Most biomechanics texts are very dense. They are filled with theory, formulas, definitions and diagrams. They often have little to directly link them to patient diagnosis and care. This book is different. Practical Biomechanics is as it says, “practical” and straight forward. It is not dependent on long discussions of joint axes or theory. In fact, I’d call it theory agnostic.
But what it does is give you insight into the thinking of someone who has mastered clinical biomechanics. Dr. Blake gives advice on how to approach the injured patient, what factors to look at, and how he approaches problems. He discusses “Occam’s razor” and the “rule of three”. Occam’s razor is a manner of looking for the simplest explanation for what is causing a problem. And the rule of three is Dr. Blake’s idea that there are often more than one factor that needs to be looked at in determining what led to a specific problem.
The book is written with a conversational tone. It has been said that a book is a conversation between the author and the reader. But that is not often said about a book on biomechanics. Perhaps years back, Galileo attempted to model a dialogue while reviewing models, in his “Dialogue Concerning the Two Chief World Systems”. Dr. Blake’s book is easier to follow and there are no arguments about what model to follow.
The book reviews much straight forward thinking. It talks to you and then poses questions. The questions are an important part of the book. Most are not quite standard knowledge. But the answers to the questions and explanations are at the end of the text. They add to your learning how Dr. Blake thinks about the analysis and treatment of the patient.
This is the first book in what is conceived as a four part series. The second book is expected in the fall. The others will follow. If you are a student or a practitioner, this is a book you’ll want to read. It is not a self-help book.
A two part interview was recently conducted over Zoom. I participated in the second part of the interview:
Sweetness has always been associated with good things. And sugar has been an obsession for many. But sugar has a good many effects that are not good. And some are affected in worse ways than others. We need a certain amount of glucose in our systems to live. That amount has been described as about a teaspoon in all of our blood at any given time. The rest has to be consumed, excreted or stored. Most of us who love sweet things rarely consider what the impact of consuming large quantities could be.
There is a national epidemic of overweight & obesity, metabolic syndrome and diabetes that was become worse over the past 30 years. While there have been many articles written and documentaries made the situation has become worse and worse. Nutritionally dense processed food tastes good and recently we have begun to realize that salt, sugar, and carbohydrates are behaviorally addictive. My belt size and weight had gone up over the past several years and my workouts did not seem to be having any impact. After several months of my youngest daughter insisting I have a physical (and stop putting so much sugar in my coffee) and signing a contract with her I listened.
On July 17 I had a physical examination and was told to lose 30-35 pounds and essentially get to a weight that I had not been at since I was running 50 miles a week. I was told to give up pasta and bread and to skip potatoes. Thinking about all the delicious fresh, home-made bread my wife makes, along with lasagna, pesto, all sorts of pasta, and my love of pizza I said “No way. My wife is Italian. I don’t think that is going to happen.” I considered the near impossibility of losing just 5 pounds. Maybe with a tremendous effort it would be possible to drop 15.
Motivation: Blood Sugar Sky High
But one day later, I was told I had a random blood sugar of 180 and an A1c of 8.5 (which indicated an average blood sugar of around 220) . My doctor suggested a low carb diet, but was doubtful I’d follow through after my response the day before. He also suggested perhaps I visit an endocrinologist and take Metformin. I said “no thank you” to the idea of Metformin and said I thought we could handle this ourselves.
I had an immediate change of heart and felt this was a great time to be motivated for a dramatic change in diet. What did I think I needed most?
Need to not be diabetic.
Need not to be on unnecessary medication.
Need to work on problems caused by being overweight:
High A1c and Blood Sugar
High Blood Pressure
Need to face up to the impact of diet health.
Need to realize that one can not live by workouts and the gym alone.
Need more energy. Lately energy had been slacking from my unknown high blood sugar
Thinking about the domestic and global epidemic of overweight and obesity, I had to face the fact that I was joining this group and needed to change.
Changes: Trim the carbs. Keep the fat
I knew there were two possible ways to handle a dietary change. One was a vegan or vegetarian diet and the other was a low carb diet which is nutritionally ketogenic also called “Keto”. I was well aware that Tim Noakes had embraced this diet and received opprobrium in return. You can google his story which he describes quite well in both book and on YouTube. But as a long time follower of his I knew he had advocated a LC/HF (low carb – high fat) diet for years. He called it the “Banting Diet” after William Banting who wrote “Letter on Corpulence, Addressed to the Public” advocating this low carb diet for weight loss back in the 1800’s. Claude Bernard, a French physiologist, known for the concept of “homeostasis” had previously described a diet for diabetes which eliminated bread, butter, milk, sugar, beer and potatoes.
