Behavioural pain measurements. Von Frey hair mechanosensitivity. Von Frey hair mechanosensitivity was used as a measure of secondary allodynia . Von Frey hair mechanosensitivity. Von Frey hair mechanosensitivity was used as a measure of secondary allodynia. Alert, unanaesthetised animals were . Von Frey (vF) filaments are a series of nylon monofilaments which are graded in .. up and down method of Dixon () (see section: ). included an animal's stood on a floor contains a mechanosensitive transducer measuring.
Von Frey hair mechanosensitivity 2.4.1.
In a preclinical model of multiple sclerosis, CBD was shown to improve clinical recovery and rotarod scores in animals, correlating with and indicative of a neuroprotective effect. Cannabidiol is a noneuphoria producing compound and has a more desirable side effect profile compared with other cannabinoid compounds and commonly prescribed analgesics.
Animal studies where CBD was administered systemically showed that the animals had no signs of adverse side effects. Successful relief of OA symptoms by peripherally administered CBD suggests a therapeutic option that has a low chance of adverse effects which is more desirable for patients. This study showed for the first time that local CBD administration inhibited pain and peripheral sensitisation in established OA. By attenuating this initial inflammatory response with CBD, end-stage OA pain and peripheral neuropathy were abrogated.
Thus, CBD may be a safe therapeutic to treat OA pain locally as well as block the acute inflammatory flares that drive disease progression and joint neuropathy. All experimental protocols were approved by the Dalhousie University Committee on Laboratory Animals, which acts in accordance with the standards put forth by the Canadian Council for Animal Care.
Availability of data and materials: Philpott conducted the pain behaviour experiments, the inflammation measurements IVM and LASCA , performed the G-ratio measurements, analysed data, and helped draft the manuscript.
O'Brien conducted all electrophysiology experiments, analysed the data, and helped draft the manuscript. McDougall conceived the study, participated in its design and coordination, helped analyse data, and helped draft the manuscript. All authors read and approved the final manuscript. Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article. National Center for Biotechnology Information , U. Published online Sep 1.
Author information Article notes Copyright and License information Disclaimer. Published by Wolters Kluwer Health, Inc.
The work cannot be changed in any way or used commercially without permission from the journal. This article has been cited by other articles in PMC. Abstract Osteoarthritis OA is a multifactorial joint disease, which includes joint degeneration, intermittent inflammation, and peripheral neuropathy.
Cannabinoids, Osteoarthritis, Pain, Neuropathy, Inflammation. Introduction The most prominent form of synovial joint disease, osteoarthritis OA , is characterised by joint degeneration, pain, and in some patients, articular neuropathy.
Experimental timeline On day 14 post-MIA induction, 3 sets of noxious rotations, each lasting 5 seconds, were applied 5 minutes apart as a baseline measurement of afferent activity. Behavioural pain measurements 2. Von Frey hair mechanosensitivity Von Frey hair mechanosensitivity was used as a measure of secondary allodynia.
Intravital microscopy Both hind limbs were immobilised and the capsule of the ipsilateral knee was exposed by surgically removing a small ellipse of the overlying skin and superficial fascia. Experimental timeline Inflammation measures were conducted on day 1 post-MIA induction, which corresponds to the peak of inflammation in this OA model. G-ratio analysis of the saphenous nerve A segment of the saphenous nerve was isolated proximal to the ipsilateral knee joint and placed in 2.
Drugs and reagents Cannabidiol 2-[ 1 R ,6 R methyl 1-methylethenyl cyclohexenyl]pentyl-1,3-benzenediol was obtained from Tocris Bioscience Bio-Techne, Abingdon, United Kingdom.
Effect of acute administration of cannabidiol on joint afferent mechanosensitivity A total of 17 afferent fibres were recorded in this study. Table 1 Characterisation of the recorded fibres in the electrophysiology experiments.
Open in a separate window. Effect of acute administration of cannabidiol on sodium monoiodoacetate—induced inflammation One day after i.
