Pain and post traumatic stress disorder – Review of clinical and experimental evidence

Moeller-Bertram, Tobias; Keltner, John R.; Strigo, Irina A.

doi:10.1016/j.neuropharm.2011.04.028

Cited by 142 publications

(110 citation statements)

References 162 publications

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“…Traumatic stress disorders such as PTSD are highly comorbid with chronic pain (Asmundson and Katz, 2009;Lew et al, 2009;Moeller-Bertram et al, 2012;Shipherd et al, 2007), and studies report lower experimental pain thresholds and acute stress-induced hyperalgesia in PTSD humans (Defrin et al, 2008;Orr et al, 2000); but see Asmundson and Katz (2009). Our laboratory uses a predator odor stress model in which rats are divided into groups that exhibit persistently high (Avoiders) or low (Non-Avoiders) avoidance of a predator odor-paired context; these animals are then compared with each other and with unstressed Controls for poststress behavioral and neural changes.…”

Section: Introductionmentioning

confidence: 99%

Traumatic Stress Promotes Hyperalgesia via Corticotropin-Releasing Factor-1 Receptor (CRFR1) Signaling in Central Amygdala

Itoga

Hellard

Whitaker

et al. 2016

Neuropsychopharmacol

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Hyperalgesia is an exaggerated response to noxious stimuli produced by peripheral or central plasticity. Stress modifies nociception, and humans with post-traumatic stress disorder (PTSD) exhibit co-morbid chronic pain and amygdala dysregulation. Predator odor stress produces hyperalgesia in rodents. Systemic blockade of corticotropin-releasing factor (CRF) type 1 receptors (CRFR1s) reduces stressinduced thermal hyperalgesia. We hypothesized that CRF-CRFR1 signaling in central amygdala (CeA) mediates stress-induced hyperalgesia in rats with high stress reactivity. Adult male Wistar rats were exposed to predator odor stress in a conditioned place avoidance paradigm and indexed for high (Avoiders) and low (Non-Avoiders) avoidance of predator odor-paired context, or were unstressed Controls. Rats were tested for the latency to withdraw hindpaws from thermal stimuli (Hargreaves test). We used pharmacological, molecular, and immunohistochemical techniques to assess the role of CRF-CRFR1 signaling in CeA in stress-induced hyperalgesia. Avoiders exhibited higher CRF peptide levels in CeA that did not appear to be locally synthesized. Intra-CeA CRF infusion mimicked stress-induced hyperalgesia. Avoiders exhibited thermal hyperalgesia that was reversed by systemic or intra-CeA injection of a CRFR1 antagonist. Finally, intra-CeA infusion of tetrodotoxin produced thermal hyperalgesia in unstressed rats and blocked the anti-hyperalgesic effect of systemic CRFR1 antagonist in stressed rats. These data suggest that rats with high stress reactivity exhibit hyperalgesia that is mediated by CRF-CRFR1 signaling in CeA.

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Section: Introductionmentioning

confidence: 99%

Traumatic Stress Promotes Hyperalgesia via Corticotropin-Releasing Factor-1 Receptor (CRFR1) Signaling in Central Amygdala

Itoga

Hellard

Whitaker

et al. 2016

Neuropsychopharmacol

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“…While it is well documented that individuals with depression and/or PTSD have a significant increase in various pain conditions. 11,15,18,40,41 little research has addressed this question among women with vulvodynia. 7,12 We found that women who …”

Section: Discussionmentioning

confidence: 99%

“…16 In particular, activation in the insula, a sensory integration region involved in pain and sensory processing, has been found to be associated with anxiety disorders such as PTSD, 17 as well as vulvar pain. [16][17][18] Serotonin and norepinephrine are neurotransmitters that have been implicated in the underlying pathophysiology of chronic pain and are known to be associated with anxiety and depressive disorders. [19][20][21] Recognizing that anxiety and depression cause a significant burden of morbidity and disability 22,23 and that the nature of the interrelationship between vulvar pain and mental health remains unclear, the aim of this paper was to describe the magnitude of the association between PTSD and/or depression and the presence of vulvodynia among a racially/ethnically diverse population-based sample of women.…”

Section: Introductionmentioning

confidence: 99%

“…PTSD and depression can be triggered by stressful life events [42][43][44] that are characterized by activation in the physiological and neuroendocrine systems. [45][46][47] Increased anterior insula activation is commonly observed in anxiety and PTSD 18 and has also been reported in patients with vulvar pain. 16 Evidence suggests that stress can also trigger the neuroinflammatory system in the brain, and inflammatory mediators such as cytokines (potent modulators of behavior and affect) that can induce depressive symptoms are also involved in the process of pathological pain.…”

