Smoking and Pain (original) (raw)
Related papers
Review: The nicotinic modulation of pain
Pakistan journal of pharmaceutical sciences, 2020
Pain is a physiological unpleasant sensation that associated with actual or potential tissue damage and affects the major part of human population. Numerous modulatory system control pain through a complex process. The drugs that regulate the modulators involving in this process are currently available; however, the studies to understand the process and develop new agents are still going on. In this review, it is aimed to relay information about how nicotinic receptors contribute the pain modulation. It is obvious that a wide variety of nicotinic receptors is located in both peripheral and central areas. Among these receptors α7, α4β2 and α9α10 receptor subtypes draw attention in terms of pain modulation. The fact that different receptor subtypes involve in different processes of different pain conditions leads to provide beneficial results from the agonism of α7, α4β2 and antagonism of α9α10. The major restraint of the usage of nAChR agonists is their adverse effects. However, nowa...
The Journal of Pain, 2012
Smoking has been associated with increased pain severity in general chronic pain populations. Less is known about the effects of smoking and nicotine on the multifaceted and often complex subtypes of pain that frequently occur following spinal cord injury (SCI). The purpose of this study was to examine the effects of nicotine on self-reported pain among individuals with SCI and to determine if the effect of nicotine varied by pain subtype. A randomized, placebo-controlled crossover design was used to determine the effect of nicotine exposure on subtypes of SCI-related pain among smokers and nonsmokers. A complex relationship emerged, such that the degree of reported pain with exposure to 2 mg of nicotine compared to placebo varied according to pain type and smoking status of the subject. Pain sites that had characteristics of both neuropathic and musculoskeletal symptoms (deemed complex neuropathic pain sites) exhibited pain reduction after nicotine exposure in nonsmokers. In sharp contrast, smokers with this form of pain exhibited an increase in pain severity. Data were also examined descriptively to determine potentially unique factors associated with complex neuropathic pain that may explain trends associated with clinically relevant changes following nicotine exposure. In sum, smoking or tobacco use history may determine the analgesic (or enhanced pain perception) effect of nicotine on post-SCI pain. Perspective: Pain characterized by both neuropathic and musculoskeletal symptoms decreased in severity after nicotine exposure in nonsmokers with SCI but increased in severity among smokers with SCI. The analgesic (or enhanced nociceptive) effect of nicotine may depend on tobacco use history.
Smoking and Chronic Pain: Compound Interactions
Background: Smoking is a major public health problem. Cigarette smoking acts as a nicotine delivery in humans, has found to produce profound changes in physiological architecture. Smoking's as well as chronic pain are one of the major challenging health concerns faced in day to day life. During smoking nicotine is quickly absorbed into the blood stream within a time gap of 30 seconds it reaches the brain. It stimulates the brain to release various chemicals namely epinephrine which will give a pleasurable euphoric effect. It is a proven fact that smoking of tobacco will cause the production of Rheumatoid factors or anti-cyclic citrullinated peptide autoantibodies which is a risk factor for the development of Rheumatoid arthritis. There is a positive relation between smoking and depression and it has been seen smokers use more number of cigarettes when depressed and smoking also caused the individual who is depressed more prone to pain than a normal smoker. Quitting of smoking is quite difficult because of unpleasant withdrawal syndrome that consists of frustration, depression, anxiety, reduced heart rate, increased weight, depressed mood, difficulty in concentration. Because of all these withdrawal symptoms individuals who try to quit start up again very soon. Smoking is a health hazard, this is a well-known fact and the noxious effects are multiple so in management of pain in theseindividual's, necessary steps has to be put forward in order to quit the habit. Cognitive behavioural therapy or antidepressant therapy in the management of pain of depressed patients who are smokers has shown good results in a rehabilitation centre on the course of the management of pain.