Discussion Pain and disease progression are poorly managed in many patients with OA because of the multifactorial nature of the disease. Conclusions This study showed for the first time that local CBD administration inhibited pain and peripheral sensitisation in established OA.
Conflict of interest statement The authors have no conflicts of interest to declare. This work was supported by an operating grant provided by The Arthritis Society. Acknowledgements The technical assistance of Allison Reid is gratefully acknowledged.
Footnotes Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article. Use of the painDETECT tool in rheumatoid arthritis suggests neuropathic and sensitization components in pain reporting.
J Pain Res ; 7: Leukocyte trafficking and pain behavioral responses to a hydrogen sulfide donor in acute monoarthritis. Molecular targets for cannabidiol and its synthetic analogues: Br J Pharmacol ; Weight bearing as a measure of disease progression and efficacy of anti-inflammatory compounds in a model of monosodium iodoacetate-induced osteoarthritis.
Osteoarthr Cartil ; Quantitative assessment of tactile allodynia in the rat paw. J Neurosci Methods ; Antihyperalgesic effect of a cannabis sativa extract in a rat model of neuropathic pain: Phytother Res ; Vanniloid TRPV1 receptor mediates the antihyperalgesic effect of the nonpsychoactive cannabinoid, cannabidiol, in a rat model of acute inflammation.
Oral anti-inflammatory activity of cannabidiol, a non-psychoactive constituent of cannabis, in acute carrageenan-induced inflammation in the rat paw. Naunyn Schmiedebergs Arch Pharmacol ; Effects of cannabinoids and cannabinoid-enriched Cannabis extracts on TRP channels and endocannabinoid metabolic enzymes.
Neuropeptides in the synovium of patients with rheumatoid arthritis and osteoarthritis. J Rheumatol ; Assessment of synovitis with contrast-enhanced MRI using a whole-joint semiquantitative scoring system in people with, or at high risk of, knee osteoarthritis: Ann Rheum Dis ; Transdermal cannabidiol reduces inflammation and pain-related behaviours in a rat model of arthritis.
Eur J Pain ; Synovitis detected on magnetic resonance imaging and its relation to pain and cartilage loss in knee osteoarthritis.
ACS Chem Neurosci ; 5: CNS Neurosci Ther ; 1: Spinal nociceptive reflexes are sensitized in the monosodium iodoacetate model of osteoarthritis pain in the rat. Osteoarth Cartil ; Increased function of pronociceptive TRPV1 at the level of the joint in a rat model of osteoarthritis pain.
Mechanisms and mediators that drive arthritis pain. Curr Osteoporos Rep ; In a preclinic al model of mult iple. Over a 3-hour time course, CBD m g. These studi es, in addition to the. Cannabidiol is a noneuphoria producing compound and has. Animal studies where CBD was administered systemically. For example, exploratory behaviour in rats was not altered by. Our study shows for the first time that CBD is an effective anti-. Successful relief of OA symptoms by. The anti-rolling effect of CBD at 30 minutes was.
This study showed for the first time that local CBD administration. By attenuating this initial. Thus, CBD may be a safe. The authors have no conflicts of interest to declare. This work was supported by an operating grant provided by The. All experimental protocols were approved by the. Dalhousie University Committee on Laboratory Animals, which. Availability of data and materials: The technical assistance of Allison Reid is gratefully acknowledged.
Philpott conducted the pain behaviour. McDougall conceived the study, participated in its design. All authors read and approved the final manuscript. J Pain Res ;7: Weight bearing as a measure of disease. J Neurosci Methods ;. Oral anti-inflammatory activity of cannabidiol, a non-psychoactive.
Naunyn Schmiedebergs Arch Pharmacol ; Effects of cannabinoids and cannabinoid-enriched. Cannabis extracts on TRP channels and endocannabinoid metabolic. Neuropeptides in the synovium of patients with rheumatoid arthritis and. Assessment of synovitis with contrast-enhanced MRI using.
