbances in vital functions are observed: bradycardia or tachycardia; arterial hypertension; disturbances in the frequency and rhythm of breathing, which may be accompanied by disturbances in the patency of the upper respiratory tract. Hyperthermia is pronounced.

Primary brainstem neurological symptoms often dominate (floating movements of the eyeballs, gaze paresis, tonic multiple nystagmus, swallowing disorders, bilateral mydriasis or miosis, divergence of the eyes along the horizontal or vertical axis, changing muscle tone, decerebrate rigidity, depression or irritation of tendon reflexes, reflexes from mucous membranes and skin, bilateral pathological foot reflexes, etc.), which obscures focal hemispheric symptoms in the first hours and days after injury.

Paresis of the limbs (up to paralysis), subcortical disturbances of muscle tone, reflexes of oral automatism, etc. can be detected. Generalized or focal convulsive seizures are sometimes observed. General cerebral and, in particular, focal symptoms regress slowly; gross residual effects are frequent, primarily in the motor and mental spheres. Severe brain contusion is usually accompanied by fractures of the vault and base of the skull, as well as massive subarachnoid hemorrhage.

In severe brain contusions, CT often reveals focal changes in the brain in the form of a zone of heterogeneous increased density. With local tomodensitometry, an alternation of areas is determined in them that have an increased density from 64 to 76 N (density of fresh blood clots) and a decreased density from 18 to 28 N (density of edematous and/or crushed brain tissue). As the data from operations and autopsies show, CT reflects a situation in the bruise zone in which the volume of cerebral detritus significantly exceeds the amount of shed blood.

In the most severe cases, the destruction of brain matter spreads in depth, reaching the subcortical nuclei and the ventricular system. Dynamic CT reveals a gradual decrease in areas of increased density against the background of their merging and transformation into a more homogeneous mass, which can become isodense with respect to the surrounding edematous substance of the brain on days 14-20.

The volumetric effect of the pathological substrate regresses more slowly, indicating that unresolved crushed tissue and blood clots remain in the focus of the bruise. The volume effect disappears by 30-40 days. after injury indicates the resorption of the pathological substrate with the further formation of atrophy in its place.

In almost half of the cases of severe brain contusion, CT reveals significant foci of intense homogeneous increase in density ranging from 65 to 76 N. As data from operations and autopsies show, tomodensitometric signs of such contusions indicate the presence of a mixture of liquid blood and its clots in the area of ​​brain damage with brain detritus, the amount of which is significantly less than the amount of shed blood.

The dynamics show a gradual decrease over 4-5 weeks in the size of the destruction area, its density and the resulting volumetric effect. Foci of crush injury are characterized by severe perifocal edema with the formation of a hypodense path to the nearest part of the lateral ventricle, through which fluid with decay products of brain tissue and blood is discharged.

Pathomorphologically, a severe brain contusion is characterized by areas of traumatic destruction of brain tissue with the formation of detritus, multiple hemorrhages (liquid blood and its coagulations) with the loss of the configuration of the grooves and convolutions and the severing of connections with the soft meninges.

Diffuse axonal brain injury

Characterized by a prolonged coma from the moment of injury. Brainstem symptoms are usually pronounced (paresis of reflex upward gaze, distance of the eyes along the vertical or horizontal axis, bilateral depression or loss of photoreactions of the pupils, violation of the formula or absence of the oculocephalic reflex, etc.).

Posnotonic reactions are typical: coma is accompanied by symmetrical or asymmetrical decerebration or decortication, both spontaneous and easily provoked painful (nociceptive) and other irritations. At the same time, changes in muscle tone are extremely variable, mainly in the form of hormetonia or diffuse hypotension.

Pyramidal-extrapyramidal paresis of the limbs, including asymmetric tetraparesis, is detected. Severe disturbances in the frequency and rhythm of breathing are often observed. Autonomic disorders are prominent: arterial hypertension, hyperthermia, hyperhidrosis, hypersalivation, etc.

A characteristic feature of the clinical course of diffuse axonal brain damage (DAB) is the transition from a long coma to a persistent or transient vegetative state, the onset of which is indicated by the opening of the eyes spontaneously or in response to various irritations (with no signs of tracking, fixing the gaze or performing at least basic instructions).

The vegetative state in DAP lasts from several days to several months and is characterized by the development of a new class of neurological signs - symptoms of functional and/or anatomical separation of the cerebral hemispheres and the brain stem. In the absence of any manifestations of the functioning of the initially grossly intact cerebral cortex, the subcortical, oral-stem, caudal-stem and spinal mechanisms are disinhibited. The chaotic and mosaic autonomization of their activity causes the appearance of unusual, diverse and dynamic oculomotor, pupillary, oral, bulbar, pyramidal and extrapyramidal phenomena.

Segmental brainstem reflexes are activated at all levels. The vivid reaction of the pupils to light is restored. Although anisocoria may persist, constriction of the pupils on both sides predominates, often with variable spontaneous or, in response to light stimulation, paradoxical dilation. Oculomotor automatisms manifest themselves in the form of slowly floating movements of the eyeballs in the horizontal and vertical planes; divergence is accompanied by a changing vertical distance of the eyeballs. There are spasms of gaze (usually downwards). Painful and especially postural irritations sometimes lead to tonic contraction of the eyes and the appearance of large converging nystagmus.

Inducing corneal reflexes, including with the help of a falling drop, often causes the appearance of various pathological responses - the corneomandibular reflex, oral automatisms, generalized uncoordinated movements of the limbs and torso. Trismus is characteristic. Facial synkinesis is often expressed - chewing, sucking, smacking, grinding teeth, squinting, blinking. Yawning and swallowing automatisms are observed. In the absence of gaze fixation, sometimes facial expressions of pain and crying appear.

Against the background of pyramidal-extrapyramidal syndrome with bilateral changes in muscle tone and tendon reflexes, a range of postural-tonic and uncoordinated defensive reactions can unfold spontaneously or in response to various irritations, including passive changes in body position: adducting tonic spasms in the limbs, turns of the body, turns and tilts of the head, paroxysmal tension of the muscles of the anterior abdominal wall, triple shortening of the legs, large-amplitude movements and complex, pretentious postures of the hands, motor stereotypies and tremor of the hands, etc.

The formula of inverted reactions changes many times in the same patient over even a short period of time. Among the infinite number of pathological reflexes detected during DAP, there may also be variants not described in the literature (for example, the phenomenon of bilateral irritation of abdominal reflexes against the background of tetraparesis with inhibition of periosteal and tendon reflexes, etc.).

In the clinic of persistent vegetative states due to DAP, along with the activation of spinal automatisms, signs of polyneuropathy of spinal and radicular origin (fibrillation of the muscles of the limbs and trunk, wasting of the muscles of the hand, common neurotrophic disorders) appear.

