INTRACRANIAL PRESSURE — pressure in a head cavity and cerebral cavities, to-rogo covers of a brain, cerebrospinal liquid, tissue of a brain, intracellular and extracellular liquid, and also the blood circulating on brain vessels participate in formation. Maintenance of EL in rather constant limits has essential value for normal life activity of a brain, its blood supply and fabric metabolism.
Arterial, venous and likvorny pressure, tension of brain fabric, hydrostatic and osmotic pressure of blood determine the level of EL. Owing to heterogeneity on structure and mechanical characteristics of contents of a skull pressure in his cavity is distributed unevenly. In horizontal position of EL 150 mm w.g. equal on average.
Arterial and venous pressure exerts very noticeable impact on the level of EL. Fluctuations of EL to 10 mm w.g. are observed., the hearts matching a systole. At contagious excitation amplitude of pulse fluctuations increases. Sharper fluctuations (from 30 to 50 mm w.g.) are caused by outflow of blood from a brain during a breath. In fluctuations of EL nasal breath has bigger value, than breath through a mouth. At a natuzhivaniye, cough, the loud speech, shout of EL raises approximately by 1,5 times.
The large role in preservation of a fixed level of EL is played by cavernous and atlantooktsipitalny sine through which there pass the main arterial highways. Expansion of the carotid and vertebral arteries supplying with blood a brain is followed by increase of inflow arterial and difficulty of outflow of a venous blood that increases a krovenapolneniye of a brain and involves increase in EL. Narrowing of the main arteries limits inflow of blood to a brain and increases its outflow that leads to decrease in EL. Difficulty of venous outflow from a head cavity leads to increase in EL. The similar changes of EL caused by a condition of reactivity of receptor devices and a tone of smooth muscles of brain arteries (the myogenetic mechanism of regulation of a brain blood-groove) are observed at changes of a brain blood-groove.
Pressure of cerebrospinal liquid in a sitting position is unequal at the different levels of likvorny system. On the convex surface of a brain it is equal or even below atmospheric, in the cerebellar and brain tank — corresponds to atmospheric pressure, in ventricles — is slightly higher in connection with secretion in them cerebrospinal liquid (see), and in subarachnoid space of a spinal cord — gradually increases and reaches the maximum in the final tank (to 300 mm w.g.).
Impact on these or those mechanisms connected with EL causes its increase or decrease. Change of osmotic pressure in a blood channel after intravenous administration of hypertonic salt solutions of glucose, fructose, sodium chloride, urea, Mannitolum, sorbitol, glycerin is followed by clear decrease in EL whereas after administration of hypotonic solutions its increase is observed. Use of diuretics leads to decrease in EL, and pharmakol, the means expanding brain vessels (nitroglycerine, amyle nitrite) — to its increase. Inhalations of gas mixture with the high content of carbonic acid (3 — 7%) are followed by increase in EL while a hyperventilation of lungs with the subsequent hypocapny — its decrease. Injections of adrenaline, Pituitrinum, a papaverine cause increase in EL.
Changes of EL under the influence of vasoactive means indicate its close dependence on a state cerebral circulation (see). However there is no full parallelism between height of arterial, venous and intracranial pressure that testifies to complexity of the mechanisms regulating EL.
In clinical conditions about EL usually judge by height of pressure of cerebrospinal liquid (see. Liquorodynamic tests ).
Permanent build-up of pressure of cerebrospinal liquid (St. 200 mm w.g.) in horizontal position of the patient confirms development of intracranial hypertensia which usually increases in process of increase of EL. However the size of pressure of cerebrospinal liquid not always precisely corresponds to expressiveness of other clinical signs of intracranial hypertensia. It is closely connected with increase in mass of a brain, disturbances of a cerebral hemodynamics (first of all due to disturbance of outflow of blood from a head cavity), increase in products of cerebrospinal liquid, deterioration in a resorption and disturbance of its outflow from cerebral cavities. Distinguish two main mechanisms of increase in EL: 1) occlusal gidrotsefalny; 2) increase in volume of the center of defeat (tumor, abscess, etc.). Disturbance of cerebral circulation plays an important role in both mechanisms of development of intracranial hypertensia.
