I had an absolutely inspiring time at the World Congress on Abdominal and Pelvic Pain in Washington recently. I was given the opportunity thanks to the Dame Josephine Barnes award from the POGP and the EPIC Scholarship from Entropy Physiotherapy in Chicago and Lorimer Moseley. I can’t thank them enough for supporting the education and development of clinicians who wouldn’t otherwise be able to attend world-leading conferences such as this one. It truly was EPIC.
I’ve gone back through my notes and pulled together some of the things I think are important and have great clinical translation. It helped me to gather and retain the information and I really wanted to share what I learned. Better informed clinicians providing up to date evidence-based therapy are going to be the best for our patients, and at the end of the day this is why we do what we do. Apologies to any of the researchers for inaccuracies, these are just a few teeny pearls of wisdom I took/understood from your fantastic talks.
The keynote on the first day was Dr Dan Clauw. He had a great analogy for chronic pain:
“Sensory nerves are like electric guitar strings. You can strum harder but the sound doesn’t increase, you can only do that by turning up the amp. The brain is the amp, and in chronic pain states it’s turned up to 11.”
FM occurs as a continuum & we have significant fMRI signatures that look at and measure the central nervous system effect on/and with pain – we know centralised pain states exist, with objective evidence of a shift in how stimuli are perceived as painful in FM. It’s real folks, let’s stop making patients feel like we think they’re crazy or non-copers. Work with their brain, their experience.
We Need to be using the FM OCM – it’s a more specific and powerful measure than the pain detector, and FM is extremely relevant to how you’ll understand and manage chronic pelvic pain. Doing the outcome measure will tell us about the underlying centralisation of pain and how and where we should be targeting our treatment.
“Trigger point injections – what are you going to do, inject everywhere?”
Lets stop looking for trigger points and start treating an underlying pain state.
We also know that pain states increase indigenous opioid release, probably to help, but this means people become non-responsive to opioids. Opioids don’t help people with an underlying pain state like FM.
FM score is greater predictor for other comorbidities. Subthreshold Fibromyalgia (measured on the outcome measure) is predictive of opioid and surgical non-responsiveness – this was shown in women with TAH for CPP. Each 1 point increase in FM score predicts an increased requirement of 9mg for oral morphine.
He discussed pelvic pain as a continuum, not a “if this, then” process – vulvodynia, IBS, MSK pelvic pain may be fundamentally different conditions but given how closely related they are it may be more useful to explore the underlying mechanisms. There are studies following patients with IBS and MSK issues who develop BPS, then within a few years the IBS was the most significant issue.
We know Tens is useful in neuromodulation, and we know the brain has a great role to play in symptoms. It may be that we get to the point of localised ECT when we know how to target brainy treatment more effectively for neuromodulation. Cool! (and slightly terrifying). Here's a great resource, the Fibroguide.
First up in the BPS cluster was Dr Jason Kutch talking about his work in brain imaging and decoding what’s happening in chronic urological pelvic pain:
“We’re not born with active BPS symptoms, they’re triggered… what happens afterwards? We get maladaptive changes in the motor coretex.”
Physios – this is great news. We’re fab at designing exercises to improve the motor planning and functioning of our patients.
We get changes in 3 key brain areas: The Peri Aqueductal Grey, Insula and Supplementary motor area. These are the core areas that control bladder filling and micturition, including autonomic regulation of PFM tone in response to bladder filling and emptying. (Griffiths et al. 2015)
In animal models acute stress creates brainy maladaptations that increase the perception of fullness, urgency and the voiding reflex. Prolonged stress can also create issues with prolonged pelvic floor muscle tension and pain, and changes to how the bladder control network is managed. (Wang et al. 2017)
There’s a spectrum of how widespread pain is. The duration of symptoms has no significance in level of pain – there’s no evidence that symptom duration is a measure of condition progressing. (Kutch 2017)
There may be two distinct separate and stable phenotypes for BPS: those with localised pain and those with widespread pain. This is also seen on MRI, with distinct differences between the adaptations seen. Importantly this is also repeated in FM.
They found a great impact of the “widespreadedness” of pain more important than it’s intensity. The more widespread the greatest reduction in SF12 score of quality of life.