Ann Rheum Dis ; Transdermal cannabidiol reduces inflammation and pain-. Eur J Pain ; Grainger A, Conaghan P. Synovitis detected on magnetic resonance. Representative sections of electron microg raphs of axons found in saphenous. B G-ratio calculations showing that MIA-induced axonal. Scale bar is 6 m m. Data are presented as mean values 6 SEM.
Spinal nociceptive reflexes are sensitized in. Increased function of pronociceptive TRPV1. Mechanisms and mediators that drive. Curr Osteoporos Rep ; The nonpsychoactive cannabis constituent cannabidiol. Neurogenic origin of joint pain. Unravelling the relationship between age, nociception and joint. Cannabinoids and pain control in the periphery. Peripheral receptor targets for analgesia: Lysophosphatidic acid provides a missing link.
The isolation and structure of. Monosod ium iodoace tate-indu ced. Osteoarth Ca rtil ; CNS Neurosci Ther ; An introduction to the pathophysiology of osteoarthritis. Neuroprotection in experimental autoimmune encephalomyelitis and. Arthritis Res Ther ; Low-grade inflammation as a key mediator of the. Nat Rev Rheumatol ; GPR55 is a novel cannabinoid receptor. Br J Pharmacol ; Electrophysiological evidence that the.
Cannabinoid-mediate d antinociception is. Grading of monosodium iodoacetate-. Paradoxical effects of the cannabinoid CB2.
Characterisation of a peripheral neuropathic component of the rat. Cannabidiol displays unexpectedly high potency as an antagonist of CB1. Szolcsanyi J, Helyes Z. Effects of the novel TRPV1 receptor antagonist. SB in vitro and in vivo in the rat.
Activation of cannabinoid CB2 receptor ameliorates. Accordingly, the pain-suppressing effect of MSC, which are considered to exert an anti-inflammatory action, and a preservation effect on the joint itself, namely their effects on prevention of disease progression as well as central sensitization of pain are worthy of further investigation. This prompted us to prepare a shoulder arthritis model in the rat using monoiodoacetate MIA to provoke pain  .
Persistent inflammation is well known to promote the progression of arthropathy. Although the experience so far with the intraarticular administration of mesenchymal stem cell MSC to induce cartilage regeneration has been disappointing, MSC implantation is now being attempted using various surgical techniques. Meanwhile, prevention of osteoarthritis OA progression and pain control remain important components of the treatment of early-stage OA.
We prepared a shoulder arthritis model by injecting monoiodoacetate MIA into a rat shoulder, and then investigated the intraarticular administration of MSC from the aspects of the cartilage protective effect associated with their anti-inflammatory property and inhibitory effect on central sensitization of pain. Moreover, expression of A disintegrin and metalloproteinase with thrombospondin motifs 5 ADAMTS5 , a marker of joint cartilage injury, was similarly elevated following MIA administration.
When MSC were injected intraarticularly after MIA, the expression of CGRP in the spinal dorsal horn was significantly deceased, indicating suppression of the central sensitization of pain. In this way, the intraarticular injection of MSC inhibited the central sensitization of pain and increased the expression of the anti-inflammatory and cartilage protective factor TSG As the least invasive conservative strategies possible are desirable in the actual clinical setting, the intraarticular administration of MSC, which appears to be effective for the treatment of pain and cartilage protection in early-stage arthritis, may achieve these aims.
Cannabis users have long reported therapeutic properties of the plant for a variety of conditions, some of which include nausea, emesis, seizures, cancer, neurogenic diseases and pain control. Research has elucidated many cannabinoid pharmacodynamic and pharmacokinetic properties, expanding the potential use of cannabinoids as a medical therapy.
Due to the inconsistent delivery and control of the active components involved with smoking, pharmaceutical companies are investigating and prioritizing routes other than smoke inhalation for therapeutic use of cannabinoids.
In this relatively new field of pharmaceutical development, ongoing drug development promises great benefit from targeted endocannabinoid receptor agonism. Available in Canada and Europe, nabiximols, a specific extract from the Cannabis plant, has demonstrated great benefit in the treatment of pain related to spasticity in multiple sclerosis, cancer and otherwise chronic pain conditions.