To me this approach made sense, although I know of people who have lost significant weight with a vegetarian approach. Eliminating most carbohydrates which would lead to higher glucose and a very variable blood glucose seemed logical. A quick literature search easily brought up dozens and dozens of academic articles. Further looking led to podcasts, online lectures, and books on the science, beginning Keto and Keto Cookbooks to read. And to my surprise, this diet had become popular and to some was known as a fad diet. I have not spent time following diet fads and trends so I had no idea.
I had at least two people tell me the “Keto” diet would kill me. Both were vegan and hopefully were not eating pesticide sprayed fruit.
The word seemed to be that this diet is a hard road to follow and difficult to sustain.
I was given the task of 1200 kcal per day and decreased carbs. The lowest recommended calories is higher than this, so don’t try this on your own.
One friend passed on a good number of presentations on the plant based diet, most of which were quite good. But I was well convinced that my path laid with the “Banting”, low carb approach. I also learned of the very hostile politics that is inherent to much of human interaction, and it was also present here in diverging nutritional opinions which should be based solely on science.
Tossing Out The Bread With the Chocolate Milk and Caramel Macchiatos
Lots had to go. The first thing that came to mind was a lifetime of daily chocolate milk and for as long as I can remember sugar, milk and a touch of cocoa in my coffee.And a good number of cups of coffee each day. In fact, my coffee consumption was enough to power enough calories for another meal each day. While much of my diet was considered healthy and included chicken, salmon, other healthy fish and vegetables, I did consume sugar chocolate milk, and would have an occasional “chip” binge. Warm, fresh, home made bread with butter was a periodic delight. But now, I can have the butter but not the bread. And over the past few years, ice cream became a joy.
So out went sugar, pasta, high fructose corn syrup, most fruits (except for certain berries), ice cream, fruit juices, chips, chocolate cake, breaded anything, most glutens, wheat flour, a good number of vegetable oils that were not olive oil.
In came whole eggs, unprocessed bacon, more salmon, fish, chicken, occasional london broil, turkey burgers, blackberries, raspberries, blueberries, 5% Greek Yogurt, a very small daily piece of dark chocolate (85%), 1/2 piece of gluten-free crisp bread with a tablespoon of humus, almond butter, almonds, macadamia nuts and pecans. Much of my vegetables are green leafy kale, spinach but also broccoli, cauliflower, avocados and zuchini.
This was done immediately, whole heartedly, and very seriously. Absolutely ZERO cheating. I obsessively read all food labels. I started going food shopping. I helped (at least a bit, like a back-seat driver, but tried to help) with food preparation. And I began weighing just about all of my portions.
And most important I have kept track of my meals in a smartphone app. There are several apps available. I am using myFitnessPal to track food groups and calories. And I used a website to determine a good set of “macros” for protein, fat, and carbohydrate which was easily incorporated into myFitnessPal.
I had great help from my wife in choosing low carb but tasty food. Some of the early options included chicken rolled in curry, pesto chicken, salmon, and tilapia with a variety of toppings. The vegetables I ate were all at her suggestion.
Short Term Results
Before my weight went had gone down 3 pounds, my blood sugar dropped to the normal range. At the start my random blood sugar was 180. A week later my fasting blood sugar was 95. And it has not been higher than this since then. My weight has steadily decreased. I was able to stop taking 2 of 3 blood pressure medicines. And I needed to use smaller belts to keep my pants up. My energy level improved. And there was not much in the way of hunger pangs. The diet has been filling without spiking sugar or adversely impacting insulin.
Longer Term Results
About three weeks in I went out for sushi with my doctor. He noticed the early but significant weight loss and was impressed with my daily blood sugars. I told him of my new found fear of carbs and how the rice in the sushi now scared me. It turned out that the restaurant would roll the sushi wrapped in cucumber without rice. But the surprise was my doctor was following the same diet and we then both happily ate sashimi.
In less than 3 months my weight went down about 28 pounds and my waist size decreased about 5 inches. My blood sugars both fasting and after eating have all been at normal levels, well below 100, usually in the 70’s and 80’s. And a home test kit for A1c showed my A1c to be down to 4.8. I will have an in office test before the end of October and I expect the then 90 day test to be no higher than that and likely a bit lower.
At a nephew’s wedding about 6 months ago, I spoke with one of my wife’s cousins. He was definitely enthusiastic about his diet which helped him lose over 100 pounds over a year or two. He didn’t just say that his low carb diet was good. He said it was great and discussed the physiology of it in more detail than most people would even think about. A few months later we met again just after I began the same nutritionally ketogenic HC/LF diet. This time I had a lot of questions to ask. He told me about the importance of electrolyte supplements, fluid replacement and foods that were helpful and those that were not. And he encouraged me to get a Ketone meter. I did, and use it every now and then. But the results are what has let me know things are working.
