Neuromodulation : journal of the International Neuromodulation Society
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The present experiments were performed on rat colon to study neurogenic and myogenic elicited propulsion induced by 0.3 and 30 msec long current pulses. The colon segments were stimulated sequentially and randomly. The obtained contractions displaced the intraluminal content in individual propulsion steps. ⋯ When inhibiting cholinergic transmission by atropine, the propulsion induced by 0.3 msec pulses was blocked, while partially inhibited when using 30 msec pulses. Inhibiting nitric oxide synthesis by N(G) -nitro-L-arginine methyl ester (L-NAME) blocked propulsion induced by both of the pulse durations. In conclusion, electrical stimulation induces propulsion when using both 0.3 and 30 msec long pulses; stimulation using 0.3 msec pulses activates neurons, whereas 30 msec pulses depolarize muscles; in the absence of nitrergic transmission, propulsion cannot be induced by electrical stimulation.
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Objective The purpose of this study was to test if the F-response can be repressed volitionally. Normally, the F-response is used for clinical diagnostics but it also has an important influence on the design of a neural prosthesis involving functional electrical stimulation (FES) and the use of volitional myoelectric signal (MES) for control. Methods Ten neurologically normal subjects were trained to reduce the level of the F-response from the anterior tibial muscle. ⋯ From the first to the last session of a trial, the change was found not significant. Conclusion The level of the F-response may change locally, but there is no indication that a subject can volitionally learn to repress the response, even when given feedback information about the actual level. Therefore the F-waves in the myoelectric signal from a stimulated muscle has to be accounted for when designing devices using a stimulated muscle response for myoelectric control such as eliminating the F-interval from the recorded signal.
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Objective To compare the technical performance of different percutaneous lead types for spinal cord stimulation. Methods Using the ut-scs software (University of Twente's spinal cord stimulation), lead models having similar characteristics such as the 3487A PISCES-Quad (PQ), 3887 PISCES-Quad Compact (PC), 3888 PISCES-Quad Plus (PP) (Medtronic Inc., Minneapolis, MN), and the AB SC2108 (AB) (Advanced Bionics Corp., Valencia, CA) were simulated in monopolar and tripolar (guarded cathode) combinations on a single lead, placed just outside the dorsal dura mater and both centered on the spinal cord midline, and at 1 mm lateral. The influence of displacing a lead dorsally in the epidural fat was examined as well. ⋯ Conclusions Complex pain syndromes are treated best with lead having a small contact spacing, being programmed as a tripole (guarded cathode) and centered on the spinal cord midline just outside the dura mater. This is because dorsal column fiber recruitment is more extensive than with any other combinations, including dual leads. Improved recruitment of dorsal column fibers is accompanied by increased energy consumption.
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Introduction. Deep brain stimulation (DBS) of the subthalamic nucleus (STN) and of the pars interna of Globus Pallidus (GPi) is used to improve parkinsonian symptoms and attenuate levodopa-induced motor complications in Parkinson's disease (PD) (DBS for PD study group, 2001). It is still not clear what the best anatomic structures to stimulate are or what the physiologic effects of DBS are. ⋯ Most patients remained were chronically treated with bilateral stimulation of both targets. Conclusion. We conclude that DBS of STN and GPi was effective, with most patients treated chronically with both targets stimulated.
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In recent years, part of the muscle resistance in spastic patients has been explained by changes in the elastic properties of muscles. However, the adaptive spinal mechanisms responsible for the exaggeration of stretch reflex activity also contribute to muscle stiffness. The available data suggest that no single spinal mechanism is responsible for the development of spasticity but that failure of different spinal inhibitory mechanisms (reciprocal IA inhibition, presynaptic inhibition, IB inhibition, recurrent inhibition) are involved in different patients depending on the site of lesion and the etiology of the spastic symptoms. ⋯ This is ensured by increasing transmission in several spinal inhibitory pathways. In spastic patients, this control is inadequate, and therefore stretch reflexes in antagonist muscles are easily evoked at the beginning of voluntary movements or in the transition from flexor to extensor muscle activity. This problem is contradicted by the fact that antispastic therapy to improve voluntary movements should be directed.