Against the described background, with DAP, paroxysmal states of a complex structure with bright vegetovisceral components can develop - tachycardia, tachypnea, hyperthermia, hyperemia and facial hyperhidrosis, etc.

As the vegetative state emerges, the neurological symptoms of dissociation are replaced predominantly by symptoms of loss. Among them, extrapyramidal syndrome dominates with severe stiffness, incoordination, bradykinesia, oligophasia, hypomimia, minor hyperkinesis, and ataxic gait. At the same time, mental disorders are clearly manifested, among which are often characterized by a pronounced lack of spontaneity (with indifference to the environment, untidiness in bed, lack of any urge to engage in any activity), amnestic confusion, dementia, etc. At the same time, gross affective disorders in the form of anger are observed , aggressiveness, irritability.

The described picture of DAP corresponds to its severe degree. It is obvious that, like focal damage, diffuse brain damage, having common biomechanics, can also be divided into several degrees according to their severity. Concussion is the mildest form of diffuse injury. With severe DAP, a deep or moderate coma lasts several days, accompanied by severe brainstem symptoms.

The CT picture of DAP is characterized by one or another increase in brain volume (due to its edema, swelling, hyperemia) with compression of the lateral and 3rd ventricles, subarachnoid convexital spaces, as well as cisterns of the base of the brain. Against this background, small focal hemorrhages can be detected in the white matter of the cerebral hemispheres, the corpus callosum, as well as in the subcortical and brainstem structures.

With the development of a vegetative state due to DAP, quite characteristic dynamics of computed tomographic data are often noted. 2-4 weeks after the injury, small foci of increased density (hemorrhages) are either not visualized or become hypodense, the ventricular system and subarachnoid spaces straighten and a clear tendency towards diffuse brain atrophy becomes apparent. Magnetic resonance imaging and its various modalities characterize DAP much more fully than CT.

Pathomorphologically, diffuse axonal damage is characterized by widespread primary and secondary axonal ruptures (with retraction balls, accumulations of microglia, a pronounced astroglial reaction) in the centrum semiovale, subcortical formations, corpus callosum, brain stem, as well as pinpoint small focal hemorrhages in the same structures.

Brain compression

It is observed in 3-5% of victims with TBI. It is characterized by a life-threatening increase - after one or another period of time after the injury or immediately after it - general cerebral (the appearance or deepening of disturbances of consciousness, increased headache, repeated vomiting, psychomotor agitation, etc.), focal (the appearance or deepening of hemiparesis, unilateral mydriasis, focal epileptic seizures, etc.) and stem (appearance or deepening of bradycardia, increased blood pressure, limitation of upward gaze, tonic spontaneous nystagmus, bilateral pathological signs, etc.) symptoms.

Depending on the background (concussion, brain contusion of varying degrees) against which traumatic compression of the brain develops, the light gap may be expanded, erased, or completely absent. Among the causes of compression, intracranial hematomas (epidural, subdural, intracerebral) come first. This is followed by depressed fractures of the skull bones, areas of crushing of the brain with perifocal edema, subdural hygromas, and pneumocephalus.

The shape and extent of epidural hematoma depends on the anatomical relationship of the skull bones and the dura mater in the area of ​​its localization, the source of bleeding, and combination with intrathecal and intracerebral hemorrhages. Acute epidural hematoma on CT examination is characterized by a biconvex, less often a plano-convex zone of increased density adjacent to the calvarium. It is limited in nature and, as a rule, is localized within one or two lobes. If there are several sources of bleeding, the hematoma can spread over a considerable distance and have a crescent shape.

A subdural hematoma on CT is often characterized by a crescent-shaped zone of altered density, but may have a plano-convex, biconvex, or irregular shape. Often subdural hematomas spread to the entire hemisphere or most of it.

Intracerebral hematomas on CT are detected as a round or irregularly shaped zone of homogeneous intense increase in density with clearly defined edges, especially when it is formed as a result of direct damage to the vessel. The density of hemorrhage is closely related to the protein component of hemoglobin and its concentration in the blood. The absorption coefficient (AC) of blood with a hematocrit of 45% is higher than the density of the brain matter and is 56 N.

As the contents of the hematoma liquefy and the blood pigments disintegrate, a gradual decrease in X-ray density occurs, making it difficult to diagnose hemorrhages, especially in cases where the coronary arteries of the altered blood and the surrounding medulla become identical (isodense hematomas). This is followed by a phase of reduced density, during which the KA of the emitted blood approaches the density of the cerebrospinal fluid.

Depressed fractures of the calvarium, as well as acute tension pneumocephalus, usually cause local compression of the brain.

The introduction of CT and MRI into clinical practice opens up fundamentally new opportunities in studying the mechanisms of dislocation processes during traumatic compression of the brain. CT and MRI make it possible not only to determine the location, nature and volume of the pathological substrate, but also to judge (due to their high resolution) the dynamics of changes in the ventricular system and cisternal spaces.

Using dynamic CT studies, it has been established that the various stages of tentorial and occipital herniations have characteristic signs and, regardless of the specific cause of brain compression, correspond to a certain phase of the clinical course of the traumatic process.

Pathomorphologically, compression of the brain is characterized by a volumetric accumulation of liquid and/or coagulated blood (supra- or intrathecal, intracerebral or intraventricular), or cerebrospinal fluid (subdural), or detritus mixed with blood (intracerebral), or air (intrathecal), causing local and general compression brain substances with displacement of the median structures, deformation and compression of the cerebrospinal fluid reservoirs, dislocation and infringement of the trunk.

Head compression

A special type of injury that occurs as a result of sequential exposure to dynamic (short-term) and static (long-term) mechanical load, morphologically characterized by damage (including long-term compression) of the soft integuments of the head, skull and brain, clinically - by the imposition and mutual aggravation of the general body, cerebral, cerebral and extracerebral focal symptoms.

In relation to the above definition, the term “long-term compression of the head” (minutes, hours, days) is more accurate, in contrast to the less significant short-term compression of the head (seconds).

Long-term compression of the head (LCH) occurs in victims of earthquakes, explosions and collapses in mines, mines, etc. The biomechanics of LCH can be represented as impact-compression. A heavy object or objects (fragments of collapsing buildings, fastening beams, rock, etc.), falling on the victim, first strikes, then presses the head to the floor or other objects.

When a traumatic object falls from a certain height, it has kinetic energy, which upon impact is transferred to the soft tissues, skull bones, and brain, exerting a dynamic short-term load on the patient’s head, resulting in a traumatic brain injury. If the object has sufficient mass, it continues the impact - creates a static load on the tissues of the head, the magnitude of which depends on the mass of the object.

