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Case Reports in Neurological Medicine
Volume 2016 (2016), Article ID 3431849, 3 pages
Case Report

Miller-Fisher Syndrome: Are Anti-GAD Antibodies Implicated in Its Pathophysiology?

3rd Department of Neurology, Medical School, Aristotle University of Thessaloniki, 57010 Thessaloniki, Greece

Received 13 March 2016; Accepted 11 April 2016

Academic Editor: Norman S. Litofsky

Copyright © 2016 Ioannis E. Dagklis et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Miller-Fisher syndrome (MFS) is considered as a variant of the Guillain-Barre syndrome (GBS) and its characteristic clinical features are ophthalmoplegia, ataxia, and areflexia. Typically, it is associated with anti-GQ1b antibodies; however, a significant percentage (>10%) of these patients are seronegative. Here, we report a 67-year-old female patient who presented with the typical clinical features of MFS. Workup revealed antibodies against glutamic acid decarboxylase (GAD) in relatively high titers while GQ1b antibodies were negative. Neurological improvement was observed after intravenous gamma globulin and follow-up examinations showed a continuous clinical amelioration with simultaneous decline of anti-GAD levels which finally returned to normal values. This case indicates that anti-GAD antibodies may be associated with a broader clinical spectrum and future studies in GQ1b-seronegative patients could determine ultimately their clinical and pathogenetic significance in this syndrome.