INVITED BLOGPOST
Much of my early professional years were spent watching competitive sports. After 1-2 years in general practice I was hired by Tulane University in New Orleans, Louisiana, as Assistant Athletic Trainer. Tulane University competed in Division I Athletics which meant that a majority of their student athletes attended on a ‘full-ride’ scholarship; our ability to keep them healthy was taken quite seriously.
The life of an athletic trainer can be a solitary experience, with many hours spent watching practice, the purpose being to prevent, or at least see the injury as it happens. As an introvert, I often enjoyed this part of the job – a lot of time was spent watching people move… and thinking about it. One phenomena I found curious was the variable effect of instability on function. A primary example of this was anterior cruciate ligament insufficiency. One athlete could perform as a linebacker (American football), cutting, pivoting and performing at full speed, while a second person would experience ‘giving way’ of the knee after stepping on a pebble. Why was that? My self-assessment indicated a lack of knowledge in motor control, so in later years, I studied for a year at Columbia University Program in Motor Learning and Control in New York City, New York, and after, PhD studies at the University of Miami in Miami Florida.
In an ACL deficient population, I found altered electromyographic (EMG) muscle activation patterns in response to unexpected platform perturbations (Courtney and Rine 2006) and with progressive challenge to gait (Courtney et al. 2005). A key finding of these studies was an increased amplitude and decreased latency of response of the hamstrings – the latency of response indicated reflexive rather than volitional activation. In addition, altered somatosensory evoked potentials were demonstrated, as had been previously reported (Valeriani et al. 1996). I proposed that these altered muscle activation patterns were a change in the motor program, generated due to altered afferent input from the knee. I thought this altered hamstring activation was a positive response, potentially serving to stabilize the knee.
Later, as an early-career faculty member at the University of Illinois in Chicago I was advised to broaden my scope to investigate osteoarthritis (OA). As I began to study the research literature, I found an interesting paper on muscle activation patterns during gait in individuals with knee OA (Childs et al. 2004). To my surprise, the EMG patterns looked very similar to what I had found in my ACL deficient population. I began to ask myself, could these heightened hamstring activation patterns be instead due to a hyperexcitable nociceptive reflex?
As is well known, the nociceptive reflex is a withdrawal response from a painful stimulus, and is characterized by inhibition of the extensor musculature (eg, quadriceps) and excitation of the flexor musculature (eg, hamstrings). Intuitively this fit my clinical pattern of knee OA and ACL injury, however this measure of spinal excitability had been little studied in non-neurological patient populations at the time (see however, Banic et al. 2004). However, an animal model study had demonstrated that the reflex could be modulated (ie, increased excitability) by inducing knee joint inflammation (Ferrell et al. 1988). I was fortunate that one of my colleagues at the time was physical therapist and neurophysiologist, George Hornby, who investigated neurophysiologic mechanisms of spinal cord injury. I approached George with my idea and he said, ‘Brilliant, let’s do it.’
We found that regardless of subjective reports of resting pain, individuals with moderate to severe knee OA demonstrated diminished thresholds to elicit the nociceptive reflex (Courtney et al. 2009). This is considered a laboratory-based indirect measure of central sensitization of nociceptive pathways. Furthermore, we were able to down-modulate the excitability of the reflex through a bout of oscillatory joint mobilization (Courtney et al. 2010). This indicated that the effects of manual therapy may be, at least in part, centrally mediated. In a later study I found that joint mobilization resulted in facilitation of descending pain inhibition in persons with knee OA and impaired conditioned pain modulation (Courtney et al. 2016). I believe that understanding the mechanisms underlying chronic musculoskeletal conditions, whether neurophysiological or biomechanical, may help direct our treatments more appropriately.
But what about the individual with ACL rupture? Through a subsequent study I was able to demonstrate that the heightened hamstring activity we had previously observed was a component of a heightened nociceptive reflex response (Courtney et al. 2011). In future studies we hope to study what role this may have in the transition to osteoarthritis and/or chronic pain.
Carol A. Courtney
Carol A. Courtney is Clinical Professor and Director of the post-professional Fellowship in Orthopedic Manual Physical Therapy at the University of Illinois at Chicago. Dr Courtney is a licensed physical therapist and athletic trainer, and has been recognized as a Fellow of the American Academy of Orthopaedic Manual Physical Therapists. In 1991 and 1992, she was chosen to serve on the USA medical staffs for the Pan American Games in Havana, Cuba, and the Olympic Games in Barcelona, Spain. Dr Courtney has over 100 peer-reviewed publications, book chapters and conference presentations and has presented both nationally and internationally on this research. She is the 2015 recipient of the AAOMPT John Mennell Service Award and the 2016 JOSPT Excellence in Research Award.
2017 Pain in Motion
References and further reading:
Courtney CA, Rine RM. Central somatosensory changes associated with improved dynamic balance in subjects with anterior cruciate ligament deficiency. Gait Posture. 2006;24:190-195.
https://www.ncbi.nlm.nih.gov/pubmed/16181781
Courtney C, Rine RM, Kroll P. Central somatosensory changes and altered muscle synergies in subjects with anterior cruciate ligament deficiency. Gait Posture. 2005;22:69-74. doi:10.1016/j.gaitpost.2004.07.002.
https://www.ncbi.nlm.nih.gov/pubmed/15996595
Valeriani M, Restuccia D, Di Lazzaro V, Franceschi F, Fabbriciani C, Tonali P. Central nervous system modifications in patients with lesion of the anterior cruciate ligament of the knee. Brain. 1996;119 ( Pt 5):1751-1762.
https://www.ncbi.nlm.nih.gov/pubmed/8931595
Childs JD, Sparto PJ, Fitzgerald GK, Bizzini M, Irrgang JJ. Alterations in lower extremity movement and muscle activation patterns in individuals with knee osteoarthritis. Clin Biomech (Bristol, Avon). 2004;19:44-49.
https://www.ncbi.nlm.nih.gov/pubmed/14659929
Banic B, Petersen-Felix S, Andersen OK, et al. Evidence for spinal cord hypersensitivity in chronic pain after whiplash injury and in fibromyalgia. Pain. 2004;107:7-15.
https://www.ncbi.nlm.nih.gov/pubmed/14715383
Ferrell WR, Wood L, Baxendale RH. The effect of acute joint inflammation on flexion reflex excitability in the decerebrate, low-spinal cat. Q J Exp Physiol. 1988;73:95-102.
https://www.ncbi.nlm.nih.gov/pubmed/3347700
Courtney CA, Lewek MD, Witte PO, Chmell SJ, Hornby TG. Heightened flexor withdrawal responses in subjects with knee osteoarthritis. J Pain. 2009;10:1242-1249.
https://www.ncbi.nlm.nih.gov/pubmed/19628435
Courtney CA, Witte PO, Chmell SJ, Hornby TG. Heightened flexor withdrawal response in individuals with knee osteoarthritis is modulated by joint compression and joint mobilization. J Pain. 2010;11:179-185.
https://www.ncbi.nlm.nih.gov/pubmed/19945353
Courtney CA, Steffen AD, Fernandez-de-Las-Penas C, Kim J, Chmell SJ. Joint mobilization enhances mechanisms of conditioned pain modulation in individuals with osteoarthritis of the knee. J Orthop Sports Phys Ther. 2016;46:168-176.
https://www.ncbi.nlm.nih.gov/pubmed/26721229
Courtney CA, Durr RK, Emerson-Kavchak AJ, Witte EO, Santos MJ. Heightened flexor withdrawal responses following ACL rupture are enhanced by passive tibial translation. Clin Neurophysiol. 2011;122:1005-1010.
