Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0184567 (acute pain)
 3,962 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Little is known about the evolution of chronic pain in primary care. Forty five patients with a four week history of musculoskeletal pain were assessed and followed up over 26 weeks by a research nurse using a structured interview and formal assessment instruments. Patients aged 18 to 65 years were recruited on presentation at two semirural Cheshire general practices and subsequently interviewed on a domiciliary visit. Twenty patients (44%) continued to have pain at 26 weeks and these patients were considered to have chronic pain. Nineteen patients had no pain after 12 weeks and a further six had no pain after 26 weeks; these patients together formed the group with acute pain. Comparing the two groups at entry into the study (pain of four weeks' duration) demonstrated significantly higher visual analogue scale scores for intensity of pain (P < 0.01) and a higher incidence of depression (P < 0.01) in the group which subsequently developed chronic pain. In this group, the presence of depression at 12 weeks was associated with higher visual analogue scale scores (P < 0.05) but at 26 weeks scores were similar in depressed and non-depressed patients. The correlation between visual analogue scale score for intensity of pain and the use of passive coping strategies to cope with pain appeared more strongly positive with duration of pain (P < 0.05 at 26 weeks). It is suggested that high pain intensity scores, the presence of depression, and the increasing use of passive coping strategies may be identifiable associations with the development of chronic pain. Areas for further research are identified.
Br J Gen Pract 1992 Nov
PMID:The evolution of chronic pain among patients with musculoskeletal problems: a pilot study in primary care. 147 92

Altered function of Na+ channels is responsible for increased hyperexcitability of primary afferent neurons that may underlie pathological pain states. Recent evidence suggests that the Nav1.9 subunit is implicated in inflammatory but not acute pain. However, the contribution of Nav1.9 channels to the cellular events underlying nociceptor hyperexcitability is still unknown, and there remains much uncertainty as to the biophysical properties of Nav1.9 current and its modulation by inflammatory mediators. Here, we use gene targeting strategy and computer modeling to identify Nav1.9 channel current signature and its impact on nociceptors' firing patterns. Recordings using internal fluoride in small DRG neurons from wild-type and Nav1.9-null mutant mice demonstrated that Nav1.9 subunits carry the TTX-resistant "persistent" Na+ current called NaN. Nav1.9(-/-) nociceptors showed no significant change in the properties of the slowly inactivating TTX-resistant SNS/Nav1.8 current. The loss in Nav1.9-mediated Na+ currents was associated with the inability of small DRG neurons to generate a large variety of electrophysiological behaviors, including subthreshold regenerative depolarizations, plateau potentials, active hyperpolarizing responses, oscillatory bursting discharges, and bistable membrane behaviors. We further investigated, using CsCl- and KCl-based pipette solutions, whether G-protein signaling pathways and inflammatory mediators upregulate the NaN/Nav1.9 current. Bradykinin, ATP, histamine, prostaglandin-E2, and norepinephrine, applied separately at maximal concentrations, all failed to modulate the Nav1.9 current. However, when applied conjointly as a soup of inflammatory mediators they rapidly potentiated Nav1.9 channel activity, generating subthreshold amplification and increased excitability. We conclude that Nav1.9 channel, the molecular correlate of the NaN current, is potentiated by the concerted action of inflammatory mediators that may contribute to nociceptors' hyperexcitability during peripheral inflammation.
J Gen Physiol 2008 Mar
PMID:Inflammatory mediators increase Nav1.9 current and excitability in nociceptors through a coincident detection mechanism. 1827 Jan 72

Opioid use disorder (OUD), a leading cause of morbidity and mortality in the USA, can be effectively treated with buprenorphine. However, the same pharmacologic properties (e.g., high affinity, partial agonism, long half-life) that make it ideal as a treatment for OUD often cause concern among clinicians that buprenorphine will prevent effective management of acute pain with full agonist opioid analgesics. Because of this concern, many patients are asked to stop buprenorphine preoperatively or at the onset of acute pain, placing them at high risk for both relapse and a difficult transition back to buprenorphine after acute pain has resolved. The purpose of this review is to summarize the existing literature for acute pain and perioperative management in patients treated with buprenorphine for OUD and to provide practical management recommendations for generalist practitioners based on evidence and clinical experience. In short, evidence suggests that sufficient analgesia can be achieved with maintenance of buprenorphine and use of both opioid and non-opioid analgesic options for breakthrough pain. We recommend that clinicians (1) continue buprenorphine in the perioperative or acute pain period for patients with OUD; (2) use a multi-modal analgesic approach; (3) pay attention to care coordination and discharge planning when making an analgesic plan for patients with OUD treated with buprenorphine; and (4) use an individualized approach founded upon shared decision-making. Clinical examples involving mild and severe pain are discussed to highlight important management principles.
J Gen Intern Med 2020 Dec
PMID:Treating Perioperative and Acute Pain in Patients on Buprenorphine: Narrative Literature Review and Practice Recommendations. 3282 9