Articles: hyperalgesia.
-
Anesthesia and analgesia · Oct 2019
The GCs-SGK1-ATP Signaling Pathway in Spinal Astrocytes Underlied Presurgical Anxiety-Induced Postsurgical Hyperalgesia.
Patients undergoing surgery often feel anxious. Accumulating evidence indicated that presurgical anxiety was related to the more severe postsurgical pain. An animal model was established that exposed Sprague-Dawley rats to a single-prolonged stress (SPS) procedure to induce presurgical anxiety-like behaviors. The experiment revealed that presurgical anxiety not only aggravated but also prolonged postsurgical pain. However, the underlying mechanisms were unknown. ⋯ These data suggested an important signaling pathway that affected the pain sensitivity after operation caused by presurgical anxiety.
-
Experimental neurology · Oct 2019
Enhanced descending pain facilitation in acute traumatic brain injury.
Acute and persistent pain are recognized consequences of TBI that can enhance suffering and significantly impair rehabilitative efforts. Both experimental models and clinical studies suggest that TBI may result in an imbalance between descending pain facilitatory and inhibitory pathways. The aim of this study was to assess the role of enhanced descending serotonin-mediated pain facilitation in a rat TBI model using selective spinal serotonergic fiber depletion with 5, 7-dihydroxytryptamine (DHT). ⋯ Additional immunohistochemical analyses of the lumbar spinal cord at 7 DPI revealed a robust bilateral microglial response in the superficial dorsal horns that was significantly reduced with DHT treatment. Furthermore, serotonin depletion also prevented the TBI-induced bilateral increase in c-Fos positive cells within the Rexed laminae I and II of the dorsal horns. These results indicate that in the weeks following TBI, pain may be responsive to 5-HT3 receptor antagonists or other measures which rebalance descending pain modulation.
-
Int. Immunopharmacol. · Oct 2019
Nrf2/HO-1 signaling pathway participated in the protection of hydrogen sulfide on neuropathic pain in rats.
Neuropathic pain is evoked by aberrant sensory processing in the peripheral or central nervous system, which is characterized by persistent pain, tactile allodynia, or hyperalgesia. Neuroinflammation is associated with the initiation and maintenance of persistent pain in both the peripheral and central nervous systems. Hydrogen sulfide plays important regulatory roles in different physiological and pathological conditions. ⋯ Mechanical allodynia, thermal hyperalgesia and the number of paw lifts were measured at different time points after operation. In the present research, neuropathic pain induced Nrf2 and HO-1 expression in the microglial cells of the spinal cord; Nrf2 and HO-1 were necessary to alleviate the hyperalgesia of CCI-induced rats; NaHS mitigated the hyperalgesia and allodynia induced by the CCI operation; and NaHS mitigated the excessive release of the cytokines TNF-α, IL-1β, IL-6 and HMGB1 via the Nrf2/HO-1 pathway in the microglial cells of the spinal cord. These results indicated that NaHS exhibited antinociceptive and anti-inflammatory effects that were associated with the activation of the Nrf2/HO-1 pathway in the spinal cord of rats with neuropathic pain.
-
Cutaneous mechanical hyperalgesia can be induced in healthy volunteers in early phase analgesic studies to model central sensitization, a key mechanism of persistent pain. However, such hyperalgesia is short-lived (a matter of hours), and is used only for assessing only single drug doses. In contrast, postsurgical peri-incisional hyperalgesia may be more persistent and hence be a more useful model for the assessment of the efficacy of new analgesics. ⋯ The findings suggest that central sensitization contributes significantly to mechanical hyperalgesia at the peri-incisional site. The prolonged duration of hyperalgesia would be advantageous as a pain model, but there was considerable variability of mechanical hyperalgesia in the cohort; the challenges of recruitment may limit its use to small, early phase analgesic studies. PERSPECTIVE: Peri-incisional mechanical hyperalgesia persists for ≥4 weeks after open inguinal hernia repair and reflects central sensitization; this may have usefulness as a model of chronic pain to assess the potential of antineuropathic analgesics.
-
There is an ethical obligation to notify individuals about potential pain associated with diagnoses, treatments, and procedures; however, supplying this information risks inducing nocebo hyperalgesia. Currently, there are few empirically derived strategies for reducing nocebo hyperalgesia. Because nocebo effects are linked to negative affectivity, we tested the hypothesis that a positive-affect induction can disrupt nocebo hyperalgesia from verbal suggestion. ⋯ In the neutral-affect conditions, there was evidence for the nocebo hyperalgesia effect: participants given the suggestion of pain displayed greater pain than participants not receiving this suggestion, P's < 0.05. Demonstrating a blockage effect, nocebo hyperalgesia did not occur in the positive-affect conditions, P's > 0.5. This is the first study to show that positive affect may disrupt nocebo hyperalgesia thereby pointing to a novel strategy for decreasing nocebo effects without compromising the communication of medical information to patients in clinical settings.