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To identify the role of age and gender in analgesic and adverse effects after administering fentanyl products for breakthrough pain (BT), given in doses proportional to opioid doses given for background pain.
Learn More >The inflammatory/immune response at the site of peripheral nerve injury participates in the pathophysiology of neuropathic pain. Nevertheless, little is known about the local regulatory mechanisms underlying peripheral nerve injury that counteracts the development of pain. Here, we investigated the contribution of regulatory T (Treg) cells to the development of neuropathic pain by using a partial sciatic nerve ligation model in mice. We showed that Treg cells infiltrate and proliferate in the site of peripheral nerve injury. Local Treg cells suppressed the development of neuropathic pain mainly through the inhibition of the CD4 Th1 response. Treg cells also indirectly reduced neuronal damage and neuroinflammation at the level of the sensory ganglia. Finally, we identified IL-10 signaling as an intrinsic mechanism by which Treg cells counteract neuropathic pain development. These results revealed Treg cells as important inhibitory modulators of the immune response at the site of peripheral nerve injury that restrains the development of neuropathic pain. In conclusion, the boosting of Treg cell function/activity might be explored as a possible interventional approach to reduce neuropathic pain development after peripheral nerve damage.
Learn More >Systematic-reviews of analgesics for low back pain generally include published data only. Obtaining data from unpublished trials is potentially important because they may impact effect sizes in meta-analyses. We determined whether including unpublished data from trial registries changes the effect sizes in meta-analyses of analgesics for low back pain.
Learn More >Itch induces a desire to scratch and leads to skin damage in some severe conditions. Much progress has been made in the peripheral and spinal level, and recent findings suggested that we need to focus on the central circuitry mechanism. However, the functional role of the thalamus in itch signal processing remains largely unknown. We showed that the posterior thalamic nucleus (Po) played a vital role in modulating facial histaminergic itch signal processing. We found that the calcium signal of Po neurons was increased during the histaminergic itch-induced scratching behavior in the cheek model, and pharmacogenetic suppression of Po neurons reduced the scratching behaviors. Retrograde mapping results suggested that the Po receives information from the somatosensory cortex, motor cortex, parabrachial nucleus (PBN), the principal sensory trigeminal nucleus (PrV) and the spinal trigeminal nucleus (SpV), which participate in itch signal transmission from head and body. Thus, our study indicates that the Po is critical in modulating facial histaminergic itch signal processing.
Learn More >Serotonin norepinephrine reuptake inhibitors (SNRIs) are commonly co-prescribed with opioids for chronic pain. The purpose of this study was to describe pain and mood response to venlafaxine among older adults with chronic low back pain (CLBP) and depression relative to opioid exposure.
Learn More >Atopic dermatitis is a common inflammatory skin disorder characterised by recurrent eczematous lesions and intense itch. The disorder affects people of all ages and ethnicities, has a substantial psychosocial impact on patients and relatives, and is the leading cause of the global burden from skin disease. Atopic dermatitis is associated with increased risk of multiple comorbidities, including food allergy, asthma, allergic rhinitis, and mental health disorders. The pathophysiology is complex and involves a strong genetic predisposition, epidermal dysfunction, and T-cell driven inflammation. Although type-2 mechanisms are dominant, there is increasing evidence that the disorder involves multiple immune pathways. Currently, there is no cure, but increasing numbers of innovative and targeted therapies hold promise for achieving disease control, including in patients with recalcitrant disease. We summarise and discuss advances in our understanding of the disease and their implications for prevention, management, and future research.
Learn More >Chronic pain has far-reaching impacts on a person's life and on society more broadly. After failure or intolerance of conservative treatments, neuromodulation may be an option for a subgroup of patients. However, little is known about the patient experience of neuromodulation. We conducted a systematic review of published qualitative research on patient experience with neuromodulation for chronic pain. Four databases were searched: MEDLINE, EMBASE, Psych INFO, and all EMB reviews, from inception to December 4, 2019. We used narrative synthesis to identify key findings from the included studies. The data were qualitatively analyzed using a modified constant comparative analysis to identify key themes across the studies. Seven thousand five hundred forty-two unique citations were retrieved. Sixty-four abstracts were selected by the reviewers and continued to full-text review. After full-text review, 57 studies were excluded with 7 studies included in this systematic review. The included studies were of high quality. Four broad themes emerged: (1) living with chronic pain, (2) expectations, (3) managing challenges, and (4) regaining normalcy. Neuromodulation should be part of an overall pain management plan that may include the need for ongoing emotional and psychosocial support. A deeper knowledge of the patient experience with neuromodulation will assist care teams in providing meaningful support to patients. The results of this study suggest that further research is needed to support neuromodulation as an option for patients living with chronic pain.
Learn More >Spinal cord injury (SCI) causes maladaptive changes to nociceptive synaptic circuits within the injured spinal cord. Changes also occur at remote regions including the brain stem, limbic system, cortex, and dorsal root ganglia. These maladaptive nociceptive synaptic circuits frequently cause neuronal hyperexcitability in the entire nervous system and enhance nociceptive transmission, resulting in chronic central neuropathic pain following SCI. The underlying mechanism of chronic neuropathic pain depends on the neuroanatomical structures and electrochemical communication between pre- and postsynaptic neuronal membranes, and propagation of synaptic transmission in the ascending pain pathways. In the nervous system, neurons are the only cell type that transmits nociceptive signals from peripheral receptors to supraspinal systems due to their neuroanatomical and electrophysiological properties. However, the entire range of nociceptive signaling is not mediated by any single neuron. Current literature describes regional studies of electrophysiological or neurochemical mechanisms for enhanced nociceptive transmission post-SCI, but few studies report the electrophysiological, neurochemical, and neuroanatomical changes across the entire nervous system following a regional SCI. We, along with others, have continuously described the enhanced nociceptive transmission in the spinal dorsal horn, brain stem, thalamus, and cortex in SCI-induced chronic central neuropathic pain condition, respectively. Thus, this review summarizes the current understanding of SCI-induced neuronal hyperexcitability and maladaptive nociceptive transmission in the entire nervous system that contributes to chronic central neuropathic pain.
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