‘It clearly can make it worse’: The connection between abuse, PTSD and chronic pain
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A considerable proportion of rheumatology patients may have a history of abuse, trauma or post-traumatic stress that contributes an emotional component to their physical pain.
The question is, how many rheumatologists are asking about it?
Source: Philip J. Mease, MD
“When you look at PTSD in the general population, the rate is approximately 7%,” Pavan Tankha, DO, of the center for spine health at the Cleveland Clinic, told Healio Rheumatology. “When you look at patients with chronic pain, those rates may increase as high as 35%, or even close to 50%.”
According to experts, this is a topic that is awash in unanswered questions. Can emotional pain or past trauma cause a de novo autoimmune or rheumatic disease? What is the extent to which that pain and trauma can exacerbate an existing condition?
The jury is out on both counts.
“It is not clear if emotional pain can actually trigger an autoimmune disease, but it clearly can make it worse,” Daniel Clauw, MD, director of the Chronic Pain and Fatigue Research Center and professor of anesthesiology, medicine and psychiatry at the University of Michigan, said in an interview.
There is considerable uncertainty about the mechanism by which emotional pain would be able to exacerbate a chronic condition, and the extent of that exacerbation.
At least part of the reason for that uncertainty is that most rheumatologists are not equipped to manage mental health comorbidities.
“The reports of trauma and abuse can be all over the map because many patients have difficulty reconstructing that history, especially in a rheumatology setting rather than a psychiatry setting,” Philip J. Mease, MD, of the Swedish Medical Center, in Seattle, and the University of Washington, told Healio Rheumatology. “It can be difficult to find the line between overt trauma and the subterranean emotional deprivation that is just part of human life.”
Regarding the potential mechanism, Tankha offered that anxiety or stress can result in the release of cortisol. Ordinarily, the release of such a steroid leads to a decrease in inflammation and some pain relief.
“In acute scenarios, this does occur,” he said. “However, chronic cortisol release has been linked to worse pain in patients with chronic conditions.”
The chronic condition that has been studied most extensively in this regard is fibromyalgia. However, while the long history of research in fibromyalgia reveals a strong trend of patients with a discernible history of abuse or trauma, the science is inconclusive when it comes to causality.
The impact of emotional pain on other conditions under the rheumatology umbrella is similarly not fully understood. However, there are data on the subject, and plenty of opinions.
‘Fan the Flames’
In a 2018 paper published in the Journal of the American Medical Association, Song and colleagues studied 106,464 individuals with stress-related disorders, 126,652 of their siblings and 1,064,640 matched controls accrued between Jan. 1, 1981, and Dec. 31, 2013.
Results demonstrated that individuals with stress-related disorders were at an elevated risk for autoimmune disease compared with controls (HR = 1.36; 95% CI, 1.33-1.4). Moreover, PTSD yielded an elevated risk for any autoimmune disease (HR = 1.46; 95% CI, 1.32-1.61) or multiple autoimmune diseases (HR = 2.29; 95% CI, 1.72-3.04).
“Psychiatric reactions to life stressors are common in the general population and may result in immune dysfunction,” Song and colleagues wrote. “Whether such reactions contribute to the risk of autoimmune disease remains unclear.”
According to Tankha, the human proclivity to suppress or avoid emotional responses to stress may provide a clue.
“Pushing down emotions is not an innocuous activity,” he said. “Over time, unexpressed emotions can cause a stress-like state.”
It does not require a physician to understand that stress can lead to adverse health outcomes. However, whether an actual autoimmune condition can be one of those potential outcomes is another matter entirely — one that is currently being explored.
Goldschen and colleagues attempted to answer the question in a data set published in Brain, Behavior, and Immunity in 2023. They investigated a possible epidemiologic link between PTSD and systemic lupus erythematosus onset.
“Perturbations in the autonomic nervous system, neuroendocrine system, and at the genomic level may cause and sustain immune dysregulation that could lower the threshold for the development and propagation of SLE,” Goldschen and colleagues wrote in the study. “Among those genetically predisposed to SLE, systemic inflammation that accompanies chronic stress may fan the flames of smoldering SLE by priming immune pathways.”
“May” is the key word in that sentence, according to Clauw.
