[Role and place of ipidacrine in the therapy of diseases of the peripheral nervous system. The resolution of the expert council]. / Rol' i mesto ipidakrina v terapii zabolevanii perifericheskoi nervnoi sistemy. Rezolyutsiya Soveta ekspertov.

The resolution of the expert council is devoted to discussing aspects of the use of ipidacrine for the treatment of mononeuropathies, polyneuropathies and radiculopathies of various etiologies. Specialists prepared recommendations for ipidacrine's application in treating peripheral nervous system disorders.

Chronic Effects of Modeled Myocardial Infarction, Thoracic Trauma, and Denervation of Hind Limb on Rheographic Parameters of Rat Femoral Arteries In Situ.

In experiments on narcotized male rats (n=85), the mean electroimpedance Z and peak-to-peak magnitudes (the swing ranges) of passive (ΔZp) and active (ΔZa) pulsatile electroimpedance oscillations of isolated segment of femoral arteries were determined in situ. These rheographic parameters (RP) were measured in intact animals and in those with modeled chronic myocardial infarction, chronic denervation of the right hind leg, as well as in rats subjected to sham operations to mimic denervation or infarction (with thoracic trauma). The rats with modeled myocardial infarction demonstrated decreasing trends of all RP. In sham-operated rats with thoracic trauma, ΔZp increased significantly on postsurgery months 2-4 by 4.3 times in comparison with the control. No essential correlation was found in denervated rats between RP of any femoral artery and severity of neuropathic pain syndrome assessed by autotomy of the operated leg. In these rats, the mean electroimpedance Z of any femoral artery was significantly greater than the control level. They demonstrated especially high values of ΔZp with significant difference between ΔZp of innervated and denervated hind leg. In denervated rats, ΔZa was significantly greater than the control value without significant difference between ΔZa of both femoral arteries. The paradoxically great increase of ΔZp (100- and 50-fold for innervated and denervated legs, respectively) and a significant 3-fold increment of ΔZa in both hind legs provoked by denervation of one of them are discussed in relation to searching for the ways of systemic influences on vascular network in clinics and experiments.

[Results of a randomized double blind parallel study on the efficacy and safety of tolpersione in patients with acute nonspecific low back pain]. / Rezul'taty randomizirovannogo dvoinogo slepogo parallel'nogo issledovaniia éffektivnosti i bezopasnosti primeneniia tolperizona u patsientov s ostroi nespetsificheskoi bol'iu v nizhnei chasti spiny.

AIM: To evaluate the efficacy and safety of tolpersione injection and oral formulations combined with NSAID over NSAID monotherapy in acute non-specific low back pain. MATERIAL AND METHODS: In this randomized double blind study 239 patients were included in the per protocol analysis. The first 5 days of treatment, patients received tolpersione or placebo injection which was followed by per os administration of tolpersione/placebo tablet up to 14 days. NSAID diclofenac tablet was used in both groups through the study. Functionality assessed by the Roland Morris Disability Questionnaire (RMDQ) at day 5 was the primary endpoint. Secondary endpoints were RMDQ at other time points, pain level change at rest and on movement assessed by the Visual Analogue Scale (VAS), the Clinical Global Impression of Improvement/Patient Global Impression of Improvement (CGI-I and PGI-I), change in the range of motion assessed by the distance from the fingertips to the floor, period of disability days, relative (%) changes in the daily dose of diclofenac from the 7th to the 14th day of therapy. RESULTS AND CONCLUSION: The primary and secondary endpoints clearly demonstrated the significant superiority of tolpersione added to NSAID monotherapy over NSAID monotherapy. The safety assessment revealed no statistically significant differences between the two groups. Based on the results, tolpersione injection and per os formulations can be considered an effective and safe drugs in the combined therapy for patients with acute nonspecific back pain.

[Contemporary approaches to the relationships between chronic pain and sleep]. / Sovremennye predstavleniia o khronicheskoi boli i ee otnoshenii k sostoianiiu sna.

Chronic pain represents the unique pathophysiological condition characterized by the sustainable chemical, morphological and behavioral patterns. Sleep facilitates many chronic pain syndromes by the blockade of nociceptive ways, release of specific neuromediators and the absence of conscious perception in this time. The restriction of sleep duration or disruption of its structure results in intensification of pain while the improvement of sleep leads to the alleviation of pain in some cases.

