The Pharmacological Treatment of Acquired Nystagmus
The Pharmacological Treatment of Acquired Nystagmus
We review the latest literature on the neuropharmacological treatments for acquired nystagmus. Nystagmus may have a significantly impact on health, yet there is little scientific evidence on which to make firm recommendations for treatment. Acquired pendular nystagmus may respond to gabapentin or memantine; downbeat and upbeat nystagmus to aminopyridines; and periodic alternating nystagmus to baclofen. To improve treatment we need multi-centre, randomised controlled trials using standardised techniques in reporting objective outcomes, with good follow-up duration and careful reporting of side effects.
Rhythmic or arrhythmic involuntary sustained to-and-fro oscillations of the eyes occur pathologically when there is a failure in the oculomotor stabilisation system. These abnormal eye movements can be either congenital or acquired. They are classified as either nystagmus or saccadic oscillations, and occur in the horizontal, vertical and/or torsional planes (Box 1). Recent data estimate the prevalence of nystagmus to be 2.4 per 1000 population. There may be reduced visual acuity (approximately a 2-line decrease in Snellen acuity) and distressing oscillopsia (the perception of constant movement of the surroundings). The impact on health is significant, resulting in lower visual functioning scores than for other visual impairments, such as age-related macular degeneration.
Numerous strategies have been tried to reduce selectively the frequency or amplitude of nystagmus, sparing voluntary eye movements ( Table 1 ). The potential advantages of pharmacological treatment over other procedures are considerable. Drugs are reversible and do not require access to specialist services. However, the available drugs have not yet been properly evaluated and there are relatively few randomised controlled trials and level 1 evidence. Indeed, much neuro-ophthalmological practice relies upon grade C and D recommendations—expert opinion, case reports and series—often without reliable measurements of the involuntary ocular movements or their visual consequences. A handful of randomised controlled trials have been published recently. However, they had only small numbers of participants and not all improved with the treatment. The follow-up duration was invariably short, precluding firm conclusions about treatment acceptability and safety. Moreover, the methods of quantifying nystagmus and its visual consequences are not standardised across studies. Thus, these isolated studies have debatable validity.
This review aims to summarise the clinical effectiveness and safety profile of drugs purported to help acquired nystagmus, and to relate the choice of treatment to pathophysiology. We do not cover peripheral vestibular nystagmus—usually associated with transient vertigo—or saccadic oscillations, since these have each been recently reviewed elsewhere.
Abstract and Introduction
Abstract
We review the latest literature on the neuropharmacological treatments for acquired nystagmus. Nystagmus may have a significantly impact on health, yet there is little scientific evidence on which to make firm recommendations for treatment. Acquired pendular nystagmus may respond to gabapentin or memantine; downbeat and upbeat nystagmus to aminopyridines; and periodic alternating nystagmus to baclofen. To improve treatment we need multi-centre, randomised controlled trials using standardised techniques in reporting objective outcomes, with good follow-up duration and careful reporting of side effects.
Introduction
Rhythmic or arrhythmic involuntary sustained to-and-fro oscillations of the eyes occur pathologically when there is a failure in the oculomotor stabilisation system. These abnormal eye movements can be either congenital or acquired. They are classified as either nystagmus or saccadic oscillations, and occur in the horizontal, vertical and/or torsional planes (Box 1). Recent data estimate the prevalence of nystagmus to be 2.4 per 1000 population. There may be reduced visual acuity (approximately a 2-line decrease in Snellen acuity) and distressing oscillopsia (the perception of constant movement of the surroundings). The impact on health is significant, resulting in lower visual functioning scores than for other visual impairments, such as age-related macular degeneration.
What Are the Treatments Available for Acquired Nystagmus?
Numerous strategies have been tried to reduce selectively the frequency or amplitude of nystagmus, sparing voluntary eye movements ( Table 1 ). The potential advantages of pharmacological treatment over other procedures are considerable. Drugs are reversible and do not require access to specialist services. However, the available drugs have not yet been properly evaluated and there are relatively few randomised controlled trials and level 1 evidence. Indeed, much neuro-ophthalmological practice relies upon grade C and D recommendations—expert opinion, case reports and series—often without reliable measurements of the involuntary ocular movements or their visual consequences. A handful of randomised controlled trials have been published recently. However, they had only small numbers of participants and not all improved with the treatment. The follow-up duration was invariably short, precluding firm conclusions about treatment acceptability and safety. Moreover, the methods of quantifying nystagmus and its visual consequences are not standardised across studies. Thus, these isolated studies have debatable validity.
What Does This Review Aim to Add to Our Approach to the Patient With Acquired Nystagmus?
This review aims to summarise the clinical effectiveness and safety profile of drugs purported to help acquired nystagmus, and to relate the choice of treatment to pathophysiology. We do not cover peripheral vestibular nystagmus—usually associated with transient vertigo—or saccadic oscillations, since these have each been recently reviewed elsewhere.
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