About 6 weeks or so into this process I contacted a friend, Mark Cucuzzella MD (https://www.drmarksdesk.com) who is a Family Physician in West Virginia, and on the faculty of the West Virginia University School of Medicine. Dr. Mark is one of the most community oriented people you could hope to meet. He owns a running shoe store, is involved in the racing community organizing and sponsoring races, and he even has a dozen bikes that are lent out to people in the community at no charge. Mark is an active lecturer nationally and around the world on diet, exercise, shoes and biomechanics and health. He has served for years as an Air Force Reserve Lieutenant Colonel. All this and he has maintained a running schedule that has had him completing 30 consecutive yearly marathons under 3 hours. His best time was 2:24. Dr. Mark’s involvement with his community, patients and students is inspirational.
I remembered from our first meeting a few years ago that Dr. Mark was an expert in nutrition in addition to being involved in the mechanics of running and training. So after finding a good number of interviews, a book and podcasts, I thought I’d drop him a note about what I had been doing. He was very supportive. We also discussed the possibility of using a CGM (continuous glucose monitor) to see what foods might be causing glucose spikes. Dr. Mark immediately sent me a presentation he had done online for physicians and a dozen or so articles on the importance of maintaining a level glucose and the impact of a low carb diet. We had the chance to spend a lot of time together at the annual American Academy of Podiatric Sports Medicine seminar in Cambridge, Massachusetts. His lectures were the best since many of them involved going outside and moving on those beautiful September days. I’ve learned much from Mark and continue to do so.
All through these past few months I’ve read journal articles, blogs, listened to dozens of podcasts and online lectures. I’ve read books on getting started on ‘Keto’, books on how the science works and how to handle athletes attempting a low carb diet (it varies), and books on low carb cooking. There are many resources available. I’d recommend researching the low carb diet thoroughly if you have reason to believe it would be helpful. Your public library is likely to have a good number of books on the shelves, surrounded by a lot of other diet books. But when I visited my library I wasn’t distracted. I knew what I was looking for.
The Impact of Nutritional Ketosis Over 11 Weeks
Total Weight Loss: 28 pounds
A1c from 8.5 down to 4.8
Fasting Blood Sugars: In 70’s and 80’s
Blood Pressure: Significantly lower on less medicine
Waist from about 39-40” to 34”
Energy level: significantly improved
So now, my blood sugar is normal. My clothes fit. My blood pressure is improved. And I don’t need to take any medicine to keep my sugar in the normal range. This worked faster and better than I would have believed.
In an upcoming post, I’ll list some of the authors, researchers and references I found helpful.
The stress of competition or even less stress can trigger eating disorders (energy intake imbalance), depression and other emotional disturbances. These need to be recognized, referred and treated as rapidly as possible.
Sports psychologists and teams that are prepared to handle all of the ramifications of these issues are critical.
Kevin Kirby, DPM has posted a biomechanical description of the orthotic modifications he uses when treating chronic peroneal tendinopathy. They mesh well with what we’ve presented here and Kevin provides an excellent diagram along with his description. Be sure to read his post.
Peroneal Tendon Complex: Injury and Rehabilitation
By Stephen M. Pribut, DPM
While ankle sprains are the most common musculoskeletal athletic injury,(1) the peroneal tendon complex (PTC) is often injured concurrently. Injury to the PTC has become widely recognized as an acute injury and a significant source of lingering pain and disability. These injuries are frequently correlated with inversion ankle sprains and chronic ankle instability (CAI).
The peroneal tendon complex (PTC) includes the peroneus longus and brevis tendons, the os peroneum, and their restraining components (Figure 1). We will discuss the anatomy, clinical significance and conservative treatment of injury to the PTC.
Peroneal Muscles and Tendons
The peroneus longus and brevis muscles are located within the lateral compartment of the leg. The vascular supply is primarily from the posterior peroneal artery. Innervation of the peroneals is from the superficial peroneal nerve. The well positioned constraints which serve to maintain proper anatomical position of the PTC include the superior peroneal retinaculum, the retromalleolar groove, the shared tendon sheath, the individual tendon sheaths, the peroneal tubercle, the inferior peroneal retinaculum, and the peroneal groove below the cuboid (Table 1).
