Cerebral compression is an acute or chronic compression of the brain tissue, which develops most often due to traumatic brain injury, volumetric formation in the cranial cavity, cerebral edema or hydrocephalus. In a narrow sense, brain compression is a form of severe TBI. This pathology is clinically accompanied by severe cerebral symptoms up to the development of coma. Topical characteristics of the pathological process affect focal symptoms. A light gap in the clinic is a characteristic, but not an obligatory sign. The basis of diagnosis is MRI and CT of the brain. Therapy is often surgical, aimed at eliminating hydrocephalus and removing the mass that has led to compression.
Description
Compression of the brain is considered a life-threatening condition that occurs due to compression of cerebral tissues and is accompanied by an increase in intracranialpressure. It is compression that causes necrosis and death of brain cells, which leads to irreversible neurological deficit. In general, compression of the brain can accompany many pathological processes occurring inside the skull.
According to statistics, a small percentage (only about 5%) of TBI is accompanied by compression of the brain. If we analyze this concept more narrowly, then under the acute type of compression of the brain we understand the clinical form of severe TBI. A fatal outcome in severe trauma can occur in half of the cases, TBI leads to disability in 30%. An important task facing modern traumatology, neurology and emergency neurosurgery is to improve the outcomes of TBI and reduce mortality.
What causes brain compression?
Compression of the brain tissue can be provoked by any volumetric formation. These include an intracerebral tumor (glioma, astrocytoma, pituitary adenoma), a tumor of the meninges, a hematoma, an accumulation of blood, which resulted in an outpouring of a brain abscess, a hemorrhagic stroke, a cerebral cyst. Severe hydrocephalus and edema lead to a significant increase in intracranial pressure and compression of the brain.
Slowly growing tumor, cyst, gradually increasing hydrocephalus, forming abscess - all this provokes compression of the brain in a chronic form. Neurons to a certain extent adapt to pathological conditions, the fault of which is the aggravated compression. In traumatic brain injury, cerebral edema, occlusive hydrocephalus, or stroke, whichaccompanied by acute compression of the brain, leading to a rapid increase in intracranial pressure and the death of brain cells begins.
Traumatic brain injury most often leads to acute compression of the brain. Its most common cause is post-traumatic hematoma. Sub- and epidural, intracerebral and intraventricular - it all depends on the location. Symptoms of brain compression will be discussed below.
Compression of the brain is caused by the indentation of fragments or intracranial accumulation of air (pneumocephalus) occurring during a skull fracture. Sometimes a hygroma that grows in volume leads to compression of the brain.
Principle of occurrence: when a valvular tear of the dura mater occurs, the subarachnoid cisterns containing the CSF are damaged. From the subarachnoid space, cerebrospinal fluid is absorbed through a hole (fissure) in the meninges. All this leads to the formation of subdural hygroma.
What are the signs of brain compression?
Symptomatics
Etiology, localization of the compressive formation, its size and rate of increase, as well as the compensatory abilities of the brain affect the clinical picture of brain compression. For post-traumatic hematomas and hygromas, a "light gap" is characteristic. This concept implies such a state of the victim when he is conscious, but there are no signs of severe brain damage.
Light gap
Light gapwith compression of the brain lasts from several minutes to four days. With subarachnoid hemorrhage and subdural hematoma, light intervals last up to one week. If a severe brain injury is recorded (such as a severe contusion, axonal damage), then there is usually no light gap.
What are the most common symptoms of cerebral compression?
Acute pressure
In case of acute compression of the brain, there is usually repeated vomiting, constant severe headache and psychomotor agitation, which is accompanied by sleep disturbance, sometimes delirium and hallucinations begin. Further, excitation is replaced by general inhibition, apathy, lethargy, lethargy begin. Consciousness is disturbed, which develops from stupor to coma. Respiratory and cardiovascular disorders due to the resulting mass effect accompany diffuse inhibition in the central nervous system.
Increased intracranial pressure during the mass effect leads to the fact that the cerebral structures are displaced towards the back of the head. As a result, the medulla oblongata in the occipital foramen is infringed and the work of the centers located in it is disrupted, respiratory and cardiac activities suffer.
