The contribution of eye movements to discriminate Parkin-linked and idiopathic Parkinson's disease

Objective: To investigate, if cerebral hemispheric eye movement disorders help to differentiate between Parkinsonian patients with Parkin mutations and those with idiopathic Parkinson's disease (PD).

Background: Parkin gene mutations are the most common cause of early-onset parkinsonism. Patients with Parkin mutations may be clinically indistinguishable from patients with idiopathic Parkinson's disease (PD). At present, there is no specific clinical feature that clearly distinguishes this monogenic form from idiopathic PD. Eye movement disorders can help to differentiate parkinsonian syndromes, but have never been systematically looked for in Parkin mutation carriers.

Design/methods: Eye movements were recorded in symptomatic (n=9) and asymptomatic Parkin mutation carriers (n=13), idiopathic PD patients (n=14) and age-matched control subjects (n=27) during established oculomotor tasks.

Results: Both PD patients and symptomatic Parkin mutation carriers showed hypometric prosaccades towards visual stimuli, as well as deficits in suppressing reflexive saccades towards unintended targets (antisaccade task). When directing gaze towards memorized target positions, PD patients exhibited hypometric saccades, whereas symptomatic Parkin mutation carriers showed normal saccades. In contrast to PD patients, the symptomatic Parkin mutation carriers showed impaired tracking of a moving target (reduced smooth pursuit gain). The asymptomatic Parkin mutation carriers did not differ from healthy control subjects in any of the tasks.

Conclusions/Relevance: Although clinically similarly affected, symptomatic Parkin mutation carriers and idiopathic PD patients differed in several oculomotor tasks. This finding may point to distinct anatomical structures underlying either condition, namely damage to cortical areas involved in smooth pursuit (V5, frontal eye field) in Parkin-linked parkinsonism and greater impairment of basal ganglia circuits in idiopathic PD.

Study supported by: Supported by the Lübeck Research grant E-32–2008.