The impact of mechanical load during DSG on the brain is realized in the following ways: due to dynamic load, concussions and brain contusions of varying degrees occur, due to static load, indirect (through soft tissues and bones of the skull) brain damage occurs. The last route of exposure is especially significant in children whose skull bones are elastic.

Prolonged compression of the head leads to a sharp and persistent increase in intracranial pressure, which naturally aggravates pathological changes in the brain. At a later stage after injury, when degenerative changes in the scalp and extensive necrosis develop, additional pathological effects on the brain are formed: intoxication with tissue decay products and wide gates for infection.

It is important to note that even if in the acute period of DSH the victim had a closed head injury, then at a later date, due to necrosis of the soft tissues of the head, it becomes open. Part of the diploic and emissary veins is also switched off from the venous network of the head, leading to a significant decrease in the outflow of intracranial blood through the external jugular vein system, which, in turn, significantly affects (due to stasis, hyperemia, etc.) pathological changes in the injured brain.

In victims with extensive unilateral and bilateral depressed fractures of the bones of the calvarium, after regression of swelling of the soft integument of the head, characteristic changes in the shape of the head are observed. The deformation of the head is then aggravated by the formation of flat scars with the absence of hair. Head deformation can be considered a pathognomonic symptom for DSH, which, depending on the size (area), localization of depressed fractures and changes in the soft integument of the head, has different severity.

Long-term compression syndrome (LCS) of the scalp is an important component of DCS. Swelling of the soft tissues of the head, which is observed in all victims, is pathognomonic for DSG. After the head is released from compression (decompression), within a short period of time (tens of minutes - hours), increasing swelling of the soft tissues appears, reaching its apogee 2-3 days after decompression.

Three degrees of severity of SDS of the scalp have been identified:

• light- compression time from 30 minutes. up to 5 hours - characterized by moderate contralateral swelling of the soft tissues of the head with minor intoxication and subsequent complete restoration of trophism;
• medium-heavy- time of compression from 2 hours to 48 hours - characterized by pronounced (with spread to nearby areas) swelling of the soft tissues of the head, followed by moderate trophic disorders and intoxication syndrome;
• heavy- time of compression from 24 hours to 58 hours or more - is characterized by sudden total swelling of the head, followed by necrosis of all layers of soft tissue and severe intoxication. The overlap of time boundaries at different degrees of SDS of the scalp is explained by the different mass of the pressing object.

Resorption into the general bloodstream of the decay products of compressed tissues of the head leads to the emergence of a complex of general body-intoxication symptoms characteristic of patients with DSH, the intensity of which depends on the severity of SDS of the scalp, as well as the mutual aggravation of SDS and TBI (impairment of consciousness is deeper and longer lasting, often not corresponds to the severity of the head injury and has an undulating nature; difficulty and disturbance of the breathing rhythm; high - up to 39-40 ° C, often hectic temperature; severe general weakness; repeated vomiting and nausea; dyspeptic symptoms, etc.).

The manifestation of the general organism-intoxication symptom complex in DSH begins after release from compression - decompression of the head, reaches its apogee with the peak intensity of trophic changes in the integument of the head and fades away along with the resolution of edema (with a mild degree - on 9-11 days, with a moderate degree - on 12 -14 days, in severe cases - for 15 or more days) and the formation of a demarcation line at the border of necrotic tissues of the head (in severe cases with prolonged compression of soft tissues).

The clinical symptoms of DSG are directly dependent on the prevalence of one of the two mandatory components of prolonged head compression - damage to the scalp or TBI, and the direction of head compression - frontal or lateral. The diversity of the clinical picture and the variability of the course of the traumatic disease in victims with prolonged compression of the head are determined by the combination of SDS of the scalp (three degrees of severity) and TBI (all forms and degrees of severity of brain damage).

In recognizing damage to the skull bones during DSG, the role of craniography is significant. However, computed tomography should be recognized as the main diagnostic method. With its help, you can simultaneously objectify and evaluate the condition of soft tissues (prevalence of edema, subgaleal hematomas, etc.), skull bones (unilateral, bilateral or multiple fractures, linear, depressed, etc.), the nature of brain damage (foci contusion, crushing, foreign bodies, edema-swelling, compression of the brain).

Gradations of the state of consciousness in traumatic brain injury

An adequate and unambiguous assessment of the clinical forms of traumatic brain injury in any medical institution and by any doctor necessarily presupposes the correct classification of disorders of consciousness. The following 7 gradations of the state of consciousness in traumatic brain injury are distinguished:

• Clear.
• Stun is moderate.
• The stun is deep.
• Sopor.
• Coma is moderate.
• Deep coma.
• Terminal coma.

Clear consciousness

Preservation of all mental functions, primarily the ability to correctly perceive and comprehend the surrounding world and one’s own “I”, actions that are adequate to the situation and useful for oneself and others with full awareness of their possible consequences. Leading signs: wakefulness, full orientation, adequate reactions.

Generalized clinical characteristics: voluntary opening of the eyes. Quick and targeted reaction to any stimulus. Active attention, extensive speech contact. Meaningful answers to questions. Follow all instructions. Preservation of all types of orientation (in oneself, place, time, surrounding persons, situation, etc.). Retro- and/or congrade amnesia is possible.

Stun

Depression of consciousness while maintaining limited verbal contact against the background of an increase in the threshold of perception of external stimuli and a decrease in one’s own activity with a slowdown in mental and motor reactions. Stunning is divided into two degrees: moderate and deep.

The leading signs of moderate stupor: moderate drowsiness, mild errors in time orientation with somewhat slow comprehension and execution of verbal commands (instructions).

Generalized clinical characteristics of moderate stunning: the ability for active attention is reduced. Speech contact is preserved, but obtaining answers sometimes requires repeating questions. Performs commands correctly, but somewhat slowly, especially complex ones. Eyes open spontaneously or immediately when addressed. The motor response to pain is active and purposeful. Increased exhaustion, lethargy, some depletion of facial expressions; drowsiness. Orientation to time, place, surroundings and persons may be inaccurate. Control over the functions of the pelvic organs is preserved.

The leading signs of deep stupor are: disorientation, deep drowsiness, and only following simple commands.

Generalized clinical characteristics of deep stunning: the sleep state predominates; alternation with motor excitation is possible. Verbal contact with the patient is difficult. After persistent requests, you can get answers, often monosyllabic, like “yes-no”. Can provide his first name, last name and other data, often with perseverations. Reacts to commands slowly. Able to perform basic tasks (open eyes, show tongue, raise hand, etc.). To continue contact, repeated calls and loud calls are necessary, sometimes in combination with painful stimulation. A coordinated defensive reaction to pain is expressed. Disorientation in time, place, etc. Orientation in one’s own personality can be preserved. Control over the functions of the pelvic organs is weakened.

