BACKGROUND: Persistent impairments in neurocognitive function have been described in patients with bipolar disorder whose disease is in remission. However, methodological issues such as the effect of residual mood symptoms and hypercortisolaemia may confound such studies. AIMS: To assess neurocognitive functioning in prospectively verified euthymic patients with bipolar disorder. METHOD: Sixty-three patients with bipolar disorder and a matched control group completed a comprehensive neurocognitive test battery. Euthymia was confirmed in the patient group by prospective clinical ratings over 1 month prior to testing. Saliva samples were collected to profile basal cortisol secretion. RESULTS: Patients were significantly impaired across a broad range of cognitive domains. Across the domains tested, clinically significant impairment was observed in 3% to 42% of patients. Deficits were not causally associated with residual mood symptoms or hypercortisolaemia. CONCLUSIONS: Neurocognitive impairment persists in patients whose bipolar disorder is in remission. This may represent a trait abnormality and be a marker of underlying neurobiological dysfunction.
BACKGROUND: Persistent impairments in neurocognitive function have been described in patients with bipolar disorder whose disease is in remission. However, methodological issues such as the effect of residual mood symptoms and hypercortisolaemia may confound such studies. AIMS: To assess neurocognitive functioning in prospectively verified euthymic patients with bipolar disorder. METHOD: Sixty-three patients with bipolar disorder and a matched control group completed a comprehensive neurocognitive test battery. Euthymia was confirmed in the patient group by prospective clinical ratings over 1 month prior to testing. Saliva samples were collected to profile basal cortisol secretion. RESULTS:Patients were significantly impaired across a broad range of cognitive domains. Across the domains tested, clinically significant impairment was observed in 3% to 42% of patients. Deficits were not causally associated with residual mood symptoms or hypercortisolaemia. CONCLUSIONS:Neurocognitive impairment persists in patients whose bipolar disorder is in remission. This may represent a trait abnormality and be a marker of underlying neurobiological dysfunction.
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