Autonomic Nervous System Function in Patients with Functional Abdominal Pain an Experimental Study

Abstract

Functional abdominal pain—that is, pain without demonstrable organic abnormalities—has often been associated with psychologic stress. The aim of the present study was to investigate whether sympathetic nervous system response to laboratory stress and basal parasympathetic neural activity were disturbed in 22 patients with functional abdominal pain (functional group) as compared with 14 healthy controls (healthy group) and 26 patients with organic abdominal pain (organic group) due to duodenal ulcer (DU), gallstones, or urinary tract calculi. Plasma adrenocorticotrophic hormone (ACTH) and serum Cortisol measurements were included, to assess the pituitary-adrenocortical axis. Heart rate, systolic blood pressure, and plasma adrenaline increased significantly in all groups in response to a stress test (mental arithmetic). Plasma noradrenaline increased in the DU patients only, and plasma ACTH and serum Cortisol did not increase at all in any of the groups. As a measure of parasympathetic neural activity, independent of sympathetic neural activity, the beat-to-beat variation of the heart rate was calculated. The functional patients had a significantly higher beat-to-beat variation expressed as the mean square successive differences of the R-R intervals (MSSD), indicating a higher basal parasympathetic neural activity (mean MSSD ± SEM = 64 ± 6 msec in the functional group, 46 ± 6 msec in the healthy group, and 49 ±6 msec in the organic group; P = 0.03). A reduced sympathetic neural response as indicated by a lesser stress-induced increment in heart rate, was seen in both patient groups (functional, 13 ± 2 beats/min; organic, 10 ± 2 beats/min) as compared with the healthy group (19 ± 2 beats/min; P = 0.003). There were no significant differences in systolic blood pressure, adrenaline, ACTH, and Cortisol. DU patients had increased levels of noradrenaline (average of all measurements, 0.3 ± 0.03 ng/ml) as compared with the healthy and calculus groups (0.2 ± 0.02 and 0.2 ± 0.03 ng/ml, respectively; P = 0.048), and DU patients alone had significant increases in response to the stressor. It is suggested that patients with functional abdominal pain have an increased basal parasympathetic neural activity and that patients with pain, whether functional or organic, have a diminished sympathetic neural response to laboratory stress. The paradox of a decreased heart rate increment and an increased noradrenaline concentration in the duodenal ulcer group is discussed.

Key Words:

• Adrenocorticotrophic hormone
• adrenaline
• automatic dysfunction
• Cortisol
• functional abdominal pain
• heart rate variation
• noradrenaline
• stress