Articles: hyperalgesia.
-
Minerva anestesiologica · Apr 2018
Randomized Controlled TrialPreventative effect of ketamine on post-surgical hyperalgesia induced at a body part remote from the surgical site: a randomized controlled trial.
It is known that pain hypersensitivity can be induced at a body part remote from a surgical site (tertiary hyperalgesia), leading to patient discomfort. Nevertheless, no reported study to date has investigated methods to attenuate such tertiary hyperalgesia. Ketamine is known to modulate hyperalgesia induced by central sensitization. Thus, we investigated whether intraoperative administration of ketamine could decrease post-surgical tertiary hyperalgesia in patients undergoing a laparoscopic hysterectomy. ⋯ These results suggest that the intraoperative administration of ketamine may decrease post-surgical hyperalgesia developing at a region remote from the surgical site.
-
Opioids are frequently used for the treatment of chronic pain, and patients taking high doses are at increased risk of complications and adverse opioid-related events. Ketamine is appealing as an opioid adjunct because of its lack of respiratory depression and potential prevention of hyperalgesia and central sensitization. We present a case in which a ketamine infusion was utilized over a 7-day period to provide rapid taper of a daily dose of 400 mg of morphine equivalents to less than one-third of that dose on discharge with unchanged pain levels and no symptoms of opioid withdrawal.
-
Chronic pain patients show hypersensitivity to sensory nonpainful stimuli. Sensory over-responsiveness (SOR) to innocuous daily stimuli, experienced as painful, is prevalent in 10% of the healthy population. This altered sensory processing may be an expression of overfacilitation, or a less efficient pain-inhibitory process in the pain pathways. We therefore aimed to investigate specifically the pain-inhibitory system of subjects with SOR who are otherwise healthy, not studied as of yet. ⋯ SOR is associated with a pronociceptive state, expressed by amplification of experimental pain, yet with sufficient inhibitory processes. Our results support previous findings of enhanced facilitation of pain-transmitting pathways but also reveal preserved inhibitory mechanisms, although they were slower to react.
-
Accumulated evidence suggests that spinal cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) may be implicated in the development of opioid-induced hyperalgesia. ⋯ Acute repeated fentanyl administration dose-dependently produced mechanical hyperalgesia and augmented surgery induced postoperative hyperalgesia. This behavioural change was paralleled with an increase in spinal COX-2 mRNA and PGE2 after fentanyl administration. Inhibition of COX-2 or blockade of EP-1R can partly or totally prevent hyperalgesia.
-
To elucidate the effects of growth differentiation factor-6 (GDF6) on: (i) gene expression of inflammatory/pain-related molecules and structural integrity in the rabbit intervertebral disc (IVD) degeneration model, and (ii) sensory dysfunction and changes in pain-marker expression in dorsal nerve ganglia (DRGs) in the rat xenograft radiculopathy model. ⋯ GDF6 injection may change the pathological status of degenerative discs and attenuate degenerated IVD-induced pain.