At least half of all people with multiple sclerosis (MS) are expected to have nystagmus at some point during the course of their illness. Nystagmus results from demyelination that involves the brainstem or cerebellar eye movement pathways. While it may be asymptomatic, it often causes blurred vision or oscillopsia. The extent of the visual disturbance is directly related to the velocity of the slow phase of the nystagmus.
In MS patients with chronic nystagmus, the most common form is an acquired pendular nystagmus (APN), which is almost always accompanied by optic atrophy, and often by internuclear ophthalmoplegia (INO).
Numerous treatment trials have demonstrated the efficacy of pharmacologic treatment of chronic symptomatic nystagmus. Treatment should be considered in individuals in whom blurred vision or oscillopsia is severe enough to warrant the potential risk of medication side effects. As a general rule, drugs used to treat nystagmus are titrated slowly upwards from a low dose to either efficacy or tolerance.
The two most effective medications for APN in MS are gabapentin and memantine. However, memantine has been shown to cause worsening of MS symptoms at daily doses of 30 mg and higher; therefore, it is a second-line treatment that is used with caution.
Some MS patients with cerebellar involvement have downbeat nystagmus, which may respond to treatment with 3.4-diaminopyridine and 4-aminopyridine (Ampyra®) or clonazepam. The aminopyridines or baclofen may also be effective at treating upbeat nystagmus in MS patients, which is common in those with bilateral INO.
In MS patients with bothersome nystagmus, the characteristics of the nystagmus must be defined. The results of this evaluation will lead to options for pharmacologic treatment that are often effective at suppressing the nystagmus, but which need to be titrated slowly due to side effects, interactions with other medications, and co-morbidities present in MS patients.