Megan Shanahan

Empirical evidence for discrete neurocognitive subgroups in bipolar disorder: clinical implications.

BACKGROUND Recent data suggest trait-like neurocognitive impairments in bipolar disorder (BPD), with deficits about 1 s.d. below average, less severe than deficits noted in schizophrenia. The frequency of significant impairment in BPD is approximately 60%, with 40% of patients characterized as cognitively spared. This contrasts with a more homogeneous presentation in schizophrenia. It is not understood why some BPD patients develop deficits while others do not. METHOD A total of 136 patients with BPD completed the MATRICS Consensus Cognitive Battery and data were entered into hierarchical cluster analyses to: (1) determine the optimal number of clusters (subgroups) that fit the sample; and (2) assign subjects to a specific cluster based on individual profiles. We then compared subgroups on several clinical factors and real-world community functioning. RESULTS Three distinct neurocognitive subgroups were found: (1) an intact group with performance comparable with healthy controls on all domains but with superior social cognition; (2) a selective impairment group with moderate deficits on processing speed, attention, verbal learning and social cognition and normal functioning in other domains; and (3) a global impairment group with severe deficits across all cognitive domains comparable with deficits in schizophrenia. CONCLUSIONS These results suggest the presence of multiple cognitive subgroups in BPD with unique profiles and begin to address the relationships between these subgroups, several clinical factors and functional outcome. Next steps will include using these data to help guide future efforts to target these disabling symptoms with treatment.

The association between childhood trauma and facial emotion recognition in adults with bipolar disorder

Many patients with bipolar disorder (BD) have difficulties in facial emotion recognition, which may also be impaired in maltreated children and in subjects who have a positive history of childhood traumatic experiences. Childhood trauma is reported with a high prevalence in BD and it is considered a risk factor for the disorder. As the relationship between facial emotion recognition and childhood trauma in BD has not yet been directly investigated, in this study we examined whether the presence of a childhood trauma in affectively stable BD patients was associated with poorer performance in emotion recognition. Seventy-five BD I and II participants completed the Childhood Trauma Questionnaire retrospectively assessing five types of childhood trauma (emotional, physical and sexual abuse, and emotional and physical neglect) and the Emotion Recognition Task evaluating the ability to correctly identify six basic facial emotions (happiness, sadness, anger, disgust, fear and surprise). Our results suggest that the presence of childhood trauma in participants with BD is associated with a more severe clinical presentation (earlier onset, longer duration of illness, and higher depressive symptom ratings) and that BD patients with a positive childhood history of emotional neglect perform worse than those without such a history in recognizing anger.

Affective temperaments and neurocognitive functioning in bipolar disorder

BACKGROUND There is evidence that patients with bipolar disorder (BD) score higher on affective temperament ratings compared to healthy controls (HCs). Moreover, unaffected relatives demonstrate similar patterns as BD patients suggesting that such temperaments are related to the genetic risk for BD and may serve as endophenotypes for the disorder. It is unknown whether affective temperaments are associated with other core features of BD, such as impairments in neurocognition. This study examined the relationship between affective temperaments and neurocognition in patients with BD and in HCs. METHODS Temperaments were evaluated using the Temperament Evaluation of Memphis, Pisa, Paris, and San Diego, Auto-questionnaire version (TEMPS-A) in 64 patients with BD and 109 HCs. Neurocognitive functioning was evaluated using the MATRICS Consensus Cognitive Battery (MCCB). Correlational analyses between temperaments and cognition were conducted in BD and HC subjects. RESULTS Data suggest that affective temperaments and neurocognition are correlated. In BD higher ratings of cyclothymia and irritability were associated with better processing speed, working memory, reasoning and problem-solving. In the HC group, increased irritability was related to worse performance on measures of attention and social cognition. LIMITATIONS Lack of functional outcome measures to evaluate the impact of temperaments and cognition on psychosocial functioning. It would be useful to test these findings on unaffected relatives of BD patients. CONCLUSIONS Cyclothymic and irritable temperaments are correlated with specific aspects of neurocognition in BD. This study is among the few exploring the dimensional relationship between temperaments and cognition in BD, and provides preliminary evidence for future studies investigating the neural and genetic mechanisms underlying the association between these variables.

