The relationship between executive dysfunction and neuropsychiatric symptoms in patients with Korsakoff's syndrome

Objective: Patients with Korsakoff's syndrome (KS) show executive dysfunction and neuropsychiatric symptoms. This study investigates whether specific executive subcomponents (shifting, updating, and inhibition) predict variance in neuropsychiatric symptoms. We hypothesized that shifting deficits, in particular, are associated with neuropsychiatric symptoms.Method: Forty-seven patients participated (mean age 61.5; 11 women). Executive function (EF) was measured using six component-specific tasks. Neuropsychiatric symptoms were measured with the Neuropsychiatric Inventory - Questionnaire (NPI-Q). General cognitive functioning was assessed with the Montreal Cognitive Assessment (MoCA). First, factor analysis was conducted to examine shared variance across the EF tasks. Subsequently, a regression analysis was performed with the EF factors and the MoCA as predictors and the NPI-Q as the dependent variable. It was also investigated whether an interaction effect between the EF factors and the MoCA was present.Results: The prevalence of neuropsychiatric symptoms was high (85.7% of the KS patients showed at least one symptom). A two-factor model was extracted with a shifting-specific factor and a combined updating/inhibition factor. The overall regression model was not significant, and no interaction was found between the EF factors and general cognitive functioning. However, a significant relationship between general cognitive functioning and neuropsychiatric symptoms (r = -.43; p <.01) was detected.Conclusions: Results point at an association between neuropsychiatric symptoms and general cognitive functioning. Possibly, diminished cognitive differentiation in these patients with severe cognitive dysfunction accounts for the absence of a significant association between EF and neuropsychiatric symptoms. While the results should be interpreted with caution due to a limited sample size, the found association highlights the need to further unravel the underlying cognitive mechanisms of neuropsychiatric symptoms in patients with KS.