Current investigative drugs, such as those developed by Cara Therapeutics and Zynerba Pharmaceuticals, are synthetic cannabinoids which show promise to specifically target neuropsychiatric conditions and chronic pain symptoms such as neuropathy and allodynia.
The objective of this review is to provide clinicians with an update of currently available and promising developmental cannabis pharmaceutical derivatives which may stand to greatly benefit patients with otherwise difficult-to-treat chronic conditions. Cannabidiol modulates serotonergic transmission and prevents allodynia and anxiety-like behavior in a model of neuropathic pain. Clinical studies indicate that cannabidiol CBD , the primary non-addictive component of cannabis that interacts with the serotonin 5-HT 1A receptor, may possess analgesic and anxiolytic effects.
However, its effects on 5-HT neuronal activity, as well as its impact in models of neuropathic pain are unknown. First, using in-vivo single unit extracellular recordings in rats, we demonstrated that acute intravenous i. Seven days of treatment with CBD reduced mechanical allodynia, decreased anxiety-like behavior, and normalized 5-HT activity. Overall, repeated treatment with low-dose CBD induces analgesia predominantly via TRPV1 activation, reduces anxiety via 5-HT1A receptor activation, and rescues impaired 5-HT neurotransmission under neuropathic pain conditions.
Several studies have indicated that CBD displays neurobiological effects, including wake promotion. Moreover, experimental evidence has shown that injections of CBD enhance wake-related compounds, such as monoamines dopamine, serotonin, epinephrine, and norepinephrine. However, no clear evidence is available regarding the effects of CBD on additional wake-related neurochemicals such as acetylcholine ACh.
Altogether, these data demonstrate that CBD increases ACh levels in a brain region related to wake control. This study is the first to show the effects of ACh levels in CBD-treated rats and suggests that the basal forebrain might be a site of action of CBD for wakefulness modulation.
Could cannabidiol play a role in the treatment of chronic pain? Emerging evidence suggests that osteoarthritis OA has a neuropathic component; however, the identity of the molecules responsible for this peripheral neuropathy is unknown. The aim of this study was to determine the contribution of the bioactive lipid lysophosphatidic acid LPA to joint neuropathy and pain.
Male Lewis rats received an intra-articular injection of 50? Saphenous nerve myelination was assessed by g-ratio calculation from electronmicrographs and afferent nerve damage visualised by activation transcription factor-3 ATF-3 expression. Nerve conduction velocity was measured electrophysiologically and joint pain was determined by hindlimb incapacitance. The effect of the LPA antagonist Ki was also evaluated. LPA caused joint nerve demyelination which resulted in a drop in nerve conduction velocity.
Sensory neurones were ATF-3 positive and animals exhibited joint pain and knee joint damage. MIA-treated rats also showed signs of demyelination and joint neuropathy with concomitant pain. Nerve damage and pain could be ameliorated by Ki pre-treatment. Intra-articular injection of LPA caused knee joint neuropathy, joint damage and pain. Pharmacological blockade of LPA receptors inhibited joint nerve damage and hindlimb incapacitance. Thus, LPA is a candidate molecule for the development of OA nerve damage and the origin of joint neuropathic pain.
Endocannabinoids inhibit neurogenic inflammation in murine joints by a non-canonical cannabinoid receptor mechanism. Neurogenic inflammation is a local inflammatory response that is driven by the peripheral release of neuropeptides from small diameter afferents which occurs in many organs including joints.
The knee joint has a rich endocannabinoid system which has been shown to decrease acute synovitis. The aim of this study was to investigate the influence of joint afferents on leukocyte-endothelial interactions within the synovial microcirculation of mice and determine the role of endocannabinoids on this inflammatory response. Electrical, antidromic stimulation of the saphenous nerve decreased leukocyte rolling at the lowest frequency tested 0.
