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The study was performed on 30 male rats of Wistar line (weight 330-360 g, age 3.5 months).In an experimental model of damage to the femur bone in the hip joint studied the effect of low frequency electrical stimulation of the damaged area on the rate of regeneration of bone. The animals were divided into two groups. Control (15 rats) and experienced (15 rats). In the experimental animals underwent stimulation of the injury site for 5 min daily for 7 days, 14 days and 21 days. Stimulation was carried out using a device "Osteon-1" generating a mixed signal of two voltage pulse of varying duty cycle, one of which is modulated to a higher frequency. Signals were not synchronized with respect to each other, unipolar with varying frequencies and amplitudes. The obtained results show the effectiveness of the electrical stimulation currents of low frequency in the restoration of bone tissue after damage. Morphological studies showed that electrical stimulation to accelerate the regeneration of damaged bone at all stages of the study (7, 14, 21 day), causes a more pronounced integration of newly formed bone with the old intact bone and promote the formation of more powerful periosteal calluses in comparison with the control.

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A comparative study of the effects of two nonsteroidal antiinflammatory drugs paracetamol and naproxen on the pain syndrome models of various etiology showed that paracetamol is more effective in the case of spinal and neuropathic pain syndromes (in which the leading pathogenic mechanisms are related to the formation of hyperactive neuron aggregates in the central nociceptive structures). Naproxen was effective in the case of adjuvant arthritis, for which the main development mechanism is related to the accumulation of inflammation mediators in tissues. It is concluded that special features of the pathogenic therapy of various pain syndromes are determined by the character of prostaglandin participation in the pathological process.

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Dopaminergic brain system plays an important role in regulation of pain sensitivity. However, the data on participation of antidopamine antibodies in the development of neurogenic pain are absent. This work was aimed at the study of the role of antidopamine antibodies in the development of pain syndrome induced by the injury of nn. ischiadic and saphenous in rats. It was shown that after the nerve injury, the behavioral reaction such as autotomy (self-injury) appeared as a feature of the experimental neuropathic pain syndrome. It was originally established that the development of neuropathic pain syndrome induced by the injury of peripheral nerves was accompanied by induction of dopamine autoantibodies. It was also shown that immunization of the animals with conjugated dopamine-protein autigen resulted in aninerease of autidopamine antibody level and an amplification of the experimental neuropathic pain syndrome, i.e., decrease in the latency of the first autotomy, increase in expression of autotomies, and increase in the number of animals with late autotomies.

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Clinical and experimental studies of formation of paroxysmal trigeminal pain are carried out in patients with typical trigeminal neuralgia (TN), TN with neuropathic disorders, TN concomitant with disseminated sclerosis, and symptomatic TN caused by vestibulo-cochlear neurinoma (VIII pair). Trigeminal, acoustic stem, and visual evoked potentials were recorded, electroencephalography (including mapping) and magnetic imaging were carried out. In experiments, bioelectric activity of the brain was recorded in rats with TN and neuropathy. Paroxysmal trigeminal prosopalgias are caused by various etiologic factors and involve mainly the sensory trigeminal radicles. Total systems' pathogenetic processes characteristic of this disease are described.

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The effect of glycine, ketamine, and their combination in chronic oral administration was studied on a model of the neuropathic pain syndrome. Glycine failed to prevent the pain syndrome but had a therapeutic effect. Ketamine possessed a marked preventive and therapeutic effect. In combined administration the drugs mutually potentiated their action. The effect of glycine and ketamine is based on intensification of spinal glycinergic inhibition, differently directed effect on the NMDA receptors, and intensification of monoaminergic inhibition.

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Serotoninergic and catecholaminergic neurotransmitter systems of the brain play an important role in the regulation of pain sensitivity. However, there are no data on the involvement of antibodies to the above neurotransmitters is the development of neuropathic pain syndromes. The authors' studies indicated that the development of neuropathic pain syndrome occurring after nerve damage is followed by the formation of serotonin antibodies and their enhanced induction caused by immunization of animals with serotonin-protein conjugated antigen aggravates the pain syndrome. Block and insufficiency of the serotoninergic antinociceptive system may be a cause of the progression of the pain syndrome due to serotonin antibodies.

