Neuromodulation : journal of the International Neuromodulation Society
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Spinal cord stimulation (SCS) has traditionally been applied to the treatment of neuropathic pain with good to excellent outcomes. Visceral pain syndromes can be just as debilitating and disabling as somatic and neuropathic pain, however, there seems to be a general lack of consensus on appropriate treatment strategies for these disorders. We present here several case studies to demonstrate the viscerotomal distribution of abdominal visceral pain pathways and the application of traditional SCS techniques for its management. ⋯ There was an overall mean reduction of 4.9 points in the VAS score for pain intensity and a substantial (> 50%) decrease in narcotic use. All patients were followed for more than one year with excellent outcomes and minimal complications. We conclude, based on these case reports, that SCS might be an effective, nondestructive, and reversible treatment modality for abdominal visceral pain disorders.
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The objective of this study was to evaluate the long-term infection risk from refilling intrathecal drug delivery devices. We studied 25 patients (14 females and 11 males) with intrathecal infusion pumps placed for spasticity (23 patients) and chronic pain (two patients). In this study group there were 890 refill procedures (mean 35.6 ± 20.5; range 8-72 times) performed on an outpatient basis by four different physicians. ⋯ All cultures, in all pumps, were negative for aerobic and anaerobic bacteria. We conclude that periodic refills of intrathecal implanted pumps do not seem to be a risk factor for infection if standard sterile refill procedures are performed. In this study, it was clear that comorbid infections from other parts of the body do not present as a risk for device contamination.
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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.