Compression of the brain is an acute or chronic compression of brain tissues that develops as a result of traumatic brain injury, the presence of a volume formation in the cranial cavity, hydrocephalus or cerebral edema. In a narrow sense, brain compression is understood as a form of severe TBI. Clinically, compression of the brain is manifested by severe cerebral symptoms up to the development of coma. Focal symptoms depend on the topical characteristics of the pathological process. A characteristic, but not mandatory, sign is the presence of a light gap in the clinic. The basis of diagnosis is CT and MRI of the brain. Treatment is often surgical, aimed at removing the formation that caused the compression, and eliminating hydrocephalus.
ICD 10
G93.5 Compression of the brain
General information
Compression of the brain is a life—threatening condition that occurs as a result of compression of cerebral tissues and a progressive increase in intracranial pressure. Compression leads to necrosis and death of brain cells, which is expressed by the formation of an often irreversible neurological deficit. In a broad sense, compression of the brain can be observed in many pathological processes occurring inside the skull. In a narrow sense, acute compression of the brain is understood as one of the clinical forms of severe traumatic brain injury.
According to statistics, about 5% of TBI occurs with compression of the brain. Mortality in severe trauma ranges from 30% to 50%, disability after TBI reaches 30%. Improving the outcomes of TBI and reducing mortality is an important task of modern traumatology, neurology and emergency neurosurgery.
Causes
Due to the limited space inside the cranium, any volumetric formation inside the skull leads to compression of brain tissues. An intracerebral tumor (glioma, astrocytoma, pituitary adenoma, etc.), tumors of the meninges, hematomas, accumulation of blood spilled as a result of hemorrhagic stroke, cerebral cyst, brain abscess can act as a similar formation. In addition, a significant increase in intracranial pressure and compression of the brain may be due to severe hydrocephalus, cerebral edema.
Slowly growing tumors, cysts, gradually increasing hydrocephalus, forming abscesses cause chronic compression of the brain, in which slowly worsening compression allows neurons to adapt to a certain extent to the pathological conditions that have arisen. Acute compression of the brain in TBI, cerebral edema, occlusive hydrocephalus, stroke is associated with a rapid increase in intracranial pressure and leads to mass death of brain cells.
Acute brain compression most often occurs as a result of traumatic brain injury. Its most common cause is post-traumatic hematoma. Depending on the location, it can be sub- and epidural, intracerebral and intraventricular. Compression of the brain can be caused by the indentation of fragments or intracranial accumulation of air (pneumocephaly), occurring with a skull fracture. In some cases, compression of the brain is caused by an increasing volume of hygroma, which is formed by valvular rupture of the dura mater and damage to subarachnoid cisterns containing cerebrospinal fluid. Through a defect of the dura mater, cerebrospinal fluid is absorbed under it from the subarachnoid space. Thus, a subdural hygroma is formed.
Symptoms
The clinical picture of brain compression depends on the etiology, localization of the compression formation, its size and rate of increase, as well as on the compensatory abilities of the brain. Pathognomonic for most post-traumatic hematomas and hygromas is the presence of the so-called “light gap”, when the victim is conscious without showing signs of severe brain damage. The duration of the light interval can vary from minutes to 36-48 hours. Subarachnoid hemorrhage and the formation of subdural hematoma may be accompanied by a light interval lasting up to 6-7 days. In severe brain damage (severe brain injury, axonal injury), the light gap is usually absent.
Acute compression of the brain is usually manifested by repeated vomiting, constant intense headache and psychomotor agitation with sleep disturbance, sometimes delusional and/ or hallucinatory syndromes. Later, the excitement turns into a general inhibition, manifested by apathy, lethargy, inhibition. There is a violation of consciousness, which progresses from sopor to coma. Diffuse inhibition in the central nervous system is accompanied by respiratory and cardiovascular disorders, which are also caused by the resulting mass effect. The latter is a displacement of cerebral structures towards the large occipital foramen, which occurs due to increased intracranial pressure. The result is prolapse and infringement of the medulla oblongata in the occipital foramen with disruption of the centers located in it that regulate respiratory and cardiac activity.
