The association between sleep and cognitive abnormalities in bipolar disorder.

BACKGROUND: Bipolar disorder (BD) is associated with attentional and processing abnormalities. Such abnormalities are also seen in healthy subjects with sleep disruption. We hypothesised cognitive abnormalities in BD patients would be worse in those with objectively verified sleep abnormalities. METHODS: Forty-six BD patients and 42 controls had comprehensive sleep/circadian rhythm assessment over 21 days alongside mood questionnaires. Cognitive function was assessed with a range of tasks including Psychomotor Vigilance Test (PVT), Attention Network Task (ANT) and Digit Symbol Substitution Test (DSST). BD participants with normal and abnormal sleep were compared with age- and sex-matched controls. RESULTS: BD patients had longer response times and made more lapses (responses >500 ms) than controls on the PVT (both p < 0.001). However, patients with normal sleep patterns did not differ from controls while those with sleep abnormalities did (p < 0.001). An identical pattern of effects were seen with the ANT response times, with the abnormality in bipolar abnormal sleepers related to the executive attentional network. Similarly, patients made fewer correct responses on the DSST compared with the controls (p < 0.001). Bipolar normal sleepers did not differ while those with abnormal sleep did (p < 0.001). All these differences were seen in bipolar abnormal sleepers who were euthymic (p < 0.01) and across the main abnormal sleep phenotypes. CONCLUSIONS: We confirm impairment in attention and processing speed in BD. Rather than sleep abnormalities exacerbating such dysfunction, the impairments were confined to bipolar abnormal sleepers, consistent with sleep disturbance being the main driver of cognitive dysfunction.

C-Reactive Protein as a Possible Predictor of Trail-Making Performance in Individuals with Psychiatric Disorders.

Cognitive dysfunction is a prominent feature of psychiatric disorders. Studies have shown that systemic low-grade inflammation is crucial in the development of cognitive deficits across psychiatric disorders. The aim of this study was to further examine the role of inflammation and inflammatory mediators in cognitive function in psychiatric disorders. This study included 364 inpatients (53% females) with International Classification of Diseases (ICD)-10 F3 (affective disorders) and F4 (neurotic, stress-related, and somatoform disorders) diagnoses. The mean age was 52 years (22 to 69 years) and the median body mass index was 27.6. Cognitive function was assessed with the Color-Word Interference Test after Stroop and the Trail-Making Test A/B. Multiple linear regression models were calculated to assess the predictive value of C-reactive protein and the kynurenine/tryptophan ratio on cognitive function controlling for age, sex, education, premorbid verbal intelligence quotient illness duration, depressive symptoms, and obesity-related parameters (e.g., body mass index, high-density lipoprotein). Our data confirm that in patients with psychiatric disorders, C-reactive protein serum concentration is a relevant and important predictor of Trail-Making Test B performance, measuring cognitive flexibility. The effect size of this association did not change much after adding clinical and metabolic variables into the regression model. The kynurenine/tryptophan ratio was not related to cognitive test scores. The involvement of C-reactive protein as a peripheral inflammatory marker in cognitive flexibility and psychomotor processing speed in psychiatric illness can be concluded.