GAD-65 Antibody Mimics Cocaine Induced Limbic Encephalopathy

Tyler G Chin, J. Colombo, S. Soloway
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Abstract

Glutamic Acid Decarboxylase 65-kilodalton isoform (GAD-65) is associated with cocaine induced limbic encephalopathy mimicking GAD-65 limbic encephalopathy in humans. A 20-year-old white female presented with a clinical picture of a limbic encephalopathy and a positive ANA. She has a hypermobility disorder with dysautonomia with POTS. Her workup revealed a GAD-65 antibody greater than 250 nmol/L, a normal lumbar puncture, and a normal brain MRI. Her GAD-65 associated limbic encephalopathy was treated with IVIG 2 g per kilogram per month. She received three treatments with no improvement. Due to arthralgias, a soft tissue rheumatic pain, she was referred to pain management. The patient admitted to using cocaine. Her IVIG was discontinued. A repeat test for GAD-65 antibody remained elevated. After a stint in drug rehabilitation and cessation of cocaine her symptoms of limbic encephalopathy abated and GAD-65 normalized. This is the 1st case report of GAD-65 antibody mimicking cocaine induced limbic encephalopathy. While GAD65 related autoimmune neuropathies are rare, one must consider cocaine toxicity as a mimic of both autoimmunity and immune neuropathies, including the spectrum of GAD-65-related disorders.
GAD-65抗体模拟可卡因诱导的边缘脑病
谷氨酸脱羧酶65千顿异构体(GAD-65)与可卡因诱导的模拟人类GAD-65边缘脑病的边缘脑病有关。一名20岁白人女性,临床表现为边缘脑病和ANA阳性。她有多动障碍和自主神经障碍。她的检查显示GAD-65抗体大于250 nmol/L,腰椎穿刺正常,脑部MRI正常。她的GAD-65相关边缘脑病接受IVIG治疗,每公斤每月2克。她接受了三次治疗,但没有好转。由于关节痛,一种软组织风湿性疼痛,她被转介到疼痛管理。病人承认使用可卡因。她的IVIG停止了。重复测试GAD-65抗体仍然升高。经过一段时间的戒毒和停止使用可卡因后,她的边缘脑病症状减轻,GAD-65恢复正常。这是第一例GAD-65抗体模拟可卡因诱导的边缘脑病的报告。虽然GAD65相关的自身免疫性神经病变很少见,但我们必须将可卡因毒性视为自身免疫和免疫神经病变的模拟物,包括与GAD65相关的疾病谱系。
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