Diffuse axonal brain damage: symptoms, signs and diagnostics

Trauma to the skull can cause serious damage to the brain, gray matter. They, in turn, can lead to the development of severe and often irreversible ailments that threaten human life. Next, consider one of these consequences - diffuse axonal brain damage, what is it, what is dangerous such a condition.

General information

To begin with, it is necessary to briefly classify the stages of skull injuries:

• Easy. Such a trauma is accompanied by a small bruise and concussion of the brain.
• Average. In this case, the degree of bruising is characterized as moderate.
• Heavy. At this stage, compression and diffuse axonal brain damage occur. Injuries are inertial in nature.

Description

Diffuse axonal brain damage (DAP) is a massive destruction of the processes of nerve cells with small predominant hemorrhages. According to the clinical picture, the pathological focus is formed at the border of gray and white substances. Diffuse axonal brain damage (DAP) significantly reduces the quality of life and mental activity of the victim. The patient's condition, without a doubt, can be considered difficult. This is mainly due to the fact that there is a serious enough threat to his life. With a bruise, hematoma occurs, puffiness develops, a subdural hygroma appears. The outflow of the cerebrospinal fluid from the ventricular zone is disturbed, and the fracture is often detected. These phenomena occur earlier than diffuse axonal brain damage develops. Trauma, as a rule, is so serious that it is far from always possible to restore the previous activity of the organ in all cases. The victim himself rarely, as practice shows, returns to his previous normal state. After passing treatment and rehabilitation to the patient with diffuse axonal brain injuries, it is necessary to visit the doctor regularly. Inspections are necessary to monitor the condition of the body and timely detection of impairments.

Diffuse axonal damage: symptoms, signs, diagnosis

How does the pathological condition manifest? Many brain lesions, diffuse axonal lesions in particular, are accompanied by a prolonged coma. This condition occurs immediately at the time of the bruise of the skull. In addition, there is a significant change in muscle tone. Diffuse axonal damage is accompanied by meningeal syndrome and gross stem manifestations. There is a sharp decrease in pressure and collapse. The patient stops all brain centers. The coma can be very long, the clinical prognosis in such a situation, as a rule, is not very favorable. There is a possibility that the patient can die without regaining consciousness. With another development of events, the patient manages to leave the coma, but after a sufficiently long time period. Unconsciousness can last 2-3 weeks. Coma can be accompanied by a change in the functions of the cerebral hemispheres. In this case, the patient experiences a characteristic pain.

Vegetative state

Diffuse axonal brain damage is characterized by a rapid change in the clinical picture. So, a coma can go into a vegetative or transistor state. Clinically diffuse axonal brain damage manifests itself in different ways. In this case, some manifestations replace others with a sufficiently high rate. The vegetative state is characterized by functional dissociation in the zone of the cerebral hemispheres. It can persist for several months. In the vegetative state, signs of functional impairment in the subcortical-stem structures of the brain are noted. Disorders in important processes provoke the appearance of bulbar, pupillary and other similar manifestations. When the muscle tone changes, latetonic and incomprehensible defensive reactions arise. These include, in particular, convulsions in the upper and lower extremities, an increase in amplitude during movements, head inclinations, trembling of the hands, complex postures of the trunk. As it was said above, the clinical manifestations change very quickly. For an hour, for example, there may be different pathological reflexes. When revealing changes in the vegetative state, dyskinesia, atactic gait appear in patients, verbal and mental disorders occur. Among the latter it is worth noting aspotannost, amnesia, moral exhaustion.

The further course of the pathological process

Diffuse axonal brain damage differs logically from a long comatose to a persistent transient vegetative state. This is indicated by new manifestations, which had not existed before. For example, a patient may overly focus his eyes, blink or react to the influence of external stimuli. If the vegetative state lasts a long period, then new signs of the disease are revealed. In particular, there is a hypotrophy of the carpal muscles, fibrillation of the musculature of the extremities. In this case there is a rapid progress of paroxysmal conditions. They are represented by tachycardia, hyperemia, hypertension and other abnormal manifestations. There is a deterioration in the condition afterwards. Diffuse axonal brain damage is now accompanied by stiffness of the muscles, discoordination, hypomyemia, oligophasia, bradykinesia, discoordination, ataxia. Headaches are frequent for the patient. The emetic syndrome begins to develop, difficulties arise with head inclinations and leg extension, stiff neck muscles are noted. Many patients are characterized by hyperthermia (from the strokes of the cortex there is a fairly sharp increase in temperature), ptyalism, increased sweating. Thus, it can be concluded that diffuse axonal brain damage provokes irreversible pathological processes in the organ.

Patient examination

Diffuse axonal brain damage is detected exclusively with MRI and CT. These research methods allow for visual observation of an abnormal increase in organ volume due to hyperemia or edema with compression of the ventricles. Other acute manifestations are also recorded. With the help of CT, specialists have an opportunity to assess the clinical picture and make an estimated prognosis for the future. MRI shows all pathological changes that are caused by extensive or partial hemorrhages that accompany diffuse axonal brain damage. The degree of pathological condition is also determined on the basis of magnetic resonance tomography indications. The results of the study make it possible to select the optimal therapy for the patient. The exact diagnosis is made on the basis of a lumbar puncture. This procedure is extremely important for the timely detection of subarachnoid hemorrhage. Together with this puncture allows to draw a conclusion about the prevalence of high intracranial pressure. This procedure is contraindicated in patients with volumetric intracranial processes that cause brain dislocation.

