Our study attempted to clarify two questions: first, whether confabulations are a critical feature of the cognitive impairment associated with long-term KS in a large sample of patients (N=42). Second, we investigated which memory domain is most likely affected by confabulations in KS. To elicit confabulations, we used a Confabulation Interview containing questions
from different memory domains. We found that KS patients overall confabulated more compared buy Anlotinib to a group of healthy subjects. Furthermore, we found that patients confabulated most within the episodic/autobiographical memory domain.
Our results imply that besides pronounced memory deficits typically associated with KS, confabulation can also be regarded as a clinical A-1210477 supplier feature of the disease.
The preponderance of episodic confabulation obtained here by using a standardized test, confirms anecdotic reports that KS patients confabulate in everyday life mainly with respect to their personal past and present.
Thus, for a detailed description of the memory profile of KS patients, the screening of confabulation tendencies may be a useful supplementary clinical tool.”
“Parkinson’s disease (PD) patients exhibit cognitive deficits, including reinforcement learning, working memory (WM) and set shifting. Computational models of the basal ganglia-frontal system posit similar mechanisms for these deficits in terms of reduced dynamic range of striatal dopamine (DA) signals in both medicated and non-medicated states. Here, we report results from the first study that tests PD patients on and off dopaminergic medications in a modified version of the AX continuous performance (AX-CPT) working memory task, consisting of three performance phases and one phase requiring WM associations to be learned via reinforcement feedback. Patients generally showed impairments relative to controls. Non-specific serine/threonine protein kinase Medicated patients showed deficits specifically
when having to ignore distracting stimuli during the delay. Our models suggest that this impairment is due to medication causing excessive WM updating by enhancing striatal “”Go”" signals that facilitate such updating, while concurrently suppressing “”NoGo”" signals. In contrast, patients off medication showed deficits consistent with an overall reduction in striatal DA and associated Go updating signals. Supporting this dichotomy, patients on and off medication both showed attentional shifting deficits, but for different reasons. Deficits in non-medicated patients were consistent with an inability to update the new attentional set, whereas those in medicated patients were evident when having to ignore distractors that had previously been task relevant. Finally, in the feedback-based WM phase, medicated patients were better than unmedicated patients, suggesting a key role of striatal DA in using feedback to update information into WM.