Pain
-
Dyspnea and pain have a number of similarities. Recent brain imaging experiments showed that similar cortical regions are activated by the perceptions of dyspnea and pain. We tested the hypothesis that an individual's pain sensitivity might parallel the individual's dyspnea sensitivity. ⋯ A significant correlation was observed between the pain threshold time and the period of no respiratory sensation in both the PT and PS groups. However, no significant association was observed between pain and dyspnea tolerance in both groups. In conclusion, an individual's pain threshold is correlated to the individual's dyspnea threshold, but the individual's pain tolerance is not consistently correlated to the individual's dyspnea tolerance.
-
The objective was to compare the Severity of Dependence Scale (SDS) score and pattern of medication use in persons with secondary chronic headache (>or= 15 days/month for at least 3 months) in a cross-sectional epidemiological survey. A posted questionnaire screened for chronic headache. Neurological residents interviewed those with self-reported chronic headache. ⋯ The sensitivity, specificity, positive and negative predictive values were 0.82, 0.82, 0.82 and 0.83, respectively. Thus the SDS score correlates with medication overuse, and a high SDS score suggests dependency-like behaviour in persons with secondary chronic headache. The use of SDS score in subjects with frequent pain episodes may contribute to the detection of medication overuse and better management of this group of patients.
-
The transcription factor nuclear factor kappa B (NF-kappaB) is a key regulator of inflammatory processes in reactive glial cells. We utilized a transgenic mouse model (GFAP-IkappaBalpha-dn) where the classical NF-kappaB pathway is inactivated by overexpression of a dominant negative (dn) form of the inhibitor of kappa B (IkappaBalpha) in glial fibrillary acidic protein (GFAP)-expressing cells, which include astrocytes, Schwann cells, and satellite cells of the dorsal root ganglion (DRG) and sought to determine whether glial NF-kappaB inhibition leads to a reduction in pain behavior and inflammation following chronic constriction injury (CCI) of the sciatic nerve. As expected, following CCI nuclear translocation, and hence activation, of NF-kappaB was detected only in the sciatic nerve of wild type (WT) mice, and not in GFAP-IkappaBalpha-dn mice, while upregulation of GFAP was observed in the sciatic nerve and DRGs of both WT and GFAP-IkappaBalpha-dn mice, indicative of glial activation. ⋯ Additionally, gene expression of TNF, CCL2, and CCR2 was reduced in the DRGs of transgenic mice compared to those of WT after CCI. We can therefore conclude that transgenic inhibition of NF-kappaB in GFAP-expressing glial cells attenuated pain and inflammation after peripheral nerve injury. These findings suggest that targeting the inflammatory response in Schwann cells and satellite cells may be important in treating neuropathic pain.
-
Multicenter Study
Distinctiveness of psychological obstacles to recovery in low back pain patients in primary care.
Many psychological factors have been suggested to be important obstacles to recovery from low back pain, yet most studies focus on a limited number of factors. We compared a more comprehensive range of 20 factors in predicting outcome in primary care. Consecutive patients consulting 8 general practices were eligible to take part in a prospective cohort study; 1591 provided data at baseline and 810 at 6 months. ⋯ Thus, a small number of psychological factors are strongly predictive of outcome in primary care low back pain patients. There is clear redundancy in the measurement of psychological factors. These findings should help to focus targeted interventions for back pain in the future.
-
Habituation to repetitive painful stimulation may represent an important protection mechanism against the development of chronic pain states. However, the exact neurobiological mechanisms of this phenomenon remain unclear. In this study we (i) explore the somatotopic specificity of pain attenuation over time and (ii) investigate the role of the endogenous opioid system in its development. ⋯ This effect was less pronounced at the untreated arm compared to the treated arm and even weaker in the leg, displaying a significant Stimulation-Site x Time interaction. The development of pain habituation was unaffected by the opioid antagonist naloxone. Taken together, these results strongly support the role of central components in the mechanism of pain habituation that do not directly involve the endogenous opioid system.