• Eva Kosek and Anna Januszewska.
• Department of Clinical Neuroscience, Karolinska Institute, MR-Center N8:00, Karolinska University Hospital, 171 76 Stockholm, Sweden. eva.kosek@ki.se
• Eur J Pain. 2008 Jul 1;12(5):650-60.

AbstractThe aim was to investigate the mechanisms of pain referral in patients with whiplash associated disorder. Pain was induced in 12 controls and 12 patients with whiplash associated disorder by intramuscular electrical stimulation in the infraspinatus muscle and the ipsilateral upper arm, i.e., the area where all subjects perceived referred pain during conditioning stimulation in the infraspinatus muscle. Conditioning stimulation amounted to a pain intensity rated as 2/10 and 4/10. During conditioning stimulation in the infraspinatus muscle, sensitivity to test stimuli was assessed in the referred pain area (i.e., upper arm) and vice versa. Test stimuli consisted of intramuscular electrical stimulation corresponding to innocuous perception threshold, electrical pain threshold, and pain intensities rated as 2/10, 4/10 and 6/10, respectively. Compared to controls, patients with whiplash associated disorder had increased pain sensitivity (p< or =0.01) and indicated larger areas of referred pain ((p< or =0.003) during stimulation at the infraspinatus muscle; p< or =0.03 during stimulation at the upper arm), including proximal referral of pain which was never reported by controls (p< or =0.05). During conditioning stimulation in the infraspinatus muscle (4/10) all subjects reported referred pain in the upper arm (corresponding to the test site) and innocuous perception thresholds (p<0.05)(patients) and electrical pain thresholds (p<0.001) (controls) decreased. Conditioning stimulation in the upper arm did not affect sensitivity to test stimuli in the infraspinatus muscle. In conclusion, patients with whiplash associated disorder had increased sensitivity to painful stimulation, reported larger areas of referred pain during the same subjectively painful conditioning stimulation (i.e., lower absolute stimulus intensities), including proximal pain referral which was never seen in controls, indicating aberrant processing of nociceptive input. The perceptual integration of nociceptive stimuli during simultaneous stimulation did not differ between groups suggesting that divergence of nociceptive input from the focal pain area leading to excitation of neurones with projected fields in the referred pain area most likely explains referred pain in both groups alike.

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