Sopor

Deep depression of consciousness with preservation of coordinated defensive reactions and eye opening in response to pain and other stimuli. Leading signs: pathological drowsiness, opening of eyes to pain and other stimuli, localization of pain.

Generalized clinical characteristics: the patient constantly lies with his eyes closed and does not follow verbal commands. Is immobile or makes automated stereotyped movements. When painful stimuli are applied, coordinated protective movements of the limbs, turning to the other side, and pained grimaces on the face, aimed at eliminating them, occur; the patient may moan. A short-term way out of pathological drowsiness is possible in the form of opening your eyes to pain or a sharp sound. Pupillary, corneal, swallowing and deep reflexes are preserved. Sphincter control is impaired. Vital functions are preserved or moderately changed in one of the parameters.

Coma

Switching off consciousness with a complete loss of perception of the surrounding world, oneself and other signs of mental activity. Depending on the severity and duration of neurological and autonomic disorders, coma is divided into 3 degrees according to severity: moderate (I), deep (II) and terminal (III).

Leading signs moderate coma (I): inability to wake up, non-opening of eyes, uncoordinated defensive movements without localization of painful stimuli.

Generalized clinical characteristics of moderate coma (I): inability to awaken. In response to painful stimuli, uncoordinated defensive motor reactions appear (usually in the form of withdrawal of limbs), but the patient does not open his eyes. Sometimes spontaneous motor restlessness is observed. Pupillary and corneal reflexes are usually preserved. Abdominal reflexes are depressed; tendon are variable, often elevated. Reflexes of oral automatism and pathological foot reflexes appear. Swallowing is very difficult. The protective reflexes of the upper respiratory tract are relatively preserved. Sphincter control is impaired. Respiration and cardiovascular activity are relatively stable, without threatening deviations.

Leading signs deep coma (II): inability to wake up, lack of protective movements in response to pain.

Generalized clinical characteristics of deep coma (II): there are no reactions to external stimuli; pathological extensor, and less often flexion, movements in the limbs may occur only in response to severe pain. Changes in muscle tone are varied: from generalized hormetonia to diffuse hypotension (with dissociation along the body axis of meningeal symptoms - disappearance of nape rigidity with a remaining Kernig symptom). Mosaic changes in skin, tendon, corneal, and pupillary reflexes (in the absence of fixed bilateral mydriasis) with a predominance of their inhibition. Preservation of spontaneous breathing and cardiovascular activity in case of severe impairments.

Leading signs terminal coma (III): muscle atony, areflexia, bilateral fixed mydriasis.

Generalized clinical characteristics of coma (III): bilateral fixed mydriasis, immobility of the eyeballs. Diffuse muscle atony; total areflexia. Critical disturbances of vital functions - severe disorders of the rhythm and frequency of breathing or apnea, severe tachycardia, blood pressure below 60 mm Hg. Art.

It should be taken into account that the proposed classification applies only to non-productive forms of disturbance of consciousness such as shutdown, deficiency, depression, quantitative decrease in mental activity (mainly due to suffering of the mid-brain structures). It does not include productive forms of disturbance of consciousness such as stupefaction, confusion, disintegration (delirium, oneiroid, twilight states, etc.), caused by a predominant dysfunction of hemispheric formations, and does not cover such usually extended post-comatose states as a vegetative state, akinetic mutism, etc. .

Glasgow Coma Scale

The so-called Glasgow Coma Scale (GCS), developed in 1974 by G. Teasdale and V. Jennet, has received recognition in world neurotraumatology. The GCS is widely used to quantify impairment of consciousness in TBI. Its undoubted advantages are simplicity and accessibility, not only for medical personnel. The condition of patients according to the GCS is assessed at the time of admission and after 24 hours according to three parameters: eye opening, verbal and motor response to external stimuli.

The total assessment of the victim’s state of consciousness according to the GCS varies from 3 to 15 points. It is accepted that 3-7 points correspond to severe TBI, 8-12 points - moderate TBI, 13-15 points - mild TBI.

Criteria for assessing the severity of the victim’s condition

It is necessary to distinguish between the concepts of “severity of traumatic brain injury” and “severity of the victim’s condition.” The concept of “severity of the patient’s condition,” although in many ways derived from the concept of “severity of injury,” is nevertheless much more dynamic than the latter. Within each clinical form of traumatic brain injury, depending on the period and direction of its course, conditions of varying severity can be observed.

The assessment of the “severity of injury” and the assessment of the “severity of the condition” in most cases upon admission of the patient coincide. But there are often situations when these estimates diverge. For example, with the subacute development of a meningeal hematoma against the background of a mild brain contusion, with depressed fractures with a moderate or even severe brain contusion, when the “silent” zones of the hemispheres are selectively affected, etc.

Assessing the severity of the condition in the acute period of traumatic brain injury, including the prognosis for both life and restoration of ability to work, can be complete only if at least three components are taken into account; namely:

• states of consciousness;
• status of vital functions;
• state of focal neurological functions.

State of consciousness:

• clear,
• moderate stun,
• deep stun,
• sopor,
• moderate coma,
• deep coma,
• terminal coma.

Vital functions:

• no violations - breathing 12-20 breaths. per minute, pulse 60-80 beats. per minute, blood pressure within 110/60-140/80 mm. rt. Art., body temperature not higher than 36.9° C.
• moderate disorders - moderate bradycardia (51-59 beats per minute) or moderate tachycardia (81 - 100 beats per minute), moderate tachypnea (21-30 breaths per minute), moderate arterial hypertension (ranging from 140 /80 - up to 180/100 mm Hg) or hypotension (below 110/ 60 - up to 90/50 mm Hg), low-grade fever (37.0-37.9 ° C).
• pronounced disturbances - sharp tachypnea (31-40 breaths per minute) or bradypnea (8-10 breaths per minute), sharp bradycardia (41-50 beats per minute) or tachycardia (101-120 beats per minute). per minute), severe arterial hypertension (over 180/100-220/120 mm Hg) or hypotension (below 90/50 - up to 70/40 mm Hg), severe fever (38.0 -38.9° C).
• gross violations - extreme degree of tachypnea (over 40 breaths per minute) or bradypnea (less than 8 breaths per minute), extreme degree of bradycardia (less than 40 beats per minute) or tachycardia (over 120 beats per minute) , extreme arterial hypertension (above 220/120 mm Hg) or hypotension (maximum pressure below 70 mm Hg), severe fever (39.0-39.9 ° C).
• critical disorders - periodic breathing or stopping, maximum blood pressure below 60 mm. rt. Art., uncountable pulse, hyperthermia (40°C and above).

