Journal of The Korean Society of Clinical Toxicology

Motor Peripheral Neuropathy Involved Bilateral Lower Extremities Following Acute Carbon Monoxide Poisoning: A Case Report: Jae-Hyung Choi, Hoon Lim; J Korean Soc Clin Toxicol. 2015;13(1):46-49. Published online June 30, 2015

Abstract PDF: Carbon monoxide (CO) intoxication is a leading cause of severe neuropsychological impairments. Peripheral nerve injury has rarely been reported. Following are brief statements describing the motor peripheral neuropathy involved bilateral lower extremities of a patient who recovered following acute carbon monoxide poisoning. After inhalation of smoke from a fire, a 60-year-old woman experienced bilateral leg weakness without edema or injury. Neurological examination showed diplegia and deep tendon areflexia in lower limbs. There was no sensory deficit in lower extremities, and no cognitive disturbances were detected. Creatine kinase was normal. Electroneuromyogram patterns were compatible with the diagnosis of bilateral axonal injury. Clinical course after normobaric oxygen and rehabilitation therapy was marked by complete recovery of neurological disorders. Peripheral neuropathy is an unusual complication of CO intoxication. Motor peripheral neuropathy involvement of bilateral lower extremities is exceptional. Various mechanisms have been implicated, including nerve compression secondary to rhabdomyolysis, nerve ischemia due to hypoxia, and direct nerve toxicity of carbon monoxide. Prognosis is commonly excellent without sequelae. Emergency physicians should understand the possible-neurologic presentations of CO intoxication and make a proper decision regarding treatment.

A Sensorimotor Polyneuropathy Caused by Chronic Phenytoin Therapy: Dong-Chul Han, Hyeon-Mi Park, Dong-Jin Shin, Yeong-Bae Lee; J Korean Soc Clin Toxicol. 2006;4(2):128-130. Published online December 31, 2006

Abstract PDF: Phenytoin has been used globally as an effective anticonvulsant. Among its adverse effects, peripheral neuropathy including polyneuropathy has sometimes been reported. We report a case of sensorimotor polyneuropathy associated with high serum level and long-term phenytoin therapy. A 29-year-old male presented with motor weakness in all extremities. He was treated with phenytoin (400 mg/day) for about eight years because of generalized tonic clonic seizure. During none conduction assessment, sensorimotor polyneuropathy was discovered.

Peripheral Neuropathy after Inhalation of Mercury: Hong Jae Chae, Hyoung Jai Lee, Sei Won Oh, Sung Kwan Lee, Jai-Dong Moon; J Korean Soc Clin Toxicol. 2004;2(1):20-22. Published online June 30, 2004

Abstract PDF: Acute mercury inhalation poisoning is a rare cause of acute peripheral neuropathy. A 44-year-old female inhaled the fume from heating mercury to treat her palmar dermatitis. For 4 days, this procedure was done for 2-3 minutes after each meal. She subsequently complained flu like symptoms, such as headache, toothache, myalgia and arthralgia. She was admitted for 9 days and then symptoms disappeared. About 3 weeks after exposure, both knee pain developed and then she could not walk. To treat mercury intoxication, she was referred to our hospital. At that time, initial laboratory data were within normal limits, but blood and urinary mercury level were 5.6 11$mu$g/dl, 132.8 $mu$g/L. After treatment with D-penicillamine for 7 days, blood and urinary mercury level were 3.9 1$mu$g/dl, 177.3 $mu$g/L. During the following 1 month, both leg symptoms remained. Nerve conduction studies were performed, both leg sensory nerve amplitude decreased. These findings were suggestive of peripheral polyneuropathy.

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