The origin of the peroneus longus muscle is from the head and upper two-thirds of the lateral surface of the fibular body and from the intermuscular septa adjacent to the muscles of the anterior and posterior leg. The musculotendinous junction occurs proximal to the lateral malleolus. The peroneus longus along with the peroneus brevis enters the fibular fibro-osseous tunnel behind the fibular malleolus and shares a common synovial sheath. The peroneus longus tendon changes direction three times in the foot: at the lateral malleolus, the peroneal tubercle, and at the cuboid notch. A hypertrophied tubercle may be a cause of injury of the PLT.(2)
An ossified os peroneum is found in approximately 20% of individuals at the cuboid notch (Figure 2).(3). The tendon runs below the cuboid and crosses obliquely to insert into the base of the first and second metatarsal and the lateral facet of the medial cuneiform bone.
The peroneus brevis muscle originates at the distal two thirds of the lateral
aspect of the body of the fibular and the adjacent intermuscular septa. It passesbehind the fibula where it lies adjacent to the fibula and deep to the peroneus longus while passing through the fibro-osseous tunnel. The insertion is at the tuberosity of the base of the fifth metatarsal bone. An os vesalianum is found near the insertion in less than 1% of people.(4)
The peroneus tertius muscle is found in approximately 90% of people and begins at the distal third of the anterior fibula. The muscle is usually confluent with the extensor digitorum muscle and ends before the inferior extensor retinaculum. The peroneus quartus is an anomalous muscle found in 6.6% to 22% of individuals. It begins at the peroneus brevis and inserts into the peroneal tubercle after travelling through the shared peroneal tendon sheath. (5)
Biomechanics and Injury
Peroneal tendon injures are a direct result of their anatomy and biomechanics. (5) The peroneal muscles are multi-joint muscles. Early in stance, the PTC is subject to passive stretch as the gastrosoleus acts proximally as a tibial decelerator. Late in stance phase, the PTC acts as a weak plantar flexor at the ankle joint.
At the subtalar joint (STJ), the peroneals act as pronators and are antagonists to the tibialis anterior and tibialis posterior muscles. Additionally, the peroneus longus muscle (PLM) plantarflexes the first ray and is a pronator at the midtarsal joint. The peroneals are most active in mid- and terminal stance, functioning to stabilize the foot. (6,7) Recent studies have demonstrated weakness of functional evertor strength in CAI. (8)
The PTC is subject to strain forces when the foot is inverted or supinated about the STJ. A sudden inversion force or chronic overuse may injure the PTC or the lateral ankle. The most frequent injuries to the PTC are traumatic tendinopathy, a tear, or a subluxation of the peroneal tendons. (9) Tendon subluxation is believed to occur with the foot in a dorsiflexed position and the peroneal tendons contracting strongly. (10)
Risk factors associated with peroneal tendon injuries may be seen in Table 2. (11, 12) Multi-directional sports, such as soccer, tennis, and basketball, are associated with these injuries. While peroneus brevis injuries are frequently suspected at the level of the lateral malleolus, injury to the distal peroneus longus is often undetected. Additional associated injuries include injury to the cuboid, the os peroneum, or fifth metatarsal. (3, 13) Differential diagnoses are listed in Table 3.
Peroneal tendon complex injury is considered a risk factor and contributor to CAI. (14, 9) A recent study showed that a brief bout of pain posterior to the lateral malleolus preceding an inversion ankle injury was associated with MRI evidence of peroneal tendinosis in 95% of cases. (13) Up to 75% of those suffering inversion ankle injuries may have a recurrence of injury or are subject to ongoing symptoms related to chronic ankle instability (CAI). (15, 16) Examination at the time of surgery for recalcitrant CAI often demonstrates injury. A retrospective review of 136 patients who underwent a Broström-Gould ankle reconstruction found that 53.3% required operative intervention for peroneal tendon pathology. (14)
Examination of sixty-four consecutive acute ankle inversion injuries by MRI revealed that 30% of the subjects suffered an associated tendon injury. (17) These injuries, when unrecognized, may contribute to ongoing symptoms. Estimates range from 30% to 70% of inversion ankle injuries may recur or have lasting symptoms. These ongoing symptoms diminish sensorimotor functioning and lead to decreased physical activity and concomitantly a diminished quality of life (18). It has been reported that 32% of ankle inversion injuries are still symptomatic seven years after the injury. (19)
Painful Os Peroneum Syndrome (POPS)
The os peroneum (OP) is a sesamoid bone found within the peroneus longus tendon (PLT) of most people. It is usually located just proximal to the cuboid tunnel. The OP is frequently fibrocartilaginous, often bipartite, and is only visible on x-ray 6–20% of the time (Figure 3).
