Unit:
Διακρατικό ΠΜΣ Κλινική Νευροψυχολογία-Νοητικές ΝευροεπιστήμεςLibrary of the School of Health Sciences
Supervisors info:
Νικόλαος Σμυρνής, Αναπληρωτής Καθηγητής, Ιατρική, ΕΚΠΑ
Κωνσταντίνος Πόταγας, Αναπληρωτής Καθηγητής, Ιατρική, ΕΚΠΑ
Σωκράτης Παπαγεωργίου, Αναπληρωτής Καθηγητής, Ιατρική, ΕΚΠΑ
Original Title:
Effect of dopaminergic treatment in inhibition of saccades in Parkinson's disease (PD)
Translated title:
Effect of dopaminergic treatment in inhibition of saccades in Parkinson's disease (PD)
Summary:
Parkinson’s disease (PD) is associated with a loss of central dopaminergic pathways in the brain leading to an abnormality of movement, including eye movements like saccades. The pathophysiology of Parkinson’s disease (PD) is considered to be the increase in the activities of basal ganglia (BG) output nuclei, which excessively inhibits the thalamus and superior colliculus (SC) and causes preferential impairment of internal over external movements. In PD, analysis of saccadic parameters and saccadic latency distributions, can provide information about how the neural decision process and inhibition are affected by dopaminergic treatment and disease state. Current study’s purpose is to examine the effects of dopaminergic treatment in inhibition of saccadic eye movements in advanced state of PD. Executive function was measured through eye movements, reflexive prosaccades and voluntary antisaccades. Ten patients with advanced idiopathic PD, “off” and “on” anti- Parkinsonian medication, were tested on a prosaccade and an antisaccade task. Saccadic eye movements were measured while patients were “off” and “on” anti- Parkinsonian medication, to study how the initiation and inhibitory control of saccades varied with the anti- Parkinsonian medication. To measure the inhibitory control of saccades, we studied the directional errors in the antisaccade task. Dopaminergic treatment was found to prolong reflexive prosaccadic latency and incorrect prosaccadic latency in antisaccade task. However, dopaminergic treatment did not suppress incorrect prosaccades during the antisaccade task. There was no improvement for voluntary cognitive processes in advanced stage PD. The saccadic parameters of reflexive and voluntary saccades showed no correlation with Unified Parkinson’s Disease Rating Scale III motor subscores reflecting dopaminergic function. The results suggest that dopaminergic treatment affects both reflexive and voluntary saccades. The impairment in reflexive and voluntary saccades may be caused by the excessive inhibition of the SC due to the increased BG output and the decreased activity of the frontal cortex-BG circuit. The impaired suppression of reflexive saccades in antisaccade task may be explained of increased SC inhibition and reduced pre-oculomotor drive due to dysfunctional frontal cortex-BG-SC circuit. Changes in saccade parameters suggest that frontal cortex-BG circuit activity decreases with disease progression.
Main subject category:
Health Sciences
Keywords:
Antisaccade task, Saccades, Latency, Inhibition, Dopaminergic treatment, Parkinson’s disease
