Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of increasing delay on the metrics of remembered saccades was studied in 10 subjects with mild Parkinson's disease, none of whom was receiving treatment with L-dopa, and nine age-matched control subjects. Delays of 1 msec, 250 msec, 1000 msec, 2500 msec, and 5000 msec were used, and reflexive saccades used as a control condition. Results were analyzed for the gain of the primary saccade and the accuracy of the final eye position (FEP gain). Reflexive saccades were normal in subjects with Parkinson's disease, but remembered saccades showed marked hypometria of primary saccade gain at all delays. FEP gain was unimpaired in Parkinson's disease, and primary saccade gain and FEP gain did not vary as a function of delay. Hypometria of primary saccades is compatible with dysfunction in striato-collicular inhibitory pathways in Parkinson's disease, arising as a functional consequence of dopamine deficiency in the basal ganglia. Maintenance of an accurate FEP gain suggests no deficit in oculomotor spatial working memory in Parkinson's disease, at least at delays of up to 5 sec.
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PMID:Remembered saccades with variable delay in Parkinson's disease. 991 48

We reviewed basal ganglia (BG) dysfunction in Parkinson's disease (PD) based on recent findings on saccade performance. Hypometria in all saccade paradigms and impaired initiation of internally triggered saccades such as memory guided saccades (MGS) are reported, whereas visually guided saccades (VGS) are relatively spared, although they are also mildly affected. The ability to inhibit unwanted saccades is also impaired. We propose that three major drives converges on SC to determine the saccade abnormalities. The impairment in VGS may be caused by the excessive inhibition of SC due to the increased BG output, whereas for MGS, decreased activity of the frontal cortex-BG circuit may also be involved. The impaired suppression of unwanted saccades may result from the "leaky" inhibition of SC. When PD patients inspect pictures, they end up exploring a smaller area of them with smaller saccades compared to normal subjects. Levodopa slightly prolongs VGS latency and shortens MGS latency, by altering the balance between the direct and indirect pathways of the BG circuit. In contrast, deep brain stimulation of the subthalamic nucleus improves saccade hypometria in both VGS and MGS, presumably by acting relatively directly on the SC-substantia nigra pars reticulata pathway to remove the excessive SC inhibition.
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PMID:New perspectives on the pathophysiology of Parkinson's disease as assessed by saccade performance: a clinical review. 2400 69