The OP is subject to both fracture and contusion. Bone callus formation during healing can lead to tendinopathy of the peroneus longus tendon and it may also play a role in tears of the tendon. When the OP is injured, the MRI may show fluid around the PLT and bone marrow edema of the cuboid. (20)
A history and physical examination will reveal the cause of many injuries. While the inversion movement which causes the injury occurs rapidly, the full effects may not be obvious for several hours. The lag between injury and effect will lead many patients to forget the inversion event. The history may reveal previous ankle sprain, fracture, or other lateral foot injury. Peroneal subluxation may be associated with a sensation of painful clicking.
A methodical physical examination follows the principles of look, touch, and move. Examine for swelling, color, general alignment, structure, and symmetry. Thoroughly palpate the lateral foot and ankle and explore the peroneal tendons through their entire course. Peroneus brevis tears often occur behind the fibula, while peroneus longus injury may occur at the cuboid groove or more distally. Note the strength of the peroneal tendons and pain during resisted ankle eversion. Also note pain in response to dorsiflexion of the first ray or an inability to resist the dorsiflexion. (5) Be sure to check the ankle for ligamentous disruption.
Peroneal subluxation may be tested by flexing the knee and asking the patient to actively dorsiflex the ankle with resisted eversion. The test is positive if the peroneal tendons are seen to subluxate anterior to the fibular malleolus. Intra-sheath subluxation is suspected if their position translates relative to each other. (5) The peroneal compression test suggests peroneus brevis tendinopathy. To perform this test, evert and dorsiflex the foot while compressing the fibular groove.(20)
The Ottawa protocol outlined in Table 4 should only be used for acute ankle injuries and not for late injury evaluation. On x-ray, carefully evaluate all the lateral boney structures. Figure 4 shows a hairline Jones fracture that went undetected the previous night at an urgent care center (Figure 4). A visible fleck of bone at the fibula indicates possible subluxation of the peroneal tendons from the fibular groove. A Harris view assists in assessing the peroneal tubercle and the retromalleolar groove. (21, 22) Be on guard for a fracture of the os peroneum or distraction of multipartite fragments (Figure 5). Fractures of the os peroneum may best be assessed using a CT scan which better reveals the border of the ossicle.
Ultrasound can be useful to detect peritendinous fluid, or partial or complete rupture, but it requires an experienced examiner.
Magnetic resonance imaging (MRI) shows the anatomy in best detail. Fluid surrounding the tendons are best seen on T2-weighted or short tau inversion recovery (STIR) images. These images are useful to assess subtle injury to the cuboid and base of the fifth metatarsal. The MRI finds more pathology than is clinically relevant in some cases while it may miss other pathology. (23) MRI has a positive predictive value of less than 50%. (24, 25)
Outline of Treatment
High level evidence-based medicine is the goal we seek to attain. However, there are times when the evidence is weak, contrary, wrong, or lacking. There is only scant material written on rehabilitation for PTC injury. Researching the rehabilitation of ankle injuries is a reasonable place to begin crafting a program for the PTC. (26) Most recent overviews have come to realize the flaw of not using adequate protection during the earliest stage of therapy. (16, 27)
The most consistently recommended therapy for rehabilitation of an acute ankle sprain, CAI, and for prevention to reduce the risk of future re-injury is balance training. (27, 28, 29, 30)
Proposed Functional Rehabilitation of PTC Injury
Phase I: Protection, rest, ice, compression, and elevation.
Initial therapy requires protection of the injured area. A removable pneumatic cast boot serves as both protection and compression and may be removed for exercise and evaluation. (21) An ankle brace alone is not effective since the stabilization achieved is inadequate. The tendons must be protected from forces that place them under stretch, including dorsiflexion moments applied to the foot. It is helpful to protect the mid-foot, mid-tarsal joint, and first ray from forces which translate into strain forces on the peroneal tendons. The removable cast boot is used for one to four weeks depending upon the severity of the injury.
Ice may be applied for 20 minutes on/40 minutes off for three to six times per day for the first 48 hours. Ibuprofen or another NSAID may be helpful.
Phase II: Motion
Do not rush the patient into vigorous muscle and strength exercises. This has been part of chronically failing regimens previously used for the ankle. Gentle range of motion exercises may be performed.
Phase III: Neuromotor
Proprioception, balance, and muscle strength are keys to successful recovery. The most efficacious tool to accomplish these goals is the 20” wobble board. This appears to reach optimal angular relationships at maximum excursion to train the neuro-facilitative responses needed in gait.
Other proprioception and balance exercises may also be used. The most popular are Romberg one leg balance exercises and the simplified STAR excursion exercises. (31, 32)
Muscular strength exercises may be augmented using exercise band therapy. Recent evidence has shown more proximal muscle training may also assist in recovery.
Limitation of dorsiflexion and equinus may be addressed by posterior muscle group stretching and active exercises such as the heel roll-up. Toe crunches strengthening the intrinsic muscles are also helpful to stabilize the mid-tarsal joint and decrease PTC forces needed for this stabilization.
