Smoking Cigarettes as a Coping Strategy for Chronic Pain Is Associated With Greater Pain Intensity and Poorer Pain-Related Function

Patterson, Alexander L.; Gritzner, Susan; Resnick, Michael P.; Dobscha, Steven K.; Turk, Dennis C.; Morasco, Benjamin J.

doi:10.1016/j.jpain.2011.11.008

Cited by 106 publications

(78 citation statements)

References 55 publications

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“…These properties of smoking are used by patients with FM as a pain coping strategy [17]. In the present study, we observed a gradually increasing prevalence of smokers in parallel with increasing TP counts (Figure 1).…”

Section: Resultssupporting

confidence: 69%

Smoking is Associated with Reduced Leptin and Neuropeptide Y Levels and Higher Pain Experience in Patients with Fibromyalgia

Bokarewa

Erlandsson

Bjersing

et al. 2014

Mediators of Inflammation

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Smoking deregulates neuroendocrine responses to pain supporting production of neuropeptide Y (NpY) by direct stimulation of nicotinic receptors or by inhibiting adipokine leptin. Present study addressed the effect of cigarette smoking on adipokines and pain parameters, in 62 women with fibromyalgia (FM) pain syndrome with unknown etiology. Pain was characterized by a visual analogue scale, tender point (TP) counts, pressure pain threshold, and neuroendocrine markers NpY and substance P (sP). Levels of IGF-1, leptin, resistin, visfatin, and adiponectin were measured in blood and cerebrospinal fluid. Current smokers (n = 18) had lower levels of leptin compared to ex-smokers (n = 25, P = 0.002), while the expected NpY increase was absent in FM patients. In smokers, this was transcribed in higher VAS-pain (P = 0.04) and TP count (P = 0.03), lower pain threshold (P = 0.01), since NpY levels were directly related to the pain threshold (rho = 0.414) and inversely related to TP counts (rho = −0.375). This study shows that patients with FM have no increase of NpY levels in response to smoking despite the low levels of leptin. Deregulation of the balance between leptin and neuropeptide Y may be one of the essential mechanisms of chronic pain in FM.

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Section: Resultssupporting

confidence: 69%

Smoking is Associated with Reduced Leptin and Neuropeptide Y Levels and Higher Pain Experience in Patients with Fibromyalgia

Bokarewa

Erlandsson

Bjersing

et al. 2014

Mediators of Inflammation

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“…78 These factors could all contribute to the increased (2Â ) risk for PTSD among tobacco users, 79 as well as the increased risk for CP in PTSD. 80,81 It will thus be important to take into account variable contributing factors from multiple domains in the pathophysiology of PTSD 11 when considering risk for particular comorbid CP conditions. Fibromyalgia provides a good example.…”

Section: Immune System Factors In Chronic Pain and Ptsdmentioning

confidence: 99%

The Shared Neuroanatomy and Neurobiology of Comorbid Chronic Pain and PTSD

Scioli-Salter¹,

Forman

Otis

et al. 2015

The Clinical Journal of Pain

104

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Chronic pain and posttraumatic stress disorder (PTSD) are disabling conditions that affect biological, psychological, and social domains of functioning. Clinical research demonstrates that patients who are affected by chronic pain and PTSD in combination experience greater pain, affective distress, and disability than patients with either condition alone. Additional research is needed to delineate the interrelated pathophysiology of chronic pain and PTSD, with the goal of facilitating more effective therapies to treat both conditions more effectively; current treatment strategies for chronic pain associated with PTSD have limited efficacy and place a heavy burden on patients, who must visit various specialists to manage these conditions separately. This article focuses on neurobiological factors that may contribute to the coprevalence and synergistic interactions of chronic pain and PTSD. First, we outline how circuits that mediate emotional distress and physiological threat, including pain, converge. Secondly, we discuss specific neurobiological mediators and modulators of these circuits that may contribute to chronic pain and PTSD symptoms. For example, neuropeptide Y, and the neuroactive steroids allopregnanolone and pregnanolone (together termed ALLO) have antistress and antinociceptive properties. Reduced levels of neuropeptide Y and ALLO have been implicated in the pathophysiology of both chronic pain and PTSD. The potential contribution of opioid and cannabinoid system factors also will be discussed. Finally, we address potential novel methods to restore the normal function of these systems. Such novel perspectives regarding disease and disease management are vital to the pursuit of relief for the many individuals who struggle with these disabling conditions.

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“…For example, smokers with chronic pain reliably endorse smoking cigarettes in response to painful episodes (Hooten, Vickers, et al, 2011; Jamison et al, 1991; Patterson et al, 2012). Data derived from ecological momentary assessment and experimental research paradigms further indicate that the experience of pain can increase urge to smoke and function as a proximal antecedent of smoking behavior (Dhingra et al, 2014; Ditre & Brandon, 2008), especially when individuals hold expectations for nicotine/tobacco-related pain reduction (Ditre, Heckman, Butts, & Brandon, 2010).…”

Section: Bidirectional Relations Between Pain and Tobacco Smokingmentioning

confidence: 99%

Anxiety and Depression in Bidirectional Relations Between Pain and Smoking

2015

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Pain and tobacco smoking are highly prevalent and comorbid conditions that impose considerable burdens on individuals and health care systems. A recently proposed reciprocal model suggests that these conditions interact in a bidirectional manner, resulting in greater pain and the maintenance of tobacco addiction. Anxiety and depression are common among smokers in pain and have been identified as central mechanisms of interest. There is emerging evidence that smokers with anxiety/depression may experience more severe pain and functional impairment, greater pain-induced motivation to smoke, and increased sensitivity to pain during periods of smoking abstinence. Based on empirical findings, we hypothesize that these experiences may engender expectations that abstaining from smoking will exacerbate both pain and negative affect, thus eroding self-efficacy for smoking cessation and increasing perceived barriers to quitting. The goal of this narrative review is to examine the role of anxiety/depression in complex pain–smoking relations so as to advance evolving theoretical perspectives and inform the development of tailored interventions.

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Smoking Cigarettes as a Coping Strategy for Chronic Pain Is Associated With Greater Pain Intensity and Poorer Pain-Related Function

Cited by 106 publications

References 55 publications

Smoking is Associated with Reduced Leptin and Neuropeptide Y Levels and Higher Pain Experience in Patients with Fibromyalgia

Smoking is Associated with Reduced Leptin and Neuropeptide Y Levels and Higher Pain Experience in Patients with Fibromyalgia

The Shared Neuroanatomy and Neurobiology of Comorbid Chronic Pain and PTSD

Anxiety and Depression in Bidirectional Relations Between Pain and Smoking

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