Corrigendum to “Short-term pre- and post-operative stress prolongs incision-induced pain hypersensitivity without changing basal pain perception”

Background Although opioids are unsurpassed analgesics, experimental and clinical studies suggest that opioids activate N-methyl-d-aspartate pronociceptive systems leading to pain hypersensitivity and short-term tolerance. Because it is difficult in humans to differentiate pain from hyperalgesia during the postoperative period, the authors performed experimental studies with fentanyl using the rat incisional pain model for evaluating relations between hyperalgesia and short-term tolerance. Because N-methyl-d-aspartate receptor antagonists oppose both pain hypersensitivity and tolerance induced by opioids, the authors examined the capability of ketamine for improving exaggerated postoperative pain management. Methods During halothane anesthesia, a hind paw plantar incision was performed in rats receiving four fentanyl subcutaneous injections (100 microg/kg per injection, every 15 min). In some groups, three subcutaneous ketamine injections (10 mg/kg per injection, every 5 h) were performed in saline- or fentanyl-treated rats. One day after surgery, the analgesic effect of morphine (2 mg/kg subcutaneous) was tested. Analgesia, mechanical hyperalgesia, tactile allodynia, and pain score were assessed for several days using the paw pressure vocalization test, the von Frey application test, and the postural disequilibrium test. Results Fentanyl induced analgesia but also produced exaggerated postoperative pain as indicated by the enhancement of hyperalgesia, allodynia, and weight-bearing decrease after hind paw plantar incision. Ketamine pretreatment prevented such a fentanyl-induced enhancement of postoperative pain and improved its management by morphine. Conclusions By opposing postoperative pain hypersensitivity and subsequent short-term tolerance induced by perioperative opioid use, ketamine not only improves exaggerated postoperative pain management but also provides better postoperative rehabilitation.

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Effect of Short-Term Use of a Centric Occlusion Stabilization Oral Appliance On Sensory and Pain Perception Thresholds in the Cervically Innervated Area: A Pilot Study

CRANIO® ◽

10.1179/crn.2005.039 ◽

2005 ◽

Vol 23 (4) ◽

pp. 278-282 ◽

Cited By ~ 2

Author(s):

Koji Kashima ◽

Mitsutaka Ogihara ◽

Naoshi Watanabe ◽

Shuichi Higashinaka ◽

Sho Maeda ◽

...

Keyword(s):

Pilot Study ◽

Pain Perception ◽

Oral Appliance ◽

Short Term ◽

Centric Occlusion

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Pain perception and short-term outcomes in totally laparoscopic colonic surgery with two different fast track programs

European Surgery ◽

10.1007/s10353-015-0343-7 ◽

2015 ◽

Vol 47 (5) ◽

pp. 258-261

Author(s):

G. Mari ◽

P. De Martini ◽

D. Maggioni ◽

A. Costanzi ◽

G. Ferrari ◽

...

Keyword(s):

Fast Track ◽

Pain Perception ◽

Colonic Surgery ◽

Short Term ◽

Totally Laparoscopic

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Short-Term Sleep Disturbance–Induced Stress Does not Affect Basal Pain Perception, but Does Delay Postsurgical Pain Recovery

Journal of Pain ◽

10.1016/j.jpain.2015.07.006 ◽

2015 ◽

Vol 16 (11) ◽

pp. 1186-1199 ◽

Cited By ~ 17

Author(s):

Po-Kai Wang ◽

Jing Cao ◽

Hongzhen Wang ◽

Lingli Liang ◽

Jun Zhang ◽

...

Keyword(s):

Sleep Disturbance ◽

Pain Perception ◽

Short Term ◽

Postsurgical Pain ◽

Induced Stress

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Cluster Headache Pathophysiology—A Disorder of Network Excitability?

Clinical and Translational Neuroscience ◽

10.3390/ctn5020016 ◽

2021 ◽

Vol 5 (2) ◽

pp. 16

Author(s):

Heiko Pohl ◽

Peter S. Sandor ◽

Lars Michels ◽

Andreas R. Gantenbein

Keyword(s):

