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)

n-Hexane and methyl n-butyl ketone share a common metabolite, 2,5-hexanedione, a potent neurotoxin. Neurotoxic effects to both peripheral and central nervous systems may occur after occupational exposure or recreational abuse of n-hexane. Initial clinical manifestations include numbness and tingling sensation in the toes and fingers, followed by progressive weakness and areflexia, particularly in the distal limbs. Chronic low-dose n-hexane exposure, often observed in industrial workers, apparently causes axonal loss with sensory impairment. Subacute high-dose n-hexane exposure, often observed in glue-sniffers, can cause axonal swelling and secondary demyelination with muscle wasting and weakness. Electrophysiological studies demonstrate prominent prolongation of distal latencies, slowing of nerve conduction velocities, and conduction block with temporal dispersion particularly in severely intoxicated patients. Pathological hallmarks include giant axonal swelling with secondary demyelination and relative loss of large myelinated fibers. Giant axons are accumulated by 10 nm neurofilaments. The clinical course tends to be biphasic with "coasting" for 2-3 months, followed by a slow recovery for about 1-2 years after cessation of exposure to n-hexane. Prognosis is usually favorable. Severely affected patients may develop sequelae of muscle wasting, foot drop, and spasticity. Increased awareness of the n-hexane neurotoxicity in industrial workers and glue sniffers as well as use of safe solvents and adequate ventilation systems are important for preventing n-hexane toxicity.
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PMID:Polyneuropathy induced by n-hexane intoxication in Taiwan. 1856 21

Neurotoxic and cytotoxic effects of venoms from Scorpio maurus palmatus taken from different populations were assessed for geographic based variability in toxicity, and to evaluate their insecticidal potency. Scorpions were collected from four regions. Three locations were mutually isolated pockets in the arid area of Southern Sinai. The fourth sample was collected from a population inhabiting the semi-arid environment of Western Mediterranean Coastal Desert. The neurotoxic (paralytic) effect of the venom from each population was assayed by its ability to induce permanent disability in adult cockroaches within 3h. Venom was applied using microinjection techniques through an intersegmental membrane. Probit analysis was used to calculate the Paralytic Effective Dose (PED(50), ng/100mg). Levels of glutathione, lipid peroxidation, protein carbonyl content and nitric oxide, as well as the activities of superoxide dismutase, catalase and cholinesterase, were measured to assess the cytotoxicity of the venom. The results show that the injected venom from each population induced obvious spasticity, followed by flaccid paralysis. All the tested biochemical parameters, except glutathione content, revealed significant differences in toxicity in venom taken from the different scorpion populations. We conclude that (i) the venom of this scorpion has significant neurotoxic and cytotoxic effects on insect cells, (ii) its efficacy, as assessed by the PED(50) unit, exhibited variation across its geographic range, and (iii) components in the venom may have the potential for being developed into effective and environmentally friendly bioinsecticides.
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PMID:Neurotoxic and cytotoxic effects of venom from different populations of the Egyptian Scorpio maurus palmatus. 1968 84