• Journal of the Korea Academia-Industrial cooperation Society
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• v.12 no.11
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• pp.5019-5026
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• 2011

The purpose of this study was to investigate the effect of the increased sympathetic outflow on the changes of muscle tone and central nervous system excitability in the chronic stroke patients. This study was conducted from October 12th 2009 to December 4th 2009. 30 patients with chronic hemiplegia for at least 6 months were participated. Before and during the mental arithmetic, static handgrip and post-handgrip ischemia tasks, the central nervous system action potentials and global synkinesis level were compared. The central nerve action potentials were measured with H/Mmax ratio and V/Mmax ratio. To obtain global synkinesis level, surface electromyography data were digitized, processed to root mean square. In our study, The global synkinesis level during knee flexion and extension was decreased in the mental arithmetic and in the post-handgrip ischemia task(p<.05) but not in the grip task. Also, V/Mmax ratio was decreased all in the three task(p<.05). In conclusion, we know that the central nervous system excitability and the muscle tone in chronic hemiplegic patients were decreased by the increased sympathetic outflow.

• The Korean Journal of Pain
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• v.22 no.1
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• pp.1-15
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• 2009

Neuropathic pain is often refractory to intervention because of the complex etiology and an incomplete understanding of the mechanisms behind this type of pain. Glial cells, specifically microglia and astrocytes, are powerful modulators of pain and new targets of drug development for neuropathic pain. Glial activation could be the driving force behind chronic pain, maintaining the noxious signal transmission even after the original injury has healed. Glia express chemokine, purinergic, toll-like, glutaminergic and other receptors that enable them to respond to neural signals, and they can modulate neuronal synaptic function and neuronal excitability. Nerve injury upregulates multiple receptors in spinal microglia and astrocytes. Microglia influence neuronal communication by producing inflammatory products at the synapse, as do astrocytes because they completely encapsulate synapses and are in close contact with neuronal somas through gap junctions. Glia are the main source of inflammatory mediators in the central nervous system. New therapeutic strategies for neuropathic pain are emerging such as targeting the glial cells, novel pharmacologic approaches and gene therapy. Drugs targeting microglia and astrocytes, cytokine production, and neural structures including dorsal root ganglion are now under study, as is gene therapy. Isoform-specific inhibition will minimize the side effects produced by blocking all glia with a general inhibitor. Enhancing the anti-inflammatory cytokines could prove more beneficial than administering proinflammatory cytokine antagonists that block glial activation systemically. Research on therapeutic gene transfer to the central nervous system is underway, although obstacles prevent immediate clinical application.