The leukocyte rolling effect of nerve stimulation was completely abolished by pre-treating the knee with the vasoactive intestinal peptide antagonist VIP; however, neither calcitonin gene related peptide nor substance P antagonism had an effect on this neurogenic inflammatory response. Treating knees with the endocannabinoid breakdown inhibitor URB completely blocked leukocyte rolling and this effect could be reversed with the non-canonical cannabinoid antagonist O Its clinical importance and relevance.
Patients with chronic pain after abdominal surgery. J Pain Palliat Care. Contemporary Cesarean delivery practice in the. Am J Obstet Gynecol , e— e If no change in sensation appeared, stimulation. The SHA index was calculated as sum of distances to. Phone number for follow-up calls: Preferred method and time of day to be contacted: What is the country of origin of your four grandparents? What is your general state of health? Have you had chronic pain that started before this pregnancy?
Were you taking daily pain medications before this pregnancy? If YES, please list the medicines and amounts:. Do any members of your family parents, brother or sister, uncle, aunt or close cousins have a problem with.
Condition name if known: Do you usually have much pain with your menstrual bleeding? If YES, have you seen a physician for evaluation of the problem? Were you seeing a doctor regularly for any medical problems in the year before your pregnancy?
If YES, the reason I was seeing the doctor was check all that apply. In the year before your pregnancy , did you smoke cigarettes more than 1 pack per week.
Have you had any problems after any previous operations? If you had a problem noted above, type of operation. Did you have any problems after the birth of any previous baby? Where did you have pain during your pregnancy? Did you take any medications regularly daily or more than 3 times a week for several weeks during your. Flow diagram, total number of patients possible to include during study period. Ho spital Santa Joana e Maternidade.
Preoperative SHA index 0. WHA at 48 h index 0. Data are presented as mean and standard deviation SD or median and quartiles [Q 25 ,Q. On the day after surgery, caesarean pain is often worse than other major surgical procedures Gerbershagen et al. The reasons are multifactorial and include the type of surgical incision, a previous negative experience, and catastrophising about pain Dehghani et al. Compared to vaginal delivery, women might also experience loss of control over decision-making Fenwick et al.
Poor postoperative analgesia and pain interference with usual activities Chin et al. Furthermore, caesarean surgery may contribute to the development of neuropathic pain due to nerve trauma Landau et al. These problems, either individually or combined, can result in chronic pain and disability Niklasson et al.
For example, the greater number of previous caesarean deliveries was predictive of more postoperative pain. This may be partly explained by the argument that scar hyperalgesia can result from previous Pfannenstiel incision and make women more sensitive to pain Loos et al. Furthermore, an experience of poor analgesia can lead to an intense fear of pain prior to a subsequent delivery and result in catastrophic thoughts about pain Keogh et al. Pain on the day after caesarean section is often treated with controlled-release oxycodone to supplement the decline in analgesia from intrathecal opioids.
Evidence suggests that caesarean birth is a biopsychosocial experience where a comprehensive approach is needed that promotes control and participation in pain management. This study compared immediate-release oxycodone integrated with supportive educational strategies to controlled-release oxycodone.
A follow-up phase aimed to explore pain over three months. This study was a two-group parallel randomised controlled trial. A metropolitan hospital in Australia with a birthing suite, operating rooms, and a postnatal unit. English-speaking women scheduled for elective caesarean section were mailed trial information. Exclusion criteria included contraindications to intrathecal analgesia, herpes simplex infection, a history of chronic pain, opioid tolerance, or substance abuse.
A total of participants were recruited and randomised out of eligible participants. Group allocation was undertaken using sequentially numbered opaque sealed envelopes. The nurse practitioner intervention commenced on the day after surgery with immediate-release oxycodone alongside supportive strategies. The control group received scheduled doses of controlled-release oxycodone.
All participants could request additional oxycodone or tramadol. Primary outcomes were pain intensity and secondary outcomes included patient global impression of change, pain interference, opioid consumption, and maternal perception of control. A follow-up phase evaluated pain outcomes over three months.