The Effect of Smoking Cessation on Acute Pain: A Systematic Review
Pain and Therapy
Smoking is a known risk factor for developing various pain-related disorders. However, acute pain often triggers the craving for cigarette consumption, resulting in a positive feedback mechanism. In addition, there is evidence of decreased pain tolerance during the early stages of abstinence. Therefore, in this study, we aimed to investigate whether a period of decreased pain tolerance and increased pain intensity occurs during smoking cessation. A systematic literature search was conducted through PubMed and Web of Science databases for controlled studies investigating the influence of smoking cessation on acute (defined as pain presentation of \ 3 months) and postoperative pain. The outcomes of interest included pain perception threshold, pain tolerance, pain intensity, and postoperative opioid requirements. The search strategy yielded 1478 studies, of which 13 clinical studies met our inclusion criteria. The included studies collectively represented data from 1721 participants from four countries. Of these, 43.3% of the included individuals were females. The mean age of the included subjects was 44.2 ± 8.2 years. The duration of smoking cessation varied considerably. The shortest duration was 2 h; others investigated the effect after more than 1 month of smoking cessation. Smokers had a history of 14.6 ± 9.9 years of nicotine abuse. The mean number of daily smoked cigarettes was 17.5 ± 10.3. Most studies examined in this systematic review show a negative influence of smoking cessation on acute pain. However, the affected pain modalities, the duration of the altered pain perception, and whether male and female smokers are equally affected could not be ascertained due to high heterogeneity and few available studies.
Nicotinic receptor involvement in antinociception induced by exposure to cigarette smoke
Neuroscience Letters, 2005
Direct exposure of rats to tobacco smoke induces antinociception. We presently investigated if this antinociception is mediated via nicotinic and/or -opioid receptors. Adult male rats were surgically implanted with Alzet osmotic minipumps that delivered either saline (control), the nicotinic antagonist mecamylamine, or the opiate antagonist naltrexone (3 mg/kg/day i.v. for 21 days). Nocifensive responses were assessed on alternate days using tail-flick reflex latency (TFL) over a 3-week period. During the second week, the rats were exposed to concentrated cigarette smoke in an environmental chamber for 6 h/day for 5 consecutive days; a control group was similarly exposed to filtered cigarette smoke. Rats receiving mecamylamine and naltrexone exhibited a significant weight loss after the first day of infusion. All treatment groups additionally exhibited significant weight loss during exposure to unfiltered or filtered smoke. The saline group exhibited significant antinociception on the first day of smoke exposure with rapid development of tolerance. The mecamylamine and naltrexone groups did not exhibit significant antinociception. Controls exposed to filtered smoke (with ∼50% lower nicotine concentration) also exhibited significant analgesia on the first exposure day with rapid development of tolerance. Exposure to high levels of cigarette smoke, or to filtered smoke with a lower nicotine concentration in the vapor phase, induces antinociception with rapid development of tolerance. The antinociceptive effect appears to be mediated via nicotinic and -opioid receptors.
Nicotine & Tobacco Research, 2010
Brody, & Birbaumer, 1993) that are mediated by nicotinic receptors (Simons et al., 2005). Specifi cally, the nicotinic acetylcholine receptor containing the beta 2 * subunit (b 2 *-nAChR, the * represents other subunits that may be part of the receptor), which is critical for the reinforcing effects of nicotine (Picciotto et al., 1998), is also necessary for nicotine-induced analgesia (Damaj et al., 2007 ; Marubio et al., 1999). A preclinical study demonstrated that the number of b 2 *-nAChRs in mouse brain is positively associated with responsivity to nicotine-induced analgesia (Damaj et al., 2007); however, the relationship between b 2 *-nAChRs in human brain and nociception is not known. During withdrawal from tobacco smoking, smokers commonly report feelings of anxiety, depression and restlessness (Hughes, 2007), and an increased sensitivity to pain (Pomerleau, Turk, & Fertig, 1984), all of which may contribute to the high rates of relapse. It has previously been demonstrated that b 2 *-nAChR availability is higher in recently abstinent smokers compared with nonsmokers (Cosgrove et al., 2009 ; Staley et al., 2006), for example, the tobacco smoking-induced upregulation of b 2 *-nAChRs is measurable in vivo with the radiotracer [ 123 I]5-IA-85380 ([ 123 I]5-IA) and single photon emission computed tomography (SPECT) brain imaging. In this preliminary study, we examined the relationship between b 2 *-nAChR availability and nociception (determined using the cold pressor task; Walsh, Schoenfeld, Ramamurthy, & Hoffman, 1989), during tobacco smoke withdrawal in human tobacco smokers using [ 123 I]5-IA and SPECT. Methods Twenty-four healthy treatment-seeking smokers (13 men, 11 women, age range 18-51 years, and mean ± SD , 34.6 ± 11.4
