scholarly journals Anger regulation style, anger arousal and acute pain sensitivity: evidence for an endogenous opioid “triggering” model

2013 ◽  
Vol 37 (4) ◽  
pp. 642-653 ◽  
Author(s):  
John W. Burns ◽  
Stephen Bruehl ◽  
Melissa Chont
1986 ◽  
Vol 92 (3) ◽  
pp. 713-722 ◽  
Author(s):  
Terence J. Coderre ◽  
Ronald Melzack
Keyword(s):  

2016 ◽  
Vol 13 (1) ◽  
pp. 1-5 ◽  
Author(s):  
Helena Eva Margareta Gunnarsson ◽  
Birgitta Grahn ◽  
Jens Agerström

AbstractBackgroundPressure pain thresholds (PPTs) in a non-painful body area are known to be affected in some chronic pain states. The aim of this study is to investigate PPTs in a pain-free body part in relation to pain persistence and intensity in patients with musculoskeletal pain.MethodsPatients with musculoskeletal pain were divided into three different pain groups: acute pain (pain duration < 3 months, n = 38), regularly recurrent pain (regularly recurrent pain duration > 3 months, n = 56), persistent pain (persistent pain duration >3 months, n = 52) and a healthy control group (n = 51). PPT measures were conducted over the tibialis anterior muscle on the right leg in all groups.ResultsThe persistent pain group showed significantly lower PPTs over the tibialis anterior muscle compared to controls. No significant differences were found between the acute and regularly recurrent pain groups compared to healthy controls. Significant correlations, albeit small, were found between pain intensity and PPTs.ConclusionsIncreased deep pain sensitivity was found in patients with persistent musculoskeletal pain, but not in regularly recurrent pain or in acute pain. Yet, a limitation of the study is that it did not have sufficient power to detect small levels of increased deep pain sensitivity among the latter groups when compared to healthy controls.ImplicationsKnowledge about increased general hypersensitivity in persistent musculoskeletal pain could be important in clinical treatment.


2021 ◽  
Author(s):  
Sydney Trask ◽  
Jeffrey S. Mogil ◽  
Fred J. Helmstetter ◽  
Cheryl L. Stucky ◽  
Katelyn E. Sadler

AbstractThe mechanisms underlying the transition from acute to chronic pain are unclear but may involve the persistence or strengthening of pain memories acquired in part through associative learning. Contextual cues, which comprise the surrounding environment where events occur, were recently described as a critical regulator of pain memory; both rodents and humans exhibit increased pain sensitivity in environments recently associated with a single painful experience. It is unknown, however, how repeated exposure to an acute painful unconditioned stimulus in a distinct context modifies pain sensitivity or the expectation of pain in that environment. To answer this question, we conditioned mice to associate distinct contexts with either repeated administration of a mild visceral pain stimulus (intraperitoneal injection of acetic acid) or vehicle injection over the course of three days. On the final day of experiments animals received either an acid injection or vehicle injection prior to being placed into both contexts. In this way, contextual control of pain sensitivity and pain expectation could be tested respectively. Both male and female mice developed context-dependent conditional pain tolerance, a phenomenon mediated by endogenous opioid signaling. However, when expecting the presentation of a painful stimulus in a given context, males exhibited conditional hypersensitivity whereas females exhibited endogenous opioid-mediated conditional analgesia. Successful determination of the brain circuits involved in this sexually dimorphic anticipatory response may allow for the manipulation of pain memories, which may contribute to the development of chronic pain states.


2019 ◽  
Vol 2 (1) ◽  
pp. 245-248 ◽  
Author(s):  
Huimin Yan ◽  
Xin Duan ◽  
Kelsey H Collins ◽  
Luke E Springer ◽  
Farshid Guilak ◽  
...  

Inflammation after joint injury leads to joint responses that result in eventual osteoarthritis development. Blockade of inflammation, by suppressing NF-κB expression, has been shown to reduce joint injury-induced chondrocyte apoptosis and reactive synovitis in vivo. Herein, we demonstrate that the suppression of NF-κB p65 expression also significantly mitigates the acute pain sensitivity induced by mechanical injury to the joint. These results suggest that early intervention with anti-NF-κB nanotherapy mitigates both structural and pain-related outcomes, which in turn may impact the progression of post-traumatic osteoarthritis.