“There are connections between brain areas that process effect and those that process pain, and these regions are more closely connected when individuals have distress or emotional pain,” he said. “There is less evidence that emotional pain directly worsens autoimmunity — that is, actually makes inflammation worse — although this is hypothesized.”
For Tankha, the chronic stress mentioned in the Goldschen paper comes back to the ongoing release of cortisol.
“There are two different mechanisms at work,” he said.
One mechanism is central sensitization of the peripheral nociceptors. The second is that there can be a hyper- or hypo-cortisolemia that occurs along the hypothalamus, anterior pituitary gland, and adrenal gland axis. However, the explanation may be simpler than that.
“Cortisol can lead to increased muscle contraction, which can lead to neck pain and back pain,” Tankha said.
Ultimately, though, the process is likely more complicated. Understanding the central nervous system’s method of responding to different types of pain may provide clues to what could be happening in patients with chronic pain who have experienced significant trauma.
‘Constant State of Pain’
Understanding how the mind and body work together to process pain can illuminate how emotional and physical pain can contribute to each other, according to Mease.
“There are upward ascending pathways and descending inhibitory pathways,” he said. “For example, if you hold your hand over a candle, the ascending pathways will signal to your brain that this is a painful feeling, and that you should pull it away.”
However, as soon as the hand is pulled away, then the descending inhibitory pathways kick in.
“Immediately, norepinephrine, serotonin, opioids and endorphins are released to mollify that pain,” Mease said.
Importantly, these processes happen in portions of the brain that deal with emotion and memory, he added. This is one part of the reason that emotional pain is implicated in the physical pain experienced by patients with chronic conditions and fibromyalgia.
However, the pathways run even deeper than that. According to Mease, the default mode network, which is a region of the brain that engages in self-referential thought, is implicated in these ascending and descending pathways.
In a 2017 paper published in the Journal of Headache Pain, Hsaio and colleagues investigated the possibility of faulty connectivity between the insula and the default mode network in patients with fibromyalgia. Results showed that, compared with controls, patients with fibromyalgia demonstrated more “tender points” in the default mode network region, along with decreased connectivity between the insula and the network.
“Dysregulation of the default mode network essentially tells fibromyalgia patients that they are in a constant state of pain,” Mease said, adding that many patients feel as though their hand is permanently over a flame, emotionally speaking. “But then they also do not have the inhibitory pathways to tell them when the painful experience is over. The default mode network does not rest in fibromyalgia patients.”
The combination of trauma, stress, cortisol release and hypervigilance of the default mode network can result in concomitant fibromyalgia in patients with SLE, as noted by Goldschen and colleagues.
“We have seen similar phenomena in rheumatoid arthritis and psoriatic arthritis,” Mease said.
Although the phenomena in these conditions have not been explored in detail, there are data showing how concomitant adverse factors can build to result in chronic pain in patients.
‘Layering Effect’
In a 2020 paper published in the Journal of Traumatic Stress, Miro and colleagues investigated the relationship between traumatic experiences and fibromyalgia. The analysis included 173 patients and 53 healthy controls. Results showed that individuals in the fibromyalgia group were more likely to report exposure to both emotional and physical trauma and more PTSD symptoms. In addition, more severe PTSD correlated with multiple parameters that impact patients with fibromyalgia, including pain, sleep disturbances, anxiety, depression, coping style and functional impairment.
Desiree Azizoddin, PsyD, of the department of family medicine at the University of Oklahoma Health Sciences Center and the Dana Farber Cancer Institute, and clinical instructor at Harvard Medical School, agreed that all of these factors may be at play, before adding another critical component.
“Genetics play a really important role,” she said. “Some patients are primed to be more reactive to trauma than others.”
These individuals may be most likely to develop fibromyalgia, according to Azizoddin.
“Their life experiences can have a compounding effect,” she said.
Emotional trauma or PTSD can lead to anxiety or depression, which can lead to sleep deprivation, which can exacerbate physical pain, according to Mease.
“It builds, and this layering effect makes it more or less likely that a person with a chronic autoimmune disease or persistent cytokine stimulation in the central nervous system will also have concomitant fibromyalgia,” he said.
Data support this hypothesis. Gardoki-Souto and colleagues aimed to determine whether psychological trauma — particularly childhood trauma — can put individuals at risk for fibromyalgia. Their 2022 study was published in Pain Research & Management.
