Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0426980 (motor symptom)
 471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxaliplatin, an effective cytotoxic treatment in combination with 5-fluorouracil for colorectal cancer, is associated with sensory, motor and autonomic neurotoxicity. Motor symptoms include hyperexcitability while autonomic effects include urinary retention, but the cause of these side-effects is unknown. We examined the effects on motor nerve function in the mouse hemidiaphragm and on the autonomic system in the vas deferens. In the mouse diaphragm, oxaliplatin (0.5 mM) induced multiple endplate potentials (EPPs) following a single stimulus, and was associated with an increase in spontaneous miniature EPP frequency. In the vas deferens, spontaneous excitatory junction potential frequency was increased after 30 min exposure to oxaliplatin; no changes in resting Ca(2+) concentration in nerve terminal varicosities were observed, and recovery after stimuli trains was unaffected. In both tissues, an oxaliplatin-induced increase in spontaneous activity was prevented by the voltage-gated Na(+) channel blocker tetrodotoxin (TTX). Carbamazepine (0.3 mM) also prevented multiple EPPs and the increase in spontaneous activity in both tissues. In diaphragm, beta-pompilidotoxin (100 microM), which slows Na(+) channel inactivation, induced multiple EPPs similar to oxaliplatin's effect. By contrast, blockers of K(+) channels (4-aminopyridine and apamin) did not replicate oxaliplatin-induced hyperexcitability in the diaphragm. The prevention of hyperexcitability by TTX blockade implies that oxaliplatin acts on nerve conduction rather than by effecting repolarisation. The similarity between beta-pompilidotoxin and oxaliplatin suggests that alteration of voltage-gated Na(+) channel kinetics is likely to underlie the acute neurotoxic actions of oxaliplatin.
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PMID:Oxaliplatin induces hyperexcitability at motor and autonomic neuromuscular junctions through effects on voltage-gated sodium channels. 1623 Oct 11

Tarsal tunnel syndrome (TTS) is defined as the entrapment of the posterior tibial nerve in the tarsal tunnel of the ankle. The etiologies of tarsal tunnel syndrome are mainly the presence of a ganglion, osseous prominence with tarsal bone coalition, trauma, varicose veins, neurinoma, hypertrophy of the flexor retinaculum, or systemic disease (rheumatoid arthritis, ankylosing spondylitis). However, no specific cause can be identified in some cases. Patients with chronic renal failure tend to develop peripheral nerve entrapment and carpal tunnel syndrome is the best-known peripheral entrapment neuropathy among them. Contrary to carpal tunnel syndrome, tarsal tunnel syndrome is observed less frequently in chronic renal failure patients. The common presenting symptoms of TTS are paresthesias and/or pain in the plantar side of the foot. Motor symptoms are rarely detected. Diagnosis is made primarily by electroneuromyographic studies and physical examination. Surgery is the treatment of choice and the outcome is generally favourable. In this report, we present a patient with tarsal tunnel syndrome complicating peritoneal dialysis.
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PMID:Tarsal tunnel syndrome in a patient on long-term peritoneal dialysis: case report. 1805 74