Tag Archives: mechanobiology

The Ice-less Management of Acute Ankle Sprains

I’ve written several articles on the use of ice on injuries, the need for inflammation, and the intricate physiological process of tissue healing.  Despite the mounds of evidence that ice is not all it is cracked up to be, there still exists a dogmatic polarization that it has magical tissue-healing properties. I often get told “Prove to me that ice does not work.” No; that is not how evidence-based practice works. You need to prove that ice does work for the reasons you use it.

Read the comments I receive, and you will recognize our ice dependency. “If I don’t ice, then what do I replace it with?” That statement screams dependency. When we take away ice, we feel that a void must be filled. It doesn’t! The treatment decision is multifactorial; the injury type, severity, tissues involved, the person, etc., all play a role in how you treat that specific injury.

A 2013 position statement made by the National Athletic Trainers’ Association on the management of ankle sprains found ice therapies had a C-level of evidence 1. Meaning little or poor evidence exists. In an interview, the author of that article said: “I wish I could say that what we found is what is really being done in a clinical setting…. Maybe our European colleagues know 20151221_102243_resizedsomething we don’t…there is very little icing over there.”

The blog shows how I treated an acute ankle sprain without ice by using all of the fun little tools learned through school and further honed with clinical experiences, trial, and error. I did what I thought was best. This protocol should not be used for every ankle injury. My treatment and rehabilitation plan changed daily. Everything I did was based on my ankle needs. I did NOT use any biophysical or electromagnetic modalities. Everything I did was manual. This is not to say that I would not use other modalities, I just chose not to. My only rule? No ice. Continue reading

Knee Osteoarthritis and ACL Injury

ACLSix months (+/- a few) is the standard time needed for an athlete to return to competition following anterior cruciate ligament (ACL) surgery. To reach this date, therapy must be thorough and exact. Range of motion, neuromuscular control, or strength deficits that go unaddressed, negatively influence return to play and can also lead to other long-term consequences.

Those who suffer from ACL injuries are at greater risk of developing knee osteoarthritis (OA). Knee OA is a condition whereby the cartilage slowly wears away. This is a painful, life-long health issue that can lead to disability. With proper rehabilitation and adequate strengthening of the quadriceps, OA can be prevented. Sounds simple, but clinicians must also deal with arthrogenic muscle inhibition (AMI).

ASpinal tractMI is a neuromuscular dysfunction that limits the ability to strengthen muscle and is common following ACL surgery. With AMI, neurological signals from the quadriceps muscle to the brain and spinal cord are interrupted or slowed. You can read more about Brain and CNS deficits here.  So the question is, how do you combat AMI to properly strengthen the quad and subsequently prevent knee OA? The answer might be vibration training.

Vibration training employs a low-amplitude, low-frequency mechanical stimulation that exercises musculoskeletal structures. Vibration training provides strength gains without joint loading and stimulates osteoblastic and chondrocyte activity through the mechanisms of  Power Platemechanobiology. Subsequently, bone and joint health are improved.

A recent article by UNC’s EXSS Impact site found that vibration training (local or whole-body) improves quadriceps function by improving central nervous system function. Following vibration training, brain activity was altered in such a way that it became easier for these subjects to activate and use their quadriceps muscles. As such, muscle vibration can be an effective method to improve quadriceps strength and reduce the risk of developing knee OA.

Below is the full article from UNC.

Why did you do this study?

Individuals with anterior cruciate ligament (ACL) injuries are at greater risk of developing osteoarthritis (OA). OA is a considerable burden on the US healthcare system and contributes to physical disability and comorbidities such as obesity and diabetes. The lifetime cost of ACL injury amounts to $7.6 billion annually for patients that undergo reconstruction, $17.7 billion for patients that undergo non-surgical rehabilitation. Quadriceps dysfunction is ubiquitous following ACL injury and reconstruction, and is a major contributor to the development of OA. The quadriceps are responsible for absorbing impact forces during everyday tasks like walking and stair climbing, and also athletic tasks like running and jumping. When the quadriceps fail to act appropriately, their ability to attenuate these forces is reduced, and cartilage within the knee joint experiences greater loading. Subtle increases in joint loading are amplified through repetitive activities like walking, and over time, greater loading contributes to a gradual breakdown of articular cartilage.

