In general, ocular motor deficits in Parkinson's disease frequently require laboratory testing to bring out abnormalities. Typically, PD is associated with similar defects as may be seen in PSP, but to a lesser degree; however, abnormalities of saccades and pursuit are common1.
Despite widespread beliefs to the contrary, at least one study suggests that analysis of the eye movements is not helpful to distinguish the various types of Parkinsonism2. It is probable that the critical role of when the eye movement examination is carried out during the course of the illness is too frequently not considered, nor the effect of medication on eye movements2. As could be predicted, eye movement abnormalities are widespread in all form of Parkinsonism, and become more severe, and clinically apparent, with progression of disease. Nevertheless, it is likely that the velocity of vertical saccades may distinguish PSP from PD. Note the frequent inaccuracy of diagnosis in the initial stages of the disease: in a study of consecutively enrolled patients, with a duration of illness of three years, and levodopa responsiveness. 10% converted to PSP-Parkinsonism over a 4 year follow up, manifesting either with a vertical gaze palsy or with slowing of vertical saccades3.
Fixation Instability: in PD, steady fixation may be disrupted by saccadic intrusions, such as square wave jerks4.
Saccades: Saccades are typically hypometric, especially vertically, and latencies are increased5.
Downward gaze paresis is not seen in PD, and if it is present, one should consider the diagnosis of progressive supranuclear palsy-Richardson’s syndrome. Hypometric voluntary saccades are supposed to be caused by increased inhibition of the superior colliculus (SC) and reduced preoculomotor drive due to dysfunction of frontal-basal ganglia-SC circuits, whereas reflexive saccades are normal (although they may also be characterized by being disinhibited).
Smooth Pursuit (SP): SP is usually impaired in PD. VOR suppression is abnormal to a similar degree as SP in most patients with PD4.
VOR: The VOR gain has been reported to be abnormally with catch-up saccades, possibly related to altered dopaminergic influences on the vestibular nuclei in the brainstem6.