Neuromodulation : journal of the International Neuromodulation Society
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Introduction. Early animal and human evidence existed for a postsynaptic dorsal column (PSDC) pathway for visceral nociception that, when lesioned, decreased pain of terminal illness. There have been recent anecdotal reports in the literature that spinal cord stimulation (SCS) reduces pain of visceral nociception. We present here a review of the literature supporting a hypothesis that SCS might work by modulating information through the spinothalamic tracts (STT) and PSDC. ⋯ Conclusions. Chronic visceral nociception may be secondary to visceral sensitization and hyperalgesia and can be affected by the spinal cord and brain, the "brain-gut" axis. There is preclinical evidence and clinical anecdotes that this nociceptive information is transmitted in the central nervous system through the PSDC pathway and LSTT and that SCS decreases pain of visceral nociception. It may be that SCS works by modulation of the above pathways.
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Repositioning of a subthalamic nucleus deep brain stimulation lead alleviated a parkinsonian patient's dyskinesias without the need for parkinsonian medication reduction. After the initial placement and programming, the patient was doing well. During repair of a skin erosion, the lead moved ventral and the patient developed severe dyskinesias and, when the deep brain stimulation system was on, diplopia. ⋯ The electrode was moved dorsally by about 6 mm. Intraoperatively the patient's dyskinesias stopped with no diplopia with the stimulator on. Two years after the revision the patient is doing very well.
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Objective. Employing [(18) F]fluorodeoxyglucose (FDG) positron emission tomography (PET) to assess the correlation between the effect of deep brain stimulation (DBS) on the subthalamic nucleus (STN) and the regional cerebral metabolic rate of glucose (rCMRGlc) in advanced Parkinson's disease patients (N = 8). Materials and Methods. On the basis of patients' diary records, we performed FDG-PET during the off-period of motor activity with on- or off-stimulation by STN-DBS on separate days and analyzed the correlation between changes in motor symptoms and alterations in the rCMRGlc. Result. When FDG-PET was performed, the motor score on the unified Parkinson's disease rating scale (UPDRS) was 64% lower with on-stimulation than with off-stimulation (p < 0.001, Wilcoxon single-rank test). ⋯ Among the items of the UPDRS motor score, the changes in resting tremor and rigidity of the left extremities showed a significant correlation with the changes in rCMRGlc observed in the right premotor area (p < 0.02 and p < 0.05, respectively, Spearman's rank correlation). Conclusions. STN-DBS either activates the premotor area or normalizes the deactivation of the premotor area. These FDG-PET findings obtained are consistent with the idea that STN-DBS modifies the activities of neural circuits involved in motor control.
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Objective. The aim of this study was to investigate the effects of spinal cord stimulation (SCS) on peripheral circulation in rats with streptozotocin (STZ)-induced diabetes. Materials and Methods. Four weeks after streptozotocin or vehicle was injected (i.p.) in male Sprague-Dawley rats, SCS-induced vasodilation was examined. Results. Plasma glucose concentration was significantly higher in diabetic rats than in the control animals. ⋯ SCS-induced vasodilation was attenuated at 90% of the MT, but not at 30% and 60% of MT in diabetic rats when compared to control rats (p < 0.001, N = 13). Furthermore, increasing SCS from 30% to 90% of MT typically produced a progressive increase in blood flow in control rats but not in diabetic rats (p < 0.01, N = 13). Conclusion. This study suggested that SCS-induced vasodilation improves peripheral blood flow, although the pathways were partially impaired in the diabetic condition.