Pain
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The thalamus plays an important role in sensory and motor information processing by mediating communication between the periphery and the cerebral cortex. Alterations in thalamic development have profound consequences on sensory and motor function. ⋯ Our findings reveal a role for first-order posterior medial thalamic neurons and their projections to layer 4 of the secondary somatosensory cortex in the transmission of nociceptive information. Together, these results establish a connection between a neurodevelopmental lesion in the thalamus and a modality-specific disruption in pain perception.
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Quantitative sensory testing (QST) is a set of methods for quantifying somatosensory functioning. Limitations of laboratory-based QST (LQST) include high cost, complexity in training, lack of portability, and time requirements for testing. Translating QST to a home setting could facilitate future research and clinical care. ⋯ The participants rated the HQST protocol as highly acceptable and safe but can be improved in future implementations. Home QST was able to detect hypoesthesia to vibration after lidocaine cream application ( P = 0.024, d = 0.502) and could detect hypoalgesia and hyperalgesia to pressure and heat pain sensitivity tests after application of lidocaine and capsaicin creams, respectively ( P -value range = <0.001-0.036, d -value range = 0.563-0.901). Despite limitations, HQST tool-kits may become a cost-effective, convenient, and scalable approach for improving sensory profiling in clinical care and clinical research.
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The concept "nociplastic pain" has been developed for patients with features of nociceptive system sensitization that are not explained as nociceptive or neuropathic. Here, we tested how well the recently published grading system differentiates between chronic primary and secondary pain conditions. We recruited patients with fibromyalgia (FMS, n = 41), complex regional pain syndrome (CRPS, n = 11), osteoarthritis (OA, n = 21), or peripheral nerve injury (PNI, n = 8). ⋯ Based on these data, specificity remained excellent (93%), but sensitivity dropped substantially (60%) due to lacking evidence for pain hypersensitivity in many patients with FMS. This low sensitivity suggests that the published grading system is not suitable for screening purposes. We suggest structural and content modifications to improve sensitivity, including placement of patient history before clinical examination and addition of a high tender point count as evidence for widespread pain hypersensitivity.
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Randomized Controlled Trial
Independent effects of transcranial direct current stimulation and social influence on pain.
Transcranial direct current stimulation (tDCS) is a noninvasive neuromodulatory technique with the potential to provide pain relief. However, tDCS effects on pain are variable across existing studies, possibly related to differences in stimulation protocols and expectancy effects. We investigated the independent and joint effects of contralateral motor cortex tDCS (anodal vs cathodal) and socially induced expectations (analgesia vs hyperalgesia) about tDCS on thermal pain. ⋯ The observed additive effects provide novel evidence that tDCS and socially induced expectations operate through independent processes. They extend clinical tDCS studies by showing tDCS effects on controlled nociceptive pain independent of expectancy effects. In addition, they show that social suggestions about neurostimulation effects can elicit potent placebo effects.
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Worse executive function (EF) is associated with chronic pain and could mechanistically contribute to pain chronification. It is unclear whether there is overall impairment in EFs or whether there are impairments in specific cognitive domains. Furthermore, the possible genetic risk underlying these associations has not been tested. ⋯ A twin model indicated that pain and Updating-specific variance share genetic risk ( r A = -0.46, P = 0.005) but not environmental risk ( r E = 0.05, P = 0.844). Updating working memory shares a phenotypic and genetic relationship with pain in young adults. Impairments in gating or monitoring pain signals may play a mechanistic role in pain development.