Miller Fisher Syndrome

Miller Fisher Syndrome

The Miller Fisher syndrome is characterized by weakness in the legs that gradually, over a period of time, spreads to the upper limbs as well. The earliest record of the disorder dates back to 1859, by French physician Jean Landry. The complete loss of reflexes of the deep tendon results in paralysis and affects the patient's quality of life severely. The condition can be treated via plasmapheresis or the administration of intravenous immunoglobulins. Supportive care plays a very important role in the treatment plan adopted for the syndrome. With correct and timely treatment the condition can be totally cured and patients are known to regain complete functional capacity of the limbs. In the face of neglect, death occurs, subsequent to the onslaught of acute dysautonomia and pulmonary complications.

What is the Miller Fisher Syndrome?

This syndrome is the result of an immune response to foreign antigens. The infectious agents attack the host nerve tissues and generate a kind of antigenic mimicry. The primary targets are gangliosides or the complex glycosphingolipids that are present within nerve tissues. The autoimmune attack results in the inflammation of myelin, on the peripheral nerves and the resultant blockage ripples on in the form of muscle paralysis. The sensory or autonomic disturbances can be life-threatening, if not addressed in time. At times, the axonal function is not affected and recovery is rapid in the presence of remyelination. However, in the case of a severe attack, axonal degeneration can only be reversed by a clinically targeted axonal regeneration.

Risks attached to the Miller Fisher Syndrome

With the occurrence of pulmonary complications, death is the fatality caused by the immunopathological reaction. Serum sickness can also manifest, damaging nerve conditions and that of the peripheral neuritis. In fact, serum sickness is a manifestation of a delayed allergic response. This autoimmune disorder is associated with a sudden loss of appetite, discomfort due to nausea and vomiting, an acute stomach pain and persistent low-grade fever. The brain involvement triggers lethargy and migraines.

Signs and Symptoms

The Miller Fisher syndrome manifests in the form of the following signs and symptoms:

• Ascending weakness in the lower limbs.
• Buckling of legs, with or without numbness or tingling.
• Bulbar weakness.
• Difficulty in swallowing.
• Respiratory difficulties.
• Eye movement abnormalities.
• Sensory loss of position, pain and temperature.
• Bladder dysfunction.
• Orthostatic hypotension.
• Cardiac arrhythmia.

Diagnosis and Treatment

The diagnosis of the Miller Fisher syndrome is usually conducted via CSF or cerebrospinal fluid testing, electromyography or EMG and nerve conduction study or NCS. These tests are conducted to assess and verify the observed symptoms. The treatment options are based on the clinical findings recorded via these dedicated mediums. At the very helm of the treatment options is dedicated supportive care. It is very important to monitor all vital limb functions, any sign of respiratory failure that usually follows the paralysis of the diaphragm and early intubation. The medication used in the treatment of the Miller Fisher syndrome includes high-dose immunoglobulins given intravenously. Plasmapheresis and physical therapy are the other treatments delivered to address motor symptoms. Rehabilitation, in the case of a Miller Fisher patient, includes monitoring of physical movement to regain lost functions. Occupational and Speech and Language therapy are usually adopted after tracheostomy.

Most Miller Fisher patients display signs of recovery within a month. Research reveals that approximately 80% patients enjoy a complete recovery within a year. In the face of neglect, areflexia, proximal motor damage and sensory axonal damage, unsuccessful axonal regeneration and even death can occur. Approximately 5% patients display relapses and are then categorized in the CIDP (chronic inflammatory demyelinating polyneuropathy) classification of the disorder.