Eye movement disorders and acquired brain injury
Acquired brain injury (ABI) can lead to eye movement disorders such as strabismus, gaze deficits and nystagmus, among many other consequences. When a person has a brain injury resulting from a stroke, for example, cranial nerves that supply the movement of the ocular muscles can be damaged, as can neurological areas that contribute to eye movement control.Studies show that 68% of people who survive stroke will have eye movement problems, a troubling number considering stroke is among the most common disabling conditions of our time. The natural progression of ABI varies depending on the cause, and the eye movement disorder may persist and require treatment to alleviate or reduce symptoms.
Existing interventions to restore eye movement function after ABI
Treatments for eye movement disorders are directed at aligning the visual axes to improve eye movements. Various treatments are associated with strabismus, eye movement disorders and nystagmus:*Restitution: These interventions involve direct training of the impaired function or repetitive stimulation of eye movement.*Compensation: These interventions aim to improve vision by compensating or adapting, using an intact function.*Substitution: These interventions involve adaptation of lost or disrupted visual faculties through the use of optic devices, extraocular surgery or botulinum toxin.*Pharmacology: These interventions aim to improve visual functioning through alteration of biochemical effects in the body. For example, gabapentin or baclofen can increase gaba and, as an inhibitory neurotransmitter, can reduce reflexes.
Are rehabilitation interventions for eye movement disorders effective?
Unfortunately, the Cochrane Review identified only 5 clinical trials, with low- to very low-certainty evidence. For a compensation strategy, the Review identified a study in oculomotor rehabilitation. But the study was small, and it is unclear whether the intervention has a permanent effect. For pharmacological intervention, three crossover studies showed that gabapentin and 4-aminopyridine may reduce oscillatory eye movements and improve visual acuity and participant-reported symptoms.Finally, for a substitution intervention, one trial evaluated the use of botulinum toxin vs observation alone. In people with sixth nerve palsy, participant symptoms may improve more quickly with botulinum toxin. Side effects were specific to each intervention, but were mainly mild and transient.These findings suggest a need for good quality trials to improve the evidence base for restitutive, substitute, compensatory and pharmacological therapies for eye movement disorders.
Comment by Sara Laxe