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Reprinted from Guillain-Barré Syndrome Support Group Miller Fisher syndrome (MFS) is also known as:
Related conditions are:
In 1956, Charles Miller Fisher, a Canadian whose specialization was stroke, described three patients with acute external ophthalmoplegia (eye paralysis), sluggish pupil reflexes, ataxia (lack of balance) and areflexia (absent tendon reflexes). Two patients had no weakness; the other had a facial palsy and possible weakness. All three recovered spontaneously. Because some patients with GBS had ophthalmoplegia and there were other similarities, Dr Fisher concluded that these patients had suffered a disorder akin to GBS. [Fisher CM. Syndrome of ophthalmoplegia, ataxia and areflexia. N Engl J Med 1956;255:57-65] Pure Miller Fisher syndrome (without generalised weakness) is rare. Electrodiagnostic abnormalities found in all patients are characteristic of an axonal neuropathy or a neuronopathy with predominant sensory nerve changes in the limbs and motor damage in the cranial nerves. [Fross RD, Daube JR. Neuropathy in the Miller Fisher syndrome: clinical and electrophysiologic findings. Neurology 1987 Sep;37(9):1493-1498] Patients described as having Miller Fisher syndrome often have a neuropathy that overlaps with GBS and demonstrate generalised weakness, sometimes paralysis, as additional symptoms. It was sometimes proposed the Miller Fisher syndrome was caused by brainstem encephalitis. It is true that the syndrome can be mimicked by a brainstem lesion, but typical cases of Miller Fisher syndrome rarely show any evidence of brainstem abnormalities either radiologically or during post-mortem examination. When clinical or radiological brainstem abnormalities are found, the condition may be referred to as Bickerstaff's syndrome or Bickerstaff's brainstem encephalopathy (or encephalitis) (BBE). Research in recent years has concentrated in identifying the antibodies that are thought to be responsible for GBS etc. It has been confirmed clinically that MFS, GBS with ophthalmoplegia, BBE, and another condition called acute ophthalmoparesis* are closely related, forming a continuous range. This is supported by immunological findings with the antibody anti-GQ1b IgG being the common factor. [J Neurol Neurosurg Psychiatry 2001 Jan;70(1):50-55] This antibody is not found in other GBS patients so it is thought that it is responsible for the ophthalmoplegia. *Acute ophthalmoparesis (AO) is characterised by acute onset of paresis of the extraocular muscles without ataxia or areflexia. Although the efficacy has not been clinically proven, treatment of Miller Fisher syndrome is much the same as 'classic' GBS though the different symptoms require modified management with emphasis on the eyes. Intravenous immunoglobulin or plasma exchange treatment is likely in all but the mildest cases. The chances of recovery are good. What is Guillain's Barre Syndrome? Guillain-Barré (Ghee-yan Bah-ray) Syndrome, also called acute inflammatory demyelinating polyneuropathy and Landry's ascending paralysis, is an inflammatory disorder of the peripheral nerves - those outside the brain and spinal cord. It is characterized by the rapid onset of weakness and, often, paralysis of the legs, arms, breathing muscles and face. GBS is the most common cause of rapidly acquired paralysis in the United States today, affecting one to two people in every 100,000.
The disorder came to public attention briefly when it struck a
number of people who received the 1976 Swine Flu vaccine. It
continues to claim thousands of new victims each year, striking any
person, at any age, regardless of gender or ethnic background.
How is GBS Diagnosed? Quite often, the patient's symptoms and physical exam are sufficient to indicate the diagnosis. The rapid onset of (ascending) weakness, frequently accompanied by abnormal sensations that affect both sides of the body similarly, is a common presenting picture. Loss of reflexes, such as the knee jerk, are usually found. To confirm the diagnosis, a lumbar puncture to find elevated fluid protein and electrical test of nerve and muscle function may be performed.
How is GBS Treated? Because progression of the disease in its early stages is unpredictable, most newly diagnosed patients are hospitalized and usually placed in an intensive care unit to monitor breathing and other body functions.
Care involves use of general supportive measures for the
paralyzed patient, and also methods specifically designed to
speed recovery, especially for those patients with major
problems, such as the inability to walk. Plasma exchange (a
blood "cleansing" procedure) and high dose intravenous
immune globulins are often helpful to shorten the course of
GBS.
What Causes GBS? The cause is not known. Perhaps 50% of cases occur shortly after a microbial (viral or bacterial) infection such as a sore throat or diarrhea. Some theories suggest an autoimmune mechanism, in which the patient's defense system of antibodies and white blood cells are triggered into damaging the nerve covering or insulation, leading to weakness and abnormal sensation. Click here for more info on GBC
Reprinted from the Mayo Clinic Web Site, by Mayo Clinic staff Encephalitis means "inflammation of the brain," but it usually refers to brain inflammation caused by a virus. This severe and potentially life-threatening disease is rare. Encephalitis takes two forms, categorized by the two ways that viruses can infect your brain:
The primary form of the disease is more serious, while the secondary form is more common. But because of the milder nature of secondary encephalitis, doctors actually see more cases of primary encephalitis.
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