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Phobic anxiety changes the function of brain-gut axis in irritable bowel syndrome
S Blomhoff1, S Spetalen, M B Jacobsen
1Department of Psychosomatic and Behavioral Medicine, National Hospital, Oslo, Norway. svein.blomhoff@riskshospitalet.no
Objective:
Disease severity in the irritable bowel syndrome (IBS) is highly influenced by psychiatric comorbidity. The mechanism of this influence is generally unknown, even if the brain-gut axis seems to be involved. Recent research has indicated that IBS patients have aberrant perception of visceral stimuli in the CNS. We compared IBS patients with and without comorbid phobic anxiety to see if the comorbid disorder influenced brain information processing of auditory stimuli, and looked for possible consequences with respect to visceral sensitivity thresholds and disease severity.
Methods:
Eleven female patients with IBS with comorbid phobic anxiety disorder were compared with 22 age-matched female IBS patients without such comorbidity. The groups were compared with respect to event-related potentials (ERP), auditory-presented words with emotional contents, barostat-assessed visceral sensitivity thresholds, and symptom levels the last week before assessment.
Results:
The comorbid group had a significantly enhanced first negative ERP wave (N1) to all stimuli, indicating increased use of brain attentional resources. It also had increased visceral threshold for the sensation of gas, and reduced gas-stool and gas-discomfort tolerances compared with the noncomorbid group. Enhanced N1 amplitude at the frontal electrode and reduced gas-stools tolerance significantly predicted subjective gas complaints, explaining 47% of the symptom variation.
Conclusions:
The study suggests an association between information processing in the frontal brain and visceral sensitivity characteristics in IBS patients, and indicates that subjective disease-related symptomatology is predicted by brain perceptual characteristics. The findings indicate that an interaction between IBS-related and anxiety-related hyperreactivity in the frontal brain may constitute a psychophysiological mechanism for the contribution of psychiatric comorbidity to severity and duration of the irritable bowel syndrome.
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