Somatosensory changes in the referred pain area following acute inflammation of the appendix

Background and aims Abdominal pain provoked by acute gastrointestinal disease may increase the sensitivity in the referred somatic pain area. The aim of this study was to examine sensory changes in the referred pain area during acute appendicitis. Subjects Twenty patients with clinical symptoms of appendicitis were included; 16 of these had appendicitis confirmed at operation. Ten healthy volunteers served as controls. Methods In patients with symptoms of appendicitis, somatic sensitivity was assessed using different stimuli presented in the area of referred pain and in a comparable non-painful area at the contralateral site of the abdomen. In healthy control subjects, the same stimuli were presented to McBurney's point and at a similar area on the left abdomen. The rating to pinprick was determined using a Von Frey hair. The rating to thermal stimuli was tested by warm and cold metal rollers. A constant current stimulator was used to measure the sensation and pain-detection threshold to single and repeated electrical stimuli. The pressure pain threshold was determined by an electronic pressure algometer. Results Patients (n = 16) with verified appendicitis showed increased ratings to pinprick (50%, P < 0.05) and thermal stimuli (56%, P < 0.05) in the referred pain area. There was a reduction in pain thresholds to single electrical (4.3 v. 8.4 mA, P = 0.001), repeated electrical (3.5 v. 4.6 mA, P = 0.005) and pressure (89 v. 243 kPa, P < 0.001) stimuli in the referred pain area versus the control area. In the control group, no difference was observed between the two areas. The pain thresholds for electrical and pressure stimuli were lower in the referred pain area in patients compared with the same area in controls (P < 0.001). Conclusion Somatosensory hyperalgesia to experimental stimuli was observed in acute appendicitis. We believe that viscerosomatic convergence mechanisms and central nervous system hyperexcitability explain these findings.

[1]  M. Giamberardino,et al.  Uterine inflammation as a noxious visceral stimulus: behavioral characterization in the rat , 1998, Neuroscience Letters.

[2]  F. Cerveró,et al.  Spinal mechanisms underlying persistent pain and referred hyperalgesia in rats with an experimental ureteric stone. , 1998, Journal of neurophysiology.

[3]  L. Arendt-Nielsen,et al.  Experimental pain in the stomach: a model based on electrical stimulation guided by gastroscopy , 1997, Gut.

[4]  Leonardo Vecchiet,et al.  Pain threshold variations in somatic wall tissues as a function of menstrual cycle, segmental site and tissue depth in non-dysmenorrheic women, dysmenorrheic women and men , 1997, Pain.

[5]  L. Arendt-Nielsen,et al.  Gut pain reactions in man: an experimental investigation using short and long duration transmucosal electrical stimulation , 1997, Pain.

[6]  F. Cerveró,et al.  Mechanisms of touch-evoked pain (allodynia): a new model , 1996, Pain.

[7]  M. Giamberardino,et al.  Changes in activity of spinal cells with muscular input in rats with referred muscular hyperalgesia from ureteral calculosis , 1996, Neuroscience Letters.

[8]  M. Giamberardino,et al.  Artificial ureteral calculosis in rats: behavioural characterization of visceral pain episodes and their relationship with referred lumbar muscle hyperalgesia , 1995, Pain.

[9]  M. A. Pozo,et al.  Selective changes of receptive field properties of spinal nociceptive neurones induced by noxious visceral stimulation in the cat , 1992, Pain.

[10]  T. Ness,et al.  Visceral pain: a review of experimental studies , 1990, Pain.

[11]  D. Albe-Fessard,et al.  Pain from renal/ureteral calculosis: evaluation of sensory thresholds in the lumbar area , 1989, Pain.

[12]  O. Rampin,et al.  Muscular hyperalgesia and hypoalgesia after stimulation of the ureter in rats , 1988, Neuroscience Letters.

[13]  M. .. Beal.  Viscerosomatic reflexes: a review. , 1985, The Journal of the American Osteopathic Association.

[14]  C. Greene,et al.  A somatic component to myocardial infarction , 1985, The Journal of the American Osteopathic Association.

[15]  F. Rogers,et al.  Palpable musculoskeletal findings in coronary artery disease: results of a double-blind study. , 1983, The Journal of the American Osteopathic Association.

[16]  L. Arendt-Nielsen.  Mechanisms of visceral pain , 2001 .

[17]  L Arendt-Nielsen,et al.  Referred pain as an indicator for neural plasticity. , 2000, Progress in brain research.

[18]  E. R. Woods.  The viscerosomatic reflex in acute abdominal disorders. , 1962, The Journal of the American Osteopathic Association.

[19]  J. Craig.  Visceral pain. , 1948, Lancet.

[20]  H. Head.  ON DISTURBANCES OF SENSATION WITH ESPECIAL REFERENCE TO THE PAIN OF VISCERAL DISEASEPART III.—PAIN IN DISEASES OF THE HEART AND LUNGS , 1893 .