Pain
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Painful temporomandibular disorders (TMDs) are both consequence and cause of change in multiple clinical, psychosocial, and biological factors. Although longitudinal studies have identified antecedent biopsychosocial factors that increase risk of the TMD onset and persistence, little is known about long-term change in those factors after TMD develops or remits. During a 7.6-year median follow-up period, we measured change in psychosocial characteristics, pain sensitivity, cardiovascular indicators of autonomic function, and clinical jaw function among 189 participants whose baseline chronic TMD status either persisted or remitted and 505 initially TMD-free participants, 83 of whom developed TMD. ⋯ In general, clinical and psychosocial variables more frequently changed in parallel with TMD status compared with pain sensitivity and autonomic measures. These findings demonstrate a complex pattern of considerable changes in biopsychosocial function associated with changes in TMD status. In particular, several biopsychosocial parameters improved among participants with chronic TMD despite pain persisting for years, suggesting considerable potential for ongoing coping and adaptation in response to persistent pain.
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Enhanced sensitivity to light (photophobia) and patterns is common in migraine and can be regarded as visual allodynia. We aimed to develop and validate a questionnaire to easily quantify sensitivity to light and patterns in large populations, and to assess and compare visual allodynia across different migraine subtypes and states. We developed the Leiden Visual Sensitivity Scale (L-VISS), a 9-item scale (score range 0-36 points), based on literature and patient interviews, and examined its construct validity. ⋯ The linear mixed model showed all factors affected the outcome (P < 0.001). The L-VISS is an easy-to-use scale to quantify and monitor the burden of bothersome visual sensitivity to light and patterns in large populations. There are remarkable ictal and interictal differences in visual allodynia across migraine subtypes, possibly reflecting dynamic differences in cortical excitability.
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We have previously demonstrated that lysophosphatidic acid (LPA) plays key roles in the initial mechanisms for neuropathic pain (NeuP) development. Here, we examined whether LPA receptor mechanisms and LPA production are related to the glial activation at a late stage after partial sciatic nerve ligation (pSNL) by use of microglial inhibitor, Mac1-saporin or astrocyte inhibitor, and L-α-aminoadipate (L-AA). Although single intrathecal injection of LPA1/3 antagonist, Ki-16425 did not affect the pain threshold at day 7 after the spinal cord injury, repeated treatments of each compound gradually reversed the basal pain threshold to the control level. ⋯ The involvement of LPA receptors in astrocyte activation in vivo was evidenced by the findings that Ki-16425 treatments abolished the upregulation of CXCL1 in activated astrocytes in the spinal dorsal horn of mice at day 14 after the pSNL, and that Ki-16425 reversed the LPA-induced upregulation of several chemokine gene expressions in primary cultured astrocytes. Finally, we found that significant hyperalgesia was observed with intrathecal administration of primary cultured astrocytes, which had been stimulated by LPA in a Ki-16425-reversible manner. All these findings suggest that LPA production and LPA1/3 receptor activation through differential glial mechanisms play key roles in the maintenance as well as initiation mechanisms in NeuP.
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The aim of this study was to determine whether upregulated cutaneous expression of α1-adrenoceptors (α1-AR) is a source of pain in patients with complex regional pain syndrome (CRPS). Immunohistochemistry was used to identify α1-AR on nerve fibres and other targets in the affected and contralateral skin of 90 patients, and in skin samples from 38 pain-free controls. The distribution of α1-AR was compared between patients and controls, and among subgroups of patients defined by CRPS duration, limb temperature asymmetry, and diagnostic subtype (CRPS I vs CRPS II). ⋯ Although less clearly associated with the nociceptive effects of phenylephrine, α1-AR expression was greater on dermal nerve fibres in the painful than contralateral limb. Together, these findings are consistent with nociceptive involvement of cutaneous α1-AR in CRPS. This involvement may be greater in acute than chronic CRPS, and in CRPS II than CRPS I.
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Movement is changed in pain, but the mechanisms remain unclear. Key questions are unresolved such as whether activation can be inhomogeneously distributed within a muscle in a manner that is specific to the location of noxious input. This study addressed this question using high-density electromyography (EMG) to study regional redistribution of muscle activation within the vasti muscles and changes in knee extension force direction in response to noxious stimulation applied to muscular and nonmuscular tissues around the knee. ⋯ Preferential reduction of activation of the distal region of vastus medialis was observed when distal vastus medialis (P < 0.001) or vastus lateralis (P < 0.05) was injected. Both adaptations persisted after pain resolution. These results support the hypothesis that specific adaptation depends on the location of a noxious stimulus and imply that recovery of pain is not necessarily concomitant with return of the EMG to prepain patterns.