Tolerance to tobacco smoke- and nicotine-induced analgesia in rats
Pharmacology Biochemistry and Behavior, 1988
Acute exposure of male Sprague-Dawley rats to either nicotine or tobacco smoke results in analgesia as measured by tall-flick latencies. A second treatment, 24 hr after the fast, failed to produce analgesia, thereby demonstrating the rapid development of tolerance. The restraint which was a necessary part of the tobacco smoke exposure also produced analgesia, although of a more transient nature and lesser magnitude than that resulting from tobacco smoke exposure. Tolerance also developed to restraint stress-induced analgesia. The long-term (43 weeks) daily exposure of rats to tobacco smoke or restraint stress resulted in the development of cross-tolerance, suggesting that these two procedures share, at least in part, a common mechanism. Additionally, long-term tobacco smoke exposure resulted in an increased tail-flick latency when the animals had been withdrawn from tobacco smoke for 24 hr, suggesting the development of tolerance. The data also suggest a differential time course for the development of tolerance and dependence. This is the first report that addresses the effect of acute and chronic tobacco smoke exposure on pain sensitivity.
The Evaluation of the Neuropathic Pain in the Smokers
Ağrı - The Journal of The Turkish Society of Algology
Nicotine addiction is one of the most important causes of the general failure of treatment and keeping the habit of smoking. Peripheral neuropathy is a leading factor of smoking. This study aimed to analyze the association of neuropathic pain and addiction levels of individuals. Methods: The study was performed on the day on which the smokers visited the hospital for any reason. The Douleur Neuropathique 4 (DN-4) Scale and Fagerström Addiction Survey were administered to the individuals after obtaining their consent. Results: In total, 444 individuals were included in the study, and 57.2% of them were males (n = 254). The age average of the individuals with neuropathic pain (46.4±12.3 years) was significantly higher than that of those without pain. The individuals with pain smoked approximately 31.8±18.3 packet/year cigarettes, whereas those without pain smoked approximately 22.4 ± 15.5 packet/year cigarettes; the difference was significant statistically (p<0.05). According to multivariate logistic regression analysis with the backward elimination method, the existence of pain was found to be PR = 2.22 (95% GA, 1.26-3.91) in terms of sex, DM existence was found to be PR = 1.97 (95% GA, 1.02-3.81), and for each standard deviation increase (2.7) in Fagerström scale, PR was 1.29 (95% GA, 1.14-1.46). Conclusion: Smoking is a risk factor for neuropathic pain. In our study, the possibility of neuropathic pain increases as the duration of smoking and addiction level increase, and with diabetes, this rate increases even more. It is extremely important that the smokers should be informed regarding these facts and possibilities.
Effects of cigarette smoking on perception of thermal pain
Experimental and Clinical Psychopharmacology, 1995
The effects of cigarette smoking on pain perception were evaluated in 18 healthy smokers. Thermal pain stimuli were used to assess pain detection threshold and tolerance and to collect subjective ratings of the intensity and unpleasantness of painful stimuli. After overnight abstinence, pain perception was evaluated before and after 3 experimental treatments. Participants smoked normal cigarettes, smoked denicotinized cigarettes, or remained abstinent. Smoking normal cigarettes produced relative increases in pain tolerance compared with abstinence. Smoking denicotinized cigarettes produced intermediate effects on tolerance not different from the other 2 treatments. Effects were not detected for pain threshold or subjective pain ratings. Results suggest that cigarette smoking can have antinociceptive effects, which may depend both on nicotine and on other factors associated with smoking.