The analysis included 88 women who were interviewed on subjects ranging from sociodemographic factors to psychiatric comorbidities, pain level, fibromyalgia impact, clinical symptoms of anxiety, depression, insomnia, quality of life, and psychological trauma. Results demonstrated that 71.5% of respondents met diagnostic criteria for current PTSD, including emotional abuse or neglect, sexual abuse or physical abuse. Moreover, these traumas correlated with clinically relevant outcomes such as anxiety, depression, insomnia, suicidal thoughts and pain. Pain levels, in turn, predicted similar outcomes such as anxiety, depression, and dissociation.
Amongst all this data, however, the answer to whether trauma can actually cause de novo autoimmunity or fibromyalgia, remains elusive.
“Ultimately, the answer right now is, ‘maybe,’” Tankha said. “In the literature there is no direct correlation between emotion and autoimmune diseases.”
That said, studies like the Gardoki-Souto data set indicate that the development of “central sensitization” may be implicated in these patients who have childhood trauma and go on to develop these symptoms.
“When traumatic events occur in childhood, there can result a dysregulation of stress response that impacts sensitization to stress or pain,” Tankha said. “But whether it can actually precipitate autoimmunity is unknown.”
Yet another consideration is that many individuals with childhood stress can demonstrate elevated levels of inflammation, according to Tankha.
“We do not know the exact mechanism for this,” he said. “We are only able to study it after the fact, when we link back to patients who have brought up to us that they have had emotional trauma.”
The thought is that peripheral sensitization and hyperalgesia can lead to chronic widespread pain, Tankha added.
As investigators continue to sort out the neurology, experts on the psychiatry side can offer clues for rheumatologists to consider in their practice.
‘The Pain Runs My Life’
A critical 2021 paper on managing chronic pain was published by Beth Darnall, PhD, director of the Stanford Pain Relief Innovations Lab, and professor in the department of anesthesiology, perioperative and pain medicine at the Stanford University School of Medicine, and colleagues in JAMA Network Open. The researchers aimed to assess how a single-session class in evidence-based pain management — called Empowered Relief — compared with eight sessions of cognitive behavioral therapy (CBT) and health education in a cohort of 263 patients with chronic back pain.
Results showed that the Empowered Relief class yielded clinically significant improvement in outcomes of interest, such as pain related distress, intensity and interference, that were noninferior to the CBT cohort.
“Empowered Relief is about skills and tools that enable participants to begin self-treatment,” Darnall told Healio Rheumatology. “Over the course of 2 hours, Empowered Relief equips individuals with actionable and evidence-based pain relief skills.”
The program includes experiential exercises and a free binaural audio app for daily calming of the nervous system, Darnall added.
“Participants take the information and skills learned and apply it to themselves as they create their own personalized plan for Empowered Relief,” she said.
Although CBT remains a standard of care for many patients hoping to manage their chronic pain, Darnall noted that this type of treatment may not be available to all patients.
“An efficient and effective one-session pain-relief skills intervention can help fill a critical gap,” she said. “Several major health care organizations offer Empowered Relief to their patients as standard care for chronic pain or surgery. It is offered at the outset to every patient as one component of their pain care plan.”
According to Azizoddin, the idea of pain-related distress is an important concept for rheumatologists to understand.
“Patients feel helpless about their pain,” she said. “Their lives are extremely difficult because they are unable to work, to have a social life, to function properly.”
It is similarly important to recognize that it is normal for patients with an autoimmune disease, fibromyalgia or other types of chronic pain to harbor some negative thoughts about their condition, Azizoddin added.
“But many patients often feel as though they will never be able to live a normal life,” she said. “They tell me, ‘The pain runs my life.’”
There is a mechanism to explain that feeling, according to Darnall. Over time, pain can create unhelpful patterns that can compound suffering.
“This is true for all types of pain conditions, including rheumatic diseases,” she said. “Although we cannot cure the rheumatic disease with a single intervention, we can help people learn ways to extinguish those unhelpful patterns, gain better control over mind and body, and steer themselves toward relief.”
It can be as simple as hope — “today was bad but tomorrow could be better” — or celebrating small accomplishments like taking a shower, added Azizoddin.
For Darnall, the other critical component to Empowered Relief is its potential impact on the various layers of life disruption that chronic pain can cause.
