[Acute-phase proteins in patients with primary stroke and prodromal transient ischemic attacks].

A study aimed at investigating of the relationship between concentrations of several acute-phase proteins and clinical course and functional outcome of ischemic stroke in patients with and without prodromal transient ischemic attacks (TIA). Eighty-five patients with baseline moderate severity of stroke (NIHSS=12+/-3,5) have been stratified into 3 groups: 1st group - with first-ever stroke, 2nd - with prodromal TIA two or three months before stroke and 3rd - with prodromal TIA within 4 weeks before stroke. Brain lesions were evaluated on conventional MRI. Clinical course of disease and stroke outcome at 1 month were assessed by the NIHSS - by the Barthel index, respectively. A control group comprised 22 healthy people. Blood free radicals (NO, LOO-) and iron transporting proteins (oxidized ceruloplasmine, Fe3+ transferine), blood nitrate levels (NO2), activity of superoxiddismutase, activity of glutathione peroxidase have been studied. No significant between-group differences in regard to blood NO and LOO- contents, activities of blood erythrocyte antioxidant enzymes were found. Baseline levels of NO2 (p<0,05) and iron transporting proteins (p<0,01) were significantly higher in the 3rd group of patients and were correlated with better clinical course of stroke and better functional outcome (r=-0,31 and r=-0,37 respectively, p<0,05). It can be supposed that the elevated level of protective proteins in the 3rd group is caused by the development of ischemic tolerance.

[Clinical-EMG characteristic of myasthenia gravis associated with thyroid pathology].

On the basis of clinical-EMG analyses, the researches have revealed the criteria characteristic of myasthenia associated with thyroid pathologies. The myasthenia process associated with thyroid pathology is mainly characterized as of generalized average intensity. Alongside with mup-s with reduced duration and amplitude characteristic of myasthenia, EMG exposes potentials with comparatively long duration and high amplitude (mainly when the process is associated with thyreotoxycosis). It should also be noted that spontaneous activity is intensively expressed. Considering all the above mentioned, we can conclude that these changes show disfunctioning of mup-s rather than the character of synapses caused by the process associated with the myasthenia. The results of the research will facilitate the timely revelation of the process associated with myasthenia and will lead to the unfailing adequate pathogenetic treatment.

[Neuropsychiatric aspects of diagnostics of nonepileptic seizures].

The outcome of nonepileptic seizures (NES) is usually poor. The early recognition suggests better prognosis. This study is undertaken to examine the value of neuropsychiatric method for making accurate diagnosis of the psychiatric disorder that underlies psychogenic NES. Multidisciplinary approach to clinical assessment of such patients with chronic or resistant course of seizure disorder was used. Out of 6 patients, who went through the neuropsychiatric evaluation, two were admitted with a diagnosis of status epilepticus, three--with acute episodes of repetitive seizures and one--with diagnoses of bettolepsy. The results demonstrated that in four cases seizures were the manifestation of dissociative disorder (F 44), in one--of somatic form autonomic dysfunction (F 45.3) and the last patient had delirium due to epilepsy. All of the four patients with the past history of epilepsy were treated with antiepileptic drugs (AED). In two cases diagnosis of epilepsy and AED therapy were withdrawn. In the remaining cases we supposed the coexistence of epilepsy and NES. Our data suggests that incorporating of neuropsychiatric methods into the diagnostic battery for people with suspected and/or intractable epilepsy help in distinguishing NES and epilepsy as well as in revealing the underlying psychic disorder, which leads to formulation specific treatment program.

[Unexplained somatic symptoms and underlying psychologic disorders in the neurology clinic].

The aim of our study was to determine pseudoneurological symptoms (PNS) and related mental disorders among patients referred to the neurology clinic. All cases of somatoform disorders (SD) as main discharge diagnosis, made on the basis of neuropsychiatric interview after exclusion of neurological disease, have been retrospectively reviewed. Among 623 patients, hospitallized to the Institute of Neurology between 2000-2001 years, SD prevalence was 3,69%, where conversion disorder accounted for 69,6% and somatization disorder - for 13%. Mean age was 27,8 (+/-10,1) and female/male ratio was 1,55. Results show that PNS appear to be a good marker of SD. We suggest that early detection of PNS would provide a correct management of patients.

[Dynamics of nitric oxide dependant oxidative stress in acute stage of ischemic stroke].

Fifty-eight patients with acute ischemic stroke have been studied. The basic neurological impairment was assessed with the National Institute of Health Stroke Scale (NIHSS) and the Glasgow Coma Scale (GCS). The patients were stratified by stroke severity into 2 groups: 1--with severe stroke (GCS> 9; NIHSS > 15) and 2--with stroke of moderate severity (GCS = 14-15; NIHSS = 10-15). Visualization of ischemic injury was performed by conventional Magnetic Resonance Imaging (MRI) 24 hours after stroke onset. Nitric oxide (NO) levels were measured by Electron Paramagnetic Resonance (EPR) method and NO2 and superoxidedismutase (SOD) levels were defined by spectrophotometer. Comparing to controls, intensive EPR signals for free NO were found in the groups of patients during 48 hours after stroke onset, though no between-group differences were detected. In group 2, CSF SOD and NO2 levels were significantly higher than in group 1 and controls. There was a significant negative correlation between initial NO2 CSF levels and ischemic lesion size as well as functional outcome 1 month after stroke onset. Thus, CSF NO2 levels in acute stage of ischemic stroke can be considered as an important predictor of the disease course and functional outcome.

