Abstract
The Miller Fisher variant is an uncommon but well known syndrome being described as a triad of areflexia, ataxia and complex ophthalmoplegia. It is characterized by antibodies against myelin that affects peripheral nerves, extraocular muscles and Schwann cells. Anti-ganglioside antibodies have been recognized in disease pathogenesis and decreasing antibody production is the mainstay of treatment. The course is usually benign with improvement after immunomodulation. This case report describes the approach to a patient suspected of having a demyelinating disorder. It delineates the subsets of immune mediated neuropathies in evaluating the diagnosis and emphasizes the need for early therapeutic intervention in achieving a good clinical outcome.
Highlights
Anti GQ1b antibodies target peripheral nerves, activate complement and cause conduction block
The clinical triad of ophthalmoplegia, ataxia and areflexia is in keeping with the Miller Fisher Syndrome discovered in 1956 [1]
The patient had a history of a recent viral infection and subsequently developed ophthalmoplegia, ataxia and areflexia
Summary
Anti GQ1b antibodies target peripheral nerves, activate complement and cause conduction block. This leads to an immune mediated neuropathy affecting extraocular muscles. Miller Fisher syndrome (areflexia, ataxia and complex ophthalmoplegia) encompasses a spectrum of immune mediated motor and sensory neuropathies. Clinical examination revealed an ataxic gait, areflexia and a complex ophthalmoplegia consistent with the clinical triad of Miller Fisher Syndrome. The hallmark of this syndrome is the presence of anti GQ1b antibodies. This condition usually has an excellent prognosis with treatment as it usually follows an uncomplicated course without remissions.
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