In the present human study, we aimed to investigate the facilitation of both the subjective pain responses, and the withdrawal reflex to consecutive transcutaneous electrical stimuli as measures of temporal summation. The frequency (0.5-20 Hz) and intensity (0.4-0.8 times the reflex threshold, xRT) of the electrical stimuli were systematically varied. When using repeated stimulation, the stimulus intensity that evoked pain was lower than that required by a single stimulus (temporal summation). Temporal summation leading to pain was found to depend significantly upon both frequency and intensity (e.g. stimulation at 1 Hz caused summation at 0.8 x RT, whereas stimulation at 20 Hz caused summation at 0.6 x RT). The strongest reflex facilitation, and hence the strongest pain intensity was obtained for stimulation at 10-20 Hz at an intensity of 0.8 x RT. In conclusion, the results of the present human study demonstrate clearly that a stimulus that is perceived as a localised, repetitive tactile tap can be integrated and cause severe pain. This suggests that pathologically generated sparse nociceptive afferent activity causes strong pain by central integration. This might be one mechanism to explain why clinical conditions can become excruciatingly painful despite the fact that the pathophysiological changes seem to be marginal (e.g. minor nerve trauma).

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The present study investigated excitatory reflex receptive fields for various muscle reflex responses and reflex mediated ankle joint movements using randomised electrical stimulation of the dorsal and plantar surface of the foot in 12 healthy subjects. Eleven electrodes (0.5-cm2 cathodes) were mounted on the dorsal side and three on the plantar side of the foot. A low (1.5 times pain threshold) and a high (2.3 times pain threshold) stimulus intensity were used to elicit the reflexes. EMG signals were recorded from tibialis anterior (TA), gastrocnemius medialis (GM), soleus (SO), biceps femoris (BF), and rectus femoris (RF) muscles together with the ankle movement measured by a goniometer. The withdrawal pattern evoked from the dorsal side consisted of two separate responses with different receptive fields: (1) early EMG responses in GM and BF (50-120 ms) evoking knee flexion, probably of purely spinal origin, and (2) a late response in GM and SO (120-200 ms) that may be under supraspinal control. The ankle flexor TA was significantly activated in both time windows, but in 11 of 12 subjects its contraction was too small to cause significant dorsal flexion. In the ankle joint inversion was the most dominant movement. Stimulation of the plantar side resulted in activation of TA when stimulating the forefoot and in activation of triceps surae when stimulating the heel. These observations show that painful stimuli activate appropriate muscles depending on stimulus location to initiate the adequate withdrawal. For proximal muscles (e.g. knee flexors) the receptive field covers almost the entire foot (dorsal and plantar sides) while more distal muscles have a smaller receptive field covering only a part of the foot. This adequate withdrawal movement suggests a more refined withdrawal reflex organisation than a stereotyped flexion of all joints to avoid tissue damage.

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