Clinical and morphological correlations in acute ischemic stroke.

We studied the clinical and histopathological changes in twenty-seven cases of acute ischemic stroke, aged between 65 and 75 years. All deaths occurred within 30 days after stroke. The aim of our study was to establish the clinical and histological correlations in acute ischemic stroke to detect prognostic factors. Brain lesions after acute stroke were observed in all regions. Our study describes the heterogeneity of brain injury after acute ischemic stroke with the participation of all brain components and the chronology in which these lesions develop and evolve. By histological and immunohistochemical studies, we identified neuronal, glial and vascular damage. The neurons had undergone in the area of lesion a process of necrosis, ballooning or condensation process. In the ischemic penumbra, we observed the presence of red neurons. Vascular lesions were represented by the discontinuity of capillaries, always associated with a marked perivascular edema. The following clinical and morphological correlations were established: liquefactive necrosis, astrocyte gliosis, phagocytosis phenomena are the more intense the later the death of the patient; apoptosis phenomena are the more intense the faster the death of the patient; the entire cerebral microcirculation presented microscopic modifications following the ischemic strokes, regardless of the time since the lesion occurred and the histological examination was made; the major neurological complications of the ischemic stroke - the hemorrhagic transformation phenomena, cerebral edema, were microscopically objectified, regardless of the time since the lesion occurred and the histological examination was made.

Histological and immunohistochemical aspects of cerebral vessels of the elderly.

The central nervous system is considered the most complex morphological structure of the human body. Between nervous tissue and cerebral circulation is a very close relationship, so transient vascular meningocerebral disturbances cause changes in neuronal function clinically expressed as various neurological signs and symptoms, especially in the elderly. In this study, we examined from the histological and immunohistochemical point of view encephalon fragments collected from 24 patients aged between 46 and 85 years. All patients exhibited changes in meningocerebral vessels, ranging from atheromatous plaques to vascular rupture. Immunohistochemical techniques have shown changes in the vascular endothelium, smooth muscle fibers of arterial walls and blood-brain barrier disruption.

Microscopic aspects of macrophage system cells in hemorrhagic stroke in humans.

Stroke is an important public health issue because it has high morbidity and mortality rates. In addition, it has one of the highest rates of disability in adults. Recent data show that macrophage system cells, especially microglial cells, are involved both in neuroprotective processes and in the neurotoxicity, depending on the type and extent of the brain damage. In our study, using histology and immunohistochemistry techniques, we evaluated the macrophage-type cell reaction in cerebral hemorrhage. We found that the number of CD68-positive cells increased 7-8 folds per square millimeter of cortical surface in the cerebral parenchyma adjacent to the hemorrhage. We identified a large number of perivascular-activated macrophages, in areas distant to the hemorrhage, showing that individuals with hemorrhagic stroke have profound and extensive alterations of the blood-brain barrier.

Study of cellular changes induced by moderate cerebral ischemia achieved through internal carotid artery ligation.

Reduced cerebral blood flow beyond the compensatory mechanisms leads to cerebral hypoxia. Hypoxia causes various lesions of neurons, glial cells and cerebral blood vessels, depending on its duration and intensity. In our study, we reduced cerebral blood flow in the experience animal on average by 30%, by right internal carotid artery ligation. Fifteen days after the onset of hypoxia, by histology and immunohistochemical studies, we identified neuronal, glial and vascular damage. Lesions of nerve and glial cells ranged from changes of cytoplasmic tinting with the development of "red neurons", to neuronal and glial cytolysis with areas of focal necrosis. Vascular lesions were represented by the collapse, fragmentation and discontinuity of capillaries, always associated with a marked perivascular edema.