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Background Optic neuritis is often the first clinical manifestation of multiple sclerosis, but little is known about the effect of corticosteroid treatment for optic neuritis on the subsequent risk of multiple sclerosis. Methods We conducted a multicenter study in which 389 patients with acute optic neuritis (and without known multiple sclerosis) were randomly assigned to receive intravenous methylprednisolone (250 mg every six hours) for 3 days followed by oral prednisone (1 mg per kilogram of body weight) for 11 days, oral prednisone (1 mg per kilogram) alone for 14 days, or placebo for 14 days. Neurologic status was assessed over a period of two to four years. The patients in the first group were hospitalized for three days; the others were treated as outpatients. Results Definite multiple sclerosis developed within the first two years in 7.5 percent of the intravenous-methylprednisolone group (134 patients), 14.7 percent of the oral-prednisone group (129 patients), and 16.7 percent of the placebo grou...

Background and Methods. The use of corticosteroids to treat optic neuritis is controversial. At 15 clinical centers, we randomly assigned 457 patients with acute optic neuritis to receive oral prednisone (1 mg per kilogram of body weight per day) for 14 days; intravenous methylprednisolone (1 g per day) for 3 days, followed by oral prednisone (1 mg per kilogram per day) for 11 days; or oral placebo for 14 days. Visual function was assessed over a six-month follow-up period. Results. Visual function recovered faster in the group receiving intravenous methylprednisolone than in the placebo group; this was particularly true for the reversal of visual-field defects (P = 0.0001). Although the differences between the groups decreased with time, at six months the group that received intravenous methylprednisolone still had slightly better visual fields (P = 0.054), contrast sensitivity (P = 0.026), and color vision (P = 0.033) but not better visual acuity (P = 0.66). The outcome in the oral-prednisone group did ...

Amaurosis fugax, a brief loss of vision in one eye, is caused by hypoperfusion of the retinal circulation. If an attack of amaurosis is prolonged, the patient is at risk of permanent visual loss. Since the 1950s, amaurosis fugax has usually been attributed to embolism from the heart or great vessels1 or to carotid occlusive disease. Because of the difficulty in differentiating between these and other causes, amaurosis fugax remains a therapeutic challenge. Depending on the patency of the internal carotid arteries, the principal treatments are anticoagulation or antiplatelet therapy2 and carotid endarterectomy3. Vasospasm is rarely reported as a . . .

To the Editor: Neurosarcoidosis occurs in less than 5 percent of patients with sarcoidosis, yet it can cause significant neurologic impairment.1,2 Although some patients have a rapid response to corticosteroids, many require prolonged treatment or additional immunosuppressants.2,3 We report the use of the antimetabolite cladribine (2-chlorodeoxyadenosine) for the treatment of neurosarcoidosis in a patient with aggressive suprasellar disease.4 A 54-year-old man received a diagnosis of nasal sarcoidosis in 1993, which was successfully treated with prednisone. In 1998, progressive blindness developed, and brain magnetic resonance imaging (MRI) studies revealed a mass-like enhancement in the suprasellar cistern. The findings on . . .

Bromocriptine in high doses (up to 100 mg per day) was administered to 14 patients with advanced Parkinson's disease whose disorder was progressing despite optimum treatment with levodopa combined with a peripheral dopa decarboxylase inhibitor (carbidopa). In 10, bromocriptine (mean dose, 57 mg) induced a statistically significant (P