The relationship between sleep quality and neurocognition in bipolar disorder

BACKGROUNDS Sleep and circadian rhythm disruptions are prominent, trait-like features of bipolar disorder (BD) which precede the onset of mood episodes. Neurocognitive impairments also characterize BD not only during acute phases of the illness but also during remission. Although the relationship between these two debilitating aspects of the illness might seem intuitive, very little is known about their relationship. We examined the association between sleep dysfunction and neurocognition in BD. METHODS In a sample of 117 BD patients (mean age=45.0±10.7; 59.0% (n=69) male), neurocognitive functioning was assessed using the MATRICS Consensus Cognitive Battery (MCCB). Sleep quality data were collected using the Epworth Sleepiness Scale (ESS) and the Pittsburgh Sleep Quality Index (PSQI). Partial Pearson correlations tested for a relationship between sleep and neurocognition. Path analyses were conducted to examine the hypothesized direct influence of sleep disruption on neurocognition. RESULTS Higher levels of sleep disruptions were associated with a more severe clinical presentation and poorer performance in social cognition, visual learning and working memory. Social cognition and working memory were directly (negatively) predicted by sleep disruptions. LIMITATIONS The study was limited by a relatively small sample size and the lack of behavioral and biological objectives measure of activity/rest cycles. CONCLUSIONS Our study suggests that in patients with BD, sleep disruptions have a detrimental effect on general level of psychopathology and contribute directly to impaired cognitive functioning in the domains of social cognition and working memory. More research using objective measurement of sleep should be pursued to support these data and to further investigate the causal relationship between these disabling aspects of the illness.

Coping strategies and real-world functioning in bipolar disorder.

BACKGROUND Bipolar disorder (BD) patients encounter significant life adversity, which has contributed to bipolar disorder being a leading cause of disability worldwide. Studies suggest BD patients have more maladaptive coping strategies, some of which can impact their illness course. Yet research on which coping strategies most influence disability is lacking. Such research could inform cognitive-behavioral targets to improve functional outcomes. Thus, we sought to identify relations between coping strategies and real-world function in BD. METHODS In 92 affectively-stable BD outpatients, we measured coping strategies via the Brief COPE, real-world disability via the World Health Organization Disability Assessment Schedule, current symptoms, illness chronicity, and neurocognitive functioning via the MATRICS. Multiple regression analysis served to identify the neurocognitive domains predictive of disability for entry into subsequent analyses. Multiple regressions assessed how adaptive and maladaptive coping strategies influenced disability. RESULTS Only one neurocognitive domain, verbal learning, significantly predicted disability and was included in subsequent analyses. Maladaptive coping significantly predicted disability while adaptive coping did not. Behavioral disengagement (giving up) and self-blame were the only remaining predictors of disability, after controlling for age, sex, illness chronicity, current symptoms, and neurocognitive functioning. LIMITATIONS The study was limited by the use of a self-report disability measure and a brief-form coping scale. CONCLUSIONS Results suggest that giving up and self-blame are significant predictors of real-world functioning beyond sub-threshold depressive symptoms. Our results in BD expand upon recent schizophrenia studies suggesting that defeatist beliefs negatively influence functional outcomes across the range of major psychiatric disorders.

The effects of cigarette smoking behavior and psychosis history on general and social cognition in bipolar disorder

Several studies have documented the prevalence and effects of cigarette smoking on cognition in psychotic disorders; fewer have focused on bipolar disorder (BD). Cognitive and social dysfunction are common in BD, and the severity of these deficits may be related both to illness features (e.g., current symptoms, psychosis history) and health‐related behaviors (e.g., smoking, alcohol use). The current study assessed the influence of cigarette smoking on general and social cognition in a BD cohort, accounting for illness features with a focus on psychosis history.

Social cognition moderates the relationship between neurocognition and community functioning in bipolar disorder

BACKGROUND Schizophrenia (SZ) studies suggest that neurocognition predicts functional outcome and that social cognition mediates this relationship. Bipolar disorder (BD) patients also have cognitive, social, and functional impairments but the relationship among these factors in BD is not well established. We assessed whether social cognition modulates the influence of neurocognition on community functioning in BD, as found in SZ. METHODS 200 BD patients and 49 healthy controls (HC) were administered and compared on a battery of tests assessing neurocognition, social cognition, and community functioning. We conducted a series of regression analyses to investigate potential mediation or moderation of social cognition on the relationship between neurocognition and community functioning. RESULTS BD patients performed worse on neurocognitive domains of processing speed, attention, verbal learning, and global neurocognition. Also, BD patients performed worse on theory of mind, the social cognition composite score, and community functioning. Neurocognition did not significantly predict functional outcome in our BD sample. However, we found a moderating effect of social cognition: among patients with poor social cognition, better neurocognition was associated with better community functioning, a relationship not seen in BD patients with good social cognition. LIMITATIONS The study was limited by a relatively small HC group and assessing one subtype of functioning status. CONCLUSIONS The relationship between neurocognition and community functioning in BD may be dependent on social cognition status, implying the presence of social cognitive heterogeneity. Results may be relevant to choosing proper treatment interventions depending on the patients social cognitive level.