“Novel treatment of muscle weakness following joint injury has sought to develop interventions that can excite the neuromuscular system and allow for more effective interactions between the nerves and muscle.”
Chad and Brent both play the same position for the same basketball team—same practice routine, same strengthening program, same injury prevention program—but Chad is suffering from left patellar tendonitis. Why is Chad injured and not Brent? We have adopted laymen medical terms such as “Runner’s Knee”, “Little Leaguer’s Elbow”, “Tennis Elbow” or “Jumper’s Knee” implying these types of injuries are caused by the activity. But are they? What if Chad’s “Jumper’s Knee” is linked to a brain or spinal cord deficit and not some musculoskeletal dysfunction?
Everything we do —touch, sense, feel, contract, move— triggers an action potential that is sensed by millions of mechanoreceptors, which follows a path to the brain.
- The action potential is picked up by peripheral nerves and carried to the dorsal root ganglion cell and travels to the spinal cord.
- The impulse goes through the dorsal column nuclei and the impulse is taken to the thalamus in the brain via the spinothalamic tract.
- In the brain, this impulse synapses with the ventroposterolateral thalamus and onto the somatosensory cortex.
- A motor response is then triggered.
This path is followed every time. Sensory or motor deficits anywhere along this path can lead to injury. Sometimes, as health care providers we get in a rut and look to treat the body part or underlying movement dysfunction. While this practice is not necessarily bad, it might not be what is needed. Correcting muscle imbalance or addressing joint dysfunction may not be the answer. Removing the athlete from activity to reduce overload may not be the answer. Our goal should aim to fix deficits along the neural path.
Over the past few years there is increased evidence that links injury to central nervous system (CNS) deficits. Data has demonstrated that some rehabilitation techniques will increase activity levels in brain centers. A recent systematic review with meta-analysis published in the British Journal of Sports Medicine evaluated involvement of the CNS on patients with unilateral tendon pain.
This review investigated evidence for sensory and motor system involvement in individuals with tendinopathy. The authors performed a comprehensive search and found twenty articles that met the study criteria. The reviews concluded that deficits in the sensory and motor systems were bilateral, not just the side of injury. These data imply central nervous system involvement and could be the cause for tendon pain.
A very recent study (April, 2015) study published in the Journal of Electromyography and Kinesiology was summarized in a post appropriately named “Turning On Your Brain to Treat Your Knee”. If you follow that link, you should also subscribe to the UNC EXSS blog page. That group turns out great stuff all the time. Lead author, Brian Pietrosimone, PhD, ATC (follow him too, because he is genius) stated quadriceps musculature, commonly develops persistent muscle weakness and in many cases this muscle weakness is due to an underlying neuromuscular dysfunction that inhibits the nerve from allowing muscle to properly contract.
In this study, Pietrosimone and team evaluated the effectiveness of biofeedback on corticomotor excitability. They found that biofeedback enhanced motor function by increasing excitability of the primary motor cortex. The authors go on to state that novel treatment of muscle weakness following joint injury has sought to develop interventions that can excite the neuromuscular system and allow for more effective interactions between the nerves and muscle. “In the future, [biofeedback] may provide a novel way of targeting disability at its origin, the brain.”
At the 2013 NATA conference, I attended a presentation by Alan Needle, PhD, ATC. In Alan’s graduate research he found that joint mobilization of the ankle increases activation of the contralateral somatosensory cortex while load is applied. This data lends support to a significant role of the brain during rehabilitation. Alan concluded that this could improve our understanding of sensory integration that must occur between the sensation of injurious loads and the formation of a reflexive response.
Returning to the example at the opening of this post – Chad’s left patellar injury – this knee pain may not be due to overload or some type of arthrokinematics dysfunction. Chad might be susceptible to injury due to CNS deficit. Therefor a traditional treatment and rehabilitation protocol for patellar pain may not fix the issue. If a particular client or athlete has recurrent or chronic injury, there might be underlying CNS deficit. You may need a multifaceted, neuromuscularly rich, therapy program that can train the central nervous system and help form a responsive line of communication between the brain, spinal cord, and muscles.
Heales, LJ, Lim, ECW, Hodges, PW, & Vicenzino, B. Sensory and motor deficits exist on the non-injured side of patients with unilateral tendon pain and disability—implications for central nervous system involvement: a systematic review with meta-analysis. Br J Sports Med 2014;48:19 1400-1406 Published Online First: 21 October 2013
Pietrosimone B, McLeod MM, Florea D, Gribble PA, Tevald MA. Immediate increases in quadriceps corticomotor excitability during an electromyography biofeedback intervention.
J Electromyogr Kinesiol. 2015 Apr;25(2):316-22.
Needle AR, Swanik CB, Baumeister J, Schubert M, Reinecke K, Higginson JS, Farquhar WB, Kaminski TW, Higginson JS. Decoupling of Laxity & Cortical Activation in Unstable Ankles during Ligamentous Loading. Eur J Appl Phys. 2014