From Big Medical Encyclopedia

PRELUM OF THE BRAIN (compressio cerebri; lat. compressio prelum; synonym compression of a brain) — the syndrome developing owing to various intracranial pathological processes — new growths, inflammatory processes, hemorrhages, and also at a craniocereberal injury, a thicket at depressed fractures of bones of a skull and intracranial hematomas; it is characterized by the accruing all-brain and focal neurologic symptomatology.

Distinguish acute and chronic m This year. Acute This year in m it is most often caused by damage of vessels of a meninx or the brain with the subsequent formation of epidural, subdural or intracerebral hematomas (see. Cerebral circulation ), an acute disorder of circulation of cerebrospinal liquid with education to hydras, a bruise crush of substance of a brain with the subsequent local or its diffusion hypostasis (see. Swelled also swelling of a brain ), to-ry on a certain phase of the development can play a role of volume education. To m acute This year gives a number of diseases and their complication in an acute stage of a current: hemorrhagic stroke (see) at a hypertension and atherosclerosis, a rupture of arterial and arteriovenous aneurisms with formation of intracranial hematomas or generalized wet brain owing to a spasm of brain vessels, a heart attack of a brain with perifocal hypostasis, etc.

Chronic This year the m arises at slowly growing tumors of a brain (see. Brain ) and its covers (see. Meninx ), torpidno the current inflammatory process leading to abscessing of a brain (see. Abscess , Brain ) or the accruing occlusion of likvoroprovodyashchy ways (see. Occlusal syndrome ). Lead the bone fragments of a skull pressed into his cavity at the time of an injury, hron to chronic m local This year. subdural hematomas and gidroma (see. Craniocereberal injury ).

The pathogeny

In a pathogeny of m matters This year not only the volume of intracranial education, but also speed of its development, plurality of the centers of defeat. Than quicker the volume of education increases and than more centers of damage of a brain, especially violently proceed m This year. The prelum of a brain at the hematoma caused by arterial bleeding develops more sharply, than at formation of the same hematoma owing to venous bleeding. A wedge, manifestations This year m arise in that case when the volume of an epidural hematoma reaches 50 — 70 ml, and subdural — apprx. 100 ml. It is explained with existence between a brain and a skull of the so-called reserve spaces caused by a difference of their volumes, edges from 8 to 15% individually hesitate. Difference of volumes of epidural and subdural hematomas, at to-rykh they cause a wedge, manifestations of m This year, is explained by the fact that the epidural hematoma usually is located rather locally and does not go beyond bone seams, to the Crimea the firm meninx is densely developped. The subdural hematoma usually spreads on the surface of a brain therefore also the mass of the blood which streamed subduralno leading to This year m shall be much more, than at epidural bleeding. In a pathogeny This year m are of great importance and other factors, in particular development of venous stagnation that causes increase in volume of a brain and it hypoxia (see). It, in turn, promotes increase in wet brain. Disturbance of outflow of blood from vascular textures of side ventricles in a big brain vein (Galen's vein) leads to increase in products of cerebrospinal liquid (see) and to reduction of its absorption. It causes increase hydrocephaly (see), strengthening a prelum of a brain. Thus there is a vicious circle: the increasing internal hydrocephaly in total with an intracranial patol. the center brings to dislocations of a brain (see) with occlusion of likvoroprovodyashchy ways and to heavy disturbances of the vital functions of a brain trunk, up to disturbance of a respiratory rhythm as Cheyn — Stokes (see. Cheyna — Stokes breath ), the Biota (see. Biotovsky breath ), development of terminal types of breath or its dead stop, cardiovascular disturbances in a look takhi-or bradycardia, arrhythmias, sharp raising or falling of the ABP, a cardiac standstill. Development of the described pathology depends as well on localization primary patol. center: at a hematoma in a back cranial pole vital disturbances arise in shorter time and at much smaller volume of a hematoma, than at its localization on the surface of a brain. The epidural hematoma on a base of skull (that happens very seldom), even of 10 — 20 ml, squeezes a brain trunk and leads to irreversible changes. The local or its general hypoxia developing owing to a prelum of a brain leads to disturbance of all types of metabolism of a brain, oxidation-reduction processes in it. At the same time intensity of anaerobic and aerobic glycolysis that, however, does not provide recovery of vysokoergichesky phosphoric connections and leads to bystry exhaustion of energy resources, accumulation milk to - you and to increase of acidosis in a brain, to its hypostasis and consequently, to a bigger increase in intracranial pressure and This year m increases. The important role in development of a vasospasm and ischemia of a brain is played by the reflex mechanisms and active chemical agents arriving from blood or the damaged tissues of a brain (oxyhemoglobin, serotonin, acetylcholine, etc.).

