In 1973 James Ritchie discovered that if a balloon is inserted in the colon and inflated, IBS patients experience pain at lower pressures than non-patients.
Ritchie concluded ‘This was probably the outcome of a low threshold for visceral pain in the section of bowel in contact with the balloon. Colonic hyperalgesia of this kind, possibly a random occurrence, may be an important contributory factor in the aetiology of the irritable colon syndrome.‘
Ritchie conjectured that hyperalgesia for visceral pain was an important factor in the aetiology of IBS. Experiments since then confirm this and show that if the balloon is repeatedly inflated and deflated, IBS patients will develop a heightened hyperalgesia. This hyperalgesia applies to other types of sensation in the colon, for example, thermal and electrical stimulation. Indeed, it is not restricted to the colon, it has been found throughout most of the gut, including the jejunum and oesophagus. In 1995 Trimble et al found that IBS and function dyspepsia (FD) patients are equally sensitive to balloon distension in the colon and the oesophagus, even though each group only experiences either IBS or FD symptoms. Furthermore, their symptom level correlates with the degree of hyperalgesia in either location.
Hyperalgesia in IBS is not even restricted to the gut. IBS patients are more sensitive to hand or foot immersion in hot (46°C) or freezing water and to heat applied to the calf, forearm or face. Conversely, they have been found to be equally or less sensitive to other pain, such as a single electric shock to the finger.
How do we make sense of this? Pain is grouped into various types, such as cutaneous or visceral, acute or chronic. The experimental data suggests that IBS patients are hypersensitive to chronic pain and to visceral pain, but not to acute cutaneous pain.
To find out why IBS patients have this curious response to pain perhaps we must look at N-methyl-D-aspartate (NMDA) receptors.