There was such deluge of important research presented at the recent World Congress on Abdominal and Pelvic pain that I’m taking time to digest it and translate it into practice. Here’s my second instalment.
There’s much more discussion in the vlog above, here are my brief notes. Starting with the end of the BPS cluster, Mr Kenneth Peters MD presented the role of peripheral nervous system on development and management of pelvic pain.
He believes there’s clearly two distinct populations in BPS: those with active Hunner’s Ulcers and those without. Those with Hunner’s Ulcers and pain/urgency symptoms (the more Type 3c, small stenotic bladder, passing small volumes at a high frequency) are the “active” Hunner’s ulcer phenotype, who tend to have less systemic pain, occur in post-menopausal women, and patients respond more readily to intensive surgical treatment. The vast majority of our BPS patients don’t fit into this bracket, but it’s important to recognise which ones do.
“Defining “IC” as a bladder disease oversimplifies the situation as nothing has shown bladder specific treatment to be effective.”
I may get cards with this made, or a tattoo (to go with my “It’s not about the Wand but what you do with it that matters” one).
“Identify what all the triggers are and chip away at them”
There’s multiple comorbidities and we need an MDT approach to resolving them.
His speech was full of great messages for his Urology colleagues:
“Treat the organ and we’re not going to do well”
Is chronic pain a symptom or a disease?
This is a great conversation starter that I feel we’ll have to run sometime. Certainly WCAPP17 has given me a lot of food for thought in the “is it a disease/underlying issue” camp with all the new work looking at immune function and regulation in pain states.
He discussed neuromodulation in BPS either from a sacral or pudendal route, and how effective it is in restoring the normal inhibitory pathways of the bladder, enabling a more normal micturition schedule and response. They’re now using this to great effect in PGAD. However, neuromodulation is not approved for pelvic pain yet – despite there being evidence for the reduction in pain levels concurrent to the reduction in voiding symptoms.
“Treat the pelvic floor before you treat anything else”
Yes! He presented his work/theories surrounding how and why the pelvic floor becomes overactive and painful in BPS: physical trauma, physiological inflammation and psychological impulses cause increasing spasm and reducing blood flow to the pelvic floor. This causes an accumulation of metabolites and the resultant ischaemia/metabolite produced therein perpetuates the cycle.
Dr Melissa Farmer did a really interesting talk about the interplay between peripheral, spinal and brain adaptations in chronic visceral pain. She’s done some incredible work that I can only begin to understand, and it was really good to have her pull it all together – it made total sense at the time, and I’m trying to piece together my understanding now a month later..
(Again, I was a little bit of an embarrassing fangirl later on with Melissa, but we’ll browse over that…)
“Pain is a primary reinforcer – do anything coupled with pain and you’ll learn it”.
Chronic pain and addiction share brainy traits – they’re both well-learned.
When rats/mice were infected with vulval Yeast and then treated 3 times it was observed that the mechanical allodynia and vulval innervation remained after treatment. If it happens enough you’ll learn to adapt to the situation. And then interestingly the site that is painful can become a large, diffuse area of pain due to how the viscera are innervated and how the brain responds to visceral pain.
In mice trials they found males were more resilient – they continued to have sex despite these changes, whereas female mice had a reduced sexual desire.
Then something with a BIG STAR next to it in my notes: In chronic pain of a year in duration the area of the brain responsible for the perception of pain shifts to the limbic system – they think this is to allow the brain to be open to manage other things. But that means our emotional centre is now managing our pain, and the pain becomes an emotionally maintained state independent of your environment. Wow. We all see this in clinical practice. So.. working with the limbic system is going to be very important in our chronic pelvic pain patients.
The mechanisms by which we initiate or initially experience pain are not the mechanisms by which it is maintained, this becomes more complexly encoded within different areas of our brain. Therefore our multifaceted treatment needs to encompass all these other areas of the brain – in the last vlog I talked about motor learning and planning, but we also need to take into consideration emotional resilience. The “Happify” website/tool was also presented at WCAPP17 and would provide you a platform to achieve more psychological inputs toward improving symptoms. Google it!
Dr Gebhart presented on Visceral Pain.
Some pearls of wisdom from him:
Convergence of visceral pain creates a widespread pain state. “Widespreadedness” in pelvic pain is important – have a watch of my last vlog from WCAPP17 to learn why. It’s important to remember that the nerves from the bowels enter the spinal cord at the sacral and thoracic levels, so the amount of potential overlap with other areas of the body is great.
Persistent organ inflammation is NOT needed to maintain visceral hypersensitivity – building on what Dr Farmer talked about – adaptations to how the tissues respond occur quickly, and may continue to present like an acute inflammation secondary to a trauma – be that physiological or psychological. Again, if you haven’t seen my last vlog have a watch of why we can’t not include the brain when we’re discussing pain at a chemical level in the body.
Dr Aziz from QMU discussed autonomic dysregulation in functional GI disorders.
He discussed the enteric nervous system – he presented that a higher resting parasympathetic tone produced a increase in the descending inhibitory subcortical network to help reduce pain in those with oesophageal pain – so we need to increase parasympathetic activity. This we’ve discussed before and is something that is hugely transferable to the clinic for us physios – Dr Chelimsky’s Interval training protocol, deep diaphragmatic breathing or even the new Vagal nerve stimulators could be helpful in this. Watch this space!
Dr Pukall discussed Vulvodynia.
She had a wealth of knowledge that would just take too long to go through! But my favourite snippets are: Women with Vulvodynia are 2-3x more likely to report an inflammatory history (hives, yeast infections etc).
There’s some evidence that they may have pro-inflammatory elements of their genetics which produce an inability to downregulate the inflammatory response, or which heighten the systemic response.
SO get asking your patients about any potential inflammatory history!
It’s been observed that women with vulval pain have an increased number of nerve fibre and are able to perceive touch at the level that normal women wouldn’t feel anything, and they will perceive pain at the level that normal women would perceive touch.
She was a big supporter of physiotherapy as a primary intervention for women with vulval pain, and noted that it is important to consider the context in which vulval pain is managed – ensure to link in with their family situation, social situation and work.
Dr Harlow built on some of the previous comments regarding immunological responses creating the situation in which pain can be expressed from the vulva:
His etiological hypothesis was that vulvodynia was the result of an immunological process.
Women with 10 or more yeast infections were 5x more likely to report vulval pain. We’ve seen from Dr Farmer’s work in mice why this could be, with both the mechanical threshold and brainy management adapting to repeat bouts.
His team are currently working on microbiome diversity in women with vulval pain, and looking at ways that this can be improved. Perhaps there’s a role for reorganising the microbiome in these women?
Dr Goldstein discussed an interesting element of vulval pain – women with umbilicus hypersensitivity.
He talked about how women can have overactivity in the left-over congenital area of the vestibule, which is now at the umbilicus. They’re more likely to get vulvodynia as they have a congenital neuroproliferation of that area. He suggested you observe for redness at the vulva and umbilicus and look at the resilience of the mucosa.
Dermal resilience is something I’ve been talking about for a while, so it’s great to see more working being done into understanding it and trying to find ways of improving it.
There you go – a few more of my highlights:
Immune function and maladaption in vulva and visceral pain syndromes
The role of tissue resilience
Changes in pain management by the Limbic system
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