The clinical picture

the Clinical picture of an acute and chronic prelum of a brain is various.

Acute This year the m is characterized by the rough beginning. At a craniocereberal injury This year the m in most cases develops against the background of its bruise. Therefore the loss of consciousness lasting from several seconds till several o'clock (see the Contusion of a brain) can be initial manifestation. This initial posttraumatic loss of consciousness is caused by a direct injury of a brain. In spite of the fact that traumatic intracranial hematomas, as a rule, develop the first minutes after an injury, the prelum owing to the compensatory mechanisms caused by existence of reserve space, elasticity of a vascular wall and tissue of a brain can come to light later — in a few minutes, hours or even days after formation of a hematoma. Therefore at a number of patients the so-called light interval * when consciousness of the patient is recovered completely is noted and the victim can make purposeful actions — to go, talk, answer simple questions, and sometimes even to carry out official duties. This light interval quite often can be reduced (extent of disturbance of consciousness decreases, but it completely is not recovered). After various, individually for each patient, time (of several minutes till several o'clock or 1 — 2 days) the patient faints already owing to immediate effect of the factor squeezing a brain again.

Chronic This year the m is characterized by the persistent, accruing headaches which are followed by nausea, vomiting, developments of stagnation on an eyeground (see) with decrease in visual acuity (see), slowly accruing focal symptoms (paresis of cranial nerves, pyramidal insufficiency, alalias, sensitivity, etc.) * At a certain stage of development chronic This year the m can gain acuity with signs of intracranial accident. It is observed at hemorrhages in a tumor of a brain, gipertenzionno-gidrotsefalny crises at hron. volume formations of a back cranial pole, etc.

Clinically This year the m has a phase current. Distinguish a phase of clinical compensation when consciousness is kept completely, all-brain symptoms are absent, secondary focal symptoms do not come to light. This phase is observed preferential at m chronic This year. The phase of clinical subcompensation corresponds to a light interval. Against the background of a satisfactory or moderately severe condition of the patient complains of a headache of various intensity, sleep disorders, unsharp psychomotor excitement are noted. At an arrangement patol. the center near a cerebral cortex there can be epileptic seizures (see. Jacksonian epilepsy ). Focal symptoms either are absent, or are expressed unsharply: tendinous raise and belly reflexes on the party opposite to the center of a prelum decrease, sometimes there is slight contralateral hemiparesis (see. Hemiplegia ). In nek-ry cases moderate bradycardia, unstable comes to light anisocoria (see). In a phase of a moderate clinical decompensation a condition of the moderately severe patient or heavy. Consciousness is broken from devocalization to a sopor (see. Devocalization ), psychomotor excitement, a sharp headache, repeated vomiting are noted. There are motive, speech, sensitive disturbances (a hemiparesis, hypesthesias), disturbances of mentality on «frontal type» (see. Psychoorganic syndrome ), sometimes anisocoria. The muscle tone changes, belly reflexes drop out, there are unilateral, seldom bilateral pathological-foot signs — Babinsky's symptom (see. Babinsky reflex ), Oppengeym's symptoms, Schaefer, etc. (see. Reflexes pathological ). In some cases meningeal symptoms (see Meningitis), bradycardia, raising of the ABP, a moderate asthma, fervescence come to light. The phase of a rough clinical decompensation is characterized by disturbance of consciousness from a sopor to expressed coma (see), gross violations of trunk functions against the background of the expressed focal damages of a brain: paresis of a look, anisocoria, disturbance of convergence, decrease in reaction of pupils to light, bilateral patol. signs, sharp disturbance of a muscle tone, disturbance of vital functions — breath, cardiovascular activity. A part of patients has an expressed bradycardia, and at a deep coma — tachycardia. Sharply the ABP to 200/120 mm of mercury raises., but at a deep coma it can decrease to subnormal figures. Body temperature increases to 40 — 41 °. Focal symptoms come to light in the form of the expressed hemiparesis or gemiplegiya on the party opposite to a prelum of a brain, and at the expressed phenomena of dislocation — gomolateralno. At a deep coma and the expressed dislocation disturbances tetraparesis can develop. The anisocoria sometimes is absent; pupils dot or evenly wide (at a deep coma), without photoharmose. The terminal state is characterized by a deep coma, an atony of muscles, lack of all reflexes, a catastrophic condition of vital functions (breath, blood circulation).