Effect of Anti-Norepinephrine Antibodies on the Development of Neuropathic Pain.

The study focuses on induction of autoantibodies directed against neurotransmitter norepinephrine during neuropathic pain syndrome and on the effect of immunization with norepinephrine-protein conjugated antigen on the development of this syndrome. The formation of anti-norepinephrine antibodies aggravated and prolonged neuropathic pain.

Analgesic Effect of Xenon in Rat Model of Inflammatory Pain.

The analgesic effects of inert gas xenon were examined on rats. The formalin model of inflammatory pain, tail-flick test, and hot-plate test revealed the antinociceptive effects of subanesthetizing doses of inhalation anesthetic xenon. Inhalation of 50/50 xenon/oxygen mixture moderated the nociceptive responses during acute and tonic phases of inflammatory pain.

[Pathogenetic mechanisms of phantom-pain syndrome].

This review considers the literature data on the epidemiology of phantom-pain syndrome (PPS) presents the results of numerous clinical studies demonstrating the lack of effectiveness of the vast majority of modem non-pharmacological and pharmacological methods of treatment of PPS. Detail presents data on the patho genetic mechanisms underlying the PPS. According to most researchers, the major role in the patho genesis of the PPS has the reorganization of the somatosensory area of the cerebral cortex of the brain. At the same time discusses the views of researchers who believe that the main reason PPS is to strengthen nociceptive and nonnociceptive afferentation in the peripheral newous system. The comparison of these conflicting data it is concluded that in the genesis of the PPS plays the role of both primary and secondary sensitization. Leading important dysfunction of the central nervous system. Details the modern understanding of the mechanisms underlying the high efficiency of suppression of PPS during stimulation of motor cortex.

[The importance of the cortex and subcortical structures of the brain in the perception of acute and chronic pain].

This review presents the current data in the literature about the importance of the cortex and subcortical structures of the brain in the perception of acute and chronic pain. Discussed the importance of various areas of the brain in perception discriminative and affective components of pain. Discusses also gender differences in pain perception depending on the functional activity of brain cortex and antinociceptive subcortical structures. Analyzed the morphological changes of cortical and subcortical structures of the brain in chronic pain syndromes. It is proved that the decrease in the volume of gray and white matter of cerebral cortex and subcortical structures is a consequence and not the cause of chronic pain syndrome. Discusses the features activate and deactivate certain areas of the cortex of the brain in acute and chronic pain. Analyzed same features the activation of several brain structures in migraine and cluster headache.

[The role of antibodies to neurotransmitters of antinociceptive system in mechanisms of neuropathic pain].

The present investigation was undertaken in order to study the role of the antibodies to neurotransmitters of antinociceptive system in pathogenesis of neuropathic pain on models of neuropathic pain. It was shown that the development of experimental neuropathic pain syndrome is accompanied with induction of autoantibodies to CABA, serotonin, noradrenalin and dopamine. It was established that the antibodies to neurotransmitters of antinociceptive system have a pronociceptive effect.

[Chronic pain: medico-biologic and sotsio-economic aspects].

In this article the role of neurobiological, psychological and social factors in pathogenesis of chronic pain is analyzed. The chronic pain is considered not as a symptom of damage of tissue and as independent illness due to non-adequate neuroplasticity of systems involved into regulation of pain sensitivity. The major role in development and maintenance of chronic pain is devoted to the primary genetically determined and/or secondary disturbance of interaction between nociceptive and antinociceptive systems at various levels--from peripheral neuron to central structures--that provides pain perception and painful behaviour development.

[Biliary dysfunctions and their prevention].

THE AIM OF REVIEW: To present the up-to-date methods of prophylaxis of biliary system pathology. ORIGINAL POSITION: The number of patients with biliary tract pathology is constantly growing up. Participation of psychovegetative state in the development of gallbladder dysfunction was confirmed. CONCLUSION: Revealing and treatment of gallbladder dysfunction, treatment of disorders of psychovegetative disorders system in patients with dysfunction of gallbladder is the necessity for successful prophylaxis of chronic cholecystitis, cholelithiasis, pancreatitis.

[Hypomotor dysfunction of gallbladder: connection between clinical symptomatic and psychovegetative state].

