“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 →
Are you an evidence-based practitioner? Think about it; are you really?
An athletic trainer working a Division 1 women’s volleyball tournament with elite Top-25 teams sent me a text: “You should do a study on the average number of ice bags used by volleyball teams after a match… Entire teams are getting ice on both knees and the hitting shoulder. No post-match mobility work, just pounds of ice. Crazy! Some athletic trainers and strength and conditioning coaches are too ignorant and too lazy to provide proper warm-up and cool-down protocols to address mobility.” This is not shocking to me. I worked with Division I volleyball for several years and I observed this too. This is where I learned ice is overused. This isn’t just a volleyball thing; this is an all-sport issue.Continue reading →
Many years ago I got tired of watching my athletes roll in to the athletic training room and slap on ice. These athletes are in a drug-like induced state of ice addiction. Their athletic trainers keep feeding the disease, by recommending cold treatment and doing the easy – here’s ice, shut-up, leave. I felt I was doing a disservice to my athletes and asked myself, “Why are we icing this injury?” I never had an answer that was supported by evidence. So I began my own case study.
I took 9 Division I athletes (6 patellar tendinopathy, 2 bicipital tendinopathy and 1 subacromial impingement) and had the athletes cease all cryotherapy and electrical stimulation.
You have an athlete with a stress fracture. The physician prescribes active rest and places the athlete in a non-weight bearing boot. Sound familiar? Suppose I told you the better option is to place some load on that bone and non-weight bearing is not recommended. Would you think I am nuts? Maybe I can convince you otherwise. Let me explain but, before you read the next paragraph and decide to leave the page, bear with me. What follows this introductory piece may provide insight to further understanding of injury pathophysiology and could revolutionize the future of rehabilitation science.
In January 2013 the Annals of Human Genetics published an article that demonstrated Achilles Tendinopathy is associated with gene polymorphism (Abrahams, et al., 2013). I am not a geneticist by any stretch of the imagination, so pardon my basic explanation. COL51A is a gene that encodes the development and organization of Type V collagen. Type V collagen is a collagen that is distributed in tissues as a component of extracellular matrix and composed of one pro alpha 2 (V) and two pro alpha 1 (V) chains. This collagen can be found in ligaments, tendons, and connective tissue. COL51A plays an integral role in development and maintenance of connective tissue. Abrahams, et al. (2013) demonstrated that polymorphisms occur in the COL51A gene causing altered structure of collagen resulting in tendionpathy. Continue reading →