The final sample size was , with 61 participants in each group. Pain intensity scores were analysed by linear mixed regression models. The follow-up analysis graded 5. The research showed that a nurse practitioner intervention can improve pain management following caesarean section.
The results underscore the influence of biological, psychological, and social factors on acute pain. Hence, this study reinforces the need for a biopsychosocial approach to acute pain management following caesarean delivery. Despite randomisation, there were differences in the numbers of twin pregnancies and previous caesarean section between Gestational age; weeks Pain management after caesarean section is still controversial.
Patient-controlled oral analgesia versus nurse-controlled parenteral analgesia after caesarean section: A randomised controlled trial. We assessed the effectiveness of early patient-controlled oral analgesia compared with parenteral analgesia in a randomised controlled non-inferiority trial of women undergoing elective caesarean section under regional anaesthesia.
Seventy-seven women received multimodal paracetamol, ketoprofen and morphine analgesia. The woman having patient-controlled oral analgesia were administered four pillboxes on the postnatal ward containing tablets and instructions for self-medication, the first at 7 h after the spinal injection and then three more at hourly intervals.
Pain at rest and on movement was evaluated using an point verbal rating scale at 2 h and then at 6-hourly intervals for 48 h. The pre-defined non-inferiority limit for the difference in mean pain scores patient-controlled oral analgesia minus parenteral was one.
After elective caesarean section, early patient-controlled oral analgesia is non-inferior to standard parenteral analgesia for pain management, and can be one of the steps of an enhanced recovery process. Particularly, in women undergoing a repeat cesar- ean section, Ortner et al. However, even with gold-standard multimodal regimens such as spinal or epidural morphine in conjunction with acet- aminophen and non-steroidal anti-inflammatory drugs NSAIDs , the proportion of women who suffer severe acute pain post-cesarean delivery is still remarkably high, 54 and women's fear of post-cesarean pain is ranked as being their most important concern.
Chronic pain after childbirth. With over four million deliveries annually in the United States alone and a constant increase in cesarean delivery rate, childbirth is likely to have a huge impact on the occurrence of acute and possibly chronic postpartum pain. Recent awareness that chronic pain may occur after childbirth has prompted clinicians and researchers to investigate this topic.
To provide a potential mechanistic explanation for the relatively low occurrence of chronic pain after cesarean delivery compared with that after other types of surgery, it has been proposed that endogenous secretion of oxytocin may confer specific protection.
Clinical interventions to reduce the incidence and severity of chronic post-surgical pain have not been consistently effective. Likely explanations are that the drugs that have been investigated were truly ineffective or that the effect was too modest because with a low incidence of chronic pain, studies were likely to be underpowered and failed to demonstrate an effect. In addition, since not all women require preventive therapies, preoperative testing that may identify women vulnerable to pain may be highly beneficial.
Further research is needed to identify valid models that predict persistent pain to allow targeted interventions to women most likely to benefit from more tailored anti-hyperalgesic therapies.
Mercier Peut-on individualiser la prise en charge de la douleur? Chronic pain issues after cesarean delivery. Peut-on individualiser la prise en charge de la douleur? The goal of preemptive analgesia is to prevent nociceptive inputs from damaged tissues to reach and to sensitize the central nervous system, thereby to reduce the expression of postinjury pain.
Although extremely attractive, the concept of preemptive analgesia has only brought deceiving results in the perioperative setting. Recent experimental models of incisional pain clearly show that any analgesic treatment administered before incision is not superior to the same treatment provided after incision because, when the effects of the analgesic treatment abate, the wound is able to reinitiate the central sensitization.
Consequently, preemptive analgesia has evolved to the concept of preventive analgesia, a broader definition, which involves any perioperative analgesic and antihyperalgesic treatments aimed to control central nervous system sensitization and to reduce the development of persistent post-surgical pain. In preventive analgesia, both the duration and the efficacy of the treatment are more important than the timing of administration of the drugs.
