[Cognitive dysfunction in bipolar disorder: determinants and functional outcome]. / Cognitieve stoornissen bij patiënten met een bipolaire stoornis: determinanten en consequenties.

BACKGROUND: Research into the nature and extent of cognitive dysfunction in patients suffering from bipolar disorder has increased greatly over the last 10 years because the dysfunction is known to persist even if the mood symptoms are in remission and can influence a patient's psychosocial functioning. AIM: To provide an overview of 1) the nature and extent of cognitive dysfunction in bipolar patients; 2) clinically relevant factors such as illness characteristics, comorbidity and psychotropic/psychoactive drugs and 3) the consequences of cognitive dysfunction. METHOD: We searched the literature in PubMed using the following search terms: bipolar disorder, neuropsychological, cognitive functioning, cognition, functional outcome, determinants, psychotropic/psychoactive drugs. RESULTS: Attentional deficits, memory lapses and aberrant executive functioning occur in both manic and depressive episodes, and may persist even in absence of mood symptoms. The precise cause of cognitive dysfunction is unknown. Persistent cognitive dysfunction frequently interferes with daily functioning. CONCLUSION: Since the treatment of bipolar patients is nowadays directed towards complete recovery rather than symptomatic remission, it is important to take into account the possibility that these patients are also suffering from cognitive dysfunction.

A 2-year naturalistic study on cognitive functioning in bipolar disorder.

OBJECTIVE: Cognitive alterations in bipolar disorder may reflect genetic influence. However, to what degree mood, medication, thyroid function and other factors impact on longitudinal cognitive functioning remains unclear. METHOD: A group of patients with bipolar (spectrum) disorder (n = 76) underwent two monthly cognitive assessments over a 2-year period in a prospective, repeated measures design. Regression models were used to investigate associations with predictors, corrected for multiple testing. RESULTS: Patients with bipolar disorder performed worse than healthy controls (n = 61) on all cognitive domains tested. Effect sizes were small, with a maximum of -0.36 for sustained attention. However, cognitive performance varied substantially over the 2-year follow-up, co-varying with subjective cognitive complaints and impacting on functioning. Alterations in sustained attention and motor speed were the only impairments that were invariant over time. Predictors had very limited explanatory power on temporal variation in cognition. Use of second-generation antipsychotics was associated with the largest negative effects on cognition, which were evident in the areas of motor speed and basic information processing (-0.35 < ß < -0.5). CONCLUSION: Cognitive function in bipolar disorder varies significantly over time, largely independent of clinical factors. The temporal stability of sustained attention is the exception, suggesting it may represent a possible candidate intermediary phenotype.

Meta-analyses of cognitive functioning in euthymic bipolar patients and their first-degree relatives.

BACKGROUND: Previous work suggests that impairments in executive function and verbal memory in particular may persist in euthymic bipolar patients and serve as an indicator of genetic risk (endophenotype). METHOD: A systematic review of the literature was undertaken. Effects sizes were extracted from selected papers and pooled using meta-analytical techniques. RESULTS: In bipolar patients, large effect sizes (d>0.8) were noted for executive functions (working memory, executive control, fluency) and verbal memory. Medium effect sizes (0.5

Cognitive alterations in groups at risk for psychosis: neutral markers of genetic risk or indicators of social disability?

OBJECTIVE: To investigate whether cognitive alterations associated with vulnerability to psychosis, are associated with expression of psychopathology and functional outcome in groups at different levels of risk for psychotic illness. METHOD: Neurocognition, psychopathology and functional outcome were measured in subjects with variable risk for psychosis: i) 29 patients with psychotic disorder, ii) 46 subjects at familial risk, iii) 41 subjects at psychometric risk and iv) 54 control subjects. RESULTS: Dose-response relationships between cognitive dysfunction and increasing risk for psychosis were found. Cognitive alterations were predicted by negative symptoms in patients and by positive psychotic experiences in the familial risk group. In both at risk groups, cognitive speed was associated with functional outcome. CONCLUSION: Some cognitive impairments serve as neutral endophenotypic marker across the psychosis continuum. However, other cognitive alterations associated with transmission of psychosis may have a direct impact on the pathway from risk to psychopathology and alterations in functioning.