Gentle foam rolling of the calf muscles may help mobilize the ankle.
Phase IV: Return to Activity
The balance and proprioceptive exercises from Phase III should all be continued for at least three months. Specific training for a return to activity may begin.
Preparation for return to full activity includes beginning with walking, progressing to running, cutting, and sideways movements needed for sport. It generally requires four to six weeks to return to most sports but occasionally twelve weeks may be needed.
Evidence has pointed to orthotics as being helpful in treating CAI. Orthotics are also helpful in treating PTC injuries. Orthotic modifications to reduce the strain on the peroneal tendons and lateral foot structures are important components of treatment. Research also indicates that orthotics produce proprioceptive and balance improvements. (33)
Feet that suffer these injuries often have a lateral shift of the STJ location, which increases the supinatory moment of ground reaction forces. The orthotic modifications I use are designed to alter these moments and allow the peroneals to function optimally. These modifications include a 0/0 rearfoot post with “no lateral bevel” (Figure 6). This makes the orthotic less prone to cause excessive supination. You may use a low level of cast inversion and medial skive depending upon the foot type. In addition, you may use about 3 degrees of lateral forefoot valgus wedging to the sulcus, especially for patients who do not contact with the rear foot. Additional modifications seen in Table 6 are based on Richard Blake’s suggestions for excessive supination. (34)
We have briefly reviewed the anatomy, injuries, and rehabilitation for injuries to the PTC (Table 7). There is much to research and write about this topic. Don’t stop learning. Your patients benefit from your knowledge.
Outline of Therapeutic Treatment for Peroneal Tendon Injuries
Figure 1. Know your anatomy. Tablet-based apps help demonstrate the anatomy to your patients. (Image courtesy 3d4Medical Ltd. “Essential Anatomy 5”)
Figure 2. Normal os peroneum.
Figure 4. Hairline Jones fracture. Tender to touch and visible on x-ray.
Figure 5. Fragmented os peroneum. Healing bone callus visible.
1. Waterman, B.R., et al., The epidemiology of ankle sprains in the United States. J Bone Joint Surg Am, 2010. 92(13): p. 2279–84.
2. Palmanovich, E., et al., Peroneus longus tear and its relation to the peroneal tubercle: A review of the literature. MLTJ Muscles, Ligaments and Tendons Journal, 2011. 1(4): p. 153–160.
3. Brandes, C.B. and R.W. Smith, Characterization of patients with primary peroneus longus tendinopathy: a review of twenty-two cases. Foot Ankle Int, 2000. 21(6): p. 462–8.
4. Vasiljevi?, V., L. Markovi?, and J. Vasi?-Vili?, Accessory bones of the feet: Radiological analysis of frequency. Vojnosanitetski …, 2010.
5. Roster, B., P. Michelier, and E. Giza, Peroneal Tendon Disorders. Clin Sports Med, 2015. 34(4): p. 625–41.
6. Perry, J., Gait Analysis: Normal and Pathological Function. 1992, SLACK, Inc.: Thorofare, NJ. p. 165–167.
7. Santilli, V., et al., Peroneus longus muscle activation pattern during gait cycle in athletes affected by functional ankle instability: a surface electromyographic study. Am J Sports Med, 2005. 33(8): p. 1183–7.
8. Terrier, R., et al., Assessment of evertor weakness in patients with chronic ankle instability: Functional versus isokinetic testing. Clin Biomech (Bristol, Avon), 2017. 41: p. 54–59.
9. DiGiovanni, B.F., et al., Associated injuries found in chronic lateral ankle instability. Foot Ankle Int, 2000. 21(10): p. 809–15.
10. Cerrato, R.A. and M.S. Myerson, Peroneal tendon tears, surgical management and its complications. Foot Ankle Clin, 2009. 14(2): p. 299–312.
11. Hyer, C.F., et al., The peroneal tubercle: description, classification, and relevance to peroneus longus tendon pathology. Foot & ankle international, 2005. 26(11): p. 947–950.
12. Mook, W.R., S.G. Parekh, and J.A. Nunley, Allograft Reconstruction of Peroneal Tendons. Foot & Ankle International, 2013. 34(9): p. 1212–1220.
13. Ziai, P., et al., Peroneal tendinosis as a predisposing factor for the acute lateral ankle sprain in runners. Knee Surg Sports Traumatol Arthrosc, 2016. 24(4): p. 1175–9.
14. Burrus, M.T., et al., Predictors of peroneal pathology in Brostrom-Gould ankle ligament reconstruction for lateral ankle instability. Foot Ankle Int, 2015. 36(3): p. 268–76.
