Recent studies into the common complaint of chronic neck pain have focused on its anatomical origin, identifying especially the cervical zygapophysial joints. However the pathophysiology of chronic neck pain remains poorly understood. In this psychophysical study, responses to electrocutaneous stimulation in subjects with chronic neck pain were examined. In an ascending method of limits design. electrical stimuli at 100 Hz with variation in current from 0 to 45 mA and in pulse width from 100 to 1000 micros were delivered transcutaneously to two points 2 cm from the midline bilaterally at the levels of C5/6 and C7/T1 in 35 subjects with chronic neck pain and 22 pain-free volunteers. There was a small difference in detection threshold between the two groups: both pain threshold and pain tolerance were significantly lower in the pain group compared with pain free controls. These findings define hyperalgesia psychophysically and, taken together with the absence of tissue damage at the sites of testing. suggest that these painful cervical regions may be examples of secondary hyperalgesia which, in turn, implies central sensitisation of nociceptive pathways. These results are compatible with studies which identify potential anatomical origins of chronic neck pain but provide evidence that central sensitisation may be the relevant mechanism of pain production.

Rational drug treatment of chronic musculoskeletal pain remains a challenge. Although commonly prescribed, the true efficacy of opioid analgesics or of nonsteroidal antiinflammatory drugs remains to be established. Using an N-of 1 design, eight patients with regional cervicobrachial pain received ibuprofen 800 mg/day, codeine 120 mg/day, or placebo during six 2 week periods. Clinical outcomes were assessed by pain diary, VAS of pain and change in pain, and uptime/downtime estimates. In none of the five subjects who completed the 12-week trial was analgesic efficacy of either drug shown. Major psychosocial and other medical influences on the subjects' status were encountered. The N-of 1 methodology is appropriated for evaluating true efficacy of pharmacotherapy in patients with regional musculoskeletal pain.

Objective. A range of functional, biochemical, and psychological indicators was used to test the concept of “responders”/“nonresponders” and to seek predictors of response to 2 nonsteroidal antiinflammatory drugs in 9 patients with rheumatoid arthritis (RA) and 11 with osteoarthritis (OA). Methods. In a balanced, randomized, doubleblind, latin‐square study design that involved four 4‐ week treatment periods, patients received ketoprofen or piroxicam (each for 2 of the 4 periods). Clinical and laboratory responses (pain, tenderness, swelling, patient and physician global assessments, acute‐phase protein levels, and disability) were assessed in the last 2 weeks of each period. Responders were those who showed >30% improvement in at least 5 of 7 measures of disease activity. Mood was also assessed. Results. At baseline, variables were higher in RA than in OA patients. The drugs produced clear improvements in patients' visual analog scale scores, physicians' overall assessments, and patients' responses to the McGill Pain Questionnaire, as well as plasma prostaglandin concentrations. In patients with either RA or OA, responders could be distinguished from nonresponders; about one‐third of patients were unambiguous responders. In RA, there were responder nonresponder differences in lymphocyte counts, erythrocyte sedimentation rate (ESR), and levels of tumor necrosis factor α, but no differences were seen in OA patients. However, caution in interpretation of the data is necessary because of the small number of patients. Responders had improved mood scores compared with nonresponders in both disease groups. Baseline ESR and white blood cell counts were correlated with responder status in RA patients. Conclusion. This study provides support for the responder/nonresponder concept. It also indicates that in RA, pretreatment ESR and lymphocyte counts are possibly useful indicators of therapeutic response.