We’ve written before about the groups that miss out on optimal pain treatment – groups in which pain is often poorly recognised at best, or not really considered an issue at worst. These include young people, people with Parkinson’s or other neurological diseases, pelvic pain and stroke.
A recent systematic review* in Stroke has highlighted just how bad the situation is for this group;
“Central poststroke pain (CPSP) is a chronic (≥3 months) neuropathic disorder that can occur after a lesion or disease affecting the central somatosensory system. The pain may be spontaneous, occurring either constantly or intermittently, or evoked in response to external stimuli. It may develop immediately after a stroke, or years later.
Eight eligible English language randomized controlled trials (459 patients) tested anticonvulsants, an antidepressant, an opioid antagonist, repetitive transcranial magnetic stimulation, and acupuncture. Results suggested that all therapies had little to no effect on pain and other patient-important outcomes. Our certainty in the treatment estimates ranged from very low to low.
Our findings are inconsistent with clinical practice guidelines by 3 major professional groups… all of whom recommend tricyclic antidepressants as first-line therapy for managing patients with CPSP. These recommendations are because of 1 trial of 15 participants that concluded that amitriptyline significantly reduced pain intensity versus placebo after 4 weeks of treatment…our reanalysis of the data found no significant effect (P=0.11).”
Research is needed – and is underway
These poor results echo the sentiments that Brendon Haslam, a NOI instructor currently undertaking a PhD looking at upper limb pain in a post-stroke population, has shared here before:
“This craziness has been driven by my frustration at the lack of effective treatment interventions for this group (and indeed many others). While there is heaps of literature out there telling us how much of a problem pain is in this population, there is hardly anything out there telling us what we can do about it, and medications just don’t seem to work adequately, with worsening NNTs over time.”
Brendan will be launching his data collection project soon, giving everyone a chance to participate in research that will help this group – we’ll certainly let you know how you can get involved.
A step back to see the commonality
A bit of reading about CPSP reveals that no one really knows what causes it. Leading theories suggest that deafferentation leads to the development of neuronal hyperexcitability (sorry, paywall), but which specific neuronal populations become sensitised is not well understood, beyond a vague they’re probably somewhere in the thalamus (open access). But, if we take a step back to think about the commonality of an individual’s experience of pain, looking for the guilty neuronal population in CPSP is a bit like looking for the ‘pain centre’ responsible for chronic low back pain. Sensitised, hyperexcitable neurones can increase their firing rate and behaviour, but this isn’t pain any more than peripheral nociception is pain. With the thinking that pain arises when there are more DIMs than SIMs, it’s not a far stretch to consider that there are multiple, terrifying DIMs post-stroke, along with all the Things happening in your body. Perhaps Explaining Pain, destroying DIMs and searching for SIMs at the right time, and in the right way, post-stroke could be an effective, risk free, low cost part of optimal pain treatment for this group desperately in need of help.
*My thanks to @NeilOConnell for pointing out the systematic review on Twitter