Given the implication for future OA development, the restoration of proper quadriceps function is extremely important in rehabilitation. However, quadriceps dysfunction is caused by a neuromuscular phenomenon called arthrogenic muscle inhibition (AM), which presents a substantial limitation to muscle strengthening. Essentially, sensory signals from the knee joint inform the central nervous system – the brain and spinal cord – that the ACL as been injured. In response, our central nervous system responds by inhibiting the quadriceps to prevent further damage of the injured joint. While this mechanism may protect the joint in short term, AMI persists for many years following the initial injury and is thought to contribute to excessive cartilage loading and the development of OA. Therefore, strengthening the quadriceps is important in rehabilitation, but traditional exercises do not address AMI. Novel rehabilitation modalities are needed to combat AMI prior to the implementation of strengthening exercises.

Previous work in our laboratory indicates that muscle vibration provided directly (local muscle vibration – LMV) and indirectly (whole body vibration – WBV) may improve quadriceps function. However, what remains unclear is the mechanism by which these vibratory stimuli actually work to enhance muscle function. Given that AMI involves alterations in central nervous system function, it is imperative to understand how muscle vibration influences characteristics of spinal cord and brain function. Therefore, the purpose of this study was to understand how both WBV and LMV influence characteristics of central nervous system function.

What did you do and what did you find in this study?

Left - Transcranial magnetic stimulation to assess cortical neuron excitability; Right - Whole body vibration platform

We recruited subjects with ACL reconstruction for this study. First, we measured various characteristics of quadriceps function (i.e. strength and activation), and also how the brain and spinal cord contribute to muscle contraction. Following baseline measurements, subjects received an intervention of WBV, LMV, or control (no vibration) treatment. We repeated the same measurements of quadriceps function and central nervous system function following the treatment.

Active motor threshold was used to assess corticomotor excitability. In this case, both WBV and LMV lowered AMT relative to the control condition. This indicates that it becomes easier for the brain to activate the quadriceps following treatment. (* indicates P<0.0083)

We found that both WBV and LMV acutely improved quadriceps function (strength and activation) relative to the control treatment, and that this improvement was likely due to greater cortical neuron excitability. In other words, muscle contraction can either be voluntary (the brain tells the muscle to contract) or involuntary (spinal reflex loops). What we found was that following WBV and LMV, brain activity was altered in such a way that it became easier for these subjects to activate and use their quadriceps muscles.

How do these findings impact the public?

These findings indicate that vibratory stimuli acutely improve quadriceps function, and could be useful in addressing deficits in central nervous system function such as AMI. As such, muscle vibration could be an effective method to improve quadriceps strengthening protocols following ACL injury, and in turn reduce the risk of developing knee OA. Overall, knee OA is a major economic burden on the US healthcare system, and these findings could have important relevance for alleviating healthcare costs and physical disability.

A comprehensive rehabilitation program is vital for an athlete’s return to competitive sport. Failure to normalize range or motion, strength, and neuromuscular control can result in performance loss, reinjury, or long-term disabilities, such as knee OA. Make sure your rehabilitation program is inclusive of all components. Of course, the best cure for ACL surgery is preventing ACL tears all-together. If you want to prevent ACL injury, read about the RIDS Program designed to prevent injury. 

10 Reasons – Icing Injuries is Wrong

iceIf you know me, you are aware of my anti-ice stance. The ice debate continues to heat up. As peer-reviewed data continues to pour in, the evidence for the use of ice to treat musculoskeletal injury still lacks. I’ve written about ice many times, but many of my anti-ice articles are science-y and focused around one topic. I wanted to do something different this time. I wanted to keep it short, sweet and comprehensive. So, I bring you 10 reasons why we shouldn’t ice injuries. Continue reading

Causes and Treatment of Achilles Tendinopathy

Overview and etiology:

Pain and injury to the Achilles tendon is often thought to be a result of inflammation.

Pain and injury to the Achilles tendon is often thought to be a result of inflammation.

The term “tendinitis” or any [insert any body part] with “itis” is tossed around as if it is the only possible cause for musculoskeletal pain. However, the “itis” is not really true. A tendon, specifically the Achilles tendon, is not really inflamed, rather it is deranged (tendiopathic / tendinopathy). In January 2013 the Annals of Human Genetics published an article that demonstrated Achilles Tendinopathy is associated with gene polymorphism (Abrahams, et al., 2013). COL51A is a gene that encodes the development and organization of Type V collagen. 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 tendinopathy.

The tendon may become fusiform or thickened, but it is due to cellular derangement rather than inflammation. Kannus and Jozsa in a controlled study of 891 patients with Achilles tendon rupture found that 97% of patients had degenerative changes in the ruptured tendon. The study also found that 34% of asymptomatic tendons also had degenerative changes (2) Continue reading

Ice: The Overused Modality?

Many years ago I got tired of watching my athletes roll in to the ice-for-injuriesathletic 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.

Continue reading