It is a rare disorder of the nervous system characterized by abnormal muscle coordination.
He also has ocular muscle weakness and an absence of tendon reflexes.
Miller Fisher syndrome is a subgroup of a more common nervous disorder. It is a rare self-limited variant of Guillain Barré syndrome; it is an anti-GQ1b immunoglobulin G antibody syndrome that affects the central and peripheral nervous system.
The anti-GQ1b immunoglobulin G antibody is a specific marker for Miller Fisher syndrome and related disorders, such as Guillain Barré syndrome with ophthalmoplegia, atypical Miller Fisher syndrome characterized by acute ophthalmoplegia or acute ataxia, and Bickerstaff brainstem encephalitis.
The antiGQ1b immunoglobulin G antibody may play some critical roles in the pathogenesis of Miller Fisher syndrome and related disorders.
Possible mechanisms are currently being discussed; the molecular mimicry between an infectious agent of the previous infection and the ganglioside may be a mechanism of antibody production.
Plasmapheresis or intravenous immunoglobulin therapy may be warranted for Miller Fisher syndrome, Bickerstaff brainstem encephalitis, and Guillain Barré syndrome with ophthalmoplegia.
It is an acute neuromuscular polyneuropathic condition, causing ascending paralysis with a classically presenting triad of ophthalmoplegia, ataxia, and areflexia.
Researchers first described the clinical triad in 1932.
Two decades later, Canadian specialist Charles Miller Fisher was the first to publish a report in 1956 describing the clinical findings and defining the condition as a limited form of Guillain Barré syndrome.
Causes of Miller Fisher syndrome
Both Guillain Barré syndrome and Miller Fisher syndrome are caused by a viral infection, most commonly the flu or stomach virus, and in some cases by bacteria, but it has not been possible to point out that they are the only causes of the disease.
Symptoms usually begin to appear one to four weeks after infection with the virus.
No one is entirely sure why Guillain Barré syndrome and Miller Fisher syndrome develop in response to these common illnesses.
Some researchers speculate that viruses may somehow change the structure of cells in the nervous system, causing the body’s immune system to recognize and eliminate them as foreign.
The nerves cannot transmit signals well when this happens, leading to muscle weakness, a common feature of both diseases.
Anyone can develop Miller Fisher syndrome, but some are more prone than others, and these include:
- Men: Men are twice as likely to have Miller Fisher syndrome as women.
- Middle-aged people: The mean age of development of Miller Fisher syndrome is 43.6 years.
- People Taiwanese or Japanese: 19 percent of Miller Fisher syndrome cases in Taiwan, which jumps to 25 percent in Japan.
Symptoms occur over several days, often in winter and spring, usually after a viral infection, and patients often experience diplopia as one of the first symptoms.
The disease destroys the immune system of the myelin sheaths of the peripheral nerves, causing the absence of this lipid substance that covers the axons of some neurons, limiting the effective transmission of nerve impulses and a decrease in their speed, as well as alterations in the central nervous system.
The GBQ1b anti-ganglioside immunoglobulin antibody is an antibody that seems to be particularly associated with the presence of ophthalmoplegia. It has been detected in the diagnosis of Miller Fisher syndrome.
The list of signs and symptoms mentioned in various sources for Miller Fisher syndrome causes symptoms that are listed below and are associated with muscle coordination and motor skills, such as ataxia, areflexia, and ophthalmoplegia:
It is the loss of motor coordination and presents as generalized muscle weakness, weakened facial muscles, an inability to smile or whistle, rambling speech, decreased gag reflex, respiratory failure, and wobbly gait.
Ophthalmoplegia and ataxia are frequently the first signs of the disease. Ophthalmoplegia is a total or partial ocular motility paralysis.
This sign appears third and primarily in the extremities; it is an absence of reflex movements or a diminished reflex when the knee or ankle is touched.
It should be noted that the symptoms of Miller Fisher syndrome generally refer to various symptoms that a patient may feel. Still, there are signs of Miller Fisher syndrome that can refer to those signs that only a doctor can detect.
When a patient has intermittent exotropia and fixed mydriatic pupils, and the neurological examination is abnormal, it is time to think about Guillain Barré syndrome, specifically Miller Fisher syndrome.
While Guillain Barré syndrome tends to produce muscle weakness in the lower body and works upward, Miller Fisher syndrome generally begins with weakness in the eye muscles and progresses downward.
Diagnosis of Miller Fisher syndrome
The first thing the doctor will do is take a complete medical history. To distinguish Miller Fisher syndrome from other neurological disorders, the doctor will ask:
- When the symptoms started.
- How quickly the muscle weakness progressed.
- If you were sick in the weeks before symptoms began.
If the doctor suspects Miller Fisher syndrome, he will order a lumbar puncture.
This is a procedure in which a needle is inserted into the lower back to remove the cerebrospinal fluid.
Many people with Miller Fisher syndrome have elevated proteins in their spinal fluid.
A blood test looking for Miller Fisher syndrome antibodies, such as proteins made by the body and used by the immune system to fight infection, can also help confirm the diagnosis.
Treatment Options for Miller Fisher Syndrome
There is no cure for Miller Fisher syndrome. The goal of treatment is to decrease the severity of symptoms and speed recovery.
The two primary forms of treatment are immunoglobulin therapy and plasmapheresis. These are the same treatments used for Guillain Barré syndrome.
This treatment consists of the administration of immunoglobulins intravenously.
This is a procedure in which antibodies are removed from the blood by filtration.
Both procedures seem to be equally effective in improving the disorder since they help neutralize the effects of pathological antibodies and reduce inflammation, which is what causes damage to the nervous system,
However, intravenous immunoglobulin therapy is easier to administer and carries fewer risks.
Sometimes sequelae may remain, so physical therapy may also be recommended to help the affected muscles regain strength.
Complications of Miller Fisher syndrome
Symptoms of Miller Fisher syndrome tend to progress for several weeks, stagnate, and then begin to improve.
Typically, Miller Fisher syndrome symptoms begin to improve within four weeks. Most people recover within six months, although some residual weakness may persist.
Muscle weakness caused by Miller Fisher syndrome can affect the heart and lungs, leading to heart and respiratory problems, requiring hospitalization and careful medical supervision during the course of the disease.
In the most severe disease cases, it can cause death due to the modification in the regular activity of the cardiac and respiratory systems.
The perspective of Miller Fisher syndrome
Miller Fisher syndrome is a low condition that is fortunately short-lived.
While there can be severe complications, such as breathing problems, most people receive successful treatment and make full or near-complete recoveries.
Relapses are rare, occurring in less than 3 percent of cases.
Talking with your doctor at the first sign of symptoms, early diagnosis, and treatment can help speed recovery.