Guillain-Barre syndrome after heat stroke

医学 格林-巴利综合征 冲程(发动机) 麻醉 横纹肌溶解症 彗差(光学) 内科学 免疫学 物理 机械工程 光学 工程类
作者
G. Pfeiffer,William M. Steffen
出处
期刊:Journal of Neurology, Neurosurgery, and Psychiatry [BMJ]
卷期号:66 (3): 408-408 被引量:11
标识
DOI:10.1136/jnnp.66.3.408
摘要

Heat stroke is usually not listed among the events triggering Guillain-Barre syndrome. Two cases of a Guillain-Barre syndrome-like polyneuropathy after heat stroke are on record, although without reference to electroneurography.1 We report on a patient, who developed Guillain-Barre syndrome 10 days after severe heat stroke. He had electrophysiological evidence of demyelination, increased CSF protein, and high anti-GM1 antibodies. Heat stroke activates the immune system by cytokine release,2 opens the blood-nerve barrier, and exposes peripheral nerve antigens and thus may induce Guillain-Barre syndrome, as suggested by results from our patient. A 28 year old drug addict was using anticholinergic drugs against sweating during levomethadone withdrawal. He was found unresponsive in a public garden on a hot summer day (ambient temperature 32°C) after ingesting cocaine. His core temperature was 42.5°C at admission. He was in deep coma with wide unreactive pupils and without corneal and pharyngeal reflexes. Tachypnoea had induced hypocapnia. Blood pressure was 85/30 mm Hg and heart rate was 165/min. He developed disseminated intravascular coagulation, thrombopenia below 10 000 MRD/ml, and metabolic acidosis. Creatine kinase rose from 128 to 751 U/l. Leucocytes and C reactive protein remained normal. After 4 days of coma he was transferred to …
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