Contribution of central sensitisation to the development of non-cardiac chest pain

Background Non-cardiac chest pain mimics angina pectoris but generally orig inates from the oesophagus, Visceral hypersensitivity may contribute, but i ts neurophysiological basis, is unclear. We investigated whether central se nsitisation, an activity-dependent amplification of sensory transfer in the central nervous system, underlies visceral pain hypersensitivity and non-c ardiac chest pain. Methods We studied 19 healthy volunteers and seven patients with non-cardia c chest pain. Acid was infused into the lower oesophagus. Sensory responses to electrical stimulation were monitored within the acid-exposed lower oes ophagus, the non-exposed upper oesophagus, and the cutaneous area of pain r eferral, before and after the infusion. Findings In healthy volunteers, acid infusion into the lower oesophagus low ered the pain threshold in the upper oesophagus (mean decrease 18.2% [95% C I 10.4 to 26.0]; p=0.01) and on the chest wall (24.5% [10.2 to 38.7]; p=0.0 1). Patients with non-cardiac chest pain had a lower resting oesophageal pa in threshold than healthy controls (45 [30 to 58] vs 64 [49 to 81] mA; p=0. 04). In response to acid infusion, their pain threshold in the upper oesoph agus fell further and for longer (mean fall in area under threshold/time cu rve 26.7 [11.0 to 42.3] vs 5.8 [2.8 to 8.8] units; p=0.04). Interpretation The finding of secondary viscerovisceral and viscerosomatic pain hypersensitivity suggests that central sensitisation may contribute to visceral pain disorders. The prolonged visceral pain hypersensitivity in p atients with noncardiac chest pain suggests a central enhancement of sensor y transfer. New therapeutic opportunities are therefore possible.