Focal neurological disorders:

Stem characteristics:

• no abnormalities - pupils are equal, with a live reaction to light, corneal reflexes are preserved;
• moderate disturbances - corneal reflexes are reduced on one or both sides, mild anisocoria, clonic spontaneous nystagmus;
• pronounced disorders - unilateral dilation of the pupils, clonal-tonic nystagmus, decreased reaction of the pupils to light on one or both sides, moderate paresis of upward gaze, bilateral pathological signs, dissociation of meningeal symptoms, muscle tone and tendon reflexes along the body axis;
• gross disorders - gross anisocoria, gross paresis of upward gaze, tonic multiple spontaneous nystagmus or floating gaze, gross divergence of the eyeballs along the horizontal or vertical axis, grossly expressed bilateral pathological signs, gross dissociation of meningeal symptoms, muscle tone and reflexes along the body axis;
• critical disorders - bilateral mydriasis with lack of pupillary reaction to light, areflexia, muscle atony.

Hemispheric and craniobasal signs:

• no abnormalities – tendon reflexes are normal on both sides, cranial innervation and limb strength are preserved;
• moderate disorders - unilateral pathological signs, moderate mono- or hemiparesis, moderate speech disorders, moderate dysfunction of the cranial nerves;
• severe disorders - severe mono- or hemiparesis, severe paresis of cranial nerves, severe speech disorders, paroxysms of clonic or clono-tonic convulsions in the extremities;
• gross disorders - severe mono- or hemiparesis, or paralysis of the limbs, palsies of the cranial nerves, gross speech disorders, frequently recurring clonic convulsions in the limbs;
• critical disorders - severe triparesis, triplegia, severe tetraparesis, tetraplegia, bilateral facial paralysis, total aphasia, constant convulsions.

The following 5 gradations of the condition of patients with traumatic brain injury are distinguished:

• Satisfactory.
• Moderate weight.
• Heavy.
• Extremely difficult.
• Terminal.

Satisfactory condition

Criteria:

• consciousness is clear;
• vital functions are not impaired;
• focal symptoms are absent or mild (for example, motor disturbances do not reach the level of paresis).

When qualifying a condition as satisfactory, it is permissible to take into account, along with objective indicators, the complaints of the victim. There is no threat to life (with adequate treatment); the prognosis for restoration of ability to work is usually good.

Moderate condition

• state of consciousness - clear or moderate stupor;
• vital functions are not impaired (only bradycardia is possible);
• focal symptoms - one or another hemispheric and craniobasal symptoms may be expressed, often appearing selectively: mono- or hemiparesis of the limbs; paresis of individual cranial nerves; blindness or a sharp decrease in vision in one eye, sensory or motor aphasia, etc. Single brain stem symptoms (spontaneous nystagmus, etc.) may be observed.

To establish a condition of moderate severity, it is enough to have the indicated violations in at least one of the parameters. For example, the detection of moderate stunning in the absence of pronounced focal symptoms is sufficient to determine the patient’s condition as moderate. Similarly, identifying mono- or hemiparesis of the limbs, sensory or motor aphasia, etc. with clear consciousness is sufficient to assess the patient’s condition as moderate. When qualifying a patient's condition as moderately severe, along with objective ones, it is also permissible to take into account the severity of subjective symptoms (primarily headache).

The threat to life (with adequate treatment) is insignificant; the prognosis for restoration of working capacity is often favorable.

Serious condition

Criteria (limits of violations for each parameter are given):

• state of consciousness - deep stupor or stupor;
• vital functions - impaired, mostly moderately, in one or two indicators;
• focal symptoms:

1. stem - moderately expressed (anisocoria, decreased pupillary reactions, limitation of upward gaze, homolateral pyramidal insufficiency, dissociation of meningeal symptoms along the body axis, etc.);
2. hemispheric and craniobasal - clearly expressed, both in the form of symptoms of irritation (epileptic seizures) and loss (motor disorders can reach the level of baldness).

To establish a serious condition, the victim is allowed to have the indicated violations in at least one of the parameters. For example, detection of stupor even in the absence or mild severity of disturbances in vital and focal parameters is sufficient to determine the patient’s condition as severe.

The threat to life is significant; largely depends on the duration of the serious condition. The prognosis for restoration of working capacity is sometimes unfavorable.

Extremely serious condition

Criteria (limits of violations for each parameter are given):

• state of consciousness - moderate or deep coma;
• vital functions - gross violations simultaneously in several parameters;
• focal symptoms:

1. stem - expressed roughly (reflex paresis or plegia of upward gaze, gross anisocoria, divergence of the eyes along the vertical or horizontal axis, tonic spontaneous nystagmus, sharp weakening of the pupillary response to light, bilateral pathological signs, decerebrate rigidity, etc.);
2. hemispheric and craniobasal - pronounced sharply (up to bilateral and multiple paresis).

The threat to life is maximum; largely depends on the duration of the extremely serious condition. The prognosis for restoration of working capacity is often unfavorable.

Terminal state

Criteria:

• state of consciousness - terminal coma;
• vital functions - critical impairment;
• focal symptoms: stem - bilateral fixed mydriasis, absence of pupillary and corneal reflexes; hemispheric and craniobasal - blocked by cerebral and brainstem disorders.

Prognosis: Survival is usually not possible.

When using the given scale for assessing the severity of a condition for diagnostic and especially prognostic judgments, one should take into account the time factor - the duration of the patient’s stay in a particular condition. Severe condition for 15-60 minutes. after an injury, it can also be observed in victims with a concussion and mild contusion, but has little effect on the favorable prognosis of life and restoration of working capacity.

If a patient’s stay in a serious and extremely serious condition continues for more than 6-12 hours, then this usually excludes the leading role of many contributing factors, such as alcohol intoxication, and indicates a severe traumatic brain injury.

With combined traumatic brain injury, it should be taken into account that, along with the cerebral component, the leading causes of a protracted severe and extremely severe condition may also be extracranial factors (traumatic shock, internal bleeding, fat embolism, intoxication, etc.).

Periodization of the clinical course of traumatic brain injury

Traumatic brain injury is characterized by a certain sequence of development and disappearance of post-traumatic changes, which indicates the presence of different periods in its course. The periodization of TBI is a content-time characteristic of the dynamics of its manifestation - from the moment of damaging effects on the brain of mechanical energy to the final result of treatment of the victim (recovery, disability, death).

This process unfolded over time is largely different in its patho- and sanogenic mechanisms, clinical manifestations, variants of possible complications, level of everyday and social-work readaptation, etc., which underlies the identification of each of the periods of TBI.

The identification of periods of traumatic brain disease is based on the sum of criteria:

• clinical (whole-organism, cerebral, brainstem, hemispheric signs and their dynamics);
• pathophysiological (edema, swelling, brain hyperemia, vascular, neurotransmitter, hormonal, enzymatic, immune and other reactions and their dynamics);
• morphological (traumatic substrate and the dynamics of its rehabilitation, organization).

