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.
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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:
Microbiome analysis is coming soon to a doctor near you. Microgenomics is going to be part of nearly everyone’s future. This week Nature magazine published an article which indicates that at least part of the action of the anti-diabetic medication Metformin may be occurring via the microbiome. At the least there is a dramatic difference between the gut microbiota between those with type 2 diabetes (T2D) treated with Metformin (T2D-Metformin+)and those not treated (T2D-Metformin-).
The article has an excellent discussion both of the direct effects of Metformin and the indirect effects and potential interactions of various gut bacteria
There is significant evidence that exercise is helpful in lowering one’s risk of dementia by regular moderate to vigorous exercise. And every month a plethora of articles appears reporting on positive impact or no impact at all on a variety of factors from diet and supplements to exercise.
A number of studies have indicated that starting and maintaining an exercise program has been helpful. But, we also need to define what may not be helpful. Exercise below a certain aerobic level, may just not count as preventative exercise for dementia and cognitive decline.
And I realize my bias in favor of exercise, so I must admit that some reviews have found the evidence is weak that exercise is helpful in avoiding cognitive decline.
Reported studies need to be subject to evaluation. One can not blindly accept the authors’ interpretation of the results. The results and protocol need to be rationally evaluated in an absence of hype.
I’m not sure that a recent study by Sink et. al. which did not find a positive correlation between activity and cognition was scrutinized thoroughly in the media. Looking closely at this study we find that they used a good number of patients and controls. But we see that the inclusion criteria of being able to cover 400 meters in 15 minutes is not what many would consider to be an aerobic exercise activity. The study was restricted to those over 70. And the data was not gathered using a Fitbit, Pedometer, GPS motion detector or observation. The data was self-reported.
So what do we know as a result of this study:
Being able to move at a speed of 1 mile/hour for 30 minutes (400 meters in 15 minutes) several times a week is not enough exercise to measurably diminish cognitive decline (it may have other benefits though).
Data acquisition by self-reporting may not be optimal. An objective measurement should be used in conjunction with a device to do and record these measurements.
The life style changes here may have been too little and too late to have an impact.
Commencing exercise prior to age 70 may be better than beginning later. If beginning later, results may only be seen if the individual is capable of exercising a moderate level.
Media coverage is often limited in interpretation and assessment of the meaning of a study’s results.
In a predefined subgroup of those aged 80 and over and with worse starting fitness they did find an improvement in “executive function”.
“Despite the lack of overall benefit, our prespecified subgroup analyses of participants aged 80 years or older and those with lower baseline physical performance demonstrated that the physical activity group had better performance on executive function tasks than those in the health education group at 24 months. This finding is important because executive function is the most sensitive cognitive domain to exercise interventions,40 and preserving it is required for independence in instrumental activities of daily living. Future physical activity interventions, particularly in vulnerable older adult groups (eg, ≥80 years of age and those with especially diminished physical functioning levels), may be warranted.”
The authors did consider as the first possible explanation that the exercise level was insufficient to produce changes in the cognitive measures, but this escaped the media blitz. In reading the article, conclusions and discussion, the study was well designed, properly randomized and controlled, used an adequate sample size. The possibilities leading to the observed results were thoroughly discussed. But again, the subtleties were not discussed in the media and the headlines you saw were that exercise was not useful in preventing cognitive decline. As with most studies the media would lead you to believe that the current study overturns all previous thinking and is the only thing to follow.
Bayesian reasoning allows for new information to be added into the mix of the prior thought and research on any topic. That should be done and the meaning of that should be clear to anyone writing about science literature. One study doesn’t usually replace all thinking, it is added to it in that successive approximation of the truth that we reach for through science.
So the same recommendation to exercise, in my mind, holds. It still has the most evidence pointing in its favor. And for those older individuals who are not able to exercise as vigorously, exercise is still likely to have positive impact on mood and other neurological and physical functions not measured in this study.And I’d suggest more education on EBM and study evaluation for those charged with distributing results of medical studies. And please read the study.
Erickson, KI, Barr, LL, Weinstein, AM, Banducci, SE, Akl, SL, Santo, NM, Leckie, RL, Oakley, M, Saxton, J, Aizenstein, HJ, Becker, JT, Lopez, OL. (in press). Measuring physical activity with accelerometry in a community sample with dementia. Journal of the American Geriatic Society.
Weinstein, AM, Voss, MW, Prakash, RS, Chaddock L, Szabo, A, White, SM, Wojcicki, TR, Mailey, E, McAuley, E, Kramer, AF, Erickson, KI. (2012). The association between aerobic fitness and executive function is mediated by prefrontal cortex volume. Brain, Behavior, and Immunity, 26:811-9.
Erickson KI, Miller DL, Roecklein KA. (2012). The aging hippocampus: interactions between exercise, depression, and BDNF. Neuroscientist, 18: 82-97.
“Cognitive decline is one of the most pressing healthcare issues of the 21st century. Worldwide, one new case of major cognitive decline (ie, dementia) is detected every 4 s. Given that no effective pharmacological treatment to alter the progress of cognitive decline exists, there is much interest in lifestyle approaches for preventing or treating dementia. Ideally, such strategies should be cost-efficient and widely accessible at a societal level to have the largest benefit for older adults with varying income and functional status levels.
One attractive solution that aligns with the above criteria is exercise. However, despite a large and consistent pool of evidence generated over the past five decades linking exercise to improved cognitive functions in older adults,2 there is a reluctance among academics, healthcare practitioners and the public alike to embrace exercise as a prevention and treatment strategy for cognitive decline. For example, the National Institutes of Health (NIH) consensus statement from 20103 concedes that there appears to be preliminary data to support the efficacy of exercise in improving cognitive function. However, they caution that there is currently no strong evidence to suggest that modifiable lifestyle factors can alter the trajectory of cognitive decline. Adding fuel to the fire are publications such as a 2013 systematic review of randomised controlled trials (RCTs) (prior to 31 October 2011) reporting ‘weak’ evidence for the effects of exercise on cognition.4 We must highlight that the search strategy used in that systematic review failed to capture many pertinent papers providing evidence from RCTs that exercise promotes cognitive and brain plasticity not only in healthy older adults but also in those with cognitive impairment. Furthermore, there are a number of animal studies that provide insight into the molecular and cellular mechanisms by which exercise promotes neuroplasticity.”