Pain
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Neurosurgical treatments for trigeminal neuralgia (TN) can provide long-lasting pain relief; however, some patients fail to respond and undergo multiple, repeat procedures. Surgical outcomes can vary depending on the type of TN, but the reasons for this are not well understood. Neuroimaging studies of TN point to abnormalities in the brainstem trigeminal fibers; however, whether this is a common characteristic of treatment nonresponse across different subtypes of TN is unknown. ⋯ We assessed treatment response using pain intensity measures and examined microstructural features by extracting pretreatment DTI metrics from the proximal pontine segment of the trigeminal nerves. We found that microstructural abnormalities in the affected pontine trigeminal fibers (notably, lower fractional anisotropy and higher radial diffusivity) highlight treatment nonresponders (n = 47) compared with responders (n = 51) and controls, and that the degree of abnormalities is associated with the likelihood of surgical response across subtypes of TN. These novel findings demonstrate the value of DTI as an objective, noninvasive tool for the prediction of treatment response and elucidate the features that distinguish treatment responders from nonresponders in the TN population.
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Low back pain (LBP) is a leading cause of disability. However, the processes contributing to disability are not well understood. Therefore, this study (1) empirically derived LBP subgroups and (2) validated these subgroups using walking performance, pain, and disability measures. ⋯ The Maladaptive subgroup had reduced walking performance (slower self-selected walking speed, TUG completion, and obstacle approach and crossing speed) and worse clinical presentation (higher pain intensity, pain interference, and disability) (moderate to large effect sizes; P's < 0.05). Findings support the construct validity of this multidimensional subgrouping approach. Longitudinal studies are needed to determine whether the Maladaptive subgroup is predictive of poor outcomes, such as pain chronicity or persistent disability.
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Randomized Controlled Trial
Brief preoperative mind-body therapies for total joint arthroplasty patients: a randomized controlled trial.
Although knee and hip replacements are intended to relieve pain and improve function, up to 44% of knee replacement patients and 27% of hip replacement patients report persistent postoperative joint pain. Improving surgical pain management is essential. We conducted a single-site, 3-arm, parallel-group randomized clinical trial conducted at an orthopedic clinic, among patients undergoing total joint arthroplasty (TJA) of the hip or knee. ⋯ Moderation analysis revealed the surgery type did not differentially impact the 3 interventions. Thus, a single session of a simple, scripted MM intervention may be able to immediately decrease TJA patients' preoperative clinical symptomology and improve postoperative physical function. As such, embedding brief MM interventions in surgical care pathways has the potential to improve surgical outcomes for the millions of patients receiving TJA each year.
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Pain and depression are episodic conditions that might take a chronic course. They are clearly related, but information on how they influence each other in the process of chronification is limited. Pain catastrophizing is hypothesized to play a role in the development of depression and chronic pain, but few longitudinal studies have investigated their association over a longer term. ⋯ The number of years lived with chronic pain was associated with a chronic course of depression, with odds ratios increasing from 1.55 (95% CI [0.87-2.91]) to 14.19 (95% CI [8.99-22.41]) when reporting chronic pain on 2 vs 5 assessments compared with none. The results suggest that when pain intensity or catastrophizing change, depressive symptoms change in the same direction. When pain and catastrophizing become chronic, they seem to be mutually reinforcing determinants for chronic depression.
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Small-fiber neuropathy (SFN), characterized by distal unmyelinated or thinly myelinated fiber loss, produces a combination of sensory dysfunction and neuropathic pain. Gain-of-function variants in the sodium channel Nav1.7 that produce dorsal root ganglion (DRG) neuron hyperexcitability are present in 5% to 10% of patients with idiopathic painful SFN. ⋯ Therefore, although these 2 Nav1.7 I228M knock-in mouse lines recapitulate the DRG neuron hyperexcitability associated with gain-of-function mutations in Nav1.7, they do not recapitulate the pain or neuropathy phenotypes seen in patients. We suggest that the relationship between hyperexcitability in sensory neurons and the pain experienced by these patients may be more complex than previously appreciated and highlights the challenges in modelling channelopathy pain disorders in mice.