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Background and Purpose: 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., Material and Methods: 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., Results: 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., Conclusions: 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.

Intracranial hypotension (IH) is a rare cause of acute headache. There are secondary IH (more frequently, after lumbar puncture, head and back trauma, brain and spine surgery) and essential (spontaneous intracranial hypotension SIH). SIH was first described by Schaltenbrand in 1938. This syndrome is characterized mainly by acute postural headache. The authors report a case of 45-year-old women with SIH. Clinical diagnosis was confirmed by lumbar puncture and characteristic MR. The symptoms completely regressed within 2 weeks. The treatment was based on bed rest, hypotonic solutions, steroids, caffeine. Pathophysiology, diagnosis and treatment of SIH are discussed.

The authors presented the results of treatment with lamotrigine (LTG, Lamictal) in 13 patients with drug resistant epilepsy (add-on therapy). There were 8f, 5m. aged 16-60 years, mean age 28.8 years. Generalized seizures occurred in 8 patients (62%). In this group there was 1 patient (aged 16 years) with the Lennox-Gastaut syndrome and 1 patient (aged 20 years) with valproate resistant juvenile myoclonic epilepsy. Complex partial seizures and complex partial with secondary generalization occurred in 5 patients (38%). Before LTG addition mean seizure frequency was from 3/month to several times/day. The mean duration of epilepsy was 16.6 years. The 8 patients were treated with CBZ and VPA, one with PHT and VPA, one CBZ and VGB. Monotherapy with VPA was introduced in 3 patients. After 6 months of treatment with LTG the efficacy was evaluated. 12 patients took LTG with VPA, 1 LTG with CBZ. Complete reduction of seizures was achieved in 3 cases (23%), at least 50% reduction in 3 patients (23%), reduction below 50% in 4 patients (31%). In 3 cases (23%) the results of treatment were negative (increase or no change in seizure frequency). Beneficial psychotropic effect was observed in 9 patients (69%). Adverse effects occurred in 2 patients (15%). Headache, vertigo, sleepness were observed in one case. Rash occurred in 1 patient (treated with LTG and VPA). After 6 months 3 patients were excluded from the study because of negative effects of treatment. LTG is helpful and well tolerated in drug-resistant epilepsy.

Hemicrania continua is a rare idiopathic headache of unknown etiology. The clinical course is characterized by usually unilateral, continuous headache. There are some clinical variants of pain character and other symptoms. Indomethacin (50-150 mg per day, rarely higher) leads to complete remission in all patients. Current diagnostic procedures (including neuroimaging) should be recommended in all cases to exclude organic cause of headache. The authors report a case of a 46-year old woman with 3 years history of drug resistant, unilateral headache. Complete remission after administration of indomethacin (75 mg TID) was achieved. Problems of diagnostic, clinical course and treatment of hemicrania continua are discussed.

The authors describe a case of a 53 years old man with myotonic dystrophy. Based on characteristic clinical symptoms and EMG results the diagnosis was established and proved on DNA examination. Myotonic dystrophy gene analysis showed on 3' untranslated region one hundred and fifty CTG triplet repeats. The accessory examinations revealed: cataract arrhythmias, gallbladder stones, impotence, cerebral atrophy on neuroimaging (CT and MRI). Apathy, somnolence, concentration troubles were present. Pedigree of the presented patient and possibility of spontaneous mutation are discussed.

Myotonic dystrophy (m.d.) is an autosomal dominant multisystem disorder involving muscles, brain, heart, eye, endocrine system, alimentary and respiratory systems. M.d. is the most frequent cause of muscle dystrophy. Unstable CTG trinucleotide repeat at 3' untranslated end of the myotonic protein kinase gene on chromosome 19q 13.3 is the molecular basis of the disease. Normal length of CTG trinucleotide repeat is 5-40. Molecular mechanism of the myotonic dystrophy is discussed. Cataract, heart dysfunction, endocrine organs dysfunction, gallbladder stones, impotence are characteristic changes in patient with m.d. Apathy, drowsiness, sometimes dementia point to central nervous system involvement. Clinical course, correlation between CTG expansion and clinical manifestation are described. Nowadays progress in molecular genetic allows to make the diagnosis by DNA examination. Prenatal diagnosis is also possible.