Cerebellar ataxia and epilepsy with anti-GAD antibodies: treatment with IVIG and plasmapheresis. (13th January 2014)

• Record Type: Journal Article
• Authors: Georgieva, Zoya; Parton, Matthew
• Is Part Of: BMJ case reports. Volume 2014
• Publication Date: 2014-01-13
• Subjects: Medicine -- Case studies -- Periodicals; 610.5
• DOI: 10.1136/bcr-2013-202314
• Languages: English
• ISSNs: 1757-790X

Abstract

Abstract : Glutamic acid decarboxylase autoantibody (GAD-65) catalyses glutamate conversion into γ-aminobutyric acid (GABA) in the central nervous system and in the pancreatic β cells. Antibodies targeting GAD-65 are of uncertain pathogenic significance and occur in stiff person syndrome, cerebellar ataxia, epilepsy, limbic encephalitis and combinations thereof and diabetes mellitus. A 45-year-old man with a cerebellar gait ataxia, dysmetria, nystagmus and mild cerebellar dysarthria was diagnosed with insulin-dependent diabetes mellitus a year after the onset of neurological symptoms. He also developed complex and tonic-clonic seizures, resistant to anticonvulsant medication and deteriorated cognitively. Blood and cerebrospinal fluid serology, and imaging supported the diagnosis of GAD-65 cerebellar ataxia and epilepsy. He was treated with intravenous immunoglobulin and subsequently plasmapheresis. We report the outcome of 3 years of treatment, which resulted in the improvement of cerebellar signs (particularly gait), with some ultimate decline of efficacy.