[Mechanisms of development of brain edema in neurosurgical pathology]

Abstract

As many as 120 neurosurgical patients were examined after the excision of hemispheric gliomas, basal and subtentorial tumors. Based on an the computer-aided analysis biochemical and clinical data, attempts have been made to unify the mechanisms responsible for brain edema development in patients with neurosurgical pathology. In the early postoperative period, brain edema occurs in 95% of neurosurgical patients. Edema development, spreading and intensity depend on the site and nature of the primary pathological focus as well as on traumatism of surgical interventions. It is proved that edema is an original, biologically expedient brain response to its injury. This response manifests in hyperhydration of all tissues, with the maximum intensity being concentrated in the focus of injury. Specific (neurogenic neurohumoral) and nonspecific (biochemical, autoimmune, mechanical, and so forth) factors of brain edema development may be distinguished. The differences in the neurogenic and neurohumoral mechanisms by which brain edema develops may be accounted for by the topography of the focus of injury. The closer the pathological focus is to the stem and diencephalic structures, the more remarkable the action of neurogenous and neurohumoral factors and the more distinct the tendency toward edema generalization are. At the diencephalic level of injury, damaged are the structures responsible for central regulation of metabolism and trophicity of nerve cells. The neurogenously precipitated diffuse impairment of permeability of the cells entails their hyperhydration, which marks cellular (cytotoxic) edema. The subtentorial process that affects the vasomotor centre of the stem triggers the neurogenic diffuse alterations in the vascular tone, manifesting in an increase of permeability for water and plasma proteins which is characteristic of vasogenic edema.(ABSTRACT TRUNCATED AT 250 WORDS)