The aim of the study was to investigate the perceptual integration of simultaneous stimulation in a focal and a referred pain area to investigate whether referred pain is mainly caused by facilitation of on-going input from the referred pain area by stimulation in the focal pain area or if referred pain is a consequence of misinterpretation of the origin of inputs from the focal pain area. Pain was induced in twelve healthy individuals by intramuscular electrical stimulation in the left infraspinatus muscle (MI) or the left dorsolateral upper arm (UA), i.e. the area of referral commonly reported from stimulation in MI. Conditioning stimulation consisted of, in a counterbalanced order, no stimulation (baseline) and pain intensity rated as 2/10 and 4/10, respectively, on a category scale. During conditioning stimulation in MI, sensitivity to test stimuli was assessed in UA and vice versa. The test stimuli consisted of i.m. electrical stimulation corresponding to the perception threshold to innocuous electrical stimulation, the electrical pain threshold (EPT), and pain intensity rated as 2/10, 4/10 and 6/10, respectively. Conditioning stimulation corresponding to 2/10 did not result in a statistically significant change in sensitivity to any test stimuli in either location. During conditioning stimulation corresponding to 4/10 in m. infraspinatus, all twelve subjects reported referred pain in the dorsolateral upper arm. Compared to baseline, EPTs decreased in the referred pain area (P<0.001), while no other statistically significant changes in sensitivity to test stimuli were seen. Conditioning stimulation corresponding to 4/10 in the dorsolateral upper arm gave rise to referred pain in one individual (area of m. biceps brachii), and no statistically significant changes were seen in the sensitivity to electrical stimuli in m. infraspinatus. In conclusion, an effect at pain threshold level only was documented during simultaneous stimulation in the focal and referred pain area, which does not support facilitation of inputs from the referred pain area as the main mechanism generating referred pain. Instead, referred pain is most likely a consequence of misinterpretation of the origin of input from the stimulated focal pain area, due to excitation of neurones somewhere along the neuroaxis with projected fields in the referred pain area. The fact that conditioning stimulation in m. infraspinatus generated referred pain in the dorsolateral upper arm, but not vice versa suggests that the divergence of the input is not reciprocally arranged.