Physical Therapists could benefit from learning the principle being taught in the following study.
Study: Increased motor cortex inhibition as a marker of compensation to chronic pain in knee osteoarthritis.
Click Here to read the study: nature.com/articles/s4159…
Summary: In short, the study suggests that as cartilage damage increases, the brain might try to compensate by increasing inhibition of muscle activity, which could help explain why pain levels don’t always match the severity of cartilage damage.
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This study aimed to examine the relationship between various social, demographic, and clinical factors and the brain's excitability as measured by motor threshold, motor-evoked potentials, cortical silent period, short-interval intracortical inhibition, and intracortical facilitation—markers identified using transcranial magnetic stimulation in individuals with chronic pain caused by osteoarthritis. It is one of the first studies to investigate the link between transcranial magnetic stimulation measurements of brain excitability and clinical as well as demographic factors in a large group of people with chronic knee osteoarthritis pain. The goal was to improve understanding of the maladaptive mechanisms associated with chronic pain and how these might be reflected in neurophysiological markers.
The main findings revealed significant connections between clinical and demographic factors and brain excitability markers identified by transcranial magnetic stimulation. The study showed osteoarthritis severity and pain—as key factors related to brain inhibition (reflected by short-interval intracortical inhibition and cortical silent period).
Additionally, anxiety and pain were associated with brain facilitation (reflected by intracortical facilitation and motor threshold) in patients with chronic knee osteoarthritis pain.
Conclusion:
A significant positive correlation has been found between the Kellgren-Lawrence Classification for OA severity and the cortical silent period, meaning that the higher severity of OA, the longer the cortical silent period, meaning more intracortical inhibition.
OA severity has been seen to respond differently to chronic pain mechanisms including the process of central pain sensitization. This is the main reason why central sensitization is still not a broadly recognized mechanism of knee OA pain.
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