Case Report Shows MG May Occur With Rare Miller Fisher Syndrome
Myasthenia gravis (MG) may occur alongside Miller Fisher syndrome, another rare autoimmune disease also characterized by weakness of the eye muscles, a recent case report highlights.
The report emphasizes the importance of careful examination for the possibility of co-occurring autoimmune disorders when a patient shows uncommon symptoms.
“Even though only five cases of overlapping [Miller Fisher syndrome] and MG so far have been described, two different autoimmune diseases may coexist,” the researchers wrote.
Titled “Case Report: A Patient Diagnosed With Miller Fisher Syndrome and Myasthenia Gravis at the Same Time,” the report was published in the journal Frontiers in Neurology.
In MG, the body’s immune system produces self-reactive antibodies that target proteins involved in nerve-muscle communication. The acetylcholine receptors (AChR), which facilitate this communication, are the most frequent targets. The thymus, an organ critical to immune response, is thought to be involved in the production of these self-targeting antibodies.
The co-occurrence of MG — itself a rare disorder — with other rare autoimmune diseases like Miller Fisher syndrome is exceedingly uncommon. In fact, only five such cases have been reported in the literature thus far. Miller Fisher syndrome is a variant of Guillain-Barré syndrome, a disorder in which the body’s immune system attacks nerves, causing muscle weakness.
In this case report, researchers in China described the case of a patient in whom both diseases were diagnosed simultaneously.
The 58-year-old man experienced sudden dizziness, which was accompanied by slurred speech, followed by a feeling of numbness in the arms. He began choking and coughing, and having eyelid droopiness in his right eye.
An MRI brain scan done at the hospital showed no abnormalities. He was, however, admitted for further examination.
A neurological examination at the time of admission confirmed eyelid droopiness in his right eye, as well as limited eye movements in both eyes. The patient lacked deep tendon reflexes in the extremities, and showed signs of weakness in several facial muscles.
Further exams, including a brain magnetic resonance angiogram — a type of MRI that evaluates blood vessels — chest CT, and ultrasound of the carotids and vertebral arteries, all were normal. Carotid arteries are blood vessels located in the neck that supply blood to the brain and head, while vertebral arteries are blood vessels running along the spine in the neck to supply blood to the brain and spine.
Blood tests were unremarkable and there were no signs of an underlying tumor or self-reactive antibodies.
“The symptoms of the patient were more consistent with the MFS [Miller Fisher syndrome] triad,” the researchers wrote. This includes eye muscle paralysis called ophthalmoplegia, lack of muscle control or coordination, known as ataxia, and lack of deep tendon reflexes, called areflexia.
Electromyography, a procedure used to assess the health of muscles and nerve cells, was conducted six days after symptom onset and showed damage to peripheral nerves on the extremities.
Further analyses of the cerebrospinal fluid (CSF) — the fluid surrounding the brain and spinal cord — showed he was positive for autoantibodies, called anti-ganglioside antibodies. These findings confirmed the diagnosis of Miller Fisher syndrome.
The patient began treatment with immunoglobulins seven days after the onset of symptoms. The therapy, lasting five days, significantly eased his symptoms.
However, he still was experiencing other symptoms — including mild facial muscle weakness, swallowing difficulties, and muscle weakness in the neck — that are not commonly associated with Miller Fisher syndrome.
A chest CT scan showed no significant abnormalities in the thymus.
To test for the presence of MG, the patient was then given neostigmine. This medication inhibits the breakdown of acetylcholine, which should ease MG symptoms if the disease is present. Of note, acetylcholine is a signaling molecule normally released by nerve cells to promote muscle contraction.
There were no significant improvements, however. Despite this, the man underwent electromyography again for the axillary nerve, which is found in the armpit.
Results showed a decrease of about 35.8% in the nerve’s response when stimulated at a low frequency (3 Hz) and about 50.6% under a high frequency (20 Hz).
Repetitive nerve stimulation (RNS), another standard diagnostic test for MG, was performed on facial and axillary nerves within one week of admission. A decreased nerve response after electrical stimulation was confirmed by these test results.
Further analysis confirmed the presence of self-reactive antibodies targeting AChR and another muscle protein called titin, confirming the diagnosis of MG.
After a course of immunoglobulin treatment, the patient’s symptoms significantly eased. At the time of discharge, he still had numbness in both hands, but no signs of slurred speech, dizziness, and headache. His neurological symptoms also were less severe.
“Because both MG and [Miller Fisher syndrome] are rare autoimmune mediated diseases, the simultaneous diagnosis of these two diseases in one patient is a rare finding,” the researchers wrote.
“We should distinguish carefully in the differential diagnosis of neurological diseases in the future and should not ignore the overlap of diseases,” they concluded.
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