This year the m not necessarily passes all listed phases. Depending on intensity and the speed of a prelum, and also the undertaken pathogenetic treatment separate phases can drop out or not come. So, at an epidural hematoma it is possible to observe all phases of development of process or their regress during timely removal of a hematoma. Acute hemorrhages at an idiopathic hypertensia after a phase of clinical subcompensation can pass into a phase of a rough clinical decompensation at once or terminal state (see).

The diagnosis

the Diagnosis is established on the basis of data of the anamnesis, by a wedge, pictures, and also the results received by means of tool researches. At ultrasound examination of a brain (see. Ekhoentsefalografiya ) note the shift of a median echo signal in the healthy party, lack of a pulsation of echo signals. On EEG it is often possible to see local decrease in bioelectric activity respectively patol. to the center and its disorganization up to a flat curve at the expressed decompensation. The angiographic picture indicates as localization and a look patol. process, and on existence of a vasomotor spasm, symptoms of hydrocephaly and dislocation of a brain (shift of the main trunks of brain arteries). At hron. process by means of a X-ray analysis of a skull it is possible to reveal symptoms of intracranial hypertensia, the expressed finger-shaped impressions, an expanded Turkish saddle. A computer tomography (see. Tomography computer ) in most cases gives exact information as about character and localization patol. the center, and about a condition of cerebral cavities and the phenomena of its dislocation.

The research of cerebrospinal liquid does not give exact data on existence of an intracranial hematoma; liquid can be both the colourless, and painted blood, likvorny pressure happens raised, is more rare normal or lowered. It should be noted danger spinal puncture (see) for diagnosis This year the m caused by an intracranial hematoma, especially in a phase of occlusion of likvoro-conduction paths as decrease in likvorny pressure in subarachnoid space of a spinal cord after a puncture can lead to emergence or increase of symptoms of a vklineniye of a brain.


Radical treatment of m is This year an operative measure, a cut shall not be limited only to removal patol. center (hematoma, tumor, etc.) or decompressive craniotrypesis (see). Operation shall provide, besides, prevention or treatment of already available dislocation and a vklineniye: a section of cerebellar it is mashed — a tentoriotomiya, a drainage of cerebral cavities (see. Hydrocephaly ), drainage of a residual cavity on site patol. center. Operational treatment is made surely against the background of intensive medicinal care (dehydrational and cardiovascular means). Apply artificial ventilation of the lungs to compensation of respiratory insufficiency (see. Artificial respiration) in the mode of a moderate hyperventilation.

The forecast

the Forecast depends on duration of the m which sharply arose This year, i.e. on timeliness of hospitalization, diagnosis and operation. The complex operational and medicinal treatment of m acute This year which is carried out in early (to 6 hours) terms after its emergence, allows to lower a lethality from 50 — 60 to 25%. At an operative measure in a phase of a deep clinical decompensation the lethality makes 60 — 75%, and in a terminal state — 100%. The forecast at m chronic This year in cases of timely recognition and elimination of a factor of a prelum (a tumor, a hematoma, abscess, etc.) favorable.

Bibliography: Arseni K. and Non an eta of N of t and N e with to at And. II. Intracranial hypertensia, the lane from Romanians., Bucharest, 1978; Isakov Yu. V. Acute traumatic intracranial hematomas, M., 1977; Beds and with L. A. Neyrofiziologiya of an acute craniocereberal injury, Vilnius, 1976; Lebedev V. V. and Goren matte D. Ya. Treatment and its organization at a craniocereberal injury, M., 1977; L and x t e r m and N of L. B. and X and t r and N of L. X. Traumatic intracranial hematomas, M., 1973, bibliogr.; The guide to neurotraumatology, under the editorship of A. I. Arutyunov, p.1, M., 1978; Self-currents of N of B. A. The principles of classification of the acute closed craniocereberal injury, Vopr. neyrokhir., century 4, page 3, 1978; With and N of at r N. A. Bruises of a brain, M., 1970; The Fazpost of a clinical course of a craniocereberal injury, under the editorship of M. G. Grigoriev and L. B. Likhterman, Gorky, 1979; Surgical treatment of bruises and dislocations of a brain, under the editorship of B. D. Komarov, M., 1974; Surgery of the central nervous system, under the editorship of V. M. Ugryumov, p.1, L., 1969; HaseU. and. lake of The influence of the decompressive operation on the intracranial pressure and the pressure-volume relation in patients with severe head injuries, Acta neurochir., v. 45, p. 1, 1978; Johnston I. H. a. Rowan J. O., Raised intracranial pressure and cerebral blood flow, J. Neurol. Neurosurg. Psychiat., v. 37, p. 585, 1974; Miller J. D. a. o. Significance of intracranial hypertension in severe head injury, J. Neurosurg., v. 47, p. 503, 1977.

V. V. Lebedev.