The association of ophthalmoplegia, ataxia and areflexia was described by M
iller Fisher in 1956. it is postulated as a variant of the Guillain Barre s
yndrome. We report 10 Miller Fisher syndrome patients admitted in an intens
ive care unit between June 1990 and February 1999 who were selected accordi
ng to clinical criteria of Ropper and Wijdicks. All patients had motor and
sensory nerve conduction studies and electromyography, nine had visual and
brainstem auditory evoked potentials and two had short latency somatosensor
y evoked potentials.
Peripheral neuropathy was found in all patients. AN had sensory nerve chang
es and some were severe. Motor nerve conduction abnormalities were observed
in 7 only cases with moderate increase of F latency in 3 cases and compoun
d muscle action potential reduction in 3 other cases. in the last case, mot
or conduction abnormalities was more severe, caracterized by conduction vel
ocity slowing in both distal and proximal sites and by temporal dispersion
of action potentials.
All brainstem auditory evoked studies were normal. In 4 patients, MRI studi
es were normal. These data support that brainstem is preserved in MFS. Only
one patient had visual evoked potential abnormalities. Optic neuropathy is
debated in Miller Fisher and in Guillain Barre syndrome.
As a conclusion, in MFS peripheral neuropathy is always present with severe
sensitive changes and moderate motor changes (This is different as compare
d to Guillain Barre syndrome according to electrophysiological data). We di
d not find involvement of brainstem in our patients with Miller Fisher synd
rome.