title: Disorders of vergence eye movements.
abstract: OBJECTIVE
  The aim is to re-interpret disorders of vergence in the light of recent studies that view disjunctive eye movements as but one component of three-dimensional gaze control.
  
  
  RESULTS
  Most natural eye movements combine vergence with saccades, pursuit and vestibular eye movements. Electrophysiological studies in epileptic patients, as well as evidence from monkeys, indicate that frontal and parietal cortex govern vergence as a component of three-dimensional gaze. Clinicians apply Hering's law of equal innervation to interpret disjunctive movements as the superposition of conjugate and vergence commands. However, electrophysiological studies indicate that disjunctive saccades are achieved by programming each eye's movement independently. Patients with internuclear ophthalmoplegia (INO) may have preserved vergence, which can be recruited to compensate for loss of conjugacy. Vergence may also enable gaze shifts in saccadic palsy. Some forms of nystagmus suppress or change with convergence; co-contraction of the horizontal rectus muscles does not appear to be the explanation. Rather, effects of near viewing on central vestibular mechanisms or differential activation of specific types of extra-ocular muscle fiber may be responsible.
  
  
  CONCLUSIONS
  Interpretation of disorders of vergence is aided by applying a scheme in which their contributions to three-dimensional gaze control is considered.
authors.affiliation: Neurology Department, Veterans Affairs Medical Center and University Hospitals, Case Western Reserve University, Cleveland, Ohio, USA.
authors.forename: Alessandro
authors.initials: A
authors.lastname: Serra
authors.forename: Athena L
authors.initials: AL
authors.lastname: Chen
authors.forename: R John
authors.initials: RJ
authors.lastname: Leigh
mesh_terms: D002526:Cerebellar Diseases / Q000150:complications; D002540:Cerebral Cortex / Q000503:physiopathology; D003290:Convergence, Ocular; D002658:Developmental Disabilities; D006801:Humans; D008636:Mesencephalon / Q000473:pathology; D015835:Ocular Motility Disorders / Q000150:complications / Q000175:diagnosis / Q000473:pathology / Q000628:therapy*; D011149:Pons / Q000473:pathology; D014786:Vision Disorders / Q000209:etiology