Traumatic brain injury

Traumatic brain injury (TBI) is a set of contact injuries of the soft tissues of the head, bones of the skull, the substance of the brain and its membranes, which coincide in time and have a single mechanism of formation. Traffic accidents (inertial trauma) are a common cause. Much less often, an injury is the result of household, sports or industrial injuries. TBI can affect any structure of the central nervous system: white and gray matter of the brain, nerve trunks and blood vessels, walls of the ventricles and cerebrospinal fluid pathways, which determines the variety of symptoms that characterize it.

Diagnostics

The diagnosis is made based on the collection of anamnesis (confirmation of the fact of injury), the results of a neurological examination and analysis of data from instrumental research methods (MRI and CT).

Classification

To assess the severity of the lesion, the Glasgow Coma Scale is used, which is based on the assessment of neurological symptoms. The scale is assessed in points, the number of which varies from 3 to 15. Based on the number of points, TBI is classified by degrees:

• easy - 13-15;
• average - 9-12;
• heavy - 3-8.

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In terms of the scale of the traumatic effect of TBI can be:

• isolated;
• combined (along with damage to other organs);
• combined (along with the effect on the human body of various traumatic factors); may result from the use of weapons of mass destruction.

By the presence of damage to soft tissues (skin, aponeurosis, dura mater), the injury is:

• closed (CCMT) - no visible damage;
• open (TBI) - damaged soft tissues of the head, sometimes together with an aponeurosis (may be accompanied by fractures of the bones of the vault or base of the skull; by origin, be gunshot or non-firearms);
• TBI of a penetrating nature - the integrity of the dura mater is violated.

A closed craniocerebral injury is dangerous because a patient without visible damage rarely seeks a doctor, mistakenly believing that "everything will be okay." Its localization in the occiput area is especially dangerous due to the fact that the prognosis for hemorrhages in the posterior cranial fossa is the least favorable.

From the point of view of the time interval since TBI, for the convenience of developing treatment tactics, it is customary to divide the damage into periods (in months):

• acute - up to 2.5;
• intermediate - from 2.5 to 6;
• remote - from 6 to 24.

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In clinical practice

Brain injuries are verified for:

Concussion (concussion)

Symptoms usually resolve within 14 days. Damage can be accompanied by the onset of a syncope from a few seconds to 6 minutes (sometimes a maximum time of 15-20 minutes is indicated), followed by antegrade, congrade, or retrograde amnesia. Probably depression of consciousness (up to stupor). Concussion can be accompanied by disorders of the autonomic nervous system: nausea, vomiting, pallor of open mucous membranes and skin, disorders of the cardiovascular and respiratory systems (short-term fluctuations in NPV and blood pressure). You may experience headache and dizziness, general weakness, clammy sweat, and a tinnitus sensation.

Possible nystagmus with extreme abduction of the eyeballs, asymmetry of tendon reflexes and meningeal signs that stop within 7 days. Instrumental studies (MRI) with concussion do not reveal pathological changes. Changes in patterns of behavior, cognitive impairment and decreased sleep depth can be observed for several months.

Contusion (contusion)

It often manifests itself by the shock-counter-shock mechanism (with a sharp acceleration and inhibition of brain movement due to external influences). Clinical symptoms are determined by the location of the injury and include changes in the state of the psyche. Morphologically confirmed by intraparenchymal hemorrhages and local edema. Subdivided into:

• Easy. It is often accompanied by loss of consciousness lasting several tens of minutes. General cerebral symptoms are more pronounced than with concussion. Characterized by vegetative disorders in the form of fluctuations in heart rate and increased blood pressure. The symptom complex is stopped within 14-20 days.
• Middle. Autonomic disorders are complemented by tachypnea and subfebrile condition. Manifests focal symptoms: oculomotor and pupillary disorders, paresis of the extremities, dysarthria and dysesthesia. Regression is more often noted after 35 days.
• Heavy. In some cases, it is accompanied by fractures of the bones of the skull and intracranial hemorrhages. Fractures of the fornix bones are usually linear. The duration of syncope ranges from several hours to 1-2 weeks. Autonomic disturbances are sharply expressed in the form of significant fluctuations in blood pressure, heart rate, respiratory rate and hyperthermia. Stem symptoms dominate. Episodes are possible. Recovery takes a long time. In most cases, it is incomplete. Disorders in the motor and mental spheres, which are the cause of disability, often persist.

Diffuse axonal injury

Injury to white matter due to shearing force.

It is characterized by moderate to deep coma. The stem symptom complex and autonomic disorders are sharply expressed. Often ends with decerebration with the development of apallic syndrome. Morphologically, according to the results of MRI, an increase in the volume of the brain substance is determined with signs of compression of the third and lateral ventricles, subarachnoid convexital space and base cisterns. Pathognomonic small-focal hemorrhages in the white matter of the hemispheres, the corpus callosum, subcortical and stem structures.

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Compression

Usually caused by rapidly developing cerebral edema and / or significant intracranial bleeding. The rapid increase in intracranial pressure is accompanied by a rapid increase in focal, brainstem and cerebral symptoms. It is characterized by the "scissors symptom" - an increase in systemic blood pressure against the background of a decrease in heart rate. In the presence of intracranial bleeding, it may be accompanied by homolateral mydriasis. "Scissors symptom" is the basis for emergency craniotomy in order to decompress the brain. Intracranial hemorrhage by localization can be:

• epidural;
• subdural;
• subarachnoid;
• intracerebral;
• ventricular.

