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AAEM case report #28: monomelic amyotrophy.

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Monomelic amyotrophy is a rare form of motor neuron disease usually presenting as painless asymmetric weakness and atrophy in the distal upper extremities of young adults. Only rarely are the legs involved and pyramidal findings are uncommon. Monomelic amyotrophy is most often observed in people of

Immediate post-dosing paralysis following severe soman and VX toxicosis in guinea pigs.

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There have been numerous studies of the central nervous system (CNS) involvement in organophosphate (OP) poisoning showing status epilepticus and/or 'electrographic seizures'. Brain damage has been demonstrated as 'neuronal necrosis' primarily in the cortex, thalamus and hippocampus. To the authors'

Mechanisms involved in the development of tolerance to DFP toxicity.

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Rats treated daily with diisopropylfluorophosphate (DFP) (0.5 mg/kg, sc), an inhibitor of acetylcholinesterase (AChE) activity, exhibited the symptoms of cholinergic hyperactivity between Days 3 and 5 similar to those observed 15 min after a single acute dosage (1.5 mg/kg, sc). A significant (p less

Quinidine prevents paraoxon-induced necrotizing myopathy in rats.

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Acute organophosphorus anticholinesterase poisoning induces a necrotizing end-plate myopathy in rats and patients. Acetylcholine (ACh) excess leads to prolonged synaptic currents and increased influx of cations including calcium through the postsynaptic ACh receptor channels with prolonged muscle

Experimental intoxication of sheep and cattle with Wedelia glauca.

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Wedelia glauca was administered experimentally to 11 sheep and 4 cattle. The minimum toxic dose for both species was of 4 to 5 g of fresh plant/kg bw. Clinical signs were depression, muscle fasciculations, increased respiratory and cardiac frequencies, opisthotonous, sternal or lateral recumbency

Diisopropylphosphorofluoridate-induced cholinergic hyperactivity and lipid peroxidation.

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In the present study, the association between acetylcholine (ACh)-induced muscle necrosis and the appearance of lipid peroxidation products was investigated. Lipid peroxidation in this injury was quantified by the malondialdehyde-thiobarbituric acid complex (TBA-MDA) using HPLC. To induce muscle

Primary hypoparathyroidism in dogs: a retrospective study of 17 cases.

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OBJECTIVE To evaluate the clinico-pathological findings, response to treatment and prevalence of complications in dogs with primary hypoparathyroidism. METHODS Retrospective study of 17 dogs presenting to the University of Melbourne Veterinary Clinical Centre and Murdoch University Veterinary

The role of diazepam in the treatment of nerve agent poisoning in a civilian population.

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The main site of action of diazepam, as with other benzodiazepines, is at the GABA(A) receptor, although it has been suggested that some of the potentially beneficial actions of diazepam in nerve agent poisoning are mediated through other means. It is likely that convulsions may have long-term

Differences in central and peripheral neural actions between soman and diisopropyl fluorophosphate, organophosphorus inhibitors of acetylcholinesterase.

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Toxic doses of acetylcholinesterase (AChE) inhibitors produce prominent motor symptoms (fasciculations, fibrillations, and body tremors) and muscle fiber necrosis. The severity and quality of motor symptoms and fiber necrosis depend upon the specific AChE inhibitor. To examine the importance of

Spin trapping agent phenyl-N-tert-butylnitrone prevents diisopropylphosphorofluoridate-induced excitotoxicity in skeletal muscle of the rat.

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Indirect evidence suggests that reactive oxygen species (ROS) may mediate muscle fiber necrosis following muscle hyperactivity induced by the anticholinesterase diisopropylphosphorofluoridate (DFP). Pronounced muscle fasciculations and muscle fiber necrosis were seen when acetylcholinesterase (AChE)

Nervous system effects of cardiac arrest in monkeys. Preservation of vision.

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Thirteen juvenile monkeys were taught two visual discrimination tasks. After 12 to 24 hours of food deprivation, ten underwent 14-minute episodes of cardiac arrest. Three served as controls. Five of the ten arrested animals survived and were tested in the discrimination box. All continued to perform

[Clinico-morphologic and histochemical changes in the neuromuscular apparatus in acute carbophos poisoning].

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Clinical analysis of 378 acute cases of Malathion insecticide intoxication and pathological and histochemical investigation of skeletal muscles in 7 autopsied victims of acute poisoning have revealed the pronounced neuromuscular disorders. Generalized paresis and paralysis of muscles were observed

Envenomation by the Mexican lance-headed rattlesnake Crotalus polystictus: a case report.

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A case of envenomation by the Mexican lance-headed rattlesnake, Crotalus polystictus, resulted in local swelling and muscle fasciculation, which abated after i.v. antivenin and an area of necrosis healed. A mild thrombocytopenia and hypofibrinogenemia with elevation of fibrin split products was

Polioencephalomalacia in a llama.

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A 5-year-old, female llama (Lama glama) developed acute, progressive neurological disease, characterized by recumbency, muscle fasciculations, intermittent convulsions/opisthotonos, and absent menace responses. Postmortem histopathologic lesions, limited to the cerebral cortex, consisted of necrosis

Seasonal pasture myopathy in horses in the midwestern United States: 14 cases (1998-2005).

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OBJECTIVE To determine clinical signs, diagnostic findings, tissue tremetone concentrations, and clinical outcome or postmortem findings in horses evaluated for acute severe nonexertional rhabdomyolysis initially attributed to white snakeroot toxicosis. METHODS Retrospective case series. METHODS 14

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