title: Pharmacological advances in the treatment of neuro-otological and eye movement disorders.
abstract: OBJECTIVE
  First, to describe the current pharmacological treatment options for peripheral and central vestibular, cerebellar, and ocular motor disorders. Second, to identify vestibular and ocular motor disorders in which treatment trials are warranted.
  
  
  RESULTS
  Peripheral vestibular disorders: In vestibular neuritis recovery of the peripheral vestibular function can be improved by treatment with oral corticosteroids. In Ménière's disease treatment strategies range from low-salt diet, diuretics, and betahistine, to intratympanic injection of corticosteroids or gentamicin. Unfortunately most of the trials on Ménière's disease do not have an up-to-date design. In bilateral vestibulopathy steroids do not seem to improve vestibular function.Central vestibular, cerebellar, and ocular motor disorders: The use of aminopyridines introduced a new therapeutic principle in the treatment of downbeat and upbeat nystagmus and episodic ataxia type 2 (EA2). These potassium channel blockers presumably increase the activity and excitability of cerebellar Purkinje cells, thereby augmenting the inhibitory influence of these cells on vestibular and cerebellar nuclei. A few studies showed that baclofen improves periodic alternating nystagmus, and gabapentin and memantine, pendular nystagmus. Many other eye movement disorders, however, such as ocular flutter, opsoclonus, central positioning, or see-saw nystagmus are still difficult to treat.
  
  
  CONCLUSIONS
  Although progress has been made in the treatment of vestibular neuritis, downbeat and upbeat nystagmus, as well as EA2, state-of-the-art trials must still be performed on many vestibular and ocular motor disorders, namely Ménière's disease, bilateral vestibulopathy, vestibular paroxysmia, vestibular migraine, and many forms of central eye movement disorders.
authors.affiliation: Department of Neurology, University of Munich, Germany. Michael.Strupp@med.uni-muenchen.de
authors.forename: Michael
authors.initials: M
authors.lastname: Strupp
authors.forename: Thomas
authors.initials: T
authors.lastname: Brandt
mesh_terms: D000818:Animals; D002524:Cerebellar Ataxia / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D002526:Cerebellar Diseases / Q000175:diagnosis / Q000188:drug therapy* / Q000503:physiopathology; D002531:Cerebellum / Q000187:drug effects* / Q000503:physiopathology; D018755:GABA Agonists / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D009759:Nystagmus, Pathologic / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D015835:Ocular Motility Disorders / Q000175:diagnosis / Q000188:drug therapy* / Q000503:physiopathology; D026902:Potassium Channel Blockers / Q000494:pharmacology / Q000627:therapeutic use; D015837:Vestibular Diseases / Q000175:diagnosis / Q000188:drug therapy* / Q000503:physiopathology; D014722:Vestibule, Labyrinth / Q000187:drug effects* / Q000503:physiopathology
chemical_list: D018755:GABA Agonists; D026902:Potassium Channel Blockers