Autonomic nervous system arousal and cognitive functioning in bipolar disorder
Article first published online: 12 DEC 2012
© 2012 John Wiley and Sons A/S
Volume 15, Issue 1, pages 70–79, February 2013
How to Cite
Levy, B. (2013), Autonomic nervous system arousal and cognitive functioning in bipolar disorder. Bipolar Disorders, 15: 70–79. doi: 10.1111/bdi.12028
- Issue published online: 22 JAN 2013
- Article first published online: 12 DEC 2012
- Received 12 January 2012, revised and accepted for publication 3 September 2012
- autonomic nervous system;
- bipolar disorder;
- cognitive impairment;
- sympathetic arousal
Levy B. Autonomic nervous system arousal and cognitive functioning in bipolar disorder. Bipolar Disord 2012: 00: 000–000. © 2012 John Wiley & Sons A/S.Published by Blackwell Publishing Ltd.
Objective: Previous theories about the etiology of cognitive dysfunction in bipolar disorder (BD) emphasized trait factors such as neurological impairment. State factors, other than mood symptoms, that may exacerbate functional deficits have not yet been considered. The purpose of this study was to examine autonomic nervous system (ANS) arousal following cognitive challenge. The study compared patients with BD and healthy controls (HC) in physiological measures and neuropsychological test scores.
Methods: Thirty euthymic patients with BD and 22 HC completed the study. Participants completed mood [Beck Depression Inventory-II (BDI-II) and Young Mania Rating Scale (YMRS)], anxiety (State–Trait Anxiety Inventory), and substance abuse (Drug Abuse Screening Test–20 item and Alcohol Use Disorders Identification Test) measures. They were connected to an electrogram, a sensitive thermometer for measuring finger temperature, and electrodes that measure galvanic skin response. After a five-min baseline measurement in a restful state, participants completed a computerized neuropsychological battery (CNS Vital Signs).
Results: The group with BD reported significantly more mood symptoms (BDI-II, t = 3.71, p < 0.001; YMRS, t = 6.73, p < 0.001) and scored higher on a measure of trait-anxiety (State–Trait Anxiety Inventory, t = 2.91, p < 0.001) than HC. A multivariate analysis of variance revealed higher arousal on all physiological measures in the BD group relative to HC at baseline [F(3,48) = 13.1, p < 0.001] and during cognitive testing [F(3,48) = 11.3, p < 0.001]. The increase in physiological arousal from a restful state to the time of testing was higher for the BD group [F(3,37) = 8.06, p < 0.001]. With respect to cognitive data, HC scored higher than patients with BD across the measures of memory (F = 8.5, p < 0.001), sustained (F = 9.5, p < 0.001) and complex (F = 2.7, p < 0.04) attention, processing speed (F = 10.0, p < 0.001), reaction time (F = 7.8, p < 0.001), cognitive flexibility (F = 19.7, p < 0.001), working memory (F = 10.8, p < 0.001), and social acuity (F = 5.7, p < 0.01), with partial eta-squared from 0.18 to 0.62. Correlational analysis revealed significant associations between various cognitive test scores and changes in physiological arousal from baseline to testing (−0.59 ≤ r ≤ 0.22).
Conclusions: Relative to HC, patients with BD experience larger changes in ANS arousal between a restful baseline and cognitive testing, and achieve lower cognitive test scores. Further research is needed to determine whether acute physiological symptoms of anxiety directly compromise cognitive functioning in BD.