Therapeutic considerations for eye movement disorders

Abstract

Advances made in understanding the pathophysiology of eye movement disorders have only recently with the publication of the first well-planned studies been translated into better treatment strategies. The following chapter summarizes the pharmacological treatment options for a variety of oculomotor syndromes. Cortisone is useful, for example, for acute vestibular neuritis to improve the restitution of the labyrinthine function. For the widespread benign paroxysmal positioning nystagmus, a series of liberating movements that free the semicircular canal from the causative otoconia is now a well-established therapy. Treatment for the central vestibular syndrome of up- and downbeat nystagmus consists of drugs like the potassium canal blocker 4-aminopyridine, which influence the cerebellar circuits involved in the disorder's pathophysiology. Acquired pendular nystagmus, one of the oculomotor syndromes often caused by multiple sclerosis, results in the severe impairment of reduced visual acuity. Memantine, a weak NMDA antagonist, has now been proven effective here. Finally, anticonvulsants like carbamazepine are the drugs of choice for disorders involving a nerve-blood vessel contact that induces symptoms of vestibular paroxysmia or superior oblique myokymia.