Articles: hyperalgesia.
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Chronic pain induced by nerve damage due to trauma or invasion of cancer to the bone elicits severe ongoing pain as well as hyperalgesia and allodynia likely reflecting adaptive changes within central circuits that amplify nociceptive signals. The present study explored the possible contribution of the mesolimbic dopaminergic circuit in promoting allodynia related to neuropathic and cancer pain. Mice with ligation of the sciatic nerve or treated with intrafemoral osteosarcoma cells showed allodynia to a thermal stimulus applied to the paw on the injured side. ⋯ Optogenetic activation of these cells produced a significant but transient anti-allodynic effect in nerve injured or tumor-bearing mice without increasing response thresholds to thermal stimulation in sham-operated animals. Suppressed activity of mesolimbic dopaminergic neurons is likely to contribute to decreased inhibition of N. Acc. output neurons and to neuropathic or cancer pain-induced allodynia suggesting strategies for modulation of pathological pain states.
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Objective Previous studies of neuropathic pain have suggested that the P2X4 purinoceptor (P2X4R) in spinal microglia is essential for maintaining allodynia following nerve injury. However, little is known about its role in inflammatory soup-induced trigeminal allodynia, which closely mimics chronic migraine status. Here, we determined the contributions of P2X4R and related signaling pathways in an inflammatory soup-induced trigeminal allodynia model. ⋯ Double immunostaining indicated that p38 and brain-derived neurotrophic factor were mainly expressed in microglial cells, whereas excitatory amino acid transporter 3 was primarily expressed in trigeminal nucleus caudalis neurons. Conclusions These data indicate that microglial P2X4R is involved in the regulation of excitatory amino acid transporter 3 via brain-derived neurotrophic factor-tyrosine receptor kinase B signaling following repeated inflammatory dural stimulation. Microglial P2X4R activation and microglia-neuron interactions in the trigeminal nucleus caudalis may play a role in the pathogenesis of migraine chronicity, and the modulation of P2X4R activation might be a potential therapeutic strategy.
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Frontiers in pharmacology · Jan 2018
Effects of Transcranial Direct Current Stimulation Block Remifentanil-Induced Hyperalgesia: A Randomized, Double-Blind Clinical Trial.
Background: Remifentanil-induced hyperalgesia (r-IH) involves an imbalance in the inhibitory and excitatory systems. As the transcranial Direct Current Stimulation (tDCS) modulates the thalamocortical synapses in a top-down manner, we hypothesized that the active (a)-t-DCS would be more effective than sham(s)-tDCS to prevent r-IH. We used an experimental paradigm to induce temporal summation of pain utilizing a repetitive cold test (rCOLDT) assessed by the Numerical Pain Score (NPS 0-10) and we evaluated the function of the descending pain modulatory system (DPMS) by the change on the NPS (0-10) during the conditioned pain modulation (CPM)-task (primary outcomes). ⋯ Thereby, tDCS could be considered as a new approach to contra-regulate paradoxical mechanisms involved in the r-IH. Clinical trials identification: NCT02432677. URL:https://clinicaltrials.gov/.
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Various spinal cord stimulation (SCS) modes are used in the treatment of chronic neuropathic pain disorders. Conventional (Con) and Burst-SCS are hypothesized to exert analgesic effects through different stimulation-induced mechanisms. Preclinical electrophysiological findings suggest that stimulation intensity is correlated with the effectiveness of Burst-SCS. Therefore, we aimed to investigate the relation between amplitude (charge per second) and behavioral effects in a rat model of chronic neuropathic pain, for both Conventional Spinal Cord Stimulation (Con-SCS) and biphasic Burst-SCS. ⋯ Biphasic Burst-SCS requires significantly more mean charge per second in order to achieve similar pain relief, as compared with Con-SCS, in an experimental model of chronic neuropathic pain.
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Migraineurs exhibit pain hypersensitivity throughout the body during and between migraine headaches. Migraine is classified as a central sensitivity syndrome, typified by fibromyalgia showing widespread pressure hyperalgesia determined by a tender point. This study was performed to examine whether: 1) there is a subgroup of episodic migraineurs with widespread pressure hyperalgesia during and between attacks; 2) if such a subgroup exists, what is the prevalence and what is the difference between groups with interictal widespread hyperalgesia and acute allodynia regarding the demographic and clinical characteristics of migraine. ⋯ Interictal widespread pressure hyperalgesia was common (42%) in the episodic migraineurs and was associated with younger age at onset, female gender, and higher frequency of headache, but not duration of migraine illness. Presence of interictal widespread pressure hyperalgesia is assumed to be an indicator of genetic susceptibility to migraine attacks. We expect that a tender point count, as an alternative to quantitative sensory testing, will become useful as a diagnostic indicator of interictal hyperalgesia in migraineurs to predict susceptibility to migraine attacks and to permit tailored treatment.