UNASSIGNED: @entity7463 and @entity191 have distinct underlying neuropathology, but both diseases affect cognitive function in addition to causing a @entity717 . They impair response inhibition and may lead to impulsivity, which can occur even in the presence of profound @entity910 and @entity2003 . The current study examined the mechanisms of @entity73 underlying @entity4943 , using horizontal saccadic latencies that obviate the impact of @entity4218 on executing response decisions. Nineteen @entity1 with clinically diagnosed @entity7463 ( @entity7463 ), 24 @entity1 with clinically diagnosed @entity191 and 26 healthy control subjects completed a saccadic Go/No-Go task with a head-mounted infrared saccadometer. @entity1 were cued on each trial to make a pro-saccade to a horizontal target or withhold their responses. Both @entity1 groups had impaired behavioural performance, with more commission errors than controls. Mean saccadic latencies were similar between all three groups. We analysed behavioural responses as a binary decision between Go and No-Go choices. By using Bayesian parameter estimation, we fitted a hierarchical drift-diffusion model to individual @entity1 ' single trial data. The model decomposes saccadic latencies into parameters for the decision process: decision boundary, drift rate of accumulation, decision bias, and non-decision time. In a leave-one-out three-way classification analysis, the model parameters provided better discrimination between @entity1 and controls than raw behavioural measures. Furthermore, the model revealed @entity51 in the Go/No-Go decision process. Both @entity1 groups had slower drift rate of accumulation, and shorter non-decision time than controls. But @entity1 with @entity7463 were strongly biased towards a pro-saccade decision boundary compared to @entity191 @entity1 and controls. This indicates a prepotency of responding in combination with a reduction in further accumulation of evidence, which provides a parsimonious explanation for the apparently paradoxical combination of @entity4943 and severe @entity910 . The combination of the well-tolerated oculomotor paradigm and the sensitivity of the model-based analysis provides a valuable approach for interrogating decision-making processes in @entity179 . The mechanistic differences underlying @entity1 ' poor performance were not observable from classical analysis of behavioural data, but were clearly revealed by modelling. These differences provide a rational basis on which to develop and assess new therapeutic strategies for cognition and behaviour in these disorders.

Different decision deficits impair response inhibition in XXXX and @entity191 .

@entity1 :: ('9606', 'Species') :: ['participants', 'patients', 'patient', 'Participants'] @entity2003 :: ('MESH:D009127', 'Disease') :: ['rigidity'] @entity73 :: ('MESH:D003072', 'Disease') :: ['cognitive impairments'] @entity4218 :: ('MESH:D017880', 'Disease') :: ['limb slowness'] @entity910 :: ('MESH:D004409', 'Disease') :: ['akinesia'] @entity191 :: ('MESH:D010300', 'Disease') :: ["Parkinson's disease", "Parkinson's"] @entity51 :: ('MESH:D009461', 'Disease') :: ['disease-specific deficits'] @entity179 :: ('MESH:D019636', 'Disease') :: ['neurodegenerative disorders'] @entity4943 :: ('MESH:D057180', 'Disease') :: ['disinhibition'] @entity717 :: ('MESH:D009069', 'Disease') :: ['movement disorder'] @entity7463 :: ('MESH:D013494', 'Disease') :: ['Progressive supranuclear palsy', 'progressive supranuclear palsy', "Richardson's syndrome"]
@entity7463 :: (MESH:D013494,Disease) :: ['progressive supranuclear palsy']