During TBI, sequential and parallel factors are intricately intertwined: biomechanics of injury, primary substrates of brain damage; pathological organ and organism reactions; age, premorbid, genetic characteristics; secondary intra- and extracranial complications; sanogenic reactions and compensatory-adaptive processes; functional and social outcomes. It should be remembered that there are often no correlations between the direction of development, severity, combination of various components and time characteristics of a particular period of traumatic brain disease.

The energetic and plastic restructuring of the brain after TBI lasts a long time (months, years and even decades). TBI triggers, among many others, two oppositely directed processes, not only local, but also distant ones - dystrophic-destructive and regenerative-reparative, which go in parallel with the constant or variable predominance of one of them, largely determining the presence or absence of certain clinical manifestations in one period or another of TBI.

In each period of TBI, all its components are important, but the clinic still plays a decisive role. It is acceptable to talk about clinical recovery - with stable good health, absence of neurological, psychopathological, somatic symptoms, complete restoration of previous working capacity and adequate social activity, even if there are morphological changes in the brain.

The modern periodization of traumatic brain disease takes into account new knowledge on the biomechanics of damage (especially in acceleration-deceleration trauma, causing diffuse axonal damage), on the pathogenesis of TBI (the concept of impaired self-regulation of cerebral metabolism), on intravital non-invasive verification of traumatic substrates and brain reactions (data from computer and magnetic resonance imaging, radionuclide studies, multimodal evoked potentials, spectral and coherence analysis of EEG, immune and biochemical tests, thermal radio imaging and others), as well as significant changes in the TBI clinic (the appearance of patients with prolonged comatose states, vegetative status, syndromes of separation of the hemispheres and brain stem, etc.) and fundamentally different possibilities for treatment and rehabilitation.

In case of TBI, three basic periods are distinguished during the course of traumatic brain disease:

• spicy(interaction of traumatic substrate, damage reactions and defense reactions)
• intermediate(resorption and organization of areas of damage and deployment of compensatory-adaptive processes),
• remote(completion or coexistence of local and distant degenerative-destructive and regenerative-reparative processes), with a favorable course - complete or almost complete clinical balancing of pathological changes caused by TBI; in case of an unfavorable course - clinical manifestation of adhesive, cicatricial, atrophic, hemo-cerebrospinal fluid-disculatory, vegetative-visceral, autoimmune and other processes triggered by trauma.

Acute period

Definition: the period of time from the moment of the damaging effect of mechanical energy on the brain with a sudden breakdown of its integrative-regulatory and local functions until the stabilization of impaired cerebral and general body functions at one level or another, or the death of the victim.

The duration of the acute period is from 2 to 10 weeks, depending on the clinical form of TBI. Approximate duration of the acute period of TBI: for concussion - up to 2 weeks; for mild brain contusion - up to 3 weeks; for moderate brain contusion - up to 4-5 weeks; for severe brain contusion - up to 6-8 weeks; for diffuse axonal damage - up to 8-10 weeks; with compression of the brain - from 3 to 10 weeks (depending on the background).

Within the acute period of TBI, several periods can be distinguished: 1) the primary maximum of brain dysfunction; 2) labile secondary disorders of brain function; 3) stabilization - at one level or another - of impaired brain functions. According to the experimental model of TBI (concussion), the acute period is characterized by an initial intensification of metabolic processes (“metabolic fire”), which turns into the development of energy deficiency in the nervous tissue and secondary changes.

Clinically, the acute period of TBI is characterized by symptoms of disintegration and loss of brain functions. Disturbances of consciousness of the type of depression and shutdown with a quantitative decrease in mental activity (stunning, stupor or coma) are typical, mainly due to the suffering of the mid-brain structures.

Among the focal neurological signs in the acute period of TBI, symptoms of loss of brain function dominate, the structure and severity of which are determined by the location and type of traumatic substrate. Severe TBI, especially brain compression, is characterized by the appearance of secondary dislocation symptoms, mainly from the brain stem, as well as distant focal pathology of vascular origin. Depending on the severity of TBI, central disturbances in metabolism, autonomic function and vital functions manifest themselves - from minor to threatening.

The acute period of TBI corresponds to post-traumatic immunosuppression and an increase in autoimmune reactions. At the same time, judging by the direction of autoantibodies to various neurospecific proteins, in mild TBI, autoantibodies are detected mainly to glial elements, while in severe TBI, antibodies to both glia and neurons are detected.

According to CT and MRI data, the acute period of TBI is characterized by various focal and diffuse changes in the brain tissue, one or another narrowing or displacement of the cerebrospinal fluid-containing spaces, reflecting the characteristics of the traumatic substrate (foci of bruise or crush, hematomas, etc.) and the brain’s reactions to it (edema, swelling , dysgemia).

Pathomorphologically, the acute period of TBI is characterized by: in case of focal bruises and crushes, destruction of brain tissue with the formation of detritus, hemorrhages (large or small focal, rectal or dipedetic), hemocerebrovascular disorders, edema and swelling of the brain, as well as developing processes of cleansing of decay products of brain tissue and shed blood ; in case of concussion - diffuse ultrastructural changes in synapses, neurons, glia; in case of diffuse axonal damage - primary axonal ruptures; with compression of the brain - microcirculation disorders, edematous and ischemic changes in neurons.

Interim period

Definition: the period of time from the stabilization of general body, cerebral, focal functions disturbed by injury to their complete or partial restoration, or stable compensation. The duration of the intermediate period: for mild TBI - up to 2 months, for moderate TBI - up to 4 months, for severe TBI - up to 6 months.

Clinically, the intermediate period is characterized by restoration of consciousness, but syndromes of its disintegration (psychotic or subpsychotic) may be observed. Asthenia is pronounced. After a long coma, a vegetative status and akinetic mutism are possible. Focal symptoms of loss (motor, speech, sensory, static coordination and other brain functions) regress completely or partially. Typically, cranial nerve palsies are more persistent. Various irritation syndromes are formed: shell-pain, trigeminal, epileptic, subcortical and others. A variety of psychovegetative symptoms begin to develop.

In the intermediate period, homeostasis is restored either in a stable mode or in a mode of tension and subsequent depletion of the activity of adaptive systems with the formation of long-term progressive consequences.

Immunologically, in the intermediate period various changes in cellular immunity indicators often persist (in particular, the level of T and B lymphocytes and their blast-transforming ability are reduced). At the same time, humoral immunity is usually normalized. It is in the intermediate period that the dynamics of immune parameters are revealed, which determines the formation of post-traumatic consequences of either a progressive or regressive nature. According to CT and MRI data, the intermediate period is characterized by the straightening and redislocation of the cerebral ventricles, basal and convexital subarachnoid spaces and the development of various focal and diffuse post-traumatic processes with multidirectional changes in the brain substance.