[Mechanisms of delayed neuronal death in experimental acute cerebral ischemia]. / Mekhanizmy otsrochennoi gibeli neironov pri ostroi tserebral'noi ishemii v éksperimente.

Delayed neuronal death or incomplete brain infarction was firstly described by two independent groups of researchers, which noted that in case of middle cerebral artery permanent and temporary occlusion two different types of lesions develop in the brain. Permanent occlusion results in infarction and coagulation necrosis. Significantly different brain lesion appears after short-term (< 30 min) middle cerebral artery occlusion followed by a long-term survival (up to 28 days). In these experiments the volume of incomplete infarction or the size of selective neuronal damage depends on time elapsed after the occlusion is removed. The authors suggest that the selective neuronal death in the areas of incomplete infarction is caused by apoptosis. Applying various methods of neuroimaging and ultrastructural study of tissue damage, the authors concluded that neuronal death in the ischemic penumbra occurs by two different mechanism. Necrosis develops promptly in the center, while apoptosis happens later in the margin of the penumbra. In experimental ischemic models, production of interleukin-1 beta and tumor necrosis factor-alpha activate the macrophagal NO-synthase (NOS-2), that leads to long-lasting NO generation. The latter causes necrosis or apoptosis depending on place of NO generation, on concentration, on glucose and growth factor quantities in paracrine media and at last on interaction and ratio between NO and superoxide anione (NO/O2-) ion concentration. NO mediated apoptosis comprises the upregulation of tumor suppressor protein P-53, activation of caspases, chromatin condensation, ladder-like fragmentation of DNA and alterations in the expression of apoptosis-associated proteins which belong to BCL-2 family. The activation of caspases is the critical signal for apoptosis. Experimental studies proved, that inhibition of caspases blocks neuronal death and diminishes the size of infarction in temporary and permanent focal cerebral ischemic rat models. If we combine antiexcitotoxic and antiapoptotic strategies by application of caspase we would significantly enlarge therapeutic window and such combinations has to become the central area of further investigations.

[Effect of alpha-tocopherol and selenium on the activity of antioxidant enzymes and level of lipid peroxidation products in erythrocytes of patients with cerebral ischemia]. / Vliianie alpha-tokoferola i selena na aktivnost' antioksidantnykh fermentov i soderzhanie produktov perekisnogo okisleniia lipidov v éritrotsitakh bol'nykh ishemicheskoi bolezn'iu mozga.

Antioxidant drugs: alpha-tocopherol acetate and "Selenium" (Finland) were used in treatment of patients with small ischemic insult and middle severity ischemic insult; the state of endogenous antioxidant system and intensity of lipid peroxidation were studied in erythrocytes within various periods of diseases. Content of diene conjugates and malonic dialdehyde was decreased, while activity of superoxide dismutase, catalase, glutathione peroxidase and reductase was increased after administration of both these antioxidants during treatment of the brain circulation impairments. Simultaneous use of the drugs caused the highest effect which occurred due to their influence on various pathways of the endogenous antioxidant system.

[Age and clinico-pathogenetic correlations in acute cerebrovascular lesions]. / Kliniko-patogeneticheskie korreliatsii pri ostrykh tserebrovaskuliarnykh parozheniiakh v vozrastnom aspekte.

A clinico-pathological analysis of 390 cases demonstrated that the clinico-pathogenetical traits of acute cerebrovascular lesions in individuals of different age groups permitted to distinguish in the group of acute cerebral dyshemia 2 nosological variants: acute disorders of cerebral circulation in the young and acute disorders of cerebral circulation in the elderly. In the young age group there is a prevalence of hemorrhagic processes, in the elderly-- ischemic lesions. An aggravating factor influencing the outcome in the younger group is the development of secondary liquid and cerebral hemocirculatory disorders, while in the other group--early appearing somatic disturbances. The important pathophysiological links due to which there may be clinical differences in the studied 2 groups are different types of the cerebral vasomotor function and the reactivity of the sino-aortal reflexogenic system.

[Comparative clinico-pathophysiologic analysis of the characteristics of juvenile and late epilepsy]. / K sravnitel'noi kliniko-patofiziologicheskoi kharakteristike detskoi i pozdnei épilepsii

Having in view the evolutional and ontogenetical traits of the bioelectrical brain activity and age types of the nervous system reactivity to endogenous and exagenous epileptic noxious factors, the authors compared the clinical and pathogenetical characteristics of an epileptic process in children and adults. Although there were several similar signs in children and late epilepsy, the authors opposed these forms on the basis of a different character in the type of development of the disease and changes in the cerebral electrogenesis, at the basis of which there lies the metabolic characteristics of a maturating and involutional brain. These regularities permitted to establish the diagnostical and prognostical criteria in respect to each separate form of the disease.