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Natural Myasthenia course

Natural history of myasthenia gravis

Generally, myasthenia gravis is a persistent disease requiring chronic treatment. Fluctuations over the long term are the norm. Some patients go into long-term remission spontaneously - approximately 15-25% after five years for those presenting with generalised disease and somewhat more for those presenting with ocular disease only. Late relapse after sustained remission also occurs, the longest reported example being after 32 years. It should be noted that the neuromuscular junction can be reformed, unlike many parts of the nervous system. Muscle strength that has been affected by myasthenia gravis for a long time often recovers with treatment. This means that the intensity of treatment for myasthenia gravis can be modulated to the current severity of the disease.

Over time, patients with clinically isolated ocular myasthenia gravis often progress to generalised myasthenia gravis. Treatment with corticosteroids can reduce the likelihood of progression, and control both ocular and generalised weakness completely in many cases. It is not known if this alters the natural history or the need for long-term treatment. It is therefore unclear whether treatment should be commenced for ocular disease or just 'as required' to control symptoms that are causing sufficient disability to justify the adverse effects of treatment. Long-standing ocular misalignment may not recover despite generalised remission.


The diagnosis must be confirmed before treatment, because the mainstay of treatment for most patients is immunosuppression. Treatments to prevent the adverse effects of immunosuppression should be started simultaneously with the therapy (see Table 1). There is no robust evidence that long-term treatment actually cures the condition, so some patients choose to avoid the adverse effects of immunosuppressive therapy and accept degrees of weakness. Coping without treatment is not always the safest strategy as patients with significant weakness, particularly in the bulbar musculature, are at risk of ventilatory failure or of needing intensive care following an intercurrent respiratory infection. Immunosuppressive treatment is therefore strongly recommended for control of significant bulbar weakness.

Initial treatment is usually with pyridostigmine, followed by prednisone and azathioprine if the response is incomplete. A combination of approaches is often useful to cover deficiencies in each available drug.

Immunosuppression produces a very slow response, often taking many months to 1-2 years.1,2 An unrealistic expectation of a speedy response is often a problem for both the patient and the doctor.

There are four main approaches to treatment, each with very different durations of effect, requirements, consequences and adverse effects.

Table 1
Prophylaxis of the complications of immunosuppression

Osteoporosis prevention Measure bone density before treatment and yearly while on treatment. Start calcium and vitamin D supplements. Bisphosphonates may reduce bone loss associated with the chronic use of glucocorticoids.
Cardiovascular risk Risk factor modification should be standard and includes advice to stop smoking, start an exercise program and manage hypertension.
Peptic ulcer prevention Helicobacter screening and prophylactic treatment with proton pump inhibitors or H2 antagonists seems appropriate for those with a past history of previous ulceration or concordant use of non-steroidal anti-inflammatory drugs.
Infection prophylaxis Use of inactivated vaccines such as influenza is recommended. Live vaccines are contraindicated. A chest X-ray should be performed prior to treatment. More specific testing for tuberculosis may be indicated depending on history and chest X-ray results.
Malignancy prevention Skin cancer rates are increased in patients using azathioprine. A full yearly dermatological survey is recommended. Exhort sun protection and cancer surveillance. Regular cervical smears are recommended. Eye protection may also limit cataract development.

Improve neuromuscular transmission by inhibiting acetylcholinesterase

Drugs that inhibit acetylcholinesterase include pyridostigmine, edrophonium (used only for testing) and neostigmine (for intravenous use in intensive care units only). These drugs take effect within minutes and last for hours. Although they are without long-term adverse effects, the efficacy of all acetylcholinesterase inhibitors is limited. As a sole drug they are not enough for most patients with generalised myasthenia gravis.


Pyridostigmine is the first-line treatment for myasthenia gravis. It is a reversible inhibitor of acetylcholinesterase so increases acetylcholine stimulation of the remaining acetylcholine receptors. If there are insufficient acetylcholine receptors remaining to trigger a muscle action potential, extra acetylcholine from the action of the drug is not going to help. The underlying autoimmune state is not altered. It is often sufficient for ptosis alone, but not for diplopia or generalised myasthenia gravis. Benefit is often not sustained, possibly due to counterproductive upregulation of acetylcholinesterase and downregulation of acetylcholine receptors. The dose required is variable, as is gastrointestinal tolerance. One approach is to start at 10 mg three times a day and titrate up to 60 mg 4-6 times daily. A 180 mg 'timespan' preparation is available for nocturnal symptoms. In practice a degree of patient control of dosing and 'when required' use is often helpful.

Doses less than 480 mg daily rarely produce depolarising crisis. Increasing weakness after an increase in the pyridostigmine dose (when high doses are already being given) suggests deteriorating disease and/or a depolarising crisis. This may require treatments such as plasma exchange and a reduction in pyridostigmine dose. The presence of gastrointestinal adverse effects and fasciculations, clinically or on electromyogram, might suggest depolarising crisis. The patient must be hospitalised and the dose of pyridostigmine reduced while they are carefully monitored. Lack of improvement with edrophonium (which has a very short half-life) indicates that further pyridostigmine will not be useful.





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