In March 2008, while vacationing, I began experiencing strange onset of symptoms.
I noticed that my jaw would start to tire (the muscles in my jaw and mouth weakened) after about a minute of so, while chewing food and speaking. Similarly, I began having trouble controlling the movement of my tongue. I attributed this odd behavior jaw to general a cold, brushed it off, and waited to see if the symptoms persisted after I got back home.
Upon retuning back to Toronto, my symptoms became oddly worse – I had little to no jaw/tongue muscle power – I could only manage to speak or chew for about 2s at a time and had to rest my jaw/tounge to regain any muscle use. Moreover, I cold not lift my neck up from a horizontal position.
Soon thereafter, I a had several choking episodes as my throat muscles stopped firing as well.
Well, I was terrified and suspected everything from stroke, to seizures.
After 10 separate diagnoses in-and-out of various hospitals, clinics and specialist, I had no answer. I had lost 20lbs in 3 weeks as I was on a liquid diet, and I felt exhausted and dejected. What should I do next? What ever was wrong with me eluded common diagnosis.
On April 2008, I walked into the emergency wing at Toronto General Hospital looking for answers – God bless Toronto General for savng my life in time…
Over the past 3 years I have been on various dosages of Prednisone
(http://www.drugs.com/search.php?searchterm=Mestinon&is_main_search=1) and Mestinon (http://www.drugs.com/prednisone.html) to manage the various symptoms of Myesthenia Gravis.
For about 1 year, post thymectomy, I was relatively symptom free and required a low dose of Predisone and Mestinon. It was really quite amazing, the thymectomy had reduced my Predisone intake from 60mg to 5mg and Mestinon from 12 x 60mg to 4 x 60mg.
Myesthenia is a disease which can go into , or come out of, remission of symptoms without warning .
Well, after about a year my symptoms returned – focused in the bulbar area – the neck, mouth, eye and throat area.
So, my Neurologist increased the dosages accordingly – my symptoms started to get better for about 6 months, at which point we decide start to decrease medications. Again, symptoms remained stable for about 3 months but them flared up again.
It is because of the relatively unreliable effect of Prednisone and Mestinon that the decision to shift to the immuno suppresant IMURAN was made by my Neurologist (http://www.drugs.com/search.php?searchterm=Imuran&is_main_search=1)
Myasthenia Gravis comes from the Greek and Latin words meaning “grave muscular weakness.” The most common form of MG is a chronic autoimmune neuromuscular disorder that is characterized by fluctuating weakness of the voluntary muscle groups. The prevalence of MG in the United States is estimated to be about 20/100,000 population. However, MG is probably under diagnosed and the prevalence may be higher. Myasthenia Gravis occurs in all races, both genders, and at any age. MG is not thought to be directly inherited nor is it contagious. It does occasionally occur in more than one member of the same family.
The voluntary muscles of the entire body are controlled by nerve impulses that arise in the brain. These nerve impulses travel down the nerves to the place where the nerves meet the muscle fibers. Nerve fibers do not actually connect with muscle fibers. There is a space between the nerve ending and muscle fiber; this space is called the neuromuscular junction.
When the nerve impulse originating in the brain arrives at the nerve ending, it releases a chemical called acetylcholine. Acetylcholine travels across the space to the muscle fiber side of the neuromuscular junction where it attaches to many receptor sites. The muscle contracts when enough of the receptor sites have been activated by the acetylcholine. In MG, there is as much as an 80% reduction in the number of these receptor sites. The reduction in the number of receptor sites is caused by an antibody that destroys or blocks the receptor site.
Antibodies are proteins that play an important role in the immune system. They are normally directed at foreign proteins called antigens that attack the body. Such foreign proteins include bacteria and viruses. Antibodies help the body to protect itself from these foreign proteins. For reasons not well understood, the immune system of the person with MG makes antibodies against the receptor sites of the neuromuscular junction. Abnormal antibodies can be measured in the blood of many people with MG. The antibodies destroy the receptor sites more rapidly than the body can replace them. Muscle weakness occurs when acetylcholine cannot activate enough receptor sites at the neuromuscular junction.
Common symptoms can include:
A drooping eyelid
Blurred or double vision
Difficulty chewing and swallowing
Weakness in the arms and legs
Chronic muscle fatigue