15. Gerber, J.P., et al., Persistent disability associated with ankle sprains: a prospective examination of an athletic population. Foot Ankle Int, 1998. 19(10): p. 653–60.
16. Richie, D.H. and F.E. Izadi, Return to play after an ankle sprain: guidelines for the podiatric physician. Clin Podiatr Med Surg, 2015. 32(2): p. 195–215.
17. Khor, Y.P. and K.J. Tan, The Anatomic Pattern of Injuries in Acute Inversion Ankle Sprains A Magnetic Resonance Imaging Study. Orthopaedic journal of sports medicine, 2013.
18. Gribble, P.A., et al., 2016 consensus statement of the International Ankle Consortium: prevalence, impact and long-term consequences of lateral ankle sprains. Br J Sports Med, 2016. 50(24): p. 1493–1495.
19. Konradsen, L., et al., Seven years follow-up after ankle inversion trauma. Scand J Med Sci Sports, 2002. 12(3): p. 129–35.
20. Sobel, M., H. Pavlov, and M.J. Geppert, Painful os peroneum syndrome: a spectrum of conditions responsible for plantar lateral foot pain. Foot & ankle …, 1994.
21. Heckman, D.S., G.S. Gluck, and S.G. Parekh, Tendon disorders of the foot and ankle, part 1: peroneal tendon disorders. Am J Sports Med, 2009. 37(3): p. 614–25.
22. Bruce, D.W., et al., Stenosing Tenosynovitis and Impingement of the Peroneal Tendons Associated with Hypertrophy of the Peroneal Tubercle. Foot & Ankle International, 1999.
23. Major, N.M., C.A. Helms, and R.C. Fritz, The MR imaging appearance of longitudinal split tears of the peroneus brevis tendon. Foot & ankle …, 2000.
24. Giza, E., et al., A clinical and radiological study of peroneal tendon pathology. Foot & ankle …, 2013.
25. Park, H.J., et al., Reliability of MRI findings of peroneal tendinopathy in patients with lateral chronic ankle instability. Clin Orthop Surg, 2010. 2(4): p. 237–43.
26. Kosik, K.B., et al., Therapeutic interventions for improving self-reported function in patients with chronic ankle instability: a systematic review. Br J Sports Med, 2017. 51(2): p. 105–112.
27. Kaminski, T.W., et al., National Athletic Trainers’ Association position statement: conservative management and prevention of ankle sprains in athletes. J Athl Train, 2013. 48(4): p. 528–45.
28. De Ridder, R., et al., Effect of a Home-based Balance Training Protocol on Dynamic Postural Control in Subjects with Chronic Ankle Instability. Int J Sports Med, 2015. 36(7): p. 596–602.
29. Hupperets, M.D., E.A. Verhagen, and W. van Mechelen, The 2BFit study: is an unsupervised proprioceptive balance board training programme, given in addition to usual care, effective in preventing ankle sprain recurrences? Design of a randomized controlled trial. BMC Musculoskelet Disord, 2008. 9: p. 71.
30. Hupperets, M.D., E.A. Verhagen, and W. van Mechelen, Effect of unsupervised home based proprioceptive training on recurrences of ankle sprain: randomised controlled trial. BMJ, 2009. 339(jul09 1): p. b2684.
31. Herb, C.C. and J. Hertel, Current concepts on the pathophysiology and management of recurrent ankle sprains and chronic ankle instability. Current Physical Medicine and Rehabilitation Reports, 2014. 2(1): p. 25–34.
32. Gribble, P.A., J. Hertel, and P. Plisky, Using the Star Excursion Balance Test to assess dynamic postural-control deficits and outcomes in lower extremity injury: a literature and systematic review. J Athl Train, 2012. 47(3): p. 339–57.
33. Sesma, A.R., et al., Effect of foot orthotics on single- and double-limb dynamic balance tasks in patients with chronic ankle instability. Foot Ankle Spec, 2008. 1(6): p. 330–7.
34. Blake, R. Orthotic Design for Excessive Supination. 2013 (cited 2017 05/05/2017); Available from: https://www.youtube.com/watch?v=hMhrTmWXfDA.
Bio: Dr. Pribut is a Clinical Assistant Professor of Surgery at George Washington University Medical School. He serves on the Runner’s World Board of Advisors. He is a past president of the American Academy of Podiatric Sports Medicine. Dr. Pribut is in private practice in Washington, DC.
A new study – online at the J Applied Physiology (August 31, 2017) – was performed to measure beneficial impact on collagen production in chronic tendinopathy. The study evaluated mRNA (and ribosomal RNA) and more along with determining the impact on gene activity.
