It’s hard to go anywhere on the interwebs without encountering something about ‘trauma-informed’ care/therapy/treatment and chronic/persisting pain management is no exception. This is the first of a series on my thoughts (based on research!) about trauma and chronic pain. Today I’ll very briefly define trauma as it’s typically used in this context, and touch on some of what research suggests is relevant to trauma and pain. Further posts will delve more deeply into therapy and suggestions for therapists and people living with pain.
Defining trauma
Trauma in the way I’m using it is “an event(s) or set of circumstances that is experienced by an individual as physically or emotionally harmful or threatening and that has lasting adverse effects on the individual’s functioning and physical, social, emotional, and/or spiritual well-being.” (Valdez, chapter 2, p. 13 in Stromberg, 2023). Valdez goes on to say ‘…extreme stress that emotionally, cognitively, and/ or physically overwhelms a person’s ability to cope, and it is an individual’s subjective experience that determines whether an event(s) is traumatic.‘ Tidmarsh and colleagues (2022) show that trauma may affect an individual directly or indirectly – that is, a person can witness events enacted on another person (indirect) and experience this as trauma personally, or they may experience direct trauma.
There is lack of clarity about how trauma is used and defined. Lumley and colleagues (2022) point to the distinction between PTSD as defined in DSM5 and the “more common but still distressing events” – and go on to discuss adversity as an even broader term that “includes potentially distressing or traumatic experiences occurring throughout life, such as abuse, neglect, parental loss, family discord, assault, partner violence, workplace abuse, national displacement, and social injustice (p. 600).” In other words, Trauma or trauma: it’s messy. Trauma as used in DSM5 PTSD or ICD-11 PTSD/CPTSD is a more restrictive term than adversity, yet adverse childhood experiences are widely studied as contributors to some forms of chronic pain.
At this point I’m going to quickly stop and say I am not going to discuss trauma and whether pain experienced by someone who has been exposed to traumatic situations is ‘psychogenic.’ Not going there – because we don’t have true experimental studies on humans because of ethics. We only have longitudinal studies (eg the Dunedin and Christchurch longitudinal studies) or correlational studies (cross-sectional studies) so our inferences must be guarded. I also hold concerns about the suggestion that any pain is ‘psychogenic’ given we have no evidence for pain without ‘activity in the nociceptive system.’ It’s way past time to put this dichotomous ‘mind’ or ‘body’ argument to bed and focus instead on understanding the person seeking help.
So just how does early childhood trauma, or really a big traumatic event, influence pain?
First, let’s look at whether there is a relationship, causal or correlational. Karimove-Zwienen conducted a systematic review exploring this question and found that… oh no, only four studies explicitly studied links between childhood exposure and pain. These studies indicated trauma involved maltreatment, emotional abuse and neglect, and that the presence of these experiences in children is associated with higher numbers of people reporting various forms of chronic pain. Some studies explictly studied PTSD and chronic pain, finding that the there was no relationship between the severity of childhood maltreatment and pain, nor a moderator effect on PTSD, but did find the direct effects of childhood trauma on pain including health impact and disability. Note that these studies specifically looked at those meeting diagnostic criteria for PTSD or CPTSD, so we may assume the trauma involved met what’s been decided by the DSM5 and ICD-11 teams.
In Tidmarsh et al’s (2022) review, the relationship between ACEs and disabling chronic pain shows an increased prevalence of chronic pain in people exposed to ACEs, as well as increased pain intensity. Note that these authors cite longitudinal court-validated ACEs as being linked to greater risk of disabling pain in people 30 years later. They consider the evidence to show that the type of ACE exposure might predict the form and severity of the pain experience (both diagnosis and intensity/interference), and that not only pain is affected – unsurprisingly, psychological wellbeing is also negatively influenced, so it’s not uncommon to see people with depression, anxiety and PTSD/cPTSD. These authors are also very clear that ‘while ACEs are potentially traumatic events, trauma may not necessarily be experienced as a result of ACEs’ as seen in the high variability of diagnoses amongst those with ACEs in early life. While having both a diagnosis of PTSD and exposure to ACES increase complexity, PTSD alone doesn’t mediate pain intensity and ACEs, so childhood adversity needs to be investigated independently from PTSD.
What’s important to note, according to Tidmarsh et al., (2022) is there is a ‘dose-response’ relationship between exposure to ACEs and higher pain intensity, pain interference, anxiety and depression.
How do ACEs/trauma influence pain?
