Pain
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Recent findings linked gastrointestinal disorders characterized by abdominal pain to gut microbiota composition. The present work aimed to evaluate the power of gut microbiota as a visceral pain modulator and, consequently, the relevance of its manipulation as a therapeutic option in reversing postinflammatory visceral pain persistence. Colitis was induced in mice by intrarectally injecting 2,4-dinitrobenzenesulfonic acid (DNBS). ⋯ By contrast, no significant alterations of colon histology, permeability, and monoamines levels were detected. Finally, by manipulating the gut microbiota of DNBS-treated animals, a counteraction of persistent visceral pain was achieved. The present results provide novel insights into the relationship between intestinal microbiota and visceral hypersensitivity, highlighting the therapeutic potential of microbiota-targeted interventions.
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One in 5 patients with diabetes suffers from chronic pain with neuropathic characteristics, but the pathophysiological mechanisms underlying the development of neuropathic pain in patients with diabetic distal symmetrical polyneuropathy (DSP) are poorly understood. Systemic low-grade inflammation has been implicated, but there is still a considerable knowledge gap concerning its scope and meaning in this context. The aim of the study was to establish the broad inflammatory signature of painful diabetic DSP in serum samples from the Pain in Neuropathy Study, an observational cross-sectional multicentre study in which participants underwent deep phenotyping. ⋯ In the exploratory cohort, additional clinical data were available, showing an association of inflammation with insomnia and self-reported psychological distress. Hence, this cross-sectional exploration-replication study seems to confirm that low-grade systemic inflammation is related to the severity of neuropathy and neuropathic pain in a subgroup of patients with diabetic DSP. The pathophysiological relevance of these proteins for the development of neuropathic pain in patients with diabetic DSP must be explored in more depth in future studies.
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Studies comparing different drug treatments for chronic neuropathic pain (NP) are very limited. We, therefore, examined 4 recommended treatments, namely, antidepressants (duloxetine, venlafaxine, and tricyclic antidepressants), antiepileptics (gabapentine and pregabalin), weak opioids, and strong opioids, among patients with NP evaluated before first visit in a tertiary pain treatment centre and 6 months later. Patients with both a clinical diagnosis of NP and a DN4 score ≥3/7 were selected from patients enrolled in the Quebec Pain Registry. ⋯ Among patients taking strong opioids (N = 288), 13.9% (N = 40/288) were improved vs 27.0% (177/656) of those who were not on opioids (P < 0.004). Inverse probability of treatment weighting confirmed that the proportion of patients who improved was significantly lower among those taking strong opioids compared with those who did not (P < 0.001). In conclusion, long-term use of strong opioids is a treatment suited for a limited proportion of patients with chronic NP.
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The transition from acute to chronic pain results in maladaptive brain remodeling, as characterized by sensorial hypersensitivity and the ensuing appearance of emotional disorders. Using the chronic constriction injury of the sciatic nerve as a model of neuropathic pain in male Sprague-Dawley rats, we identified time-dependent plasticity of locus coeruleus (LC) neurons related to the site of injury, ipsilateral (LCipsi) or contralateral (LCcontra) to the lesion, hypothesizing that the LC→dorsal reticular nucleus (DRt) pathway is involved in the pathological nociception associated with chronic pain. LCipsi inactivation with lidocaine increased cold allodynia 2 days after nerve injury but not later. ⋯ Furthermore, chemogenetic inactivation of the LCcontra→DRtcontra pathway induced depressive-like behaviour in naïve animals, but it did not modify long-term pain-induced depression. Overall, nerve damage activates the LCipsi, which temporally dampens the neuropathic phenotype. However, the ensuing activation of a LCcontra→DRtcontra facilitatory pain projection contributes to chronic pain, whereas global bilateral LC activation contributes to associated depressive-like phenotype.
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There is a need to further develop telemedicine approaches because of the immediate and perhaps long-term consequences of the coronavirus disease 2019. Thus, a remote protocol for assessment of patients with temporomandibular disorders (TMD) was developed, and the agreement of this protocol was compared with the guidelines of the Diagnostic Criteria for TMD (DC/TMD). A total of 16 individuals were first assessed by a reference standard examination (RSE) and 3 other examinations applied in a random order by 3 examiners: standard physical examination (standard examination), physical examination keeping 2-m distance (physical distanced examination), and examination conducted with the aid of video communication technology (video communication examination). ⋯ There was substantial to almost perfect agreement between the RSE and all the examination protocols for the diagnoses of myalgia (0.86-1.00) and arthralgia (0.74-0.87) (P < 0.001). On the other hand, there was an overall poor agreement (0.30-0.58) between the RSE and all the protocols for the diagnosis of disk displacement with reduction. Remote assessment of patients with pain-related TMD is feasible and presents a high degree of accuracy.