Development in a head cavity of volume education or process leads to increase in EL. Initial build-up of pressure is a push to inclusion of compensatory reactions of an organism owing to what pressure in a head cavity is completely normalized for some time. At a certain stage of development of volume process compensation increasing EL becomes insufficient that begins to be shown by the corresponding signs making so-called. hypertensive syndrome (see). In this regard in development of intracranial hypertensia distinguish stages of compensation, sub-compensation and a decompensation passing into the terminal period. Increase in EL extends in a head cavity unevenly and is followed by fluid displacement from reserve likvorny spaces, and in particular from tanks of a brain. In this regard intracranial hypertensia in the presence of volume education or okklyuziruyushchy process leads to dislocation of various departments of a brain and formation of gryzhevidny vklineniye of marrow (see. Dislocation of a brain ).
Treatment at intracranial hypertensia is defined by character of a basic disease. The symptomatic treatment consists in carrying out dehydrational therapy (see), promoting dehydration of tissues of brain and the strengthened removal of liquid from an organism.
Permanent decrease in EL. — intracranial hypotension — quite often arises later craniocereberal injury (see), at different types liquorrheas (see). Development of intracranial hypotension is connected: 1) with the expiration of cerebrospinal liquid in the quantities exceeding its products (a fracture of base of the skull with a liquorrhea); 2) with the reflex reactions caused by increase in a tone of a sympathetic nervous system. In this case long and permanent narrowing of brain arteries leads to reduction of volume of the circulating blood, decrease in functional activity of vascular textures of a brain and reduction of products of cerebrospinal liquid; reduction of inflow of an arterial blood is followed by pressure decrease in venous vessels that promotes increase in a resorption of liquid from perivascular and intercellular spaces in a vascular bed. Clinical display of intracranial hypotension is hypotensive syndrome (see). Distinguish moderated (pressure of cerebrospinal liquid of 100 — 80 mm w.g.) and the expressed intracranial hypotension (pressure of cerebrospinal liquid from 80 mm w.g. to zero). At true hypotension pressure is equally reduced in likvorosoderzhashchy spaces of a brain and in spinal subarachnoid space. At false hypotension because of quickly coming blockade of likvorny ways pressure in spinal subarachnoid space goes down, and EL remains raised. The extreme degree of quickly developed intracranial hypotension caused by sharp reduction of volume of a brain owing to neuroreflex falling of a brain blood-groove and oppression of products of cerebrospinal liquid is designated by the term «collapse of a brain».
Treatment at intracranial hypotension is defined by etiopatogenetichesky factors. At the hypotension connected with reflex reactions apply vasodilators, administration of isotonic solutions, and also intravenous administration of 10 — 20 ml of the bidistilled water. The positive effect renders subarachnoidal administration of air in number of 15 — 30 cm3. It is in the presence long the liquorrhea existing and not giving in to conservative treatment the surgical treatment directed to closing of fistula or defect of a firm meninx is shown.
Bibliography Arutyunov A. I. Nodal questions of the doctrine of intracranial hypertensia and a way of its further studying, in book: Probl, neyrokhir., under the editorship of A. I. Arutyunov, t. 2, page 5, Kiev, 1955; H u b e of R. and. lake of Electromagnetic flowmeter study of carotid and vertebral blood flow during intracranial hypertension, Acta neurochir. (Wien), v. 13, p. 37, 1965; Intracranial pressure, Experimental and clinical aspects, ed. by M. Brock a. H. Dietz, B., 1972; Zwetnow N. N. Effects of increased cerebrospinal fluid pressure on the blood flow and on the energy metabolism of the brain, Lund, 1970, bibliogr.
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