[Cerebellum, postural tonus, and reticular discharge].
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As many as 8 patients aged 8-19 years suffering from infantile cerebral paralysis (ICP) with torsion dystonia, akinetic, rigid, spastic and hypotonically atactic syndromes were examined for the maximum amplitude of EMG activity of the musculus tibialis anterior in voluntary rear flexion of the foot and in Strümpell's tibial synkinesia before treatment and after intake of small doses of L-DOPA (nakom, 62 mg/day). It has been established that the amplitude of voluntary EMG activity and the rate of impulse transmission in efferents of the tibial nerve remained practically unchanged during treatment; in all the cases, the synergic EMG activity, discharges of EMG and prolonged activity decreased; the scope of active movements in the talocrural joint increased by 10-20 degrees. The greatest decrease of synergic EMG activity (by 40%) was recorded in patients with rigid muscle tone, the mean in patients with spastic and spastic -dystonic (by 25-33%), the least one (17%) in muscle hypotonia. It is assumed that voluntary and synergic automatic movements have varying neuromediator supply. The effect of L-DOPA is realized via changes in the function of suprasegmental brain structures regulating polysynaptic postural reflexes with primary action on extensors. The effects of the subcortical nuclei, stem and cerebellar systems are made possible by dopamine neuromediation to a different measure.
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The mammalian brain contains anatomically distinct dopaminergic neuronal systems that subserve a variety of functions which include maintaining postural reflexes, modulating basic psychic processes, and controlling the secretion of hormones from the pituitary. In turn, these various dopaminergic neuronal systems are regulated by different mechanisms that are appropriate for the functions that they control. This is illustrated by comparing the responses to endocrinological and pharmacological manipulations of the nigrostriatal dopaminergic neuronal system that is involved with sensorimotor integration and the tuberoinfundibular dopaminergic neuronal system that tonically inhibits the release of prolactin.
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BACKGROUND: Green tea catechins possess potent antioxidative properties, and the preventive effects against various oxidative diseases have been reported. The purpose of this study is to examine preventive and protective effects of green tea catechins on various deteriorative processes following stroke. MATERIAL/METHODS: Male Wistar rats were given ad libitum water with or without 0.25 and 0.5% tea catechin extract for 5 days prior to the operation and during the experiment. Right middle cerebral artery was occluded for 2 h, then reperfused for 22 h. Brain slices were stained with triphenyltetrazolim chloride to assess infarct area. Concentrations of plasma EGCg, and serum NOx were analyzed by HPLC. Detection of iNOS expression, neutrophil infiltration and peroxynitrite formation in the penumbra was performed by immunostain. Neurologic deficit was scored by posture reflex. RESULTS: Tea catechins dose-dependently reduced the brain infarct area and volume. Infarct volume was inversely correlated with plasma EGCg concentration. Dark staining for iNOS, neutrophils and peroxynitrite were observed in vessel wall of small arteries in control ischemic hemisphere, while in catechins (0.5%)-treated rats iNOS was detected slightly, and staining for neutrophils and peroxynitrite was not seen. Catechin ingestion blocked a 3-fold increase in serum NOx concentration in the jugular vein, and also reduced by 35% a 2-fold increase of plasma lipid peroxide level seen in control rats after reperfusion. Neurologic deficits were significantly alleviated by 0.5% catechin ingestion. CONCLUSIONS: Daily intake of green tea catechins efficiently protects the penumbra from irreversible damage due to cerebral ischemia, and consequent neurologic deficits.
There is little information concerning the effects of passive exercise training in healthy humans. This prompted an investigation to evaluate muscle activity and the associated changes in strength and lean body mass resulting from a passive exercise program. Twenty-eight healthy volunteers, aged 26 to 44 years, participated in this six-week study. Lean body mass changes were evaluated by tetrapolar bioelectric impedance measurements, strength changes by isokinetic strength evaluation, and muscle activity by surface EMG techniques. Reproducible muscle activity was recorded in all three muscles studied during two of three preselected exercises. This involuntary muscle activity was attributed to fusimotor and postural reflexes. No significant change (p greater than .05), however, occurred in muscle strength or lean body mass at the end of the six weeks. Lack of these physiologic changes in light of the documented muscle activity is attributed to insufficient training effect.