2015 ◽  
Vol 34 (5) ◽  
pp. 547-555 ◽  
Author(s):  
John W. Burns ◽  
James I. Gerhart ◽  
Stephen Bruehl ◽  
Kristina M. Peterson ◽  
David A. Smith ◽  
...  

2016 ◽  
Vol 35 (1) ◽  
pp. 29-40 ◽  
Author(s):  
John W. Burns ◽  
James I. Gerhart ◽  
Stephen Bruehl ◽  
Kristina M. Post ◽  
David A. Smith ◽  
...  

Author(s):  
М.Н. Карпова ◽  
Л.В. Кузнецова ◽  
Н.Ю. Клишина ◽  
М.Л. Кукушкин

Цель исследования - изучение особенностей действия ипидакрина («Ипигрикс» Эйч Би Эм Фарма с.р.о., Словакия) на острую боль и динамику развития невропатического болевого синдрома у крыс линии Вистар. Методика. Проведено 2 серии опытов. В 1-й серии влияние ипидакрина изучали на моделях острой боли. Пороги болевой чувствительности определяли до внутримышечного введения ипидакрина (0,5 и 1 мг/кг), а также через 30 и 60 мин после введения. Оценку изменения индивидуальной болевой чувствительности у животных проводили с помощью 2 стандартных тестов: «Tail flick» и «Hot plate». Во 2-й серии изучали влияние ипидакрина на развитие невропатического болевого синдрома, который воспроизводили перерезкой опытным и контрольным животным левого седалищного нерва на уровне подколенной ямки. Интенсивность невропатического болевого синдрома у животных оценивали в баллах по выраженности аутотомии на оперированной конечности, времени появления аутотомий и количеству животных с аутотомией. Внутримышечное введение ипидакрина осуществляли ежедневно (1 мг/кг) в течение 20 сут. Результаты. Введение ипидакрина (0,5 мг/кг) не оказывает антиноцицептивного действия: порог болевой чувствительности не менялся по тестам «Tail flick» и «Hot рlate». Введение ипидакрина (1 мг/кг) за 30 мин до тестирования также не влияло на порог болевой чувствительности по тестам «Tail flick» и «Hot рlate», а через 60 мин после введения ипидакрина порог болевой чувствительности увеличился на 15,8 % (*р=0,033) по тесту «Tail flick» по сравнению с показателем до введения препарата. Заключение. Ипидакрин значительно задерживал развитие невропатического болевого синдрома НБС, но не оказывал влияния на острую боль в тестах «Tail flick» и «Hot plate». The aim of the study was to elucidate specific features of the effect of ipidacrine (IPIGRIKS, Slovakia) оn acute pain and development of neuropathic pain syndrome (NPS) in Wistar rats. Methods. Two series of experiments were performed. In the first series, effects of ipidacrine were studied on models of acute pain. Thresholds of pain sensitivity (PS) were determined before and 30 and 60 min after ipidacrine injection (0.5 and 1 mg/kg, i.m.). Changes in individual pain sensitivity were assessed with two standard tests, tail flick and hot plate. In the second series of experiments, the effect of ipidacrine on the development of NPS was studied. NPS was induced by transection of the left sciatic nerve at the level of popliteal fossa in experimental and control animals. The NPS intensity was evaluated in scores based on severity of autotomy on the operated extremity, time of autotomy emergence, and number of animals with autotomy. Ipidacrine (1 mg/kg, i.m.) was injected daily for 21 days. Results. Ipidacrine at a dose of 0.5 mg/kg did not exert an antinociceptive effect - the PS threshold did not change in the tail flick and hot plate tests. Ipidacrine at a dose of 1 mg/kg 30 min before testing did not affect the PS thresholds in the tail flick and hot plate tests; at 60 min after the ipidacrine injection, the PS thresholds increased by 15.8% (*p = 0.033) in the tail flick test compared to the value before the ipidacrine injection. Conclusion. Ipidacrine significantly delayed the development of NPS but did not affect acute pain in the tail flick and hot plate tests.


Sign in / Sign up

Export Citation Format

Share Document