“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. Continue reading