Abstract
Fisher syndrome (FS) is characterized by triad of ataxia, areflexia, and ophthalmoplegia. To elucidate the pathophysiology of ataxia in FS, we reviewed extensively electrophysiological data of FS patients. We reviewed results of sensory nerve conduction studies, soleus H-reflex, postural body sway analysis and somatosensory-evoked potentials (SEP) in consecutive 47 FS patients. Reduction of SNAP amplitudes was only seen in 32% of the patients in routine nerve conduction studies. In contrast, the absence of soleus H-reflex was shown in 67%. 1 Hz peak of postural body sway analysis was in 57%. SEPs were abnormal in 17%. This abnormal pattern of sensory electrophysiology is characterized by predominant involvement of group 1a afferents with relatively preserved cutaneous afferents. Our findings suggest that involvement of group 1a fibers could be responsible for ataxia as well as areflexia in FS.
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