Smoking and Chronic Pain
The prevalence of smoking in those with chronic pain is up to double that of the general population. In the short term smoking is an analgesic, however in the long-term it is deleterious for pain as it exacerbates nociceptive, neuropathic, and psychosocial pain. Smokers have higher pain intensities, number of painful areas, levels of disability, and opioid use to nonsmokers. There is a positive correlation even when controlling for confounding demographic, socioeconomic, and mood disorder factors. Many smokers identify coping with pain and anxiety as reasons for smoking. There is therefore a bidirectional relationship with smoking and pain. Pain increases the desire to smoke, and smoking increases pain.
Tobacco smoke contains nicotine and over 4000 other compounds. Nicotine plays a role in pain-related pathophysiology.
Nicotine binds to nicotinic acetylcholine receptors (nAChRs) which are found throughout the central and peripheral nervous systems and are involved in the physiology of arousal, sleep, anxiety, cognition, and pain. Nicotine also binds to opioid receptors.
Short Term Use
Cigarette smoking results in increased brain concentrations of nicotine within 7-10 seconds. It binds to nAChRs in the midbrain as well as in the peripheral nervous system. nAChR activation results in the release of noradrenaline, endogenous opioids, dopamine, and other neurotransmitters. This results in the feelings of euphoria and analgesia. The analgesic effect is from activation of the descending pain modulatory pathways and inhibition of afferent input to the dorsal horn.
A meta-analysis for intranasal or transdermal nicotine found a small beneficial analgesic effect when used in the short-term for post-operative pain.
Long Term Use
However inhaled nicotine has a half-life of approximately 30 minutes. This leads to a rapid decrease in the levels of the above neurotransmitters. This then leads to increased withdrawal, greater pain intensity, and cravings. Increased pain sensitivity occurs because long term use of nicotine results in neuroplastic changes with nAChR desensitisation and upregulation. The only way to overcome this would be to smoke constantly, which is not typically possible, and it would have other deleterious effects.
Therefore with use in the longer term pain is worsened, and the short term analgesic effects are outweighed by increased pain sensitivity from nicotine withdrawal due to rapid brain elimination of nicotine. There may also be reduced endogenous opioid release, blunting of the hypothalamic-pituitary-adrenal axis during stress, and altered connectivity of the basal ganglia.
Furthermore smoking has other deleterious effects on the musculoskeletal system. It increases the risk of disc degeneration, fractures, delayed tissue healing, and osteoporosis. From a psychosocial perspective it can further intensify depressive and anxiety symptoms and cause sleep disturbance. Smokers are also more likely to abuse alcohol, other substances, and have suicidal ideation.
In rat models nicotine exposure results in improved pain thresholds after 1 to 3 weeks of exposure. However after 6 weeks of use pain thresholds are worsened. Chronic exposure leads to decreased pain thresholds in a neuropathic pain model following withdrawal.
Effect on Pain Interventions
In the surgical setting, smokers have a higher incidence of inadequate post-operative pain control than nonsmokers and higher rates of chronic post-surgical pain regardless of the type of surgery (including arthroplasty and spinal surgery), as well as higher risk of chronic opioid use post surgery. Smokers also have poorer outcomes with nerve blocks and spinal cord simulators.
Smokers may have poorer outcomes in MDT pain management programmes as well as lower rates of return to work. Smokers may benefit from a high-intensity programme, with one study of a 15 day 8-hour a day programme finding that smokers had similar or better outcomes than non-smokers.
Few smokers with pain are successfully able to quit and are often refractory to smoking cessation treatment. After initial withdrawal of nicotine, even after a few hours, there is rapid recovery of excess nAChRs from desensitisation which results in hyperexcitability of the nicotinine cholinergic system. This results in agitation driving the craving for nicotine to desensitise the nAChRs.
This is why In the short term nicotine withdrawal worsens pain, however in the long term cessation may be beneficial. Patience may be needed to see the benefits of smoking cessation on pain. and some of the harmful effects may not be reversible. Regardless of whether smoking cessation improves pain, continuing to smoke may worsen pain and outcomes in the long-term.
The prevalence rates of chronic pain in ex-smokers is higher than nonsmokers. However chronic pain is more severe in smokers than nonsmokers and ex-smokers when looking at pain frequency, intensity, duration, and number of painful sites.
Pain intensity may start to decrease after about 3 weeks of abstinence. However in the surgical literature, postoperative pain is worse than nonsmokers even if abstinence occurs 3 weeks before surgery. However one randomised trial of veteran smokers with chronic illness found no difference in pain at 5 months in those who quit versus those who continued to smoke. But several other studies have found that patients who quit smoking have improvements in pain and improved response to various treatments. It is probably imperative to address underlying psychological issues.
Vaping is not a good alternative because it also negatively impacts pain perception due to containing which increases pain sensitivity.
Prescription options to assist with smoking cessation include nicotine replacement therapy, bupropion, nortriptyline, and varenicline. As of December 2022 varenicline has been unavailable in New Zealand for many months. Bupropion and nortriptyline can be good options due to their mild analgesic effects.
Exercise should be promoted as a healthier alternative to analgesia through exercise induced hypoalgesia.
Not only is opioid use more common in smokers compared to non-smokers, there is also an increased quantity of opioid use per individual. Even with higher use of opioids pain control is still worse than non-smokers. This association holds when controlling for confounding factors. It is also more difficult for smokers who use opioids to quite smoking. The analgesic effect of opioids is enhanced by supraspinal nicotinic acetylcholine receptors.
Smoking is harmful in a variety of pain conditions including but not limited to headache disorders, low back pain, fibromyalgia, inflammatory arthritis, neuropathic pain, and cancer. It likely contributes to the development of these conditions.
Low Back Pain
Smoking is a risk factor for disc degeneration and the development of chronic low back pain. The prevalence of smoking in this group reported to be between 16-40%. One large cohort study of over 70 thousand Canadians found a clear relationship between smoking and chronic low back pain risk. The prevalence was 23.3% in daily smokers compared to 15.7% in non-smokers. The association was stronger amongst younger individuals and the effect was dose dependent. The rates of low back pain are higher even in passive smokers.
The rate of smoking amongst patients with fibromyalgia is higher than the general population. For example one study of 1566 patients reported a smoking prevalence of 38.7% in those with fibromyalgia compared to 24.7% of patients without fibromyalgia.
Rheumatoid arthritis is approximately twice as more prevalent in smokers compared to nonsmokers, and four times more prevalent for rheumatoid-factor positive rheumatoid arthritis.
The rates of sciatica and postherpetic neuralgia are approximately twice that of nonsmokers.
Smoking is harmful in those with cancer for several reasons. It causes increased pain sensitivity, increased need for opioids, increased rates of chemotherapy induced peripheral neuropathy, and increased pain with radiation.
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