Acquired nystagmus occurs frequently in patients with
multiple sclerosis and is often the cause of illusory motion of the environment (oscillopsia), and blurring of vision. Based primarily on the beneficial effect of
gabapentin on acquired
pendular nystagmus (APN), a GABAergic mechanism in controlling nystagmus has been hypothesised. If increasing
GABA concentrations in the CNS are critical for the treatment of nystagmus, then a selective GABAergic
drug should be highly successful. However, as
gabapentin is not a selective
GABAergic agent,
vigabatrin, a "pure" GABAergic medication, and
gabapentin, were compared in a single blind cross over trial in eight patients with definite
multiple sclerosis. Patients were randomly assigned to begin with
gabapentin (1200 mg daily) or
vigabatrin (2000 mg daily). Neuro-ophthalmological and electro-oculographic (EOG) evaluations were performed four and three times, respectively. Treatment efficacy was based on improving visual acuity and EOG indices (amplitude or frequency of nystagmus, or both) by at least 50% of pretreatment values. Three out of eight patients dropped out due to adverse effects. In the remaining five patients
gabapentin improved symptomatic pendular or gaze evoked
jerk nystagmus in four. Three patients decided to continue
gabapentin therapy. Importantly,
vigabatrin proved useful in only one out of five patients, suggesting that
gabapentin effectiveness may be related to additional non-GABAergic mechanisms of action. Interaction with cerebral
glutamate transmission by inhibition of
NMDA receptor might be an alternative hypothesis for the therapeutic action of
gabapentin.