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The authors carried out estimation of analgetic effect of tisanidin by double blind test in patients with phantom limb pain syndrome. 14 patients took the medicine in a dose of 12 mg/day and 5 patients took placebo at the same dose. Characteristics and intensity of pain were estimated in accordance with McGill pain questionnaire and visual analogue scale. Pain possessed more than one sensory characteristics in the majority of patients. Tisanidin had a significant analgetic influence on all type of phantom limb pain: "neuralgic"--acute, shooting, transitory, "causalgic"--hot, burning, searing, "cramping" pain. Pain sensation did not decrease only in one of 14 patients treated with tisanidin. The authors explain the effectivity of the drug for treatment of phantom limb pain of different sensory modality by variety of the mechanisms of its therapeutic action, the capacity to decrease the releasing of excitatory neurotransmitter amino acids and the influence on alpha 2-adrenoceptors.

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The effect of hydrocortisone on the neurogenic pain syndrome induced by damage to the peripheral nerves was studied in 40 male Wistar rats. Intraperitoneal administration of 10 mg/kg of the drug caused both hyperalgesia and hypoalgesia. The direction of the hydrocortisone effect on the neurogenic pain syndrome depended on the time of administration: chronic administration before the damage to the nerves promoted the development and intensity of the syndrome; treatment applied after the nerve damage delayed the development of the syndrome. It is suggested that the mechanism of the hydrocortisone effect on the neurogenic pain syndrome may be realized via the central link through the effect of the hormone on the glucocorticoid receptors of the brain structures.

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The central mechanisms of analgesic action of phentanyl and moradol are compared using analysis of changes in the early and late components of somatosensory evoked potentials (SSEP) of the brain in normal volunteers in response to pain stimulation. Phentanyl and moradol differently affect the changes in the early components of SSEP: phentanyl reduces their amplitude, whereas moradol increases it. Both drugs similarly influenced changes in the late components of SSEP. Specific effects of the drugs on the sensory and psychoemotional components of pain perception by man are discussed.

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Changes in the somatosensory evoked potentials (SSEP) were studied in patients with amputated limbs with and without phantom pain syndrome (PPS). Patients with PPS were found to develop hypersynchronous postdischarges following the components of SSEP, the amplitudes of the early components of SSEP (N1, P2, and N2) increase in response to stimulation of the stump nerves and the median nerve on the side of amputation, and EEG shows paroxysmal activity. The results indicate a stable increase of the excitability and reactivity of the central structures of the brain, reflecting the formation of a pathologic algic system in the structures regulating pain sensitivity.

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The authors consider that failures in the treatment of phantom pain syndrome (PPS) are explained by the lack of individual approach to the clinical manifestations of the syndrome. Three main clinical forms of PPS are distinguished using McGillow's questionnaire: causalgic, neuralgic, and spastic. Differentiated therapy for each form is proposed: combinations of amitriptyline, propranolol, and phenazepam for the first form, carbamazepine, propranolol, and phenazepam for the second, and tizanidine monotherapy for the third form. The efficacy of such therapy is approximately 75.2%, incidence of relapses during a year's follow up 12.4%.

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Ipsilateral evoked potentials in the caudal trigeminal nucleus, ventrobasal thalamus, and cortex during electrical stimulation of the injured and opposite intact nerves were studied in rats with trigeminal neuropathy caused by partial compression of the infraorbital nerve. In spite of abnormally increased long latent evoked activity in the caudal nucleus ipsilaterally to compression, amplitude asymmetry of the ipsilateral thalamic and cortical evoked potentials in rats with pain syndrome was shown to be absent during nerve stimulation of the snout sides. In rats without pain-evoked potentials in the caudal nucleus during injured nerve stimulation had small differences as compared with the latter group. At that time, the increased magnitude of ipsilateral evoked potentials at uninjured nerve stimulation was recorded in all structures in rats without pain syndrome as compared with the pain syndrome group and sham-operated rats, and as compared with ipsilateral evoked potentials during injured nerve stimulation in rats without pain syndrome. The neuropathic pain syndrome is considered to result from the formation of the pathologic algic system with a generator of abnormality enhanced excitation which arises in the nonspecific nociceptive structures in response to specific structural injury. This alternative process is the compensative increase in the ipsilateral input of agents into the brain cortex from the intact nerve that prevents the development of its abnormal activities.

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