Now we head into somewhat murky territory as researchers try to explain how ACEs influence chronic pain in adulthood. Tidmarsh and colleagues (2022) provide a summary suggesting that because the years from birth to around six years old are a period of rapid neuroendocrine development (and yeah, brain development, immune system physiology) these systems can be dysregulated by prolonged exposure to ACEs. Of course, neuroendocrine development also occurs during adolescence – and for women, menopause is another time of neuroendocrine change. These authors detail the biological effects of prolonged exposure to adversity (ie ‘stress’) on altered stress reactivity, physiological sensitisation to stress and immunological dysregulation – perhaps via elevated inflammatory biomarkers. They point to epigenetic changes in the stress response system (increased reactivity in the HPA axis), along with cortisol dysregulation and concurrent amygdala activity – and we know the amygdala is involved in threat ‘detection’ and response – and both neuroinflammatory activity and functional and structural changes in the brain, because this exposure occurs during brain development. Thankfully, for my sanity, Tidmarsh and colleagues clearly state that ‘much evidence is based upon animal experimentation’ and that the role of cortical modulation and human psychology ‘are not yet elucidated’ meaning yes, more research.
I’ve leaned into Tidmarsh et al’s paper because it includes biopsychosocial mechanisms. This is important given there are some commentators who eschew psychosocial factors and prefer to focus exclusively on ‘the bio.’ Tidmarsh and colleagues state ‘there is an empirically grounded link between ACEs and threat detection through stress-induced HPA axis dysregulation, increasing amygdala activity and fear-based memory formation. Moreover, the link between heightened threat detection and chronic pain is also well-established’ (p. 5) in their argument for including psychological models of threat detection in their paper. They describe the relevance of ‘catastrophising’ (see my posts on this construct here) – despite the vexed definition and language around this construct, the evidence strongly supports that pain-related anxiety/fear/vigilance is relevant, and catastrophising is the strongest psychosocial predictor of chronic pain. Pain is a salient experience – and is perceived as ‘a cognitive-emotionally salient threat’, mediating the link between being exposed to stress and chronic pain. It’s not surprising that exposure to threat leads to learning (in the biological and psychological sense of this word) to detect potential threat (better be safe than sorry). Especially if the individual is young because this is when we’re learning how the world works.
The final psychological model is pain-related avoidance. I’ll refer you back to Vlaeyen and Crombez (2020) paper “Behavioral Conceptualization and Treatment of Chronic Pain”
for one of the most useful papers describing why ‘undoing’ avoidance is so difficult yet so important. I’ll be digging into this when it comes to looking at what we do as clinicians for people with ACEs or trauma. Essentially, if our nervous system likes to be ‘better safe than sorry’ it’s HARD to train it to be less twitchy in the face of potential threat.
To summarise
Trauma can be direct or indirect, and much trauma-related research is about PTSD-style Trauma with a big T. Short answer: yes there’s a relationship but it’s a bit complicated.
Most of the research into ACEs has shown this broader set of traumatic experiences (trauma with a small t) are linked to greater rates of chronic pain and that exposures to different types of ACEs have different effects on an adult’s chronic pain.
ACEs include many socioeconomic, cultural, social and contextual factors so the prevention (and probably management) requires a broad approach to equity and attending to social factors including poverty.
There are many biological mechanisms thought to be involved in chronic pain linked to ACEs, but most of the studies have been carried out in animals – so we’re extrapolating a lot when we apply this to humans. Suffice to say, neuroendocrine and neuroinflammatory mechanisms are involved, along with the plasticity of cortical structures involved in detecting threat and maintaining both attention and salience towards potential threat. Reward mechanisms in the cortex help maintain this learning – note that ‘reward’ here doesn’t mean it feels good. Not experiencing a negative is rewarding and repeated neural activity myelinates those pathways, strengthening their connection.
Attending to potential threat, negatively interpreting said threat, and the resultant behavioural learning (catastrophising and behavioural avoidance) are clearly involved in what we see in clinical practice. Highly distressed people, with lots of impact on their lives from their pain, and plenty of mental health problems along with not a lot of trust in relationships – a perfect storm, especially if this pattern has been there since childhood.
Out next step? At what point do we start looking at ACEs and trauma (how much do we need to delve into trauma in therapy?), and what are the implications for the way we work with people experiencing pain? Keep reading, there’s a whole lot more to come!
In the meantime, this blog from MelloJonny is pretty spot on.
Karimov-Zwienenberg, M., Symphor, W., Peraud, W., & Decamps, G. (2024). Childhood trauma, PTSD/CPTSD and chronic pain: A systematic review. PLoS ONE, 19(8), e0309332. https://doi.org/10.1371/journal.pone.0309332
Stromberg, E. (Ed.). (2023). Trauma-Informed Pedagogy in Higher Education: A Faculty Guide for Teaching and Learning (1st ed.). Routledge. https://doi.org/10.4324/9781003260776
Tidmarsh LV, Harrison R, Ravindran D, Matthews SL and Finlay KA (2022)
The Influence of Adverse Childhood Experiences in Pain Management: Mechanisms, Processes, and Trauma-Informed Care. Front. Pain Res. 3:923866.
doi: 10.3389/fpain.2022.923866
Vlaeyen, J. W. S., & Crombez, G. (2020). Behavioral Conceptualization and Treatment of Chronic Pain. Annual Review of Clinical Psychology, 16, 187-212. https://doi.org/10.1146/annurev-clinpsy-050718-095744