Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0026838 (spasticity)
 6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty-two patients with spinally originated muscle spasticity were treated with a transcutaneous electrical nerve stimulator, the Han's acupoint nerve stimulator (HANS) via skin electrodes placed over the acupoints on the hand and leg. High frequency (100 Hz), but not the low frequency (2 Hz), stimulation was effective in ameliorating muscle spasticity. While the therapeutic effect lasted for only 10 minutes in the first treatment, it became consolidated after consecutive daily treatment for 3 months. The anti-spastic effect induced by high frequency electrical stimulation can be partially reversed by a high dose of naloxone. The results suggest that the anti-spastic effect elicited by peripheral electrical stimulation is mediated, at least in part, by the endogenous opioid ligand interacting with the kappa opiate receptors, most probably dynorphin, in the central nervous system.
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PMID:Transcutaneous electrical nerve stimulation for treatment of spinal spasticity. 818 75

To study the effect and mechanism of electrical stimulation in treating spinal spasticity, we used electroacupuncture (EA) on the surface of 2 couples of acupoints. The short term application (30 min) of high-frequency EA (100 Hz) produced an immediate antispastic effect in contrast to the low-frequency EA (2 Hz). After application of high-frequency EA (2 times/day, 30 min/time) for 3 months, antisplastic effect was stable. To keep this antispastic effect, the high-frequency EA must be used permanently. Recent experimental results showed that low and high frequency EA release MEK and dynorphin respectively from the spinal cord in humans. We infer that by enhancing the production of dynorphin in CSF, high-frequency EA decrease the excitability of the motor neurons in the anterior horns through the kappa opiate receptors, thus ameliorating the muscle spasticity of spinal origin.
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PMID:[Transcutaneous electric stimulation at acupoints in the treatment of spinal spasticity: effects and mechanism]. 831 80

Spasticity in rat hindlimbs was induced by compressing cervical spinal cord with a wax ball. Ashworth score and H-reflex were measured 1 week after the surgery. The results showed that: (1) muscle spasm was detected in the hindlimbs a week after the operation and maintained at least 8 weeks, (2) in the spastic animals, dynorphin A (1-17)-ir decreased significantly in thoracic and lumbar segments of the spinal cord and (3) peripheral administration of kappa receptor agonist U50488H and electrical stimulation at 100 Hz effectively relieved the muscle spasm. Our data supported the note that the reduction of endogenous dynorphin A (1-17) might play an important role in the pathogenesis of spinally induced muscle spasticity and the replenishment of its shortage might relieve the spasticity.
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PMID:Decreased dynorphin A (1-17) in the spinal cord of spastic rats after the compressive injury. 1614 54