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.
Incomplete compression of the infraorbital nerve in rats leads to spontaneous netlronal activity in the form of bursts in the caudal trigeminal nucleus and to epileptiform activity in the ventrobasal thalamus and cerebral cortex. From the latter, afterdischarges are also recorded.
Analgesic activity of a new anticonvulsive agent lamotrigin was studied on the model of neurogenic pain syndrome produced in rats by penicillin applied to the dorsal surface of the spinal cord and by dissection of the sciatic nerve. Lamotrigin was shown to have a profound analgesic activity. It can be used as an efficient prophylactic agent for prevention of chronic pain syndromes by suppression of the generators of pathologically enhanced excitation in the nociceptive structures which are the pathophysiological basis of the chronic pain syndromes.
Key Words: lamotrigin; neurogenic pain syndromes; nociceptive neuronsNeurogenic pain syndromes appear due to damage to peripheral or central structures of the nervous system that participate in conduction of nociceptive signal [7]. They are characterized by prolonged painful seizures which cannot be arrested by conventional analgesics [2,3]. The pathophysiological basis of neurogenic pain syndromes is formation of the generators of pathologically enhanced excitation which are the aggregates of interacting hyperactive neurons producing an anomalous impulse traffic in the structures responsible for regulation of pain sensitivity. Formation of such generators results from suppression of inhibitory reactions in the central nervous system structures, which is mediated by glycin and -/-aminobutyric acid [2] and enhancement of the effect of excitatory amino acids on the nociceptive neurons via NDMA and non-NDMA receptors [7,11]. Logically, the treatment of the neurogenic pain syndromes by administration of antiepileptic drugs (carbamazepine, phenytonin, clonazepam, diazepam, etc.), which eliminate the pathological hyperactivity In this work we study the effect of a novel antiepileptic preparation lamotrigin (LT) on the development of neurogenic pain syndromes, which were elicited by application of a convulsive agent (penicillin) to the dorsal surface of the spinal cord as well as by transection of the sciatic nerve.
MATERIALS AND METHODSExperiments were carried out on 73 outbred albino rats weighing 180-200 g. The ethic requirements of International Association of Study of Pain were adhered to in the experiments. The spinal pain syndrome (SPS) was produced with the help of benzyl penicillin sodium salt dissolved in 1% agar, which was applied under ether narcosis unilaterally to the dorsal surface of the lumbar segments in the spinal cord (Liv-Lv). After application of the convulsant, the wound was sutured, and the animal was placed into a glass cage for observation. The degree of SPS was evaluated by a 3-point scale [ 1].The neuropathy pain syndrome (NPS) was produced by transecting of the sciatic nerve under ether narcosis at the level of the popliteal fossa and placing
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