There is a disorder of the breathing rhythm. Tachypnea (increased breathing) reaches 60 per minute, accompanied by noisy inhalation and exhalation, Cheyne—Stokes breathing is observed. Heart rate gradually decreases, bradycardia reaches 40 beats / min. and lower, the blood flow rate drops significantly, arterial hypertension is observed. The lungs develop congestive pneumonia, pulmonary edema. Multiple wet wheezes are heard auscultatively. The skin of the limbs and face becomes cyanotic. Body temperature rises to 40-41 ° C. Meningeal symptoms are determined. In the terminal stage, tachycardia, arterial hypotension appears. The pulse becomes thready, episodes of apnea (breath retention) appear, the duration of which increases.
In parallel, against the background of general cerebral symptoms, focal ones arise and worsen. They entirely depend on the topic of the pathological process. On the side of the focus, there may be drooping of the upper eyelid, diplopia, strabismus, mydriasis, central facial paresis (facial asymmetry, lagophthalmos, “sailing” cheek), on the opposite side (heterolateral) — paresis, paralysis, tendon hypo- or areflexia, hypesthesia. Epileptic seizures, hormonal seizures (paroxysms of muscle hypertension), tetraparesis, coordination disorders, bulbar syndrome (dysarthria, swallowing disorders, dysphonia) may be noted.
Diagnostics
In the diagnosis of brain compression, the neurologist relies on the data of anamnesis and neurological examination. If, due to his condition, the patient cannot be interviewed, if possible, relatives or persons who were near the victim at the time of the injury and in the period after it are interviewed. The neurological status may indicate the topic of the pathological process, but it does not allow to accurately determine its nature. In cases where compression of the brain is caused by TBI, the patient should be examined by a traumatologist.
The list of instrumental diagnostic methods should be limited only to the most necessary and urgent studies. Previously, it included echoencephalography and lumbar puncture. The first allowed to reveal the mass effect – the displacement of the median M—echo, the second – increased cerebrospinal fluid pressure, the presence of blood in the cerebrospinal fluid. Today, the availability of neuroimaging methods eliminates the need for such studies. Depending on the patient’s indications, an MRI or CT scan of the brain is performed, and sometimes both of these studies are performed. In emergency situations, spiral CT of the brain can significantly reduce the time of tomography.
CT of the brain makes it possible to determine the type, location and size of intracranial formation, assess the degree of dislocation of cerebral structures and diagnose the presence of cerebral edema. Perfusion CT allows to assess cerebral perfusion and blood flow, to identify secondary ischemia. MRI of the brain is more sensitive in determining areas of cerebral ischemia and injury foci, the direction of dislocation of brain tissues. Diffusion-weighted MRI makes it possible to examine the state of the brain’s pathways, to determine the degree of their compression.
Treatment
The choice of therapeutic tactics is based on clinical and tomographic data. Conservative therapy includes dehydration and hemostatic treatment, normalization of hemodynamics, relief of respiratory disorders (if necessary, ventilation), preventive antibacterial therapy, in the presence of convulsions — anticonvulsant treatment, etc. Blood pressure and intracranial pressure must be monitored.
Indications for surgical treatment are determined by a neurosurgeon. These include: a large volume of hematoma, dislocation syndrome, displacement of cerebral structures of more than 5 mm, compression of the encircling cerebral cistern, persistent uncupable increase in intracranial pressure of more than 20 mm Hg, occlusive hydrocephalus. With respect to hematomas, transcranial or endoscopic evacuation is possible, with intracerebral hematoma of complex localization, its stereotactic aspiration is possible.
When a post-traumatic hematoma is combined with brain tissue crushing, the operation is supplemented by the removal of areas of crushing, which is carried out using microsurgical techniques. With a cerebral abscess, its total removal is performed, with a tumor, its as radical excision as possible. In the presence of hydrocephalus, the cause of which cannot be eliminated, bypass surgery (venticuloperitoneal or lumboperitoneal bypass surgery) is indicated.
Prognosis and prevention
Compression of the brain always has a serious prognosis. The correlation of compression outcomes with the assessment of patients’ condition on the Glasgow scale was noted. The lower the scores, the higher the probability of death or transition to a vegetative state — the impossibility of productive mental activity while maintaining vegetative and reflex function.
There is a high percentage of disability among the surviving patients. There may be severe motor disorders, epiprimes, mental disorders, speech disorders. At the same time, thanks to modern approaches to diagnosis and treatment, it was possible to reduce mortality rates and increase the volume of neurological deficit recovery in patients with brain compression. Prevention of cerebral compression is reduced to injury prevention, timely and adequate treatment of intracranial pathology.
