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Biomedical subjects

V I Skvortsova

Publications and source records attributed to V I Skvortsova.

83 records · Page 5Linked to original sources
PubMed1994

[The clinico-neurophysiological study of the effect of cerebrolysin on brain function in the acute and early recovery periods of hemispheric ischemic stroke].

Thirty patients with acute ischemic stroke and at early terms of postapoplectic recovery received cerebrolysin in daily doses 10, 20 and 30 ml for 5 days or 10 ml, i. v. for 10 days, respectively. The patients were examined for neurological status and cerebral function. In acute stroke the highest effect occurred in the affection of moderate severity. In severe stroke the drug stimulated recovery of impaired functions which tended to restore more quickly than in control subjects. In early convalescents cerebrolysin improved motor functions. Details of the results of the combined neurophysiological examination in the course of the treatment are discussed.

Acute Disease↗
PubMed1992

[Clinico-neurophysiological studies of the conductive affective and effective systems of the brain in the acute period of ischemic stroke].

As many as 43 patients aged 44 to 79 years with acute ischemic brain stroke of hemispheric (n = 30) and stem (n = 13) localization underwent clinical and neurophysiological examinations including noninvasive transcutaneous cortical pacing and investigation of short-latent somatosensory evoked brain potentials. This made it possible to exercise objective dynamic control over the motor and sensitive conductive brain systems. Certain common regularities were revealed in the functional reconstruction of motor (pyramid) and sensitive conductors in the acute period of brain stroke. Quantitative criteria for estimating the degree of the functional motor and sensitive defect were determined together with those for predicting its recovery.

Acute Disease↗
PubMed1988

[The genesis of early clinical forms of cerebral circulatory failure and the effectiveness of different courses of therapeutic measures].

The authors have examined 214 patients with early clinical forms of cerebral circulation insufficiency. It has been established that discirculatory encephalopathy (DE) may be formed in two ways. One way is angiogenic and it leads to DE through a stage of initial manifestations of cerebral circulation insufficiency (IMCCI), the other way is related to the neurovascular nature of the disease (vegetovascular dystonia) and may lead to DE, bypassing the stage of IMCCI. It is concluded that therapy with vasoactive drugs is the basic therapy for patients with an angiogenic origin of the disease whereas in patients with a neurovascular genesis of the disease the basic approach is the administration of metabolism-correcting drugs.

Adult↗
PubMed1986

[Electroneuromyographic characteristics of the initial manifestations of cerebral circulatory insufficiency].

A clinico-electroneuromyographic examination covered 50 patients with initial manifestations of cerebral circulation insufficiency. The results are compared with the electroneuromyographic characteristics of discirculatory encephalopathy (20 patients), transient disorders of the cerebral circulation (28 patients) and ischemic strokes (30 patients). The parameter of "the sum of maximum amplitudes of M-responses" in the musculi manus and musculi pedis upon stimulation of the median, ulnar, tibial and fibular nerves at both sides developed by the authors was found to be diagnostically effective. This parameter proved to be significantly decreased in all cases of initial manifestations of cerebral circulation insufficiency. With increasing severity of cerebral circulation insufficiency in ischemic stroke the parameter reduced to the minimal values in a step-wise manner.

Adolescent↗
PubMedDate not supplied

Levels of neurotransmitter amino acids in the cerebrospinal fluid of patients with acute ischemic insult.

The dynamics of excitatory (glutamate, aspartate) and inhibitory (GABA, glycine) neurotransmitter amino acid contents in the cerebrospinal fluid were studied in 110 patients with hemispheric ischemic insult. These studies revealed significant increases in the levels of glutamate and aspartate in the first six hours of illness, and the level and duration of these changes correlated with the severity of the insult. Peak GABA and glycine levels were seen at the end of the first day after strokes, reflecting the delayed activation of the mechanisms of protective inhibition. The insufficiency of GABAergic mediation in strokes located in the hemispheres to a significant extent mirrored the severity of clinical features and the potential of restorative processes. Early significant biochemical criteria were identified for objective assessment of the severity of brain ischemia, and these had prognostic value for the course and outcome of strokes. The most unfavorable prognostic signs were the presence of low (or undetectable) GABA levels in the first days after insult and progressive increases in aspartate levels to the third day on the background of sharp reductions in glutamate levels (after initial elevation on the first day).

Aspartic Acid↗
PubMedDate not supplied

Neuroprotective effects of glycine for therapy of acute ischaemic stroke.