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confidence: 99%

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Depression and Posttraumatic Stress Disorder Among Women with Vulvodynia: Evidence from the Population-Based Woman to Woman Health Study

Iglesias-Ríos

Harlow

Reed

2015

Journal of Women's Health

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Background: Psychological disorders may affect the pain experience of women with vulvodynia, but evidence remains limited. The present study aimed to describe the magnitude of the association of depression and posttraumautic stress disorder (PTSD) with the presence of vulvodynia in a nonclinical population from southeastern Michigan. Methods: Baseline data from 1,795 women participating in the Woman to Woman Health Study, a multiethnic population-based study, was used for this analysis. Validated screening questionnaires were conducted to assess vulvodynia, depression, and PTSD. Modified Poisson regression models with a robust variance estimation were used to estimate prevalence ratios (PR) and their 95% confidence intervals (CI) for the association between vulvodynia status and two mental health conditions, depression and PTSD. Results: In the adjusted models, women who screened positive for depression had a 53% higher prevalence of having vulvodynia (PR = 1.53; 95% CI: 1.12, 2.10) compared with women who screened negative for depression. Women who screened positive for PTSD had more than a two-fold increase in the prevalence of having vulvodynia (PR = 2.37; 95% CI: 1.07, 5.25) compared with women who screened negative for PTSD. Conclusions: The increased prevalence of vulvodynia among those screening positive for depression or PTSD suggests that these disorders may contribute to the likelihood of reporting vulvodynia. Alternatively, vulvodynia, depression, and PTSD may have a common pathophysiological and risk profile. Prospective studies are needed to improve our understanding of the temporal relation between mental health conditions and vulvar pain.

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“…Not surprisingly, the prevalence of PTSD (~10 %) is considerably lower than that of PTSD symptoms (~50 %) in patients with chronic pain [ 7 ]. The higher prevalence rates (up to 50 %) of PTSD symptoms in chronic pain populations are typically found in high-risk populations, including motor vehicle collision victims and hospitalized burn patients [ 88 ]. Approximately 35 % of patients referred to a pain clinic subsequent to a work-related injury also suffer from PTSD symptoms [ 14 ].…”

Section: Prevalence Of Ptsd and Ptsd Symptoms In Chronic Pain Patientsmentioning

confidence: 99%

Chronic Pain and the Anxiety Disorders: Epidemiology, Mechanisms and Models of Comorbidity, and Treatment

Katz

Pagé

Fashler

et al. 2014

Mental Health and Pain

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Chronic pain was traditionally defi ned by the length of time that pain persists [ 54 ] but more recent conceptualizations have introduced a more nuanced approach [ 85 ]. The International Association for the Study of Pain (IASP) currently defi nes chronic pain variously as " pain without apparent biological value ", " that has persisted beyond the normal tissue healing time … as determined by common medical experience ", and/or as " a persistent pain that is not amenable, as a rule, to treatments based upon specifi c remedies " [ 85 ]. Moreover, some chronic pain syndromes, such as rheumatoid arthritis, will likely never heal and others, such as migraine headaches, remit (i.e., heal) and then recur [ 85 ]. Notwithstanding the challenges associated with defi ning chronic pain and the problems with a solely, time-based defi nition, for research purposes, chronic non-malignant pain is typically defi ned as pain that persists for longer than 3 or 6 months [ 58 , 59 , 74 , 126 ].Recent epidemiologic studies reveal considerable variability in prevalence estimates for chronic pain (using a liberal time frame of 3 months or longer). These studies show that between 11.5 and 55 % of the population worldwide report chronic

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Pain and post traumatic stress disorder – Review of clinical and experimental evidence

Cited by 142 publications

References 162 publications

Traumatic Stress Promotes Hyperalgesia via Corticotropin-Releasing Factor-1 Receptor (CRFR1) Signaling in Central Amygdala

Traumatic Stress Promotes Hyperalgesia via Corticotropin-Releasing Factor-1 Receptor (CRFR1) Signaling in Central Amygdala

Depression and Posttraumatic Stress Disorder Among Women with Vulvodynia: Evidence from the Population-Based Woman to Woman Health Study

Chronic Pain and the Anxiety Disorders: Epidemiology, Mechanisms and Models of Comorbidity, and Treatment

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