When Paul Biegler injured his knee training on his bicycle, the pain persisted for months longer than he anticipated.
Biegler, a former doctor, academic and science journalist, started investigating chronic pain after he was given pain medication and told he'd need surgery on his knee.
He came upon the information that your brain can think you have an injury when you no longer do, something called central sensitisation.
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His book new book is Why Does It Still Hurt?
“I developed a condition called patellofemoral pain syndrome, which is pain in my left knee.
“This went on for some months and I became concerned, what's going on here? Am I going to end needing potentially surgery, injections and so on and so forth,” he tells Nine to Noon.
He stopped “doing everything” he says, riding, running and swimming, because they all “seemed to bring on the pain”.
Eventually a sports and exercise physician told him about neuroplasticity.
“Pain lasting beyond about 10 or 12 weeks is no longer a very good marker of damage to the tissues.
“We know that in short term acute injuries, pain is a very useful marker that you've done damage and that you need to stop and rest it and get help and do things to ensure that the injury heals.
"But in chronic pain, that kind of one-to-one matching of the pain with tissue damage starts to break down.”
The pain becomes a much less accurate marker of tissue damage courtesy of a process of neuroplasticity, he says.
“This is where there is a strengthening in the sensory nerve pathway, in my case leading to the knee, such that you could now experience things that shouldn't be painful, like a breeze blowing on my knee when I rode the bike, as painful.
“And things that normally shouldn't hurt too, much pressure on the area and so on, would start hurting a lot more.”
The pain is 100 percent real, he says.
“But what's really likely to have happened now is that it's no longer coming from the knee itself, the pathology there has in all likelihood healed, it's resolved.”
A significant contributor to his pain was coming from sensitised nerve pathways and from changes in the brain, he says.
Central sensitisation happens as soon as an injury occurs, he says
“It's part of that strengthening of the sensory pathway. There's a number of changes that happen with receptors, NMDA receptors, and changes in neurotransmitters to sensitise those pathways.”
It’s the body’s ‘better safe than sorry’ response, he says.
“This kind of helicopter parent approach to getting you to do everything possible to stop re-injuring and to aid recovery.”
Significant changes to the brain occur in people with persistent pain according to research at Northwestern University, Chicago, he says. Researchers there took a cohort of people with lower back pain and monitored them over a year.
“About 50 percent of those people got better, their pain went away, and those brain changes disappeared. But the other 50 percent went on to develop persistent back pain and they had ongoing brain scan changes.”
The changes moved from the sensory cortex to other parts of the brain; the amygdala, which registers anxiety and fear; the hippocampus, which registers sadness and depression and the medial prefrontal frontal cortex, part of our reward pathways, he says
“And what [researcher] Apkarian discovered as a result of these brain changes, was that the emotions you normally get as a sequel to chronic pain, you feel anxious, you feel miserable, you feel sad, those emotions aren't just consequences of pain, they can actually perpetuate pain.”
Understanding what central sensitisation is, can help people recover, he says.
“Simply understanding that the pain is far less likely now to be indicative of ongoing tissue damage can be a huge relief to people, that understanding can be therapeutic in and of itself.”