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Biomedical subjects

G N Kryzhanovskiĭ

Publications and source records attributed to G N Kryzhanovskiĭ.

At least 19 recordsLinked to original sources
PubMed2006

[Therapeutic effect of dexalgin on disturbances of vertebrogenic and nonvertebrogenic mechanisms in back pain].

To evaluate the effect of Dexalgin on dysregulation mechanisms in the complex therapy of dorsalgia, 39 patients have been studied. They were divided into 2 groups: with vertebrogenic (23 patients) and without vertebrogenic (16 patients) pain syndrome. Dexalgin was prescribed in dosage 75 mg daily during 5 days. Its efficacy was measured using the Visual Analogue Scale (VAS), Mc Gill Pain Questionnaire, OBPDQ in case of low back pain. Electromyographic (EMG) and magnetic resonance imaging (MRI) examination was performed in radiculopathic patients receiving dexalgin. The results revealed a statistically significant decrease of the VAS values at the control examination in both groups of patients (p<0,001) with background RI values being 18,4 +/- 9,7 and 21,2 +/- 11,7, respectively. The considerable reduction of RI to 14,6 +/- 9,2 was observed in the second group (p=0,044) on day 5. Dynamic examination showed the predominant decrease of OBPDQ percentage values in patients with myofascial back pain (p=0,038). The EMG data demonstrated a tendency to reduction of spontaneous activity in muscular fibers and normalization of the H-reflex latency during the tibial nerve conduction study in patients with vertebrogenic dorsalgia (p=0,058 and p=0,064, respectively). Dexalgin is the new generation of nonsteroid analgesics possessing potential in treatment of both, acute and exacerbations of chronic dorsalgias. No significant between-group differences were found in the MRI study. The study revealed dexalgin efficacy in patients with myofascial low back syndrome.

Back Pain↗
PubMed2003

[Insufficiency of nigrostriatal dopaminergic system as a disregulation mechanism of dopamine-dependent depression syndrome].

Considered here, is a role of insufficiency of central dopaminergic systems in the pathogenesis of depression. Experimental data have been obtained in a rat model of depression-like syndrome caused by administration of specific-for-dopamine-neurons neurotoxin 1-methyl-4phenyl-1,2,3,6-tetrahydropyridine. Along with literature data, these results suggest a reduction of dopaminergic system activity in striatum, accompanied by the latter's hyperactivation, as a pathophysiological mechanism for development of certain depressive disorders.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2002

[Pathological dominant and determinant in pathogenesis of nervous and mental disorders].

The dominant (A.A. Ukhtomsky) and the determinant (G.N. Kryzhanovsky) are different working principles and basic mechanisms underlying nervous system function in health and disease. The main feature of the dominant is related inhibition of other structures or systems. This inhibition provides normal functioning of physiological system, which is dominant at the given time. The pathology of the dominant relationships consists in insufficient or excessive coupled inhibition. The structures which determine and form a corresponding functional premise to the efferent system structures for achieving the present result play a role of the determinant in physiological system. The role of the pathological determinant is performed by hyperactive CNS structure which determines a functional state of other structures connected with it and forms, along with them, a pathological system underlying the corresponding neuropathological syndrome.

Animals↗
PubMed2002

[Pathological systems in CNS performance].

The occurrence of new pathological integrations from the altered nervous structures in the central nervous system (CNS) is a highly important mechanism of nervous disorders. At the level of systemic relations, such an integration represents a new pathodynamic arrangement from the primarily and secondary altered formations of the CNS. The results of its performance are of a biologically negative, pathogenic value for the body. So such a pathodynamic arrangement is determined by the author as a pathological system (PS). PS substantially and basically differs from the physiological system in the mechanisms of occurrence, clinical manifestations, and performance results. PS is formed and fixed due to the plastic processes intrinsic to the nervous system, under the influence of the pathological determinant the hyperactive CNS formation that can also determine the nature of PS activity. The pathological systems are a pathobiological basis and a pathophysiological mechanism of neuropathological syndromes that are a clinical manifestation of PS performance. Each neuropathological syndrome has its PS. The pathological systems may consist of different formations, levels, and spheres of CNS performance, which determines the content of neuropathological syndromes, including those applied to higher nervous performance, behavior, and the mental sphere.

Animals↗
PubMed2002

[The general theory of pathophysiological mechanisms of neurological and psychopathological syndromes].

Besides structural and functional deficits, central nervous system (CNS) damage causes another effect in the form of novel pathological integrations consisting of CNS primarily and secondarily changed structures. At the neuronal level, the integration presents as aggregation of hyperactive uncontrollable neurons, which produces enhanced uncontrolled impulse flow and acts as a generator of pathologically enhanced excitation, network type. At the system interrelation level, the integration is represented by a new pathodynamic organization including damaged CNS regions, which constitutes a pathological system (PS). The hyperactive CNS structure plays a role of a pathological determinant promoting PS formation may determine a type of PS activity. A clinical manifestation of PS activity is a corresponding neurological or psychopathological syndrome.

Cell Aggregation↗
PubMed1999

[Neuroimmunopathology].

The paper deals with a part of neuroimmunopathology which is concerned with the role of the pathologically altered nervous system in the pathology of the immune system and vice versa and considers disturbances in the interconnection of nervous and immune systems. Antibodies against neuromediators and nervous tissue can produce both pathogenetic and sanogenic effects depending on the neurotransmitter function or the nervous structure which they are specifically directed towards. The effects of systematically administered antibodies against nervous tissue and neuromediators demonstrate that antibodies can penetrate into the central nervous system (CNS). The adoptive transfer of the signs of a pathological condition by immunocytes from CNS abnormalities illustrates the role of the immune system in nervous diseases.

Animals↗