Morphologically, in the intermediate period, in response to TBI, reparative and regenerative processes fully unfold. Damage to a neuron, glia or nerve fiber causes intracellular regeneration. The destruction of individual fields and layers of the cortex leads to increased functioning, due to hypertrophy or hyperplasia, of cells in neighboring areas. In the intermediate period, local and distant processes of demyelination, fragmentation of axons, formation of cysts, adhesions, etc. also continue.

Remote period

Definition: a period of clinical recovery, or the maximum achievable rehabilitation of impaired functions, or the emergence and/or progression of new pathological conditions caused by a TBI. The length of the long-term period: with clinical recovery - up to 2 years, with a progressive course - not limited.

Clinical symptoms, if they do not disappear, become persistent and residual, combining signs of loss, irritation and disconnection. New neurological symptoms may appear.

Immunologically, in the long term, autoantibodies to neurons and glial cells are detected in 50-60% of cases. Taking this into account, two forms of post-traumatic development are distinguished: immune-dependent and immune-independent. The first is characterized by secondary immunological reactions.

According to CT and MRI data, the long-term period is characterized by post-traumatic focal and diffuse changes in the brain tissue, intrathecal spaces and ventricular system of mild, moderate and severe degrees (depending on the nature, severity, location of brain damage, the presence of surgical intervention, purulent-inflammatory complications and consequences TBI). Plastic restructuring of the brain after TBI continues in the long-term period, complexly combining destructive and regenerative processes in various proportions.

Age and premorbid characteristics

When characterizing the periods of TBI, pre-traumatic neurological pathology, concomitant somatic diseases and age factors should be taken into account. In the pediatric and geriatric contingents of victims, the age-related characteristics of the body, the causes and biomechanics of injuries are very significant for the content-time qualification of the course of TBI.

Childhood is distinguished by the special vulnerability of the immature brain, the tendency to generalize edema, the tendency to diffuse axonal damage, and at the same time, the high compensatory capabilities of the developing brain.

Elderly and senile age are distinguished by torpid reactions with a predominance of intracranial hypotension and vascular disorders, the dominance of focal symptoms, a comparative frequency of intracranial hematomas, and tropism for focal lesions.

In children, the acute period is often much shorter than in adults (for mild TBI - up to 10 days, for moderate trauma - up to 15-20 days, for severe TBI - up to 21-28 days). At the same time, in children the intermediate (for mild TBI - up to 6 months, for moderate TBI - up to 1-1.5 years, for severe TBI - up to 2 years) and long-term (for mild and moderate severity - up to 1.5-2.5 years, with severe cases - up to 3-4 years) periods.

In elderly and elderly people, the acute period of TBI is often prolonged compared to young and middle-aged people, which is due to the appearance or exacerbation of vascular and visceral pathology; The intermediate and long-term periods also lengthen, coinciding with the frequent worsening of involutional disorders after TBI.

In the intermediate and long-term periods, and sometimes even in the acute period, various consequences of TBI develop. At the same time, purulent-inflammatory complications of TBI often develop in the acute period, less often in the intermediate period.

Without at all downplaying the importance of various morphological and functional indicators, we emphasize that their use in isolation from the clinic is unproductive. It is the clinical picture that more accurately reflects the compensatory and adaptive capabilities of the body, when, for example, with the same substrate (atrophic, cicatricial adhesive process, liquor cysts, etc.) there is either almost complete social and labor readaptation and the absence of gross neurological and psychiatric symptoms , or severe disability of the victim with severe cerebral and focal symptoms.

Symptoms of traumatic brain injury often develop immediately after the injury, but they may also appear over time.

• Loss of consciousness: develops immediately after injury. Depending on the severity of the injury, it can last from a few minutes to several hours (or even days). In this case, the victim does not answer questions (or answers slowly and with a delay), and may not respond to calls or pain.
• Headache: occurs after a person regains consciousness.
• Nausea and vomiting that does not bring relief (usually one-time, after regaining consciousness).
• Dizziness.
• Facial redness.
• Sweating.
• Visible damage to the bones and soft tissues of the head: bone fragments, bleeding, and skin defects may be visible.
• Hematoma (bleeding) into soft tissues: formed due to fractures of the skull bones. It may be located behind the ear, as well as around the eyes (symptom of “glasses” or “raccoon eyes”).
• Leakage of cerebrospinal fluid from the nose or ears (cerebrospinal fluid rhinorrhea). Liquor is a cerebrospinal fluid that provides nutrition and metabolism to the brain. Normally, it is located in the slit-like cavity between the bones of the skull and the brain. With fractures of the base of the skull, defects in the bones of the skull are formed, the dura mater adjacent to the bones is torn, and conditions are created for the leakage of cerebrospinal fluid into the nasal cavity or into the external auditory canal.
• Convulsive seizure: involuntary contractions of the muscles of the arms and legs, sometimes with loss of consciousness, tongue biting and urination.
• Memory loss (amnesia): Develops after injury, usually involving pre-injury amnesia (retrograde amnesia), although anterograde amnesia (loss of memory of events that occurred shortly after injury) is also possible.
• With traumatic damage to the superficial vessels of the brain, the development of traumatic subarachnoid hemorrhage (blood entering the space between the membranes of the brain) may develop, and the following symptoms develop:
  • sudden and severe headache;
  • photophobia (painful sensations in the eyes when looking at any light source or when being in a lit room);
  • nausea and vomiting that does not bring relief;
  • loss of consciousness;
  • tension of the suboccipital muscles of the neck with tilting the head back.

• Damage to the frontal lobe can cause the following symptoms:
  • speech disorders: the patient’s speech is slurred (like “porridge in the mouth”). This is called motor aphasia;
  • unsteadiness of gait: often the patient tends to fall on his back when walking;
  • weakness in the limbs (for example, according to the hemitype - in the left arm and left leg, in the right arm and right leg).

• Damage to the temporal lobe can cause the following symptoms:
  • speech disorders: the patient does not understand the speech addressed to him, although he hears it (his native language sounds like a foreign language to him). This is called sensory aphasia;
  • loss of visual fields (lack of vision in any part of the visual field);
  • seizures that occur in the limbs or throughout the body.

• Damage to the parietal lobe can cause a loss of sensitivity in one half of the body (a person does not feel touch, does not feel temperature and pain during painful stimulation).

• Damage to the occipital lobe can cause visual impairment—blindness or limited visual field in one or both eyes.

• Damage to the cerebellum can cause the following symptoms:
  • impaired coordination of movements (movements are sweeping, unclear);
  • unsteadiness of gait: the patient deviates to the side when walking, there may even be falls;
  • large-scale horizontal nystagmus (pendulum-like eye movements, “eyes dart” from side to side);
  • decreased muscle tone (muscle hypotonia).