“Salience network” area detects and decides which areas are deserving of our attention – patients with widespread pain may be treating more areas as if they are deserving of attention than patients without pain.
The neurotags (connected regions of the brain that light up in response to stimuli or to create a thought/response) connections are stronger in patients about to improve than in those who aren’t (Rushworth 2001). Connectedness matters. The right brain is interested in special attention (proprioception) and the left brain is deciding what’s the best action plan to achieve motion – patients who are about to improve seem to have a better ability to motor plan, not so many motor maladaptations.
Sooo… Can we bias symptom improvement with this? Can we work more on motor planning and attention to make people better? This is a really exciting idea. It might make a PhD question ? My current thoughts?
Possibly. I have a great case study of a patient with a 46 year history of pelvic pain with widespread pain that I treated with more of a CRPS protocol after she had a huge autonomic response to discussing her symptoms and potentially looking at a model of a pelvis (sweating, mottling and erythema, nausea). I used progressive laterality testing with images of clothes pelvises, then medical diagrams of vulvas to centrally desensitise her to the pelvis. Within 3 months she was able to go through an assessment without an autonomic response, and with minimal internal “treatment” (I think it was my physical presence in the area not the actual stuff I was doing) she had near complete resolution of her symptoms. I’m currently writing this up for publication, I’ll pop it on the blog when it’s done too.
Next up was Dr Thomas Chelimsky talking about autonomic features of chronic pelvic pain:
He discussed the “new model” for chronic pelvic pain involving an awareness of its frequent non-bladder comorbidities – BPS sufferers are known to have a higher rate of dyspepsia and chronic idiopathic nausea than controls. We know IBS etc higher prevalence.
Is the comorbidity a driver or a precursor?
Having 2 pelvic pain conditions increases the odds ratio of having certain comorbidities such as chronic fatigue, FM, Panic and dyspepsia.
They looked at the sequence of onset versus the Clemens at al (2012) data: PTSD, Depression and Migraine were early predictors of then developing BPS or myofascial pelvic pain later. Should we be intervening earlier – prevention is better than cure!
They’ve studied the autonomic function in people with BPS using a sweat test: they found patients with BPS were similar to healthy controls in the amount they sweat in response to stimuli, but those with myofascial pelvic pain had reduced sweat output. They concluded that this was evidence of an autonomic neuropathy, similar to FM. He discussed how we know there is a loss of sympathetic nerve activity in fibromyalgia and also loss of sympathetic fibres in intestinal endometriosis.
He discussed further autonomic testing, this time measuring heart rate variability to positional change. They found patients with non-bladder syndromes had reduced parasympathetic activity, but contra to the previous testing there were more effects in those with BPS, less with those with myofascial pelvic pain, and in between in people with a mixed picture.
The conclusion/hypothesis was:
MPP – autonomic neuropathy
MPP sympathetic vascular dysfunction + how the vascular system feeding the systems., creating local muscle disorders.
BPS – vagal function was diminished
BPS there are a number of disorders involving hollow organ dyfunction related to the vagal nerve – we know they overlap – and how it relates to brain activity.
The Peri Aqueductal Grey (primary control centre for descending pain modulation) is smaller in those with endometriosis and pelvic pain than healthy controls. If there’s the potential for chronic pain the PAG needs to grow to do it’s job, deciding the best response to threat. This isn’t happening in CPP.
We know that if you activate the dorsal lateral column you get an increase in heart rate and BP. Activating the ventral column you get a reduction in BP and heart rate. So in patients with CPP they suggest that stimulating the PAG may effect chronic pain experience, but that we also need to increase parasympathetic activity and do to this via Vagal nerve stimulation.
He suggests that Interval training for this can be really effective. When I asked him he said his protocol was to work for 20 seconds, rest 70 seconds. Do 5 to 7 cycles of this, building to 150second total cycles. Patients to do this daily. He starts them off in the pool then progresses from there to land as able.
This is so clinically applicable! I’ve been playing with it for a few weeks and will report back on how it goes.
I hope you’ve found this useful. Learning in a vacuum is boring – sharing and debating is how we get better at things. Any thoughts? Catch me @Jilly_Bond on Twitter or Jilly Bond Physiotherapy on Facebook.