Abstract
BackgroundThe basal ganglia (BG) are thought to play an important role in the control of eye movements. Accordingly, the broad variety of subtle oculomotor alterations that has been described in Parkinson's disease (PD) are generally attributed to the dysfunction of the BG dopaminergic system. However, the present study suggest that dopamine substitution is much less effective in improving oculomotor performance than it is in restoring skeletomotor abilities.MethodsWe investigated reactive, visually guided saccades (RS), smooth pursuit eye movements (SPEM), and rapidly left-right alternating voluntary gaze shifts (AVGS) by video-oculography in 34 PD patients receiving oral dopaminergic medication (PD-DA), 14 patients with deep brain stimulation of the nucleus subthalamicus (DBS-STN), and 23 control subjects (CTL);In addition, we performed a thorough review of recent literature according therapeuthic effects on oculomotor performance in PD by switching deep brain stimulation off and on in the PD-DBS patients, we achieved swift changes between their therapeutic states without the delays of dopamine withdrawal. In addition, participants underwent neuropsychological testing.ResultsPatients exhibited the well known deficits such as increased saccade latency, reduced SPEM gain, and reduced frequency and amplitude of AVGS. Across patients none of the investigated oculomotor parameters correlated with UPDRS III whereas there was a negative correlation between SPEM gain and susceptibility to interference (Stroop score). Of the observed deficiencies, DBS-STN slightly improved AVGS frequency but neither AVGS amplitude nor SPEM or RS performance.ConclusionsWe conclude that the impairment of SPEM in PD results from a cortical, conceivably non-dopaminergic dysfunction, whereas patients' difficulty to rapidly execute AVGS might be related to their BG dysfunction.
Highlights
The basal ganglia (BG) are thought to play an important role in the control of eye movements
Some studies show no effect of dopaminergic medication [4], whereas other studies do show effects on latency, gain or amplitude of saccades (e.g. [5])
In this study we investigated whether an accurate assessment of oculomotor changes in Parkinson’s disease (PD) patients - subdivided in a group with oral dopaminergic medication and a group of STN-DBS patients in the DBS “on” and “off” condition with additional oral dopaminergic medication - may allow a conclusion as to the pathomechanism of oculomotor dysfunction in PD
Summary
The basal ganglia (BG) are thought to play an important role in the control of eye movements. The broad variety of subtle oculomotor alterations that has been described in Parkinson’s disease (PD) are generally attributed to the dysfunction of the BG dopaminergic system. A broad variety of oculomotor alterations have been described in Parkinson’s disease (PD) such as an increased latency of visually guided reactive saccades, reduced saccadic gain, impaired smooth pursuit and difficulties to inhibit unwarranted reactions [1]. Regarding the effects of STN-DBS on saccadic function, there exist only a few studies, so far. Most of these report a reduction of the latency of visually elicited reactive saccades (RS) [2] as well as an increase in gain [7,8], whereas another study found no effect on latency and gain of RS [9] but an improvement of the amplitude of memory guided saccades [8]. Since STNDBS is generally accepted to be highly effective in reducing the levodopa sensitive parkinsonian motor symptoms [11], these observations suggest that oculomotor deficits in PD might to a considerable part be caused by a dysfunction of non-dopaminergic systems
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