Osteoarthritis (‘OA’) is a $3.5 billion burden in Australia and a leading cause of pain and disability globally. Pain and impairment from OA means extensive time-loss from work, with people relying on pain medication and in some circumstances major surgery to manage the condition.
A/Prof Myles Murphy is a Sport and Exercise Physiotherapist and researcher at the University of Notre Dame Australia. His research explores what drives pain and impairment in people with lower-limb musculoskeletal injury, and how we can better prevent and treat these conditions.
Fresh perspective on an old problem
Best-practice management for OA involves building strength, increasing range of motion and improving proprioception (body awareness). But despite doing all of these things, not everyone achieves a satisfactory outcome. During his work as a sports physiotherapist, A/Prof Murphy knew there had to be more to this condition and that thinking ‘outside the box’ was needed to improve outcomes for people with OA.
“This suggested to me that looking at the joint structure and function alone was too narrow a view, and we weren’t seeing the complete picture.”
Therefore, his latest research has demonstrated that people with hip OA not only have peripheral issues with the joint structure and function, but they also experience changes in the brain that are associated with their OA pain.
Misconceptions about pain at the heart of OA
“There’s a misconception about OA that pain severity and function are related to the degree of structural damage,” says Murphy.
“Evidence actually shows that pain severity with OA has a poor relationship with the degree of structural damage visible on imaging.”
Working with elite athletes, Dr Murphy saw this play out time and time again: people with ‘bone-on-bone’ OA living completely pain-free with full function, and others with only minor degeneration rating their pain 11 out of 10.
“What we were seeing on the x-ray or MRI wasn’t accurately reflecting how clients were feeling, or how their limb was functioning.”
“Improvements in pain can even occur while visible “damage” on a scan remains completely unchanged. We have seen this in other musculoskeletal conditions, where changes in disability aren’t necessarily tied to improvements in muscle function either.”
Research has shown that imaging has a poor relationship to function in many musculoskeletal conditions, such as lower back pain or tendinopathy.
OA brains are hitting the ‘brakes’
“People with OA are unable to fully activate the muscles around their affected joint, because the brain is actively applying a ‘brake’ to stop them from using the muscle,” Dr Murphy explains.
“We don’t yet know why that is. But the brain seems to be doing this to protect the joint by reducing the ability of the muscle to produce force. However, this is a maladaptive change as strong muscles actually help reduce joint pain.”
“If we describe this in clinical terms, when people with persistent OA pain try to actively contract muscles around the affected joint, they show impaired voluntary muscle activation. To produce maximum strength, the motor cortex, which is the part of the brain that activates muscles, needs to send a clear signal down through the spinal cord to the muscle. When that signal is reduced, the result is muscle weakness that has nothing to do with damage in the muscle itself.
The exact mechanism driving these changes in the brain, and the lack of activation in the muscle, are not yet fully understood.
“What we know is that the pain associated with OA is complex and not solely related to signals sent by damaged joint tissue. The central nervous system plays an important role.”
“Understanding the different ways in which the nervous system contributes to muscle dysfunction in OA, will help inform the design of more targeted treatments for pain, muscle weakness, and function.
Measuring the brain’s role: Transcranial Magnetic Stimulation (TMS)
To measure the degree of inhibition and facilitation of the brain’s motor cortex researchers use transcranial magnetic stimulation (TMS). Magnetic pulses stimulate the motor cortex, and EMG sensors on the leg muscles record the level of activation. This provides insight into whether the brain-to-muscle pathway is underactive, or overactive.
“Think of inhibition and facilitation as a brake and accelerator,” says Dr Murphy. “TMS lets us see how those pathways are working — whether they’re operating normally, or whether activity is excessive.”
With alterations in these brain pathways, resulting in a lack of strong signal to the muscles, people with OA cannot properly activate their muscles and this limits their ability for improvements in pain and restoring normal function. A/Prof Murphy’s research is now looking at how innovative technological approaches can be used to normalise brain pathways.
Turning measurement into treatment: the ACL study
Similarly to OA even with best-practice exercise rehabilitation, patients commonly struggle to recover following Anterior Cruciate Ligament (ACL) Injury and Reconstruction. Previous research has shown the changes that occur in the brain in people with OA, are also present in people following ACL reconstruction.
“This is largely because the brain ‘dials down’ the drive to those leg muscles, making rehab less effective,” says Dr Murphy.
Dr Colin Sylvester, a physician with the Fremantle Football Club, investigated this under the supervision of A/Prof Murphy, and discovered these changes in the brain occur as early as two weeks following the ACL surgery.
A/Prof Murphy, alongside Dr Casey Whife, West Coast Eagles Chief Medical Officer, tested whether they could reverse these changes by applying a small, externally-delivered electrical current to the brain region controlling the leg muscles, at the same time as standard rehab exercises. This is a simple approach, and all participants feel is a light tingling or itchiness at the site of the electrodes on the head.
Findings indicated that muscle strength could be maintained while reducing the brain’s inhibitory “brake”. Marking a substantial step forward in our understanding of how to best rehabilitation people with musculoskeletal injuries.
What’s next
Myles is now trialling the same electrical stimulation approach for people with hip OA, testing whether the positive changes he has observed following ACL surgery can be replicated in people with hip OA.
“This is early-stage research, and brain stimulation isn’t yet a standard clinical tool. But it’s paving the way for a potentially simple, low-cost, accessible add-on to existing exercise rehab — not a replacement for it, but a way to help rehab actually work the way it’s supposed to.”
Read about Myles Murphy’s latest work here:
https://www.sciencedirect.com/science/article/pii/S266633762400101X
https://eor.bioscientifica.com/view/journals/eor/8/12/EOR-23-0092.xml
https://www.sciencedirect.com/science/article/pii/S266633762500099X
https://bmjopensem.bmj.com/content/10/4/e002080
Dr Myles Murphy is open to speaking on the topics of ankle, knee and hip pain as well as musculoskeletal injury prevention in physically active populations.