Article presents data on connection between disorders of psychovegetative state and clinical symptomatic in the patients with hypomotor dysfunction of gallbladder. Participation of disorders of psychovegetative state in the development clinical symptomatic of hypomotor dysfunction of gallbladde was confirmed.

[Analgesic effects of cannabinoids on central pain syndrome].

It was shown that cannabinoids anandamide, HU210 and WIN 55,212-2 inhibit both spontaneous episodes of pain and mechanical allodynia in rats with central pain syndrome caused by disturbance of inhibitory processes in the dorsal horns of lumbar spinal cord. The analgesic effect is most pronounced in the intrathecal route of administration. The intensity of analgesic actions of cannabinoids on the central pain syndrome in rats, depending on the drug is as follows: HU210 > WIN 55,212-2 > anandamide.

Experimental model of combined pain and depression status in rats.

Combined pain and depression status in rats was created by inducing experimental depressive syndrome (by subchronic injection of MPTP proneurotoxin) in animals with manifest and developing neurogenic pain syndrome induced by preliminary crossing of the sciatic nerve in the hind limb. The neurogenic pain syndrome augmented by some parameters the depressive symptoms and provoked manifestation of signs of depressive behavior in animals treated with saline.

Autoantibodies against glutamate, gamma-aminobutyric acid, and norepinephrine in mechanisms of neuropathic pain syndrome.

The production and role of autoantibodies against neurotransmitters glutamate, gamma-aminobutyric acid, and norepinephrine were studied in rats with experimental neuropathic pain syndrome induced by sciatic nerve transection. Nerve transection in rats was followed by behavioral reaction of autotomy (self-mutilation of the operated limb), which often accompanies neuropathic pain syndrome. The development of neuropathic pain syndrome was accompanied by increased production of autoantibodies against glutamate, gamma-aminobutyric acid, and norepinephrine. A negative correlation was found between the amount of autoantibodies against neurotransmitters and severity of neuropathic pain syndrome. Our results suggest that antibodies against glutamate and norepinephrine exhibit protective activity.

Role of cannabinoid receptor agonists in mechanisms of suppression of central pain syndrome.

We studied the effect of cannabinoid receptor agonists anandamide and WIN 55,212-2 on the central pain syndrome induced by intraspinal injection of penicillin sodium salt in rats. Cannabinoids suppressed allodynia and spontaneous attacks in rats with the central pain syndrome. The analgesic effect was most pronounced after intrathecal injection of cannabinoid receptor agonist in a dose of 100 microg in 10 microl. After systemic treatment the analgesic effect was produced by only WIN 55,212-2 in a dose of 1 mg/kg. WIN 55,212-2 was superior to anandamide by the duration and intensity of the effect on allodynia and spontaneous attacks.

Mechanisms of pefloxacin-induced pain.

In electrophysiological and behavioral experiments on rats we studied the effects of pefloxacin, a member of fluoroquinolone family, on the nociceptive system. Intraperitoneal injection of pefloxacin (80 mg/kg) decreased the thresholds of nociceptive response to noxious stimulation in the hot-plate test. In addition, it decreased the threshold of the late component of nociceptive flexor reflex. Intrathecal application of pefloxacin in a dose of 20 microg provoked allodynia, while the higher dose of 400 microg induced behavioral pattern characteristic of central pain syndrome. It was hypothesized that pain induced by pefloxacin results from disturbances in GABAergic inhibition in the central subdivisions of the nociceptive system.

Role of 5-HT3 receptors in the mechanisms of central pain syndrome.

Electrophysiological and behavioral studies showed that spinal 5-HT3 receptors are involved in the regulation of pain sensitivity in rats. Intrathecal administration of the 5-HT3 receptor antagonist tropine (200 microg) produced allodynia, reduced the threshold, decreased the latency, and increased the number of spikes in the late component of the nociceptive flexion reflex. Intrathecal administration of 5-HT3 receptor agonist quipazine (200 mg) abolished nociceptive flexion reflex and alleviated spinal pain syndrome produced by impairment of GABAergic inhibition in the lumbar spinal segments. Our results indicate that spinal 5-HT3 receptors are involved in the modulation of pain sensitivity: activation of these receptors inhibits nociceptive reactions, while blockade of 5-HT3 receptors potentiates the nociceptive response via modulation of excitability of GABAergic interneurons.