Pain
-
Randomized Controlled Trial
Effects of open-label placebo on pain, functional disability and spine mobility in chronic back pain patients: a randomized controlled trial.
Chronic back pain (CBP) is a major global health problem, while its treatment is hampered by a lack of efficacy and restricted safety profile of common frontline therapies. The present trial aims to determine whether a 3-week open-label placebo treatment reduces pain intensity and subjective and objective functional disability in patients with CBP. This randomized controlled trial, following a pretest-posttest design, enrolled 127 patients with CBP (pain duration >12 weeks) from the Back Pain Center, Neurology, University Hospital Essen, Germany. ⋯ Open-label placebo treatment did not affect objective mobility parameters, anxiety and stress. Our study demonstrates that a 3-week open-label placebo treatment is safe, well tolerated and reduces pain, disability, and depressive symptoms in CBP. Trial registration: German Clinical Trials Register, DRKS00012712.
-
While the contribution of social processes to pain perception is well documented, surprisingly little is known about the influence of pain on social perception. In particular, an important question is how pain modulates the processing of other people's actions. To address this question, the current study tests, using automatic imitation, the hypothesis that pain interferes with motor simulation-that is, the processing of observed actions in the motor system. ⋯ Automatic imitation was measured in a pain-free context, a context where pain was coupled to the execution of a movement (experiment 1), and a context where pain occurred randomly (experiment 2). The results revealed that automatic imitation, indexed by slower responses on incongruent compared with congruent trials, was reduced when experiencing pain, both when pain was linked to movement execution and when it was not. Thus, the current study shows that pain leads to reduced motor processing of others' behavior and, as such, has important implications for understanding the social difficulties associated with pain.
-
Pain catastrophizing has been shown to predict greater pain and less physical function in daily life for chronic pain sufferers, but its effects on close social partners have received much less attention. The overall purpose of this study was to examine the extent to which pain catastrophizing is an interpersonal coping strategy that is maladaptive for patients and their spouses. A total of 144 older knee osteoarthritis patients and their spouses completed baseline interviews and a 22-day diary assessment. ⋯ Multilevel mediation models showed that patients' morning pain catastrophizing indirectly impacted spouses' negative affect and punishing responses through patients' own greater negative affect throughout the day. There was no evidence that spouses' empathic or solicitous responses either followed or preceded patients' catastrophizing. These findings suggest that cognitive-behavioral interventions that reduce pain catastrophizing should be modified for partnered patients to address dyadic interactions and the spouse's role in pain catastrophizing.
-
Chemotherapy-induced peripheral neuropathy (CIPN) is a serious adverse side effect of cancer treatment with no Food and Drug Administration-approved medication for its prevention or management. Using RNA sequencing analysis of dorsal root ganglia (DRG), we identify critical contributions of histone deacetylase 6 (HDAC6) and mitochondrial damage to the establishment of CIPN in a mouse model of cisplatin-induced neuropathy. We show that pharmacological inhibition of HDAC6 using ACY-1215 or global deletion of HDAC6 is sufficient to prevent cisplatin-induced mechanical allodynia, loss of intraepidermal nerve fibers (IENFs), and mitochondrial bioenergetic deficits in DRG neurons and peripheral nerves in male and female mice. ⋯ We further reveal a critical role of T cells in the protective effects of HDAC6 inhibition on these signs of CIPN. In summary, we show that cisplatin-induced mechanical allodynia is associated with mitochondrial damage in DRG neurons, whereas the loss of IENFs is related to bioenergetic deficits in peripheral nerves. Moreover, our findings identify cell-specific contributions of HDAC6 to mechanical allodynia and loss of IENFs that characterize cisplatin-induced peripheral neuropathy.