Breathing
There are also characteristic signs of brain compression. The rhythm of breathing is disturbed. Tachypnea (acceleration) reaches sixty breaths per minute, inhalation and exhalation are accompanied by noise, Cheyne-Stokes breathing occurs. Decreased heart rate, bradycardiais fixed at the level of forty beats per minute and below, the blood flow rate drops, which leads to arterial hypertension. All this is accompanied by congestive pneumonia, pulmonary edema. The patient has wet rales. The skin of the extremities and face becomes cyanotic. Body temperature rises to 41 degrees. There are meningeal symptoms. The terminal stage is characterized by tachycardia, arterial hypotension. The pulse is thready, there are episodes of apnea (breathing occurs with delays), the duration of which increases. Bruising and compression of the brain are also manifested by other signs.
Focal symptoms
Cerebral symptoms accompany focal symptoms that arise and worsen. They are influenced by the pathological process. This leads to drooping of the upper eyelid, diplopia, strabismus, mydriasis, central facial paresis (facial asymmetry, lagophthalmos, "floating" cheek) on the side of the focus.
The opposite side heterolaterally suffers from paresis, paralysis, tendon hypo- or areflexia, hypoesthesia. Often the manifestation of epileptic seizures, hormetonic convulsions (paroxysms of muscle hypertension), tetraparesis, coordination disorders, bulbar syndrome (dysarthria, swallowing disorders, dysphonia). How to diagnose cerebral contusion with compression?
How to detect pathology?
Data from a neurological examination and anamnesis help a neurologist diagnose brain compression. If, due to the patient’s condition, it is impossible to interview the patient, theyrelatives or persons who were close to the victim at the time the injury occurred. The nature of the pathology does not allow to accurately determine the neurological status. If TBI resulted in compression of the brain, the patient should be examined by a traumatologist. What is included in the diagnosis of cerebral compression?
Instrumental methods of diagnostics
Instrumental diagnostic methods should be limited to only the most urgent and necessary research. For example, echoencephalography and lumbar puncture have proven their informative value. The first can detect a mass effect with a shift in the middle M-echo, the second will reveal that the CSF pressure is increased, and there is blood in the cerebrospinal fluid. But now neuroimaging methods are available, so there is no need for such studies anymore. An MRI or CT scan of the brain is prescribed to the patient depending on the indications, and sometimes both of these studies are performed. Spiral CT of the brain is connected in emergency situations, which reduces the time of diagnosis.
Intracranial formation, its location, type and size, CT helps to assess the dislocation of cerebral structures and diagnose cerebral edema. With the help of perfusion CT, cerebral perfusion and blood flow, secondary ischemia are detected. Areas of cerebral ischemia, foci of contusion and dislocation of brain tissues are determined on MRI of the brain, which is more sensitive. Diffusion-weighted MRI is used to study the state of the conduction pathways of the brain and determine the degree of theircompression.
Treatment of cerebral compression
Clinical and tomographic data determine the choice of methods of therapy. Conservative therapy consists of dehydration and hemostatic treatment, normalization of hemodynamics, relief of respiratory disorders (if necessary, artificial lung ventilation), preventive antibiotic therapy, anticonvulsant treatment in the presence of seizures. It is necessary to keep arterial and intracranial pressure under control.
Surgical treatment
Indications for surgical treatment are determined by the neurosurgeon. Most often, it is prescribed for a large volume of hematoma, dislocation syndrome, displacement of cerebral structures, compression that covers the brain center, a persistent intractable increase in intracranial pressure, occlusive hydrocephalus. Endoscopic evacuation is performed in relation to hematomas. With complex localization of intracerebral hematoma, stereotaxic aspiration is indicated. If a post-traumatic hematoma is combined with crushing of the brain tissues, during the operation, areas of crushing are additionally removed, which requires the use of microsurgical techniques. In the case of a cerebral abscess, it is completely removed, the tumor is radically excised. Hydrocephalus involves bypass surgery (venticuloperitoneal or lumboperitoneal shunting).
Prevention of pathology and prognosis
Compression of the brain always has a serious prognosis. ScaleGlasgow coma helps to correlate predicted outcomes. Low scores indicate a high probability of death or a vegetative state, that is, the inability to think productively while maintaining reflex functions. Many surviving patients become disabled. Pathology leads to severe motor disorders, epileptic seizures, mental disorders, and speech disorders. But modern approaches to diagnosis and therapy reduce mortality rates and increase the frequency of recovery of neurological deficits. Preventive measures include injury prevention, as well as timely and adequate treatment of intracranial pathology.