The aim of this randomized, double-blind, placebo-controlled trial was to assess the safety and the efficacy of the pharmaceutic drug glycine in 200 patients with acute (<6 h) ischaemic stroke in the carotid artery territory. Fifty patients received placebo, 49 glycine 0.5 g/day, 51 glycine 1.0 g/day and 50 glycine 2.0 g/day for 5 days in each group. The efficacy of glycine was assessed by clinical analysis, by an enzyme-linked immunosorbent assay of levels of blood serum autoantibodies to NMDA-binding proteines, by detection of excitatory (glutamate, aspartate) and inhibitory (glycine, GABA) amino acid concentrations and lipid peroxidation products (TBARS) in CSF. The trial confirmed the safety profile of the glycine treatment. Slight sedation was observed in 9 patients (4. 5%) as a side-effect. Other marked side-effects or adverse events were absent. The glycine treatment at the dose of 1.0-2.0 g/day was accompanied by a tendency to a decreased 30-day mortality (5.9% in 1. 0 g/day glycine and 10% in 2.0 g/day glycine groups vs. 14% in the placebo and 14.3% in 0.5 g/day glycine groups), to an improved clinical outcome on the Orgogozo Stroke Scale (p < 0.01) and the Scandinavian Stroke Scale (p < 0.01) and to a favourable functional outcome on the Barthel index (p < 0.01 in 1.0 g/day glycine vs. placebo group in patients with no or mild disability). An early normalization of autoantibody titres to NMDA-binding proteins in serum was found (p < 0.01 vs. placebo), a reduction of glutamate and aspartate levels (p < 0.05 vs. placebo), an increase in GABA concentrations (p < 0.01 vs. placebo in severe stroke patients) and also a reduction of TBARS levels (p < 0.05 vs. placebo) in CSF by day 3. Thus, the trial suggests that sublingual application of 1.0-2. 0 g/day glycine started within 6 h after the onset of acute ischaemic stroke in the carotid artery territory is safe and can exert favourable clinical effects. These results will be verified in further trials with a larger number of patients.

Acute Disease↗
PubMedDate not supplied

[Secondary prevention of stroke: advantages of work under the conditions of a neurological center using specialized course ambulatory treatment].

A neurologic center of specialized course outpatient treatment provides a higher level of medical service to patients with prior stroke as compared to general outpatient treatment. A continuous use of antiaggregants and currently available antihypertensive agents caused a considerable decrease in the incidence of recurrent stroke as compared to the conventional treatment of such patients in the outpatient setting (4.6% versus 24% during the year, p < 0.05). A combined treatment in the neurological center induced a decrease in neurologic deficit in 96.2% of cases. Some positive experience of a secondary stroke prevention room deserves a wider introduction into clinical practice.

Ambulatory Care↗
PubMedDate not supplied

[Glutamate neurotransmission and calcium metabolism in cerebral ischaemia and under normal conditions].

This article is dedicated to the mechanisms of ischaemic brain damage. The processes of glutamate-calcium cascade connected with formation of focal brain necrosis within the period of therapeutic window (the first 3-6 h after the induction of cerebral ischaemia) are discussed. The basis mechanisms of energy-dependent ionic pumps failure, development of glutamate excitotoxicity, disorders of calcium metabolism are analyzed. The results of own investigations are presented. The significant increases in the concentrations of excitatory aminoacidergic neurotransmitters (glutamate and aspartate) in the cerebrospinal fluid were demonstrated in patients with acute ischaemic strokes from the first hours of illness with no dependency on vascular origin of strokes. The extent and duration of these increases were of prognostic value for determining the severity and outcome of the stroke. It was showed that along with "excitotoxicity", the pathogenesis of ischaemic stroke also involves a deficiency of protective inhibitory GABAergic mechanisms and developing imbalance between the excitatory and inhibitory neurotransmitters systems. The significant increase of the level of the specific autoantibodies to phencyclidine-binding protein of glutamate NMDA-receptors was found out in blood serum of patients beginning from the first 3 h after stroke onset and it directly correlated with the severity of ischaemic stroke. The great attention is paid to the role of astroglia in energy metabolism and glutamate neurotransmission, to the mechanisms of regulation of concentrations of neurotransmitter amino acids in the synaptic cleft, as well as to the mechanisms of spreading depression waves and zinc neurotoxicity.

Aspartic Acid↗
PubMedDate not supplied

[Syndromology and differential treatment of secondary cochleovestibulitis in patients with early clinical forms of cerebral circulatory insufficiency].

Altogether 136 patients with cochleovestibulitis and early clinical forms of cerebral circulation insufficiency were examined. Two types of syndrome were identified that were associated with the pathogenetic development: vascular and metabolic. Different diagnostic criteria and therapeutic approaches as applied to each type of syndrome were developed.

Adult↗