What is Miller Fisher Syndrome: Causes, Symptoms, Treatment, Diagnosis, Prognosis
What is Miller Fisher Syndrome?
Miller Fisher syndrome (also known as Fisher’s syndrome, Cranial variant of Guillain-Barré syndrome and Cranial variant of GBS) is an acquired disease of the nerves and is a rare disease. Miller Fisher syndrome is considered to be a variant of Guillain-Barré syndrome.
Why the Name Miller Fisher Syndrome?
Miller Fisher Syndrome is named after Dr. C. Miller Fisher who had first described this condition as a limited variant of Guillain-Barré syndrome (GBS).
What Causes Miller Fisher Syndrome?
The exact cause of Miller Fisher Syndrome is not clear. The waddling gait of the patient is thought to occur as a result of loss of myelin around the nerves. There can also be involvement of other sensory fibers, autonomic and motor fibers which innervate the muscles which move the face and eyes along with controlling the function of the eye, pupil and bladder. There is evidence of auto-immune mechanism where the triggering/preceding infection stimulates the production of an antibody which reacts to sugar found on both the surface of peripheral nerve and the infectious organism causing demyelination and loss of nerve function.
What are the Symptoms of Miller Fisher Syndrome?
The characteristic symptom of Miller Fisher syndrome is abnormal muscle coordination where the patient’s walk becomes clumsy or sloppy; absence of deep tendon reflexes (ankle jerk and knee jerk); and paralysis of the muscles of the eye where the patient also experiences blurry or double vision, facial weakness and droopy eyelids. As Miller Fisher syndrome is a variant of Guillain-Barré syndrome, the symptoms of Miller Fisher syndrome are also preceded by a viral illness just as in Guillain-Barré syndrome. Other symptoms of Miller Fisher syndrome include respiratory failure and generalized muscle weakness.
How is Miller Fisher Syndrome Diagnosed?
The majority of the patients suffering from Miller Fisher syndrome will have a unique antibody which is characteristic of this disease. Other than this, the characteristic symptoms of Miller Fisher Syndrome such as of rapid deterioration of the vision and difficulty in walking which are preceded by a diarrheal illness or viral illness helps with the diagnosis. The patient also has difficulty in swallowing, slurred speech and abnormal facial expression with loss of ability to whistle and smile. Pure Fisher syndrome occurs rarely. Most of the patients develop the characteristic widespread weakness of GBS.
Neurological exam reveals poor coordination and balance of the hands along with loss of deep tendon reflexes. There is weakness of the eye muscles, facial muscles with dilated pupils. Some patients also have a decreased gag reflex on stimulation of the throat.
Nerve conduction tests can be done which reveal decreased nerve activity, which transmit sensory information to the brain and spinal cord.
Magnetic Resonance (MRI) Imaging of the spinal cord and brain are often normal.
Lumbar Tap: There is elevation of spinal fluid protein.
How is Miller Fisher Syndrome Treated? And What Is The Recovery Period From Miller Fisher Syndrome?
Treatment for Miller Fisher syndrome is similar to that of Guillain-Barré syndrome. Miller Fisher syndrome is often a short lived disorder which is good news for patients suffering from it. This condition progresses for a few weeks after which there is an improvement seen. The symptoms of MFS can also indicate the beginning of GBS where the patient experiences breathing difficulties and needs to be hospitalized and kept under observation.
Patients suffering from pure MFS usually recover within 2-3 months. Rarely, in patients who have symptoms which cause impairment of function, other treatments which neutralize or limit immune system activity are considered such as plasmapheresis or intravenous immunoglobulin (IVIg).
What is the Prognosis of Miller Fisher Syndrome?
For majority of the patients suffering from Miller Fisher syndrome, the prognosis is good. Many patients recover within 2 to 4 weeks of the onset of symptoms and are almost completely normal within 6 months. There are some patients who are left with residual deficits. Rarely there may be a relapse of this disease.