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Biochemical markers offer a new strategy in the diagnosis, estimation of clinical prognosis and monitoring of treatment in patients with brain damage. At present, two specific brain originated proteins play a major role: S100B protein and neuron-specific enolase (NSE). S100B comes from astrocytes and NSE has been found in neuronal cytoplasm. The aim of this study was to evaluate dynamics of protein S100B level changes in blood in stroke patients.The material consisted of 67 patients, 53 with ischemic stroke (mean age 67.7) and 14 with hemorrhagic stroke (mean age 66.7). The diagnosis of stroke was made on the basis of clinical symptoms and computed tomography (CT). Plasma concentration of S100B was measured using the immunoluminometric test (Lia-Mat Sangtec 100(R)) on the 1st, 3rd, 7th and 14th day after stroke onset.The highest levels of protein S100B were found in ischemic stroke predominantly on the 3rd day and in hemorrhagic stroke on the 1st day. The concentrations of protein S100B were similar in ischemic and hemorrhagic stroke on the 3rd, 7th and 14th day but they were significantly higher on the 1st day in hemorrhagic stroke. Serum levels of protein S100B after stroke onset have shown a correlation with infarct volume, especially in patients with large or medium stroke. In small stroke lesions, concentrations of protein S100B were under the cut-off level. In hemorrhagic stroke protein S100B levels were higher in patients with midline shift visible in brain CT, but the differences were not significant.Ischemic and hemorrhagic strokes lead to release of protein S100B into the blood. A good correlation between the release pattern of S100B and volume of vascular lesion has been found. S100B protein is the marker of brain damage during stroke. It is possible to use protein S100B measurements in monitoring the stroke treatment.

Primary intracranial sarcomas are very rare and aggressive tumors. A case of a 40-year-old woman with primary leptomeningeal sarcomatosis is presented. Initially her clinical symptoms resembled those of a pseudo tumor cerebri. Neuroimaging did not allow establishing a diagnosis of leptomeninges neoplastic infiltration. The patient died 8 months since the onset of symptoms. A neuropathological examination revealed diffuse thickening of leptomeninges. Microscopically a widespread sarcomatous infiltration of the subarachnoid space was shown, as well as a neoplastic infiltration of the choroid plexus and of some perivascular spaces in the cerebral cortex. On the grounds of a review of the literature diagnostic problems, differential diagnosis and clinical course of primary leptomeningeal sarcomatosis are discussed.