Can J Neurol Sci
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A decrease in spinal cord blood flow (SCBF) is a known sequela of spinal cord injury. The radioactive microsphere technique permits repeated measurement of spinal cord blood flow (SCBF) and cardiac output (CO) in the same experimental animal. The purpose of this study was to adapt the radioactive microsphere technique for use in the rat extradural clip compression injury model used in our laboratory. ⋯ Radioactive microspheres were used for two blood flow and CO determinations in both groups. MSAP fell 59% in the injured animals (p less than 0.01), but this was not accompanied by significant changes in heart rate or CO. There was a 50% reduction in SCBF in the injured cord (p less than 0.02), and there were significant reductions in cerebral blood flow (p less than 0.05) and cerebellar blood flow (p less than 0.02) following spinal cord injury.
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A solid phase radioimmunoassay was used to detect anti-myelin basic protein (MBP) antibodies in the CSF and serum of multiple sclerosis (MS) patients and controls. CSF and serum samples were assayed prior to acid hydrolysis in order to detect free anti-MBP as well as after acid hydrolysis to measure the total (free and bound) amount of antibody. ⋯ The anti-MBP index is also significantly increased in MS patients with both forms of active disease. Anti-MBP antibodies are intrathecally produced in MS patients with active disease.
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The authors report a case of Charcot-Marie-Tooth disease that mimicked Friedreich's ataxia and featured impaired tendon reflexes in the limbs, incoordination mimicking cerebellar disease in the extremities, extensor plantar responses on both sides, bilateral foot deformity, imparied position sense in the toes, absent vibratory sense in the distal parts of the legs and minimal distal weakness with wasting. Motor conduction velocity in the upper limbs was substantially reduced. Other cases similar in nature reported in the literature resemble spino-cerebellar degeneration in general, and Friedreich's ataxia, in particular. ⋯ It is also emphasized that patients similar to the one reported here may also resemble, and should be differentiated from, cases of familial dorsal column ataxia (Biemond type). Stress is put upon the fact that when Charcot-Marie-Tooth disease mimicks spino-cerebellar degeneration, substantial slowing of motor conduction in the upper limbs is generally sufficient to establish the diagnosis. The relation between Friedreich's ataxia an Charcot-Marie-Tooth disease is reviewed and it is concluded that these two disorders are distinct clinical and pathological entities.
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In this brief review it will be possible to mention only superficially the bioclinical, behavioral, neurochemical, neuropharmacological and neurophysiological evidence to support the view that some of the trace amines [meta- and paratyramine (m-TA, p-TA), beta-phenylethylamine (PE) and tryptamine (T)] may play a significant role in the propagation of nervous impulses and perhaps be involved in the etiology of certain mental disorders. More detailed comments will be found in some recent papers and reviews (Axelrod et al., 1976; Boulton, 1974, 1976, 1978, 1979; Boulton and Baker, 1975; Boulton and Juorio, 1979, Faurbye, 1968; Mosnaim and Wolfe, 1978, Sandler and Reynolds, 1976; Wyatt et al., 1977).
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Injury to peripheral nerves complicating deep intramuscular injections of antibiotic and other agents is well recognized and can result in significant permanent neurological deficit. The purpose of this paper is to review the subject of nerve injection injuries, and report on a series of recent experimental studies carried out in this laboratory designed to improve our understanding of the pathophysiology of this condition and help provide a rational basis for its treatment. A wide variety of chemotherapeutic, prophylactic, and local anaesthetic agents in common use were injected into the sciatic nerve of the adult Wistar rat. ⋯ Pathological alterations in the nerve were evident as early as 30 minutes following injection injury. Regeneration was a constant finding in nerve damage by injection of the various agents. The mechanism of injury appeared to be a direct toxic effect of the injected compound on neural tissue, with an associated break down of the blood-nerve barrier.