Abstract
ObjectiveTo study the neurocognitive profile and its relationship to prefrontal dysfunction in non-demented Parkinson's disease (PD) with deficient haptic perception.MethodsTwelve right-handed patients with PD and 12 healthy control subjects underwent thorough neuropsychological testing including Rey complex figure, Rey auditory verbal and figural learning test, figural and verbal fluency, and Stroop test. Test scores reflecting significant differences between patients and healthy subjects were correlated with the individual expression coefficients of one principal component, obtained in a principal component analysis of an oxygen-15-labeled water PET study exploring somatosensory discrimination that differentiated between the two groups and involved prefrontal cortices.ResultsWe found significantly decreased total scores for the verbal learning trials and verbal delayed free recall in PD patients compared with normal volunteers. Further analysis of these parameters using Spearman's ranking correlation showed a significantly negative correlation of deficient verbal recall with expression coefficients of the principal component whose image showed a subcortical-cortical network, including right dorsolateral-prefrontal cortex, in PD patients.ConclusionPD patients with disrupted right dorsolateral prefrontal cortex function and associated diminished somatosensory discrimination are impaired also in verbal memory functions. A negative correlation between delayed verbal free recall and PET activation in a network including the prefrontal cortices suggests that verbal cues and accordingly declarative memory processes may be operative in PD during activities that demand sustained attention such as somatosensory discrimination. Verbal cues may be compensatory in nature and help to non-specifically enhance focused attention in the presence of a functionally disrupted prefrontal cortex.
Highlights
Non-demented Parkinson's disease (PD) has been associated with a number of neurocognitive deficits including executive and memory dysfunction [1,2]
Recent work indicates that encoding deficits [12,13,14] and even hippocampal atrophy [15,16,17,18] may develop in nondemented PD, independent of verbal retrieval
While encoding deficits likely mirror mesio-temporal dysfunction, it has been suggested that the verbal retrieval deficit, the hypothetical cause of delayed free recall, is explained by ineffective search strategies normally executed by the intact prefrontal cortex [19], reflecting impaired prefrontal processing
Summary
Non-demented Parkinson's disease (PD) has been associated with a number of neurocognitive deficits including executive and memory dysfunction [1,2]. While encoding deficits likely mirror mesio-temporal dysfunction, it has been suggested that the verbal retrieval deficit, the hypothetical cause of delayed free recall, is explained by ineffective search strategies normally executed by the intact prefrontal cortex [19], reflecting impaired prefrontal processing. Strategic or executive deficits are associated with both encoding and retrieval processes, thought to predominantly involve left dorso-lateral prefrontal cortex in the former and right dorsolateral prefrontal cortex in the latter function [20]
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