Cluster Headache ◽

Pain Threshold ◽

Pain Perception ◽

Case Reports ◽

Epileptic Seizures ◽

Short Term ◽

Factors Influencing ◽

Continuous Activity ◽

Electrophysiological Studies ◽

Autonomic Reflex

Patients’ accounts of cluster headache attacks, ictal restlessness, and electrophysiological studies suggest that the pathophysiology involves Aδ-fibre nociceptors and the network processing their input. Continuous activity of the trigeminal autonomic reflex throughout the in-bout period results in central sensitization of these networks in many patients. It is likely that several factors force circadian rhythmicity upon the disease. In addition to sensitization, circadian changes in pain perception and autonomic innervation might influence the excitability of the trigeminal cervical complex. Summation of several factors influencing pain perception might render neurons vulnerable to spontaneous depolarization, particularly at the beginning of rapid drops of the pain threshold (“summation headache”). In light of studies suggesting an impairment of short-term synaptic plasticity in CH patients, we suggest that the physiologic basis of CH attacks might be network overactivity—similarly to epileptic seizures. Case reports documenting cluster-like attacks support the idea of distinct factors being transiently able to induce attacks and being relevant in the pathophysiology of the disorder. A sustained and recurring proneness to attacks likely requires changes in the activity of other structures among which the hypothalamus is the most probable candidate.

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Application of Theory in Chronic Pain Rehabilitation Research and Clinical Practice

The Open Sports Sciences Journal ◽

10.2174/1875399x02114010106 ◽

2021 ◽

Vol 14 (1) ◽

pp. 106-113

Author(s):

Zakir Uddin ◽

Joy C. MacDermid ◽

Fatma A. Hegazy ◽

Tara L. Packham

Keyword(s):

Chronic Pain ◽

Pain Perception ◽

Pain Modulation ◽

Pain Mechanisms ◽

Pain Hypersensitivity ◽

Gate Control Theory ◽

Controlling Mechanism ◽

Measurement Tools ◽

Gate Control ◽

Chronic Pain Conditions

Introduction: Chronic pain has multiple aetiological factors and complexity. Pain theory helps us to guide and organize our thinking to deal with this complexity. The objective of this paper is to critically review the most influential theory in pain science history (the gate control theory of pain) and focus on its implications in chronic pain rehabilitation to minimize disability. Methods: In this narrative review, all the published studies that focused upon pain theory were retrieved from Ovoid Medline (from 1946 till present), EMBAS, AMED and PsycINFO data bases. Results: Chronic pain is considered a disease or dysfunction of the nervous system. In chronic pain conditions, hypersensitivity is thought to develop from changes to the physiological top-down control (inhibitory) mechanism of pain modulation according to the pain theory. Pain hypersensitivity manifestation is considered as abnormal central inhibitory control at the gate controlling mechanism. On the other hand, pain hypersensitivity is a prognostic factor in pain rehabilitation. It is clinically important to detect and manage hypersensitivity responses and their mechanisms. Conclusion: Since somatosensory perception and integration are recognized as a contributor to the pain perception under the theory, then we can use the model to direct interventions aimed at pain relief. The pain theory should be leveraged to develop and refine measurement tools with clinical utility for detecting and monitoring hypersensitivity linked to chronic pain mechanisms.

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Food Deprivation Sensitizes Pain Perception

Journal of Psychophysiology ◽

10.1027/0269-8803/a000062 ◽

2012 ◽

Vol 26 (1) ◽

pp. 1-9 ◽

Cited By ~ 2

Author(s):

Olga Pollatos ◽

Beate M. Herbert ◽

Jürgen Füstös ◽

Katja Weimer ◽

Paul Enck ◽

...

Keyword(s):

Heart Rate ◽

Food Deprivation ◽

Pain Sensitivity ◽

Pain Perception ◽

Control Group ◽

Sympathovagal Balance ◽

Short Term ◽

Pressure Algometer ◽

Healthy Female ◽

Experimental Group

While food deprivation has known effects on sympathovagal balance, little is known about hunger’s influence on the perception of pain. Since autonomic activities influence many cognitive and emotional processes, this suggests that food deprivation should interact with the perception of pain. This study analyzed the possible effects of short-term food deprivation on pain sensitivity in healthy female participants. This study was comprised of 32 healthy female participants who underwent a 48-hr inpatient hospital investigation. Prior to testing, heart rate and heart rate variability were assessed. After a standardized breakfast, day 1 measurements were taken. Food intake was then not allowed again until the following evening for 22 participants (experimental group), while 12 participants were served standard meals (control group). Pain threshold and tolerance were assessed at 10:00 a.m. on both days using a pressure algometer. Additionally pain experience was examined. Food deprivation significantly reduced pain thresholds and tolerance scores in the experimental group. Additionally, the sympathovagal balance changed, characterized by a decrease in parasympathetic activation. Higher vagal withdrawal after food deprivation was associated with higher pain sensitivity in the experimental group. Furthermore, perceived unpleasantness and pain intensity increased for threshold and tolerance stimuli in the experimental group. We conclude that short-term food deprivation sensitized pain perception in healthy females. An imbalance in sympathovagal activation evoked by food deprivation accounted for this effect. Our results might be a pathogenic mechanism for the development of emotional difficulties associated with disturbed eating behavior.

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