Swelling of cerebral swelling presentation

Edema of GM is considered to be one of the most serious tangatogenetically significant complications. The edema of the brain can be confined to the area adjacent to the pathological focus, or it can be diffuse.

this is the most acceptable technique in the diagnosis and treatment of tension that exists in the anteroposterior direction of crescent formation headbrain. In the framework of craniosacral therapy on the anteroposterior system of crescent formation headbrain easy to work by performing.

There are three main mechanisms for the development of cerebral edema:

  • hemodynamic, caused by violation of venous outflow;
  • membranogenic, which increases the permeability of the blood-brain barrier;
  • the so-called "cytotoxic", resulting from metabolic disorders of brain cells, with a disturbance of water-electrolyte metabolism and accumulation of fluid in cells.

The latter state is also called "swelling"brain. However, this distinction is often conditional, since most often there is a combination of swelling and swelling of the brain in different ratios.

It is known that the intercellular space in whitesubstance is narrower than in gray, and is 15-20 nm and 80 nm, respectively. This creates conditions for a different distribution of water in norm and with swelling or swelling of the brain in white and gray matter (in the intercellular and intracellular spaces).

Hemodynamic edema, very often developingin GM at sudden death from acute heart failure is one of the causes of changes in the microcirculation system of GM (Dronnikova IS 1989, Cole G. Cowie V. A. 1987).

In this case, the lumen of the capillaries may be narrowed due to their compression by both edematous fluid and swollen outgrowths of astrocytes. This was noted in the experimental brain edema of GI Mchedlishvili (1989).

N.K. Bogdanovich (1987), investigating the state of neurosecretory cells of the hypothalamus died of OCH, indicates the presence in the structure of the microcirculatory channel of the hypothalamus features that affect the functional activity of the hypothalamic-pituitary neurosecretory system, which is the central point in the deployment of adaptation processes.

Reduction of neurosecretory activity of cellshypothalamus, receiving information from various receptors regulating the activity of the cardiovascular system (baro-, press-, volumo- and osmoreceptors), leads to the fact that its efferent activity may be inadequate arising situation (sudden hypotension, rhythm disturbances) and, therefore, the possible occurrence of death as a consequence of insufficiently realized adaptive processes in the body.

Morphological marker of edematous changes of GMis the expansion of perivascular and pericellular spaces, the severity of which has an important prognostic significance as an indirect indicator of the state of filtration-adsorption processes at the level of the blood-brain barrier.

The existing concept (Voino-Yasenetsky M.V. Zhabotinsky Yu. M. 1970) about perivascular and pericellular spaces as artifacts arising from the wiring and pouring of GM tissues into paraffin is not supported by data obtained by AS Esipov (1993) and SA Povzun (1994). In particular, they show that the specific volume of these voids, on the one hand, correlates with the number of vessels in the cut (its increase can not be official), and on the other, does not depend on the time from death to the moment of fixation of tissues at the time of autopsy .

Permeability of capillaries of GM is not only related tothe state of the endothelium, but also with the peculiarity of the basal membrane (Bradbury M. 1983). It is established that in the capillaries of the brain it is continuous and homogeneous, unlike the capillaries of other organs, where it has a lattice structure (Matavkin PA et al., 1983).

Basal membrane of the capillaries of the brain especiallydense, often consists of two layers that are closely adjacent to the endothelium, and sometimes merge into one membrane. Edema of the brain tissue with the formation of perivascular and pericellular optically empty spaces is associated not with the release of plasma beyond the capillaries, but with disturbances in outflow from these spaces of tissue fluid. In this case, the violation of the close relationship between the capillary and astrocyte, on the one hand, and also the astrocyte and neuron, on the other, is one of the main factors of ischemic damage and necrosis of nerve cells due to the lengthening of the diffusion pathway of oxygen and glucose, which occurs along the concentration gradient, and not active transfer.

Edemas in neurons are expressed inappearance around the nucleus of small areas of rarefaction of the cytoplasm, forming an optically empty bright rim. The nucleus in these cells decreases, assumes an irregular, angular shape and becomes hyperchromic, the Nislevian substance disappears quickly, and obscure mesh structures that are also disappearing soon appear on the periphery in the form of a narrow rim (Zhabotinsky Yu. M. 1965).

Acute "swelling" of the brain (extreme variantedema) during neurosurgical operations accompanied by sudden increase of its volume and dislocation syndrome with hemorrhage and secondary ischemia compression. This phenomenon is the result of a complex neurovascular reaction arising during stimulation of certain areas of the midbrain, and thalamus (Permyakov N. K. et al. 1986). Hemorrhages in reticular formations of the GM, arising from irritation of the vasomotor centers during an acute displacement of the trunk, according to LM Popova (1983), underlie coma in pathological processes in the posterior cranial fossa.

Today, pathoanatomical diagnosis of edemathe brain practically reduces to determining the magnitude of the wedging of the brain into the tentorial and large occipital orifices, as well as to subjective methods of evaluation (the humidity of the cut surface, the adhesion of the brain substance to the knife, etc.).

However, the most objective way to solve the problem of the degree of hydration of the GM tissue is the direct determination of the water content in the relevant departments of the GM (Medvedev, Yu. A., et al., 1988).

Differential clinical diagnostics of edema anddehydration of the GM is extremely complicated, since it manifests itself mainly as a coma. Thus, according to ON Gaikova (1984), more than half of the deceased, according to clinicians, from "edema and swelling of the GM," dehydration, sometimes very significant, was found at the autopsy. When comparing the states of hydration of various brain structures, it is established that the mosaic distribution of water (i.e., the alternation of sites of hyper-, normo- and dehydration) occurs most often (42%). When comparing the state of brain hydration with general disturbances of the water-electrolyte balance, no correlation was obtained (Gaikova, ON 1996).

The deceased from severe closed craniocerebral(40,1%) and local (51,4%) signs of water exchange disturbances (in 59,3% - dehydration, in 32,2% - hyperhydration), as well as electrolyte imbalance in GM tissue (Reynus K.B. 1986).

It was shown that the lipid content in GM affectsindicators of water and electrolyte content in the brain tissues, which can increase both due to the true increase, and by reducing the dry residue. Therefore, the true edema of the GM is isolated when there is an absolute increase in the water content and the associated increase in the volume of brain tissue and also false when the lipid content in the tissue of GM is reduced (Gaykova ON et al 1996).

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