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Cognitive performance in irritable bowel syndrome: evidence of a stress-related impairment in visuospatial memory

  • P. J. Kennedy (a1) (a2), G. Clarke (a1) (a2), A. O‘Neill (a1), J. A. Groeger (a3), E. M. M. Quigley (a1) (a4), F. Shanahan (a1) (a4), J. F. Cryan (a1) (a5) and T. G. Dinan (a1) (a2)...



Central nervous system (CNS) dysfunction is a prominent feature of the functional gastrointestinal (GI) disorder, irritable bowel syndrome (IBS). However, the neurobiological and cognitive consequences of key pathophysiological features of IBS, such as stress-induced changes in hypothalamic–pituitary–adrenal (HPA)-axis functioning, is unknown. Our aim was to determine whether IBS is associated with cognitive impairment, independently of psychiatric co-morbidity, and whether cognitive performance is related to HPA-axis function.


A cross-sectional sample of 39 patients with IBS, a disease control group of 18 patients with Crohn's disease (CD) in clinical remission and 40 healthy age- and IQ-matched control participants were assessed using the Paired Associates Learning (PAL), Intra-Extra Dimensional Set Shift (IED) and Spatial Working Memory (SWM) tests from the Cambridge Neuropsychological Test Automated Battery (CANTAB) and a computerized Stroop test. HPA-axis function was determined by measuring the cortisol awakening response (CAR).


IBS patients exhibited a subtle visuospatial memory deficit at the PAL six- pattern stage (p = 0.03), which remained after psychiatric co-morbidity was controlled for (p = 0.04). Morning cortisol levels were lower in IBS (p = 0.04) and significantly associated with visuospatial memory performance within IBS only (p = 0.02).


For the first time, altered cognitive function on a hippocampal-mediated test of visuospatial memory, which was related to cortisol levels and independent of psychiatric co-morbidity, has been identified in IBS. Visuospatial memory impairment may be a common, but currently neglected, component of IBS. Further elucidation of the nature of this impairment may lead to a greater understanding of the underlying pathophysiology of IBS, and may provide novel therapeutic approaches.

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The online version of this article is published within an Open Access environment subject to the conditions of the Creative Commons Attribution licence .

Corresponding author

* Address for correspondence: Professor T. G. Dinan, M.D., D.Sc., Ph.D., Department of Psychiatry, GF Unit, Cork University Hospital, Wilton, Cork, Ireland. (Email:


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