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September 1983

Proposed Mechanism of Ataxia in Fisher's Syndrome

Author Affiliations

From the Department of Neurology (Drs Ropper and Shahani), Neurological/Neurosurgical Intensive Care Unit (Dr Ropper), and Clinical Neurophysiology Laboratory (Dr Shahani), Massachusetts General Hospital, Boston.

Arch Neurol. 1983;40(9):537-538. doi:10.1001/archneur.1983.04050080037004

• A patient with Fisher's variant of Guillain-Barré syndrome had severe limb ataxia. Joint position sense was diminished proximally but normal distally. In contrast, muscle proprioceptive function, studied electrophysiologically by recording silent periods in proximal muscles, appeared to be normal. A disparity between proprioceptive information from muscle spindles and kinesthetic information from joints and other proprioceptors may be a mechanism of ataxia, based solely on abnormalities of peripheral nerve function. A CNS lesion is, therefore, not necessary to explain cerebellar ataxia in Fisher's syndrome.

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