Adjustment to chronic pain in back pain patients classified according to the motivational stages of chronic pain management.

UNLABELLED: According to Prochaska's transtheoretical model, the Freiburg Questionnaire stages of chronic pain management (FQ-STAPM) were used to classify chronic back patients into 4 distinct motivational stages. The FQ-STAMP was completed by 163 chronic back pain patients. Pain chronicity was measured by the Mainz Pain Staging System; pain intensity was measured by the numeric rating scale. Healthcare system expenses were considered as number of consulted physicians, number of stays in hospital, and number of rehabilitation programs. As psychometric tests, the lower pain disability index (PDI), the Hospital Anxiety and Depression Scale (HADS), and a quality of life score (SF36) were used. Patients were in the following motivational stages: precontemplation in 30%, preparation in 19%, action in 30%, maintenance in 21%. The intensity of pain in the precontemplation stage patients was significantly higher compared to patients in the maintenance stage. A lower pain chronicity was related to a significantly higher motivation. Moreover, there was a significant increase in healthcare system expenses by the lesser motivated patients. Patients in the maintenance stage used significantly less opioids than patients in the precontemplation stage. The higher motivated patients had a significantly lower PDI, a significantly lower HADS, and a significantly higher quality of life compared to less motivated patients. PERSPECTIVE: The study indicates that the FQ-STAPM might be a useful tool to classify chronic back pain patients and to work out a strategy together with the patient relevant to the outcome of pain management among chronic back pain patients.

Neuropathic pain activates the endogenous kappa opioid system in mouse spinal cord and induces opioid receptor tolerance.

Release of endogenous dynorphin opioids within the spinal cord after partial sciatic nerve ligation (pSNL) is known to contribute to the neuropathic pain processes. Using a phosphoselective antibody [kappa opioid receptor (KOR-P)] able to detect the serine 369 phosphorylated form of the KOR, we determined possible sites of dynorphin action within the spinal cord after pSNL. KOR-P immunoreactivity (IR) was markedly increased in the L4-L5 spinal dorsal horn of wild-type C57BL/6 mice (7-21 d) after lesion, but not in mice pretreated with the KOR antagonist nor-binaltorphimine (norBNI). In addition, knock-out mice lacking prodynorphin, KOR, or G-protein receptor kinase 3 (GRK3) did not show significant increases in KOR-P IR after pSNL. KOR-P IR was colocalized in both GABAergic neurons and GFAP-positive astrocytes in both ipsilateral and contralateral spinal dorsal horn. Consistent with sustained opioid release, KOR knock-out mice developed significantly increased tactile allodynia and thermal hyperalgesia in both the early (first week) and late (third week) interval after lesion. Similarly, mice pretreated with norBNI showed enhanced hyperalgesia and allodynia during the 3 weeks after pSNL. Because sustained activation of opioid receptors might induce tolerance, we measured the antinociceptive effect of the kappa agonist U50,488 using radiant heat applied to the ipsilateral hindpaw, and we found that agonist potency was significantly decreased 7 d after pSNL. In contrast, neither prodynorphin nor GRK3 knock-out mice showed U50,488 tolerance after pSNL. These findings suggest that pSNL induced a sustained release of endogenous prodynorphin-derived opioid peptides that activated an anti-nociceptive KOR system in mouse spinal cord. Thus, endogenous dynorphin had both pronociceptive and antinociceptive actions after nerve injury and induced GRK3-mediated opioid tolerance.