Journal
MUSCLE & NERVE
Volume 26, Issue 6, Pages 845-849Publisher
WILEY
DOI: 10.1002/mus.10246
Keywords
anti-GQ1b antibody; Bickerstaff brainstem encephalitis; Bickerstaff encephalitis; blink reflex; Fisher syndrome; nerve conduction study; somatosensory evoked potential
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We describe a 27-year-old woman who showed the clinical triad of Fisher syndrome (ophthalmoplegia, ataxia, and areflexia), a disturbance of consciousness, facial diplegia, and hemisensory loss. Her serum was positive for anti-GQ1b immunoglobulin G (IgG) antibody. The electroencephalographic findings (diffuse slow activity), median somatosensory evoked potential (absent cortical N20 with normal cervical N13), and blink reflex studies (absent R2) suggested central dysfunction, whereas results of facial nerve conduction studies (low amplitudes of compound muscle action potentials), F-wave and H-reflex studies (absent F-waves and soleus H-reflexes), and brainstem auditory evoked potentials (prolongation of wave I latency) suggested peripheral abnormalities. This case supports the hypothesized continuity between Fisher syndrome and Bickerstaff brainstem encephalitis. These two conditions may represent a single autoimmune disease mediated by anti-GQ1b antibody, usually involving the peripheral and occasionally the central nervous systems. (C) 2002 Wiley Periodicals, Inc.
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