Cutaneous vibration is able to reduce both clinical and experimental pain, an effect called vibratory analgesia. The traditional explanation for this phenomenon is that it is mediated by lateral inhibition at the segmental (spinal cord) level, in pain-coding cells with center-surround receptive fields. We evaluated this hypothesis by testing for two signs of lateral inhibition-namely (1) an effect of the distance between the noxious and vibratory stimuli and (2) an inhibition-induced shift in the perceived location of the noxious stimulus. The experiment involved continuous ratings of the pain from pressure applied to the back of a finger, alone and in the presence of vibration delivered to sites on the palm of the hand both near to and far from the site of painful stimulation. Neither prediction of the segmental hypothesis was supported. There was also little evidence to support the view (widely held by subjects) that distraction is the primary mechanism of vibratory analgesia. The results are more consistent with a recently proposed theory of interactions between two cortical areas that are primarily involved in coding pain and touch, respectively.

Vibratory antinociception: effects of vibration amplitude and frequency.http://www.ncbi.nlm.nih.gov/pubmed/14622680

Abstract

The ability of cutaneous vibration to compromise detection of a nociceptive stimulus was examined in 2 sets of psychophysical experiments. The noxious stimulus was a 10-millisecond burst of radiant heat from a CO2 laser; at the near-threshold levels used it generally yielded a mild pricking sensation. In both experiments, the detectability (de′) of the laser was measured in the presence of different vibratory stimuli and in the absence of vibration. Periods of vibration lasted 10 seconds, bracketing the time of occurrence of the laser. Vibratory and laser stimuli were presented 2.3 cm apart on the dorsal surface of the forearm. Confidence rating procedures yielded receiver operating characteristic curves from which detectability of the laser was calculated. In an amplitude study, vibrations ranging from 10 to 45 dB above threshold were used; results indicated that nociceptive sensitivity gradually declined as vibration amplitude increased. In a frequency study, vibrations ranging from 20 to 230 Hz were used; all interfered with nociception. Combining the results of the 2 studies permitted the conclusion that signals in multiple vibrotactile channels are able to modulate nociception. No one mechanoreceptive channel appears to have a privileged role.