The authors of this paper do not have any commercial associations that might pose a conflict of interest in connection with this manuscript.
Neuropsychological impairment in bipolar disorder: the relationship with glucocorticoid receptor function
Article first published online: 12 JAN 2006
Volume 8, Issue 1, pages 85–90, February 2006
How to Cite
Watson, S., Thompson, J. M., Ritchie, J. C., Nicol Ferrier, I. and Young, A. H. (2006), Neuropsychological impairment in bipolar disorder: the relationship with glucocorticoid receptor function. Bipolar Disorders, 8: 85–90. doi: 10.1111/j.1399-5618.2006.00280.x
This study was presented as an abstract and poster at the Third European Stanley Foundation Conference on Bipolar Disorders, Freiburg, Germany, September 12–14, 2002 (Bipolar Disord 2002, 4, Suppl. 1:138).
- Issue published online: 12 JAN 2006
- Article first published online: 12 JAN 2006
- Received 18 February 2005, revised and accepted for publication 29 July 2005
- bipolar disorder;
- dexamethasone suppression test;
- glucocorticoid receptor;
- neuropsychological performance;
- working memory
Objective: Basal levels of glucocorticoids, such as cortisol, are generally unaltered in bipolar disorder. However, neuroendocrine tests of glucocorticoid receptor (GR) function such as the dexamethasone suppression test (DST) are frequently abnormal. Neuropsychological impairment is well documented in healthy volunteers after administration of glucocorticoids and in patients with bipolar affective disorder. This suggests a potential link between neuropsychological and hypothalamic-pituitary-adrenal axis function. We examined the hypothesis that neuropsychological impairment in bipolar disorder is associated with abnormal GR function.
Methods: Seventeen euthymic bipolar patients and 16 controls completed tests of verbal declarative and working memory (WM) tests and the DST. The correlation between neuroendocrine and neuropsychological function was examined.
Results: Bipolar patients made significantly more errors of omission and commission on the WM paradigm and demonstrated impaired verbal recognition memory. Patients’ post-dexamethasone cortisol correlated with WM commission errors (rs = 0.64, p = 0.0006). No such relationship was evident in controls.
Conclusion: Deficits in declarative memory and WM are evident in patients with bipolar disorder. The deficit in retrieval accuracy from WM appears to be correlated with abnormal GR function.