[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.

Effect of selective blockade of M4 cholinoreceptors by tropicamide on blood supply in brain, splanchnic azygous organs, and hindlimbs in intact rats.

Experiments on anesthetized rats carried out with a high-frequency ultrasonic system and tropicamide, a highly selective blocker of M4 cholinoreceptors, showed that the vasodilator effects observed after selective blockade of M4 cholinoreceptors are not organ-specific. Intravenous tropicamide (0.1 µg/kg body weight) transiently decreased systemic BP, elevated the linear and volume fl ow rates, and diminished vascular resistance in common carotid, superior mesenteric, and femoral arteries. At the same time, in most rats (76%) the fl ow rate in the portal vein did not change, while in 25% rats it insignificantly and temporarily increased. The hypothesis on possible involvement of M4 cholinoreceptor structures in cholinergic vasoconstriction is discussed.

[The role of M4-subtype of cholinoreceptors in acethilinecholine vasoconstriction].

In experiments on rats using high frequency ultrasonic measurement technique and selective M4-cholinoreceptor antagonist tropicamide it was shown that i/v injection of the cholinolitic block agent in large doses exceeding of its selective threshold (1 mg/kg) causes pronounced inhibition of the cardiovascular system in rats. Severe transitory hypotension and bradycardia are developed, general vascular resistance, minute cardiac output, are decreased. The block of M4-cholinoreceptors with smaller doses of tropicamide (0.1-0.001 mg/kg) causes transitory dose-depended effect on hemodynamic--system blood pressure and vascular resistance, pulse, minute cardiac output, as soon as velocity of aortic blood flow, strike cardiac output are increased on the contrary. The following decrease the dose of the high selective M4-cholinolitic antagonist (0.0001 mg/kg) reveals that its negative chronotropic effect are not detected practically but tropicamide vessel action (decrease of system blood pressure and vascular resistance) are preserved distinctly. The obtained data are discussed in aspect of the possible involvement of M4-muscarinic receptor subtype in acetylcholine-induced vasoconstriction in rats.

Role of various subtypes of muscarinic cholinergic receptors in the development of posthemorrhagic abnormalities in systemic and portal circulation in rats.

The experiments employing high-frequency ultrasonic technique and selective blockers of M1, M3, and M4 muscarinic cholinergic receptors pirenzepine, 4-DAMP, and tropicamide, respectively, revealed individual roles of these receptors in the development of severe posthemorrhagic hypotension in rats with low or high individual resistance to circulatory hypoxia. The study showed that M1 and M4 muscarinic receptors are involved in shock-limiting and shock-activating processes, respectively, while M3 receptors exert no effect on the course of posthemorrhagic abnormalities in systemic and hepatic portal circulation and on the posthemorrhagic lifespan. Poor resistance of the cardiovascular system to circulatory hypoxia during shock development is considered to be dysregulatory pathology.

Non-invasive interactive neurostimulation in the post-operative recovery of patients with a trochanteric fracture of the femur. A randomised, controlled trial.

We undertook a trial on 60 patients with AO 31A2 fractures of the hip who were randomised after stabilisation of the fracture into two equal groups, one of which received post-operative treatment using a non-invasive interactive neurostimulation device and the other with a sham device. All other aspects of their rehabilitation were the same. The treatment was continued for ten days after operation. Outcome measurements included the use of a visual analogue scale for pain, the brief pain inventory and Ketorolac for post-operative control of pain, and an overall assessment of outcome by the surgeon. There were significantly better results for the patients receiving treatment by active electrical stimulation (repeated measures analysis of variance, p < 0.001). The findings of this pilot trial justify a larger study to determine if these results are more generally applicable.