Depending on the type of damaged vessel, they are arterial and venous. The greatest danger is arterial intracranial bleeding. Hemorrhages are best seen on CT. Spiral CT allows you to assess the volume of an intracranial hematoma.

At the same time, various types of damage can be combined, for example, contusion and ventricular hemorrhage, or additional damage to the brain matter on the processes of the meninges. In addition, the central nervous system can experience stress caused by trauma, CSF shock.

Five conditions of the sick

In neurotraumatology, five conditions of patients with TBI are distinguished:

First aid

If an episode of loss of consciousness is indicated, the victim needs emergency transportation to a hospital, since syncope is fraught with complications that are dangerous for the body. When examining the victim, you should pay attention to:

• the presence of bleeding or liquorrhea from the nose or ears (a symptom of a fracture of the base of the skull);
• the position of the eyeballs and the width of the pupils (unilateral mydriasis may result from homolateral intracranial hemorrhage);
• physical parameters (try to record as many indicators as possible):
  • skin color;
  • NPV (respiratory rate);
  • Heart rate (heart rate);
  • HELL;
  • body temperature.

If the patient is unconscious, in order to exclude retraction of the tongue and prevent possible breathing difficulties. If you have the skills, you can push the lower jaw forward, placing your fingers behind its corners, and stitch your tongue with thread and tie it to a shirt button.

Consequences and complications

Complications from the central nervous system are divided into:

• infectious:
  • meningoencephalitis;
  • encephalitis;
  • brain abscess;
• non-infectious:
  • arterial aneurysms;
  • arteriovenous malformations;
  • episyndrome;
  • hydrocephalus;
  • apallic syndrome.

The clinical consequences can be temporary or permanent. Determined by the volume and location of the alteration. These include:

• General cerebral symptoms - headaches and dizziness - caused by a violation of the innervation of the dura mater, alteration of the vestibular apparatus or cerebellar structures, a persistent increase in intracranial and / or systemic blood pressure.
• The emergence of pathological dominants (overactivity of neurons) in the central nervous system, which can manifest as convulsive seizures (post-traumatic episodic syndrome) or changes in behavior patterns.
• Symptoms caused by damage to areas associated with the motor, sensory and cognitive spheres:
  • memory loss, disorientation in time and space;
  • mental changes and mental retardation;
  • various disorders in the work of analyzers (for example, olfactory, visual or auditory);
  • changes in the perception of the sensitivity of the skin (dysesthesia) different in area;
  • coordination disorders, decreased strength and range of motion, loss of acquired professional skills, dysphagia, various forms of dysarthria (speech disorders).

Disorders in the work of the locomotor system are manifested by paresis of the extremities, much less often by plegias, often accompanied by a change, decrease or complete loss of sensitivity.

In addition to complications caused by disturbances in the work of the brain, pathological changes can be of a somatic nature and affect the work of internal organs due to a violation of innervation. So, if swallowing is difficult, food can enter the trachea, which is fraught with the development of aspiration pneumonia. Damage to the nuclei of the vagus nerve leads to disruption of the parasympathetic innervation of the heart, digestive organs and endocrine glands, which negatively affects their work.

Rehabilitation

An adequate complex of rehabilitation measures directly affects the results of treatment and the severity of post-traumatic neurological deficit. Rehabilitation is carried out under the supervision of the attending physician and a group of specialized specialists. Usually they are: a neurologist, a rehabilitation therapist, a physiotherapist, an occupational therapist, a speech therapist and a neuropsychologist.

Doctors strive to create favorable conditions for the patient to return to normal life and relieve neurological symptoms. For example, the efforts of a speech therapist are aimed at restoring speech function.

Rehabilitation methods

• Bobath therapy - stimulates physical activity due to changes in body position.
• Vojta therapy is based on encouraging the patient to make directional movements by stimulating certain areas of his body.
• Mulligan therapy is a type of manual therapy aimed at reducing muscle tone and relieving pain.
• Using the "Exart" design, which is a harness designed to develop hypotrophic muscles.
• Performing exercises on cardiovascular equipment and a stabilization platform in order to improve coordination of movements.
• Occupational therapy is a set of techniques and skills that allow the patient to adapt to the social environment.
• Kinesio taping is a branch of sports medicine, which consists in the application of elastic adhesive tapes along the muscle fibers and increasing the effectiveness of muscle contractions.
• Psychotherapy - aimed at neuropsychological correction at the stage of rehabilitation.

Physiotherapy:

• drug electrophoresis;
• laser therapy (has an anti-inflammatory and regeneration-stimulating effect);
• acupuncture.

Admission-based drug therapy:

• nootropic drugs (Picamilon, Phenotropil, Nimodipine) that improve metabolic processes in neurons;
• sedatives, hypnotics and tranquilizers to normalize the psycho-emotional background.

Forecast

Determined by the severity of TBI and the patient's age. Young people have a more favorable prognosis than older people. Injuries are conventionally distinguished:

• low risk:
  • scalped wounds;
  • fractures of the bones of the skull;
  • concussion;
• high risk:
  • any type of intracranial bleeding;
  • some types of skull fractures;
  • secondary damage to the brain substance;
  • damage accompanied by edema.

High-risk injuries are dangerous by the penetration of the brainstem (SHM) into the foramen magnum with compression of the respiratory and vasomotor centers.

The prognosis for mild disease is usually good. With moderate and severe - assessed by the number of points on the Glasgow Coma Scale. The more points, the more favorable it is.

With a severe degree, neurological deficit almost always persists, which is the cause of disability.

Watch the video: Living with a Traumatic Brain Injury (November 2024).