• Journal of The Korean Dental Society of Anesthesiology
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• v.11 no.1
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• pp.45-50
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• 2011

Bell's palsy is an isolated facial paralysis of sudden onset caused by a neuritis of the seventh nerve within the facial canal. It occurs often in the adult man with a history of recent exposure to local cold, such as sleeping next to an open window, or in some cases it occurs after infections of the nasopharynx or masticator spaces. Especially, this neuropathy have linked with the major collagen disorders (diabetes mellitus). A segmental demyelination develops rapidly, with vascultitis in microinfarcts and ischemia to the nerve segment. The authors experienced about the bizarre neurological symptom of Bell's palsy after inferior alveolar nerve block anesthesia and TMJ dislocation in diabetic mellitus. The early and correct consultation with the multiple medical and dental departments was important to prevent the inadequate care & medicolegal problems.

• Journal of Environmental Health Sciences
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• v.24 no.3
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• pp.35-40
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• 1998

This study was conducted to examine the pathological changes of rat peripheral nervous system during exposure to tellurium known to be a demyelinating agent by using teasing nerve fiber method and quantitative light microscopic analysis by image analyzer. The pellet containing 1.2% of tellurium were fed for 3, 5, 7, 9, 13 days to male wistar rats (21 days old) and then neurologic symptom and the feature of nerve fiber myelination were studied. From this study, following results were obtained. In 3 days treated group, it showed various neurologic symptom and teased nerve fiber showed slight irregularity of the myeline sheath. In 5 days and 7 days treated groups, it showed the segmental demyetination in larger size fiber and widening of nodes of ranvier. In 9 days and 13 days treated groups, the remyelinated fibers were observed and it was generally small in size. We consequently suggest that teasing nerve fiber method and quantitative analysis of nerve fiber were useful pathologic screening method of neurotoxicity of the peripheral nervous system.

• Journal of Veterinary Clinics
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• v.10 no.1
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• pp.111-130
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• 1993

Lead toxicity was evaluated in forty-five cats on a balanced diet, Treated with 0(control), 10, 100(low), 1, 000, 2, 000, and 4, 000(high) ppm of lead acetate orally on a body weight basis. The objectives were to establish toxic dosage level of leaf in cats, to characterize changes in behavior and clinical pathology, and to demonstrate what blood lead concentrations correlate with the known dosages of lead. Some high dose cats showed projectile vomiting, hyperactivity, and seizures. The growth rates did not appear to be altered in any of the dosed groups. Normal blood lead concentration in cats were lower than that of humans, dogs, and cattle. Blood lead concentrations of 3 to 20$\mu\textrm{g}$/100$m\ell$ could be termed a 'subclinical' range in the cat. Clinical lead toxicity in cats may have blood lead concentrations ranging 20 to 120$\mu\textrm{g}$/100$m\ell$. Zinc protoporphyrin concentrations were proportional to lead dosages and a significant ZPP elevation, greater than 50$\mu\textrm{g}$/100$m\ell$, may be indicative of clinical lead toxicity. The enzyme aminolevulinic acid dehydratase showed an inverss dose response relationship for all lead dosages and a significant ZPP elevation, greater than 50$\mu\textrm{g}$/100$m\ell$, may be indicative of clinical lead toxicity. The enzyme aminolevulinic acid dehydratase showed an inverse dose response relationship for all lead dosages and appears to be a good indicator of lead exposure in cats. Urinary aminolevuliruc acid concentrations generally increased with lead dosage, but individual values varied. Hair lead concentrations rose proportionately to lead dosages. Lead at least in high doses appears to inhibit chemotactic activity of polymorphonuclear cells and monocytes. No consistent dose response relationships were observed in hemoglobin, RBC, WBC, neutrophil, lymphocyte, monocyte, and eosinophil counts. There were no consistent dose related changes in total protein, plasma protein, BUN, and ALT values. Reticulocyte counts did not increase significantly in most lead dosage levels, and are probably of little value in diagnosing lead toxicity in cats. The fact that no significant changes were found in nerve conduction velocities may support that there was no segmental demyelination resulting from lead ingestion. The lethal dose in cats appear to range from 60 to 150mg/kg body weight. A reliable diagnosis of lead poisoning can be made utilizing blood lead, ZPP, and ALAD, and hair lead.