Recent clinical studies have highlighted the fact that an optimal control of preoperative, peroperative and postoperative pain is mandatory to ensure the success of preventive analgesia. Furthermore, progresses made in the assessment of endogenous mechanisms of pain processing should allow to improve even more preventive analgesia by an individualization of analgesic and antihyperalgesic perioperative treatments.
Hyperalgesia and temporal summation of pain after heat injury in man. Temporal summation of pain occurs when repeated stimuli become increasingly painful in spite of unchanged stimulus intensity. Summation can be quantified as the difference in pain between the first and the last stimulus in a train of stimuli.
The aim of the study was to compare temporal summation of pain in normal skin with summation of pain in skin with primary and secondary hyperalgesia evoked by a heat injury. Measurements were made before, and 0, 1, 2, and 4 h after the heat injury, in three areas: Temporal summation of pain was induced by repeated electrical stimuli five stimuli at 2 Hz and assessed by visual analog scale VAS. Primary hyperalgesia was evaluated by von Frey hairs and electrical stimuli, and the areas of secondary hyperalgesia with a rigid von Frey hair mN.
The pain responses to single and repeated electrical stimuli were not significantly altered by the injury. We found no correlation between either temporal summation and area of secondary hyperalgesia, or temporal summation and pain intensity during the induction of heat injury. We conclude that the development of primary and secondary mechanical hyperalgesia after heat injury in man was not associated with changes in temporal summation of painful electrical stimuli.
Wind-up of spinal cord neurones and pain sensation: Much ado about something? Wind-up is a frequency-dependent increase in the excitability of spinal cord neurones, evoked by electrical stimulation of afferent C-fibres. Although it has been studied over the past thirty years, there are still uncertainties about its physiological meaning. Glutamate NMDA and tachykinin NK1 receptors are required to generate wind-up and therefore a positive modulation between these two receptor types has been suggested by some authors.
However, most drugs capable of reducing the excitability of spinal cord neurones, including opioids and NSAIDs, can also reduce or even abolish wind-up. Thus, other theories involving synaptic efficacy, potassium channels, calcium channels, etc. Whatever the mechanisms involved in its generation, wind-up has been interpreted as a system for the amplification in the spinal cord of the nociceptive message that arrives from peripheral nociceptors connected to C-fibres.
This probably reflects the physiological system activated in the spinal cord after an intense or persistent barrage of afferent nociceptive impulses. On the other hand, wind-up, central sensitisation and hyperalgesia are not the same phenomena, although they may share common properties.
Wind-up can be an important tool to study the processing of nociceptive information in the spinal cord, and the central effects of drugs that modulate the nociceptive system. This paper reviews the physiological and pharmacological data on wind-up of spinal cord neurones, and the perceptual correlates of wind-up in human subjects, in the context of its possible relation to the triggering of hyperalgesic states, and also the multiple factors which contribute to the generation of wind-up.
The effect of post-surgical neuroplasticity on the stability of systemic pain perception: It remains unclear whether the systemic pain perception measured outside the incision area remains unchanged and whether it is affected by the presence of cAPOP.
This study explored whether the systemic perception of experimental pain would be altered towards hypersensitivity following elective gynecological surgery unmasked by opioids. A perioperative psychophysical evaluation of heat pain thresholds HPT and pain estimations were obtained in a remote bodily area before and after surgery among 35 women. The ratings for both pain dimensions of intensity and unpleasantness remained stable following surgery.
However, there was a reduction found in HPT the day after surgery
Von Frey hair tactile sensitivity .. 40 . Von Frey hair mechanosensitivity. Drugs and reagents. Colonic Mucosal Viability Other Specific Novel Mechanosensitivity and Classification of Colonic Afferent fibres 3. Abstract . Response of a mucosal afferent to calibrated Von Frey hairs and two chemical stimuli. Table Conduction velocity, von Frey hair thresholds, heat Mechanical stimulation. The mechanical threshold of each unit was determined with heat-cold sensitive nociceptor; CLTM, C low threshold mechanosensitive fibre;.