• Symptoms indicating damage to the cranial nerves are also possible:
  • strabismus;
  • asymmetry of the face (“the mouth is skewed when smiling, palpebral fissures of different sizes, smoothness of the nasolabial fold);
  • hearing loss.

Forms

• Depending on the presence of damage to the skin of the head, the following forms of traumatic brain injury are distinguished:
  • open traumatic brain injury - damage to the scalp;
  • closed craniocerebral injury - there is no damage to the scalp (damage is present in the brain itself).

• Depending on the presence of damage to the dura mater (separating the bones of the skull from the substance of the brain itself), the following forms of traumatic brain injury are distinguished:
  • penetrating traumatic brain injury - damage to the dura mater;
  • non-penetrating traumatic brain injury - no damage to the dura mater.

• The following types of traumatic brain injury are distinguished:
  • isolated - damage to the head only;
  • combined - in addition to the head, other parts of the body are damaged (for example, chest, pelvis).

• Depending on the severity of damage to the skull and its contents, the following forms of traumatic brain injury are distinguished:
  • A concussion is the mildest form of traumatic brain injury. Accompanied by short-term loss of consciousness (several seconds or minutes), weakness and autonomic disorders (rapid heartbeat, sweating) without focal symptoms (that is, associated with damage to a specific area of ​​the brain);
  • mild brain contusion - loss of consciousness for several minutes or hours, there are mild focal symptoms (weakness in the limbs, nystagmus (pendulum-like eye movements, “eyes dart” from side to side)).
  • moderate brain contusion - loss of consciousness for several hours, there are pronounced focal symptoms (weakness in the limbs, slurred speech, facial asymmetry), possible intrathecal hemorrhage (subarachnoid hemorrhage);
  • severe brain contusion - there is no consciousness for several days or even weeks, characterized by impaired muscle tone (a sharp increase in the extensor muscles of the arms and legs), strabismus, prolonged increase in body temperature, floating eye movements, convulsive seizures (contractions of the muscles of the arms and legs, sometimes with tongue biting);
  • diffuse axonal damage is a consequence of severe brain damage. The person is in a coma (there is no reaction to a call, pain stimulation), there are breathing disorders (irregular breathing rhythm, respiratory arrest), maintaining arterial (blood) pressure (a sharp decrease in it), as well as a characteristic posture (a sharp increase in tone in extensor muscles of the arms and legs), strabismus, prolonged increase in body temperature, floating eye movements;
  • compression of the brain - characterized by the so-called “lucid interval” after injury.
    • Moreover, after the restoration of consciousness, the person feels more or less satisfactory, although at this time the volume of the intracranial hematoma (accumulation of blood) increases.
    • The condition worsens sharply when it puts enough pressure on the brain, causing focal symptoms: weakness in the limbs, facial asymmetry, dilated pupil on the side of the hematoma, convulsive seizures.

• There is a classification of periods of traumatic brain injury:
  • acute period: 2-10 weeks;
  • intermediate period: 2-6 months;
  • long-term period: up to 2 years from the moment of injury.

Causes

• Trauma to the skull:
  • traffic accidents;
  • blows to the head for criminal purposes (fights, beatings);
  • falling from height;
  • gunshot injuries to the skull;
  • non-gunshot penetrating injuries (melee weapons).

Diagnostics

• Analysis of complaints and medical history:
  • what is the nature of the head injury: car accident, blow to the head, fall, gunshot wound;
  • How long did the loss of consciousness last?

• Neurological examination:
  • level of consciousness - assessment of the patient’s reaction to a call, pain stimulation (in the absence of a reaction to a call);
  • assessment of the size and symmetry of the pupils: you should especially pay attention to the asymmetry of the pupils with a lack of reaction to light on one side (this may indicate compression of the brain by a hematoma on one side);
  • the presence of symptoms of irritation of the meninges (headache, photophobia (painful sensations in the eyes when looking at any light source or when being in a lit room), tension in the suboccipital muscles of the neck with throwing the head back);
  • the presence of neurological focal symptoms (associated with damage to a specific area of ​​the head): weakness in the limbs, facial asymmetry, slurred speech, convulsive seizures (contractions of the muscles of the arms and legs, sometimes with tongue biting).

• CT (computed tomography) and MRI (magnetic resonance imaging) of the head: allows you to study the structure of the brain layer by layer, detect signs of damage to brain tissue, the presence of blood in the brain (hematoma - accumulation of blood) or in its membranes (subarachnoid hemorrhage).

• Echo-encephaloscopy: the method allows you to assess the presence of displacement of the brain relative to the bones of the skull under the influence of pressure from intracranial hemorrhage.

• Lumbar puncture: using a special needle, a puncture is made in the subarachnoid space of the spinal cord at the lumbar level (through the skin of the back) and 1-2 ml of cerebrospinal fluid (the fluid that provides nutrition and metabolism in the brain and spinal cord) is taken. Since the subarachnoid space of the spinal cord communicates directly with the subarachnoid space of the brain, in the presence of hemorrhage between the membranes of the brain, blood or its remains can be detected in the cerebrospinal fluid.
• A consultation with a neurosurgeon is also possible.

Treatment of traumatic brain injury

• Hospitalization in a neurological or neurosurgical department.
• Life support: artificial ventilation, oxygen supply, maintenance of arterial (blood) pressure.
• Dehydration therapy (removing fluid from the body): necessary for the development of cerebral edema (swelling of its tissue).
• Hyperventilation when intracranial pressure increases: Reducing the amount of carbon dioxide in the blood reduces intracranial pressure.
• Muscle relaxants (drugs that relax muscles) and anticonvulsants for seizures.
• Antipyretic drugs, cooling blankets - for a sharp increase in temperature.
• Adequate nutrition, if necessary, through a tube (a tube inserted into the stomach through the nose or mouth).
• Surgery:
  • removal of destroyed brain tissue or blood collections;
  • wound treatment, suturing soft tissue.

Complications and consequences

• Post-traumatic illness: prolonged persistence of increased fatigue, memory impairment after a traumatic brain injury.
• Post-traumatic epilepsy: periodic convulsive seizures (involuntary contractions of the muscles of the arms and legs, sometimes with loss of consciousness, tongue biting and urination).
• Vegetative state: develops with severe traumatic brain injury.
  • It is a consequence of the death of the cerebral cortex (or an extreme violation of its function), while the person opens his eyes, but there is no consciousness.
  • The prognosis for this condition is unfavorable.
• Risk of death.

Prevention of traumatic brain injury

Compliance with safety rules in production (wearing helmets) and when driving a car (fastening a seat belt, following traffic rules).