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in a few patients with azathioprine alone. Treatment begins with 50 mg (1 tablet) twice daily for a few days; if this is tolerated, the dosage is raised to 2 to 3 mg/kg per day (150 to 250 mg daily). The number of positive responses is much the same as with prednisone. However, improvement occurs much more slowly with azathioprine, and a signi cant response may not be evident for many months to a year (Witte et al). Liver function tests and blood cell count should be checked regularly. The Myasthenia Gravis Clinical Study Group found that the most severe forms of the disease, particularly those resistant to prednisone or azathioprine alone, bene t from the combination of the two medications. Many neurologists, including the present authors, begin by prescribing both medications early in the illness with the plan of reducing the corticosteroid dose in the third or fourth month. Mycophenolate (CellCept) is currently being used as an adjunct to corticosteroids and has been bene cial in several small trials. The clinical improvement suggested by these studies has generally occurred sooner than it does with azathioprine (Meriggioli and colleagues). Diarrhea was the main adverse effect. Our initial impression is that mycophenolate may be preferable to most of the adjunctive medications and, in some milder cases, may be effective alone. Cyclophosphamide, administered in intravenous pulses, has been used by De Feo and coworkers; they were able to remove 5 of their 12 patients from steroids but the appropriate use of this potent agent is not clear and we have resorted to it infrequently. Drachman and colleagues and others describe a regimen of highdose cyclophosphamide (50 mg/kg/d for 4 consecutive days) followed by granulocyte-stimulating factor to reboot the immune system in refractory cases. This approach has risks but may be justi ed if all other measures have failed in severe instances of the disease. Liver function and white blood cell count should be monitored regularly. The clinical effects of the immunosuppressive agent cyclosporine are much like those of azathioprine but become evident more rapidly, in a matter of a month or two (Tindall et al). It is given in two divided doses daily, to a total of about 6 mg/kg but not often used currently because of serious side effects (hypertension, nephrotoxicity) and its high cost. Because of the success of alternative regimens, we have had occasion over the years to use cyclosporine only once for myasthenia. Plasma Exchange and Intravenous Immune Globulin For severe myasthenia that is refractory to treatment with anticholinesterase drugs and prednisone, or during an acute worsening, one must resort to other measures. Striking temporary remissions (2 to 8 weeks) may be obtained by the use of plasma exchange. This form of treatment may be lifesaving during a myasthenic crisis, as noted later. It is also useful before and after thymectomy and at the start of immunosuppressive drug therapy. The number and volume of exchanges required in these circumstances is somewhat arbitrary, but they tend to be less than those required for GBS; several exchanges of 2 to 3.5 L each (totaling approximately 125 mL/kg), performed over a week, usually suf ce. The removed plasma is replaced with albumin and saline. It has been estimated that a 2-L exchange will remove 80 percent of circulating antibodies and that this will be re ected in reduced ACh antibody levels in 3 to 5 days. However, there is only an approximate correlation between a reduction in the titer of anti-AChR antibody and the degree of clinical improvement. In a crisis requiring plasma exchanges and mechanical ventilation, it has been our practice to discontinue or curtail the use of anticholinesterase drugs and resume them as the patient is being weaned from the ventilator. Also, it may be that sensitivity
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