“Participants find they are less reactive to pain, sleep improves so they have more energy and less next-day pain, and overall that pain occupies less of their mind space,” she said.
However, Azizoddin cautioned that for any intervention targeting something as complex as chronic pain, managing expectations is critical.
“Their lives are unlikely to be completely changed,” she said. “But they can improve. For many patients, that is a huge achievement.”
This achievement can feel particularly profound for patients who have cycled through so many other therapies without success.
‘It Goes a Long Way to Simply Ask’
“Some patients have failed on biologics, biosimilars, opioids, OTC pain medications, steroids [and] injections,” Azizoddin said.
For these patients, the intervention described by Darnall and colleagues can be an especially good option. They may also benefit from combination therapy with a non-therapeutic intervention, along with selective serotonin reuptake inhibitors (SSRIs) and other anti-depressants or anti-anxiety medications.
“More and more evidence is coming out to support the possible impact of SSRIs in reducing neuroinflammatory responses,” Azizoddin said.
Further data from the Song study demonstrated that persistent use of SSRIs during the first year after PTSD diagnosis was associated with an attenuated relative risk for autoimmune disease for durations of 179 days or less (HR = 3.64; 95% CI, 2-6.62), 180 to 319 days (HR = 2.65; 95% CI, 1.57-4.45), and more than 320 days (HR = 1.82; 95% CI, 1.09-3.02).
According to Azizoddin, further research is necessary to accurately describe the mechanism behind this trend.
“Theoretically, we think they help with neuroinflammatory processes associated with mood and pain,” she said.
According to Clauw, rheumatologists, for the time being, may be best served by simply asking patients if they have a history of trauma or emotional pain that they would like help with.
“If the patient acknowledges this, then to refer to a therapist,” he said.
Clauw argued that many rheumatologists lack the appropriate training to truly handle the types of stress and emotional trauma that result from a history of abuse or extreme experiences, like military service.
“If they simply identify this and refer, they will be doing the patient a huge favor,” he said. “Typically, though, no one asks.”
Tankha, likewise, suggested that if a patient is suffering but cannot describe exactly where the pain is, it might be a good time to send them to see a mental health professional.
Physicians with such a patient should be careful not to insert blame, according to Azizoddin.
“Telling a patient, ‘I know your pain is real, and it is not your fault,’ can be so powerful,” she said.
Azizoddin added that she is confident the evidence describing the mechanisms discussed above and the connections between emotional and physical pain will soon catch up with the hypotheses.
“Until then, we should all try to remember that when we tell a patient they are no longer to blame for their pain, it is very empowering and validating information,” she said. “We need to help them understand that this is the way the brain and the body work for all of us. And yet, there is a lot within their own control that can they do to modify their pain and stress. Learning those pain coping skills can be life changing.”
- References:
- Darnall B, et al. JAMA Netw Open. 2021;doi:10.1001/jamanetworkopen.2021.13401.
- Gardoki-Souto I, et al. Pain Res Manag. 2022;doi:10.1155/2022/2114451.
- Goldschen L, et al. Brain Behav Immun. 2023;doi:10.1016/j.bbi.2022.12.012.
- Hsaio, FJ, et al. J Headache Pain. 2017;doi:10.1186/s10194-017-0799-x.
- Miro E, et al. J Trauma Stress. 2020;doi:10.1002/jts.22550.
- Song H, et al. JAMA. 2018;doi:10.1001/jama.2018.7028.
- For more information:
- Desiree Azizoddin, PsyD, can be reached at 75 Francis St., Ste 13 Thorn, Boston, MA 02115; email: drazizoddin@bwh.harvard.edu.
- Daniel Clauw, MD, can be reached at 24 Frank Lloyd Wright Dr., Ann Arbor, MI 48105. email: dclauw@med.umich.edu or karbro@med.umich.edu.
- Beth Darnall, PhD, can be reached at 450 Broadway St., Pavilion A 1st Fl MC 5340, Redwood City, CA 94063; email: likim@stanfordhealthcare.org.
- Philip J. Mease, MD, can be reached at 601 Broadway, Seattle, WA 98122; email: pmease@philipmease.com.
- Pavan Tankha, DO, can be reached at 9500 Euclid Ave., Cleveland, Ohio 44195; email: bishoph@ccf.org.
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