Turning On Your Brain to Treat Your Knee

Many thanks to Dr. Brian Pietrosimone for providing this week’s EXSS Impact blog post, which summarizes recent work examining the influence of biofeedback on a person’s ability to activate their muscles.  This work has many applications in the areas of injury prevention and rehabilitation, as well as performance enhancement.

This is a summary of a recently published article in the Journal of Electromyography and Kinesiology entitled, “Immediate Increases in Quadriceps Corticomotor Excitability during an Electromyography Biofeedback Intervention.”

Dr. Pietrosimone’s co-authors on this paper include EXSS alumni Dr. Michelle McLeod and Dr. Phillip Gribble.

pietroarticle1) Why Did We Perform this Study?

Knee injury or pain is a common cause of disability for many people in the United States. In part, the disability associated with knee injury and joint disease is influenced by muscle weakness in the lower extremity. The quadriceps musculature, or the group of muscles on the front of the thigh, commonly develops persistent muscle weakness immediately following a joint injury or slowly and concurrently as chronic joint pain progresses. The exact cause of muscle weakness may vary among people, but in many this muscle weakness is due to an underlying neuromuscular dysfunction that inhibits the nerve from allowing muscle to properly contract. This means the muscle weakness that occurs in combination with joint injury is due to the inability for the nerves to “turn on” the muscle. 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.

There is evidence that areas of the brain (primary motor cortex) that are responsible for sending messages to the muscle during voluntary muscle contraction are less excitable following joint injury. A less excitable primary motor cortex inhibits a person from properly contracting a muscle or performing movements that individuals were previously able to preform before injury. People will often explain this feeling as, “ I know how I want to move my leg, but I’m just unable to do it.”

Biofeedback is a commonly used modality that focuses a person’s attention away from the internal physiology of the task, such as contracting a muscle, and toward a more external goal, like moving a body part to a target. Electromyographic biofeedback (EMG-BF) measures electrical activity in the quadriceps muscles, which represents how the nerves are “turning on” the muscles during a contraction; EMG-BF then provides the user with a real-time illustration of the amount of electrical activity in the muscle during a contraction with an easy to understand bar graph. The clinical utility of EMG-BF stems from its ability to teach the patient to “turn on” muscles better than conventional instructions used by clinicians to cue a muscle contraction. Without an EMG-BF device, the idea of “turning on” electrical activity in a muscle may be too abstract of an instruction for people to effectively accomplish this task. Therefore, EMG-BF may be important for cueing patients to excite areas of the brain that influence voluntary muscle contraction. There have not been any studies that have evaluated if EMG-BF treatments used in conjunction with muscle contractions can increase excitation of the primary motor cortex compared to only performing muscle contractions without an external cue.

The primary motor cortex of the brain is responsible for executing the relay of neural information from pre-motor areas of the brain (involved in planning movements) to descending tracts in the spinal cord, which terminate on alpha motor neurons that direct excite the muscle. The excitability of the primary motor cortex is decreased in patients with certain knee injuries. Individuals with diminished excitability of the primary motor cortex may be able to plan voluntary movements, yet lack the ability to easily execute those same voluntary movements.

The primary motor cortex of the brain is responsible for executing the relay of neural information from pre-motor areas of the brain (involved in planning movements) to descending tracts in the spinal cord, which terminate on alpha motor neurons that direct excite the muscle. The excitability of the primary motor cortex is decreased in patients with certain knee injuries. Individuals with diminished excitability of the primary motor cortex may be able to plan voluntary movements, yet lack the ability to easily execute those same voluntary movements.

2) What we did in this study

We used transcranial magnetic stimulation to excite areas on the primary motor cortex of the brain that “turn on” the quadriceps muscles. Briefly, transcranial magnetic stimulation is applied over the scalp with a coil that induces a brief stimulus to a specific area in the brain. The magnetic stimulation depolarizes neurons (nerve cells) in the brain causing a measurable twitch in the quadriceps, which we measured in the quadriceps musculature using electromyography. These twitches that we measured in the quadriceps muscle provide an estimate of excitability of the primary motor cortex.

Healthy participants were secured into a chair and performed maximal contractions against a dynamometer, which is an instrument that measured the force produced by the quadriceps. Participants reported to the laboratory on two separate occasions, where they performed a series of maximal contractions with EMG-BF or a series of maximal contractions without EMG-BF. When the participants produced a maximal contraction we administered transcranial magnetic stimulation to the primary motor cortex of the brain and evaluated the size of the response in the quadriceps to determine if EMG-BF enhanced the excitability of the primary motor cortex during a maximal muscle contraction.

kneepain3) What we found and how it impacts the public.

As we hypothesized, providing an external focus of attention during a maximal quadriceps contraction with EMG-BF enhanced motor function by increasing excitability of the primary motor cortex. Additionally we found that participants were able to produce more force when augmenting maximal contractions with EMG-BF. We expect that the current research will have both future research and clinical implications. Currently, the large body of evidence on the EMG-BF remains relatively inconclusive regarding its benefits for improving muscle function. There has not been adequate study on the potential neuromuscular mechanisms that may be influenced by EMG-BF. Our study provides some fundamental knowledge on how EMG-BF affects brain excitability, which may allow researchers to determine how to utilize EMG-BF to elicit the most advantageous neuromuscular benefits. Clinically, EMG-BF may be a viable intervention for treating persistent neuromuscular deficits following a variety of knee injuries and conditions including: 1) anterior cruciate ligament rupture, 2) meniscal injury, 3) patellofemoral pain, and 4) osteoarthritis. In the future, EMG-BF may provide a novel way of targeting disability at its origin, the brain.

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