Results of CT in acute period

Diffuse axonal brain injury is characterized by a pronounced or moderate increase in organ volume. There is also a narrowing, and in some cases, complete compression of the III and lateral ventricles, base tanks and convectional subarachnoid spaces. Changes in tissue density tend to have a normodensitive character, but there may be increases or decreases. In white matter, corpus callosum, stem and subcortical structures, small-focal hemorrhages are often found. It is necessary to take into account that the CT picture in patients can remain in the range of age norms. Dynamics in patients with diffuse axonal brain damage is characterized by the development of an atrophic process. In particular, there is ventriculomegaly, an expansion in the convectal and basal subarachnoid spaces. At later terms after the injury (after about 3-4 weeks), clusters of cerebrospinal fluid in the frontal zones, interhemispheric fissure (in its anterior regions in particular) can often be observed. It can be eliminated in the course of stabilizing the mental and neurological status. This is an indirect evidence of volume recovery after brain damage. Craniocerebral injury in children is much more often and better than in adults, is amenable to therapy.

Conclusions based on CT results

According to the picture can be tentatively judged on the lack or presence of intracranial hypertension. If CTs do not visualize the base and ventricles, or if there is a manifestation of their coarse compression, the likelihood of HFG is high. It may be quite justified to install a sensor for measuring intracranial pressure and its subsequent correction. If CT scans are clearly visible on the CT, especially from the ventricle and cisterns, ICP is most likely within the burrow. It is unlikely that activities aimed at reducing it will be useful for the victim. Patients have a significant disorder of osmotic homeostasis due to primary or secondary damage to stem and hypothalamic-pituitary structures. In patients with hyperosmolar moderate status, more favorable outcomes are noted, with more pronounced very often death occurs.

Pathogenesis

Macroscopic examination of tissues does not show destructive changes on the basal and external surfaces. Along with this, white matter contains areas of deep damage. Local zones of hemorrhages in different parts of the brain can also be detected. A histological examination is also performed. It allows to detect the presence of "axonal balls". These elements are areas of rupture in nerve endings. In addition, histological examination reveals changes in the cylinders of a destructive nature with the appearance of varicose thickening. A month after the injury, the disappearance of the balls and the proliferation of macrophages in the alteration zone are observed. There are further changes in the myelin sheath, pathological processes in the neurons of the peripheral part of the nervous system continue. Also, lesions of nerve fibers of the spinal cord and brain develop.

Therapy: general information

Patients who have diffuse axonal brain damage are treated, the treatment is complex, involving several methods. In particular, patients need a prolonged ventilation (ventilation) in a moderate mode of hyperventilation. Complex therapy is prescribed, including the use of vasoactive and nootropic drugs, maintenance of stability in metabolic processes using probe (enteral) and parenteral nutrition. Operative intervention, as a rule, is not appointed, since there is no substrate that is to be removed. Surgical manipulations are advisable in detecting other progressive anomalies that exert high pressure on the brain and its components. In connection with the high incidence of extracranial complications (pulmonary and purulent-inflammatory, mainly), the therapeutic course includes preparations of antibacterial and immunocorrective action.

Scheme of therapeutic measures

Patients with diffuse axonal brain damage are hospitalized in a hospital. The institution carries out a complex of therapeutic and rehabilitation measures. The scheme, in particular, includes:

• IVL to maintain a stable functioning of the respiratory system.
• Probe food.
• Intensive therapy with medicines.
• Maintaining a normal water-electrolyte balance.
• In some cases, the use of neurotransmitters, biogenic stimulants.
• Medical gymnastics, which contributes to the restoration of the normal functioning of the limbs, prevention of joint diseases.
• Logopedic exercises for stabilization of speech activity.

After the operation, a short recovery period is necessary with prolonged hospitalization. To stabilize the functions of the central nervous system, compensate for impaired brain activity, accelerate the pace of rehabilitation, it is necessary to appoint vascular and nootropic drugs. It may also be necessary to use biogenic stimulants, drugs that affect tissue metabolism, as well as, according to indications, neurotransmitters (Madopar, L-Dopa, Nakom and others) and anticholinesterase medications. With the WCT, there is no need for hormonal therapy.

Forecast

The probability of curing a patient with a WCT will depend on the extent of damage in the axons, the presence of edema, the possibility of joining the pathological processes of the extracranial divisions. When an effective complex of therapeutic measures is carried out in short time intervals, a more favorable outcome is more likely. In the case of prolonged coma, the risk of complications increases. When it lengthens, the probability of unfavorable outcomes increases, and, accordingly, the possibility of recovery decreases. Of great importance is the depth of the coma. The harder it is, the worse the outcome. The possibility of complete or partial recovery of lost mental functions can be considered as fundamental, in the case of a regression of neurological disturbances, even in cases of damage, when the patient develops a vegetative position lasting several weeks to months after a prolonged coma. This phenomenon may indicate a probability of reversibility and compensation of neurotransmitter and structural disorders that underlie the persistent impairment of functional activity in the brain after diffuse axonal injury.