Treatment of abnormal eye movements that impair vision: strategies based on current concepts of physiology and pharmacology

Ann Neurol. 1994 Aug;36(2):129-41. doi: 10.1002/ana.410360204.


Certain abnormal eye movements, especially pathological nystagmus, degrade vision and cause illusory motion of the seen environment. These symptoms are due to excessive movement of images of stationary objects on the retina. Recently, the pathophysiology underlying several types of nystagmus and saccadic oscillations was better defined by the development of animal models and by experimental pharmacological studies. Despite this, few reliable therapies are currently available for these abnormal eye movements. In clinical studies, a number of drugs reportedly helped individual patients, but few drugs have been subjected to double-blind trials. An alternative approach to pharmacological suppression of abnormal eye movements is optical stabilization of images on the retina, which is helpful in selected patients. Weakening of the extraocular muscles, using botulinum toxin or surgery, is prone to cause diplopia and may induce plastic-adaptive changes that render the effect temporary. In some patients, treatment of an underlying condition, such as the Arnold-Chiari malformation, reduces nystagmus and improves vision. There is a need for multicenter trials to evaluate systematically potential treatments of abnormal eye movements that impair vision.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Clinical Trials as Topic
  • Double-Blind Method
  • Eye / physiopathology*
  • Eye Movements*
  • Fixation, Ocular
  • GABA Antagonists
  • Haplorhini
  • Humans
  • Nystagmus, Pathologic / physiopathology*
  • Nystagmus, Pathologic / therapy
  • Vision Disorders / physiopathology*
  • Vision Disorders / therapy
  • gamma-Aminobutyric Acid / physiology


  • GABA Antagonists
  • gamma-Aminobutyric Acid