Miller Fisher syndrome (MFS), also called Fisher’s syndrome, usually begins with the rapid development, over days, of 3 problems: 1) weak eye muscles, with

double or blurred vision, and often drooping eyelids with facial weakness; 2) poor balance and coordination with sloppy or clumsy walking; and 3) on physical examination, loss of deep tendon reflexes, such as the knee and ankle jerk.

MFS is named after Dr. C. Miller Fisher who described it in 1956 as a limited variant of ascending paralysis, Guillain-Barré syndrome (GBS).

Patients typically seek medical attention because of a rapid decrease in vision over days and/or difficulty walking. These

changes are frequently preceded by a viral or diarrheal illness 1 to 4 weeks earlier. Slurred speech, difficulty swallowing and abnormal facial expression with inability to smile or whistle may also occur. Examination shows poor balance and coordination of the hands as well as loss of deep tendon reflexes and eye muscle weakness. Facial weakness, enlarged or dilated pupils and a decreased gag reflex on stimulation of the throat can be present in some patients. Tests of nerve conduction may show diminished activity of nerves that carry sensory information to the spinal cord and brain.

Magnetic resonance (MRI) or other imaging of the brain and/or spinal cord are usually normal. Spinal fluid protein is often elevated.

Pure Fisher syndrome is uncommon, with many patients going on to develop the prominent widespread weakness of GBS.

Fortunately, this disorder is often short lived, progressing for only a few weeks and then improving. MFS symptoms can signal the beginning of GBS,

with breathing difficulties, so patients are often hospitalized for observation. In pure MFS, a near full recovery typically occurs within 2-3 months. In rare cases when symptoms substantially impair function, various treatments that limit or neutralize immune system activity may be considered. These include high dose immune globulins or plasma exchange.

The cause(s) of Fisher’s syndrome is not completely understood. The waddling, duck-like gait is likely due to the loss of a fat rich insulating material called myelin around nerves,

designated as 1A, that innervate the major sensory organ of muscle called the muscle spindle. These fibers send information to the spinal cord about the speed and extent of muscle stretch without which skeletal muscles can not properly function. As the clinical course progresses, other sensory fibers can be involved as well as motor and autonomic fibers that respectively innervate muscles that move the eyes and face and control function of the eye, pupil and the bladder. Multiple lines of evidence support an auto-immune mechanism in which the preceding/triggering infection stimulates

Honorary Board

Rachel Chagall*	Marjorie H. Downey*
Andy Griffith*	Joseph Heller*#

Executive Director

Estelle L. Benson

Officers

Sara Voorhees Pessel,* President

Joel S. Steinberg, MD, PhD,* Vice President

Sue D. Baier,* Secretary

Henry Friedman,* Treasurer

Jerry R. Jones, Treasurer

Board of Directors

Robert Benson, CLU, ChFC*	Patricia H. Blomkwist-Markens*
Patricia Bryant*	Thomas S. Butler
Elizabeth B. Emerson	Thelma Gifford, RN*
Susan Keast*	Philip H. Kinnicutt
Kim Koehlinger*	Harriette Lion
Glennys Sanders*	Laura E. Stegossl, Esq.

Medical Advisory Board

Barry G. W. Arnason, MD

Arthur K. Asbury, MD

Richard J. Barohn, MD

Mark J. Brown, MD

Kopel Burk, MD*

David Cornblath, MD

Marinos C. Dalakas, MD

Jonathan Goldstein, MD

Kenneth C. Gorson, MD

Michael G. Graves, MD

John W. Griffin, MD

Angellka F. Hahn, MD

Hans-Peter Hartung, MD

Thomas L. Hedge, Jr., MD*

Prof. R.A.C. Hughes

Jonathan S. Katz, MD

Carol Lee Koski, MD

Richard A. Lewis, MD

Robert Lisak, MD

Robert G. Miller, MD

Gareth J. Parry, MD

Allan H. Ropper, MD

John T. Sladky, MD

Joel S. Steinberg, MD, PhD*

Pieter A. van Doorn, MD

Prof. Hugh J. Willison, PhD

*Former GBS or CIDP patients

# Deceased