The study showed that one week of 1800 mg per day of Ibuprofen seemed to not have a measurable impact. The authors propose that the impact in vivo and in vitro may be dramatically different for one of several reasons. The tendon cells may not be sensitive to ibuprofen or they may not be exposed to a high level of ibuprofen in the body
The study did demonstrate that there was a decrease in pain compared to placebo and suggested that the pain reduction pathway may work in ways not yet well described.
The best news was that although it may not have a dramatic impact on chronic Achilles tendinopathy (which we suspected and perhaps knew all along), it did not destroy tendon cells.
Special Topic: Orthotic Modifications for Over Supinated Feet
In most cases I am not designing a foot to correct a “foot type” but to provide a solution for a specific clinical problem. While having a high arched, over supinated, under pronated foot may predispose to certain problems other “foot types” can have many of the same problems.
Some problems that can occur and are related to supination movements (or even “moments”) include:
chronic and repeated ankle sprains
peroneus brevis tendinopathy
peroneus longus tendinopathy
cuboid stress fractures
4th and 5th metatarsal stress fractures
5th metatarsal base or midshaft fractures
lateral leg pain (peroneal muscle group)
In many instances with problems like these, immobilization may be necessary for a time. Wobble board training should be incorporated into rehabilitative programs. The purpose of the wobble board training is to have the neuromuscular system adapt the peroneal muscles to performing repetitive firing for stabilization. The angles that the wobble board makes with the ground and the motion and angular relationships that it engenders in your ankle and leg are ideal to training the peroneals to fire appropriately.
The wobble board assists in training muscle strength, balance, and improving joint position sense. There is nothing that beats this 3 in 1 training.
For patients who do not have a dramatic Pes Cavus foot there are a few specific corrections I include in the orthotic:
Accurate cast of the foot.
I do not want a 2D pressure scan. I want to hold the foot in neutral subtalar joint position. And I want to plantar flex the first ray by either light dorsal pressure over the first metatarsal or by slight dorsiflexion of the great toe during the casting.
Minimal cast correction.
I want the cast to reflect the shape of the foot to mirror it so that when I want to alter forces, they will be altered by the shape and adjustments to the orthotic. I want the forces distributed through a large surface area and need conformity between the shape of the foot and the shape of the orthotic.
No lateral bevel.
This resists over supination directly. It is like an outrigger on a boat. It also changes moments of force going into the foot.
3 degree lateral forefoot wedge.
This is often used to prevent over supination of the foot after the heel as left the ground or as weight is transferred towards the forefoot.
These are often my starting steps to deal with the problems listed above when they are resistent to treatment.
For a Pes Cavus, high arched, over supinated foot podiatrist Richard Blake, DPM has put a great video on line. It details his 8 steps to deal with this foot type using specially customized orthotics. The modifications made for this problem are not found in over the counter orthotics. And many specialists do not see enough patients with high arches to be adept at treating the problems associated with this foot type. It is important to find a physician that has experience with sports medicine, high arch feet, and biomechanics.
The Blake 8 Steps (only slightly modified) follow:
First an accurate cast is required as described above.
A) Rounding of the lateral border of the cast or via CAD/CAM to have the orthotic better grip the foot.
B) Lateral Kirby Skive. Often 2 to 4 mm.
C) Deep Heel Cup – up to 25 mm.
D) Extended lateral heel cup or “lateral flange”
E) Eliminate “medial heel grind off” and/or add No Lateral Bevel in rearfoot posting instructions.
F) Lateral arch fill to add more surface contact area
G) Narrower orthotic (sometimes) to limit any antipronatory forces. (note: some will go for wide or nomal width for increased stability and contact)
H) Forefoot modifications such as lateral wedge
Those two recommended set of injections at $6,000 per series for your Achilles tendinitis hasn’t sounded very good for the past few years. Ever since a controlled, prospective comparison study demonstrated there was absolutely no difference in the efficacy of PRP over saline injected in the same manner, there has been doubt about the use of PRP in the office. But instead of falling by the wayside, like a bad political candidate, it has spread by meme and scheme far and wide and even infiltrated some of the best offices in the country and world.
The British Medical Journal has recently posted an article strongly recommending against the in office use of PRP (platelet rich plasma) outside of established studies.
The article was titled: “How effective are platelet rich plasma injections in treating musculoskeletal soft tissue injuries?” The answer, at this time, seems to lie somewhere between “we have no clue” and “not very”. This study mentions a previous review by the Cochrane review (2014) which examined 19 studies and found insufficient evidence of the usefulness of PRP. This study reviews 10 additional studies and reaches the same conclusion.
The article is readily available and worth a read: