Recently an article was published in JAMA by Mez, Daneshvar, and Kiernan et al that investigated the frequency of Chronic Traumatic Encephalopathy (CTE) in football players. It has become a topic of controversy because CTE has become a red flag for the public eye. It is now known to be correlated with repetitive trauma from popular impact sports such as hockey, football, and even soccer. While many hope to avoid or prevent the progression of this disease, there is currently no definitive causation and therefore no cure-all. CTE is a post mortem diagnosis that requires evidence of an accumulation of certain proteins along with other neurological criteria.
Mez, Daneshvar, and Kiernan et al used current classification systems to evaluate and assess 207 donated brains of football players. An overwhelming majority of them (87%) met the criteria for neuropathological diagnosis of CTE and the article detailed severity of symptoms (pre-mortem) associated with severity of CTE as well as mean age of death. While the article suggested a relationship between higher level of football participation (NFL) and worse disease presentation, the authors were definitely not stating a cause and effect relationship. The conveniance sample was for investigating possible relationships between activity levels and disease burden. This was an observational study with no constant or variables to compare.
Studies have shown that while living, a person with CTE may present with similar behaviors and cognitive impairments to that of a person with mood disorders, dementia, or Alzheimer’s disease. Mez, Daneshvar, and Kiernan et al outlined common characteristics and behaviors of the people that were diagnosed with CTE and therefore provided a foundation for future studies to help eventually determine causation, a sensitive and specific means of evaluation, and prevention. Until then, athletes of all levels must try their best to avoid repetitive and unecessary microtaumas. Playing smart and competitively, not aggresively, can help minimize repeated impact and trauma in every game.
Elizabeth Lamontagne PT, DPT, SCS, CKTP
We’ve all heard much about the dangers of football and the alarming incidence of concussions in the sport. Also about the NFL’s initial resistance to acknowledging the probable relationship of concussions to Chronic Traumatic Encephalopathy (CTE), which currently can only be diagnosed on autopsy.
CTE – as defined by the Boston University CTE Center16 – is “a progressive degenerative disease of the brain found in athletes (and others) with a history of repetitive brain trauma, including symptomatic concussions as well as asymptomatic subconcussive hits to the head… This trauma triggers progressive degeneration of the brain tissue, including the build-up of an abnormal protein called tau. These changes in the brain can begin months, years, or even decades after the last brain trauma or end of active athletic involvement. The brain degeneration is associated with memory loss, confusion, impaired judgment, impulse control problems, aggression, depression, and, eventually, progressive dementia.”
The concern many have is not only for the health and safety of the athletes. Others who have suffered mild traumatic brain injury want to know if they are susceptible to CTE as well. No one really has that answer yet. However, lets look carefully at the information that is out there and how it can be interpreted.
First, scary as it may be, recognize that the high incidence of CTE reported in studies reflects several biases. The most significant of these is self-selection. The brains that have been examined on autopsy are primarily those of athletes who have donated their brains for research due to symptoms they’ve experienced, or those whose family has suspected the diagnosis. This clearly inflates the percentages of athletes diagnosed with the condition.
One such study done by Boston University and the US Department of Veteran’s Affairs17 established that 87 of 91 football players had signs of CTE on autopsy, while Boston University also found the condition in 79% (131 of 165) of football players across all levels.17
These frightening results are mildly contrasted by another study18 that looked at 60+ former NFL players – all aged 60-69 – to try to identify symptoms of CTE in living people. Their age range indicates that these were players who played before heightened concussion awareness and before protocols were initiated by the NFL. The results showed that 60% had completely normal age-appropriate cognitive decline. Of the remaining 40%, 6% met the criteria for dementia. It would be interesting – and possibly revealing – to be able to correlate the findings on these men with how their brains subsequently present on autopsy.
Though this group also played before helmets were improved, the sturdier helmets may even have encouraged harder hitting. The NFL’s response has included recent rule changes to modulate direct hits to the head, though the game will likely see an even greater proportion of debilitating but less threatening lower body injuries as a result. The players of today are also typically stronger, bigger and faster than those in the era of those tested in this study. This too likely influences the frequency and outcomes of traumas that they experience.
Though the brain has the ability to recover from one injury, long-term effects are more likely after multiple incidents.
However, keep in mind that football players sustain blows to the head (direct and/or indirect) on almost every play. This cumulative subconcussive microtrauma may be as much or more of a factor in causing CTE than one or few isolated incidents of concussive trauma. Not at all good for football or soccer players, but an encouraging note for others who fear the long term effects of having sustained a concussion, or even several of them.
Vulnerability differs amongst athletes on the field. Dr. Steven Erickson noted that offensive linemen face forces “that are generally linear and the players know they are coming. Consequently, the head doesn’t move very much, so the brain doesn’t move very much. This may still represent brain trauma, but less often to the degree of causing concussion.”
He contrasted this with receivers. Though the “magnitude of the forces they sustain may be lower, the rotational component to the trauma, the player not being able to anticipate the nature of the hit and the degree of subsequent brain motion all make it more likely they will sustain a clinical concussion.”
A study by the Mayo Clinic, published in December 2015, found that one in three amateur athletes who participated in contact sports while in school developed CTE. 19 That statistic will likely cause even more scrutiny of the games and cause some to weigh the risk-reward of participation differently than before. Again though, this study also reflected issues of self-selection.
I asked Dr. Erickson about the cheating (underperforming) on baseline screening that we have read about occurring in the NFL, and whether this effort by some players to lessen the likelihood that a subsequent concussion will be diagnosed can be detected.
His response was that “though it may be possible, there are internal checks with ImPACT™ whereby validity scores can generally identify when an individual is cheating.”
Dr. Erickson commented that “this is another advantage of the vestibular test (see Part 2 of this series) advocated at the Banner Concussion Center, because a non-physiologic response is detected with intentional underperformance or anxiety responses to testing, We benefit from the fact that athletes don’t know how to cheat to underperform on the test.”
He added that “of course, best medicine is for an athlete to put in best effort at baseline as well as post injury. The motivation factor is very real. Sometimes those not particularly motivated in baseline testing are very motivated to achieve in order to return to play,”
Hopefully more athletes and their coaches are acknowledging that playing through will not serve them well either in the short or long term.
So, does the Banner Concussion team advocate keeping kids from playing sports? Most definitely not… Each member acknowledges the many benefits of sport, such as exercise, physical development and emotional growth. Developing mental toughness and learning life lessons such as teamwork and how to deal with adversity while enjoying a healthy social outlet that is fun, challenging and productive trumps fear.
They stress that concussion can happen almost any time – even to those who don’t play sports – and that sports can be made safe. The key to addressing concussion is education and diligence. It is important to be able to identify concussion if/when it happens and seek appropriate assessment and care. By managing the symptoms, recovery is accelerated and the likelihood of recurrence minimized. The value of baseline testing cannot be stressed enough nor can the importance of not allowing an athlete of any age to return to play after sustaining a head trauma resulting in symptoms without undergoing an evaluation.
Though most who suffer a concussion recover fully and within a four-week period, the caution is to understand that symptoms left untreated – can result in long lasting consequences.
As for those who sustain multiple head traumas and, quite possibly – or especially – those who have also suffered repeated microtrauma, the long term effects are coming into better focus with the further study of CTE.
References for Parts 1-3 of the Concussion Series:
- Centers for Disease Control and Prevention (CDC), National Center for Injury Prevention and Control. Report to Congress on mild traumatic brain injury in the United States: steps to prevent a serious public health problem. Atlanta (GA): Centers for Disease Control and Prevention; 2003.
- Lescohier I, DiScala C. Blunt trauma in children: causes and outcomes of head versus intracranial injury. Pediatrics 1993;91(4):721-5.
- Langlois JA, Rutland-Brown W, Wald M. The epidemiology and impact of traumatic brain injury: a brief overview. Journal of Head Trauma Rehabilitation 2006;21(5):375-8
- Finkelstein E, Corso P, Miller T and associates. The Incidence and Economic Burden of Injuries in the United States. New York (NY): Oxford University Press; 2006.
- Fung M, Willer B, Moreland D, Leddy J. A proposal for an evidence-based emergency department discharge form for mild traumatic brain injury. Brain Injury 2006;20(9):889-94.
- Alexander, Andrew L., Lee, Jee Eun, Lazar, Mariana, Field, Aaron, S.
Diffusion Tensor Imaging of the Brain. Neurotherapeutics. 2007 Jul; 4(3): 316–329.doi: 10.1016/j.nurt.2007.05.011
- Field M, Collins M, Lovell M, Maroon J. Does age play a role in recovery from sports-related concussion? A comparison of high school and collegiate athletes. The Journal of Pediatrics 2003;142(5):546-53.
- Bryan Kolb, PhDand Robbin Gibb, PhD: Brain Plasticity and Behaviour in the Developing Brain . J Can Acad Child Adolesc Psychiatry. 2011 Nov; 20(4): 265–276.
- Guskiewicz K, et al. Cumulative effects associated with recurrent concussion in collegiate football players: the NCAA Concussion Study. JAMA 2003;290(19):2549-55.
- Pellman EJ, Lovell MR, Viano DC, Casson IR. Concussion in professional football: recovery of NFL and high school athletes assessed by computerized neuropsychological testing–Part 12. Neurosurgery 2006;58(2):263-74;discussion 263-74
- Kashluba S, Casey JE, Paniak C. Evaluating the utility of ICD-10 diagnostic criteria for postconcussion syndrome following mild traumatic brain injury. Journal of the International Neuropsychological Society 2006;12(1):111-8.
- Dean PJ, O’Neill D, Sterr A. Post-concussion syndrome: prevalence after mild traumatic brain injury in comparison with a sample without head injury. Brain Inj. 2012;26(1):14-26. doi: 10.3109/02699052.2011.635354.Epub 2011 Nov 22
- McManus, C. Stress-Induced Hyperalgesia: Clinical Implications for the Physical Therapist Orthopedic Physical Therapy Practice. 2012;24(3):165-168. (http://carolynmcmanus.com/publications/mcmanus-stress-induced-hyperalgesia.pdf)
- UPMC Sports Medicine Website
- Boston University CTE Center: http://www.bu.edu/cte/about/what-is-cte/
- Hart, J.J., JAMA Neurology 2013
- Mayo Clinic Press Release: Mayo Clinic: Evidence suggests contact sports played by amateurs increase risk of degenerative disorder http://newsletter.carehubs.com/t/ViewEmail/j/2B6E3073A3AD413C/59F3204D88C0AFA89A8E73400EDACAB4
- Aubry M, et al. Summary and agreement statement of the first International Conference on Concussion in Sport, Vienna 2001. Clinical Journal of Sports Medicine 2002 Jan;12(1):6-11
Giants fourth-year running back, Ahmad Bradshaw, underwent three surgeries last January â€“ one to remove spurs from his right ankle, and one on each foot to repair fractures of both his right and left fifth metatarsals with the insertion of a screw.Â Bradshawâ€™s first post-op running session was in April and until yesterday, when
he reportedly ran in both practices, his immediate football future was questionable. All accounts Iâ€™ve read since then have been enthusiastic.Â A piece in the NY Post stated that Bradshaw was running well and will likely return kickoffs and punts once the season begins.Â However, though I hate to be the spoiler, I can only remain guardedly optimistic.
Which of Bradshawâ€™s surgeries was the bigger deal?
Wear and friction at a joint can promote changes in bone, which
responds to stresses by growing more bone.Â The irregular shape of the joint surfaces that results is due to this extra bone, or spurring.Â The spurs then take up space in the joint and, when the joint moves through the range of motion required for function, impingement occurs.Â This is painful, as nerve endings and other structures are pinched.Â Add impact from running, especially with the cutting patterns involved in football, and the situation can become untenable.Â Removing the spurs arthroscopically, if that is all that Bradshawâ€™s ankle surgery entailed, is a fairly routine procedure, and he likely healed well.Â Is it always this simple? â€“ Absolutely not.Â Sometimes there is more that might have contributed to an athleteâ€™s condition.Â Perhaps there are additional diagnoses that may or may not have been addressed.Â Or, there could be underlying factors that predisposed an individual to the formation of spurs, such as structural mal-alignment, mechanical flaws in the manner in which an athlete runs, or even consistently running in one direction on a banked surface.Â Â Simply stepping up a training program too aggressively can create undue stress on the weight-bearing joints.Â These and other issues might persist once spurs are removed.Â If so, with return to competition, the long-term result would be that over time the spurs will reappear.Â I donâ€™t know the specifics of Ahmad Bradshawâ€™s circumstances and so I make no predictions.Â
Fifth Metatarsal Fracture Fixation
Surgical fixation of fractures of the fifth metatarsal (MT), the long bone of the midfoot that connects the little toe to the bone just in front of the heel, can be tricky.Â These fractures come in several varieties, based on their exact location and whether they are acute (from a recent trauma) or chronic (typically this is due to an unhealed stress fracture).Â The most common fracture of the fifth metatarsal is an avulsion fracture, where a small portion of the base of the bone is pulled away from the body of the bone. At the fifth MT, avulsion is most often due to the pull of the connective tissue at the base of the foot or tension from a particular muscle of the lower leg that attaches at the fifth MT.Â Â A â€œDancerâ€™s fractureâ€ of the fifth metatarsal typically occurs with twisting of the ankle, otherwise known as an inversion sprain (Oâ€™Malley, 1996).Â These MT fractures may be accompanied by fractures of the outer ankle.Â Though Iâ€™ve not seen detailed reports of his injuries, I would guess that Bradshawâ€™s fractures were most likely of the Jonesâ€™ variety rather than avulsions.Â Jonesâ€™ fractures occur in an area connecting the base of the fifth metatarsal with the shaft of the bone, and they often prove to be stubborn injuries.
Studies have demonstrated that only about two-thirds of acute fifth metatarsal fractures heal well with non-operative treatment (Wheelessâ€™ Textbook of Orthopaedics).Â Conservative care
initially entails wearing a non-weight-bearing cast for about 6-8 weeks followed by therapy.Â Surgery is the treatment of choice for those with delayed healing or incomplete healing of the bone, known as non-union.Â In these chronic cases, only a percentage of the fractures will mend without surgical intervention, and those that do require prolonged treatment during which time an individual cannot participate in sports.Â Likewise, when a fracture is displaced (where the two ends of the bone donâ€™t line up) or where an avulsion entails a large piece of bone being pulled away, surgery is warranted.Â An athlete, such as Ahmad Bradshaw, may opt for surgery rather than risk being out for an extended period only to find out that his fracture still hasnâ€™t healed.Â Post-operatively you can be sure that he was monitored carefully and only allowed to return to activity once full union (mending) of the bone was established.Â This is because a premature return to activity can result in failure of the fixation (Larson, 2002).Â Some athletes, even after surgery and a carefully executed rehabilitation plan, suffer from re-fracture.
So, the answer to my question is clearly that the fixation of Bradshawâ€™s metatarsals was the more sensitive of his surgeries.Â After working to control his post-operative inflammation and pain, regain his strength, range of motion, endurance, flexibility and balance, Mr. Bradshaw began to run again.Â Iâ€™ve read that he has been trying to adjust his running technique â€“ attempting to place less stress on the outer border of his feet â€“ to avoid re-injury.Â That may be a tough go.Â Weâ€™ll keep an eye on himâ€¦
If you experience the onset of pain at the side or outer edge of your foot, seek treatment.Â The pain may seem to have been unprovoked or might have increased gradually.Â Donâ€™t hesitate if you find that the pain is more pronounced with walking and is exacerbated by running or sports participation.Â A negative x-ray doesnâ€™t even mean that you are in the clear.Â Remain on alert because stress fractures often donâ€™t show up on initial x-rays and may only be evident once they begin to heal.
Fifth seeded Michigan State managed a huge win on Sunday over fourth seeded Maryland on a three-point buzzer-beater by Korie Luscious. The biggest surprise was that the Spartans did it without the services of Kalin Lucas who went down with 2:28 left in the first half while clutching his left foot. Though reports have not yet clarified the details of Lucas’ newest injury, Coach Tom Izzo was quoted after the game as having said that he was 99% certain that his star would be out for the balance of the season after what appeared to be an Achilles tendon rupture.
If his coach is correct, Kalin Lucas should give David Beckham a call for a Q & A on what to expect next.Â Mr. Beckham was headed to his fourth World Cup,
a record for an English soccer player, when he left the field in tears on March 14th after he too suffered an Achilles rupture.Â Beckham wasted no time in having surgery, flying to see a specialist in Finland early the next morning for an Achilles repair.
Both Lucas’ and Beckham’s injuries were non-contact, typical of Achilles ruptures. Lucas claimed not to have felt or heard the “pop”, often associated with Achilles injury, though he reportedly did think he might have been kicked — a sensation that is also classic for a rupture. Beckham looked behind him when his injury occurred, as though he too may have suspected a kick to the calf. Both players also likely experienced sharp pain. Post-game, a teammate said that Beckham felt the muscle begin to come up. This too is common; it is almost like firmly pulling an elastic band until it breaks and seeing the top half retract. Surgery is often performed quickly, exactly for that reason to approximate the two ends of the tendon it is often recommended to act before the tissue can shorten permanently.
What is the Achilles tendon?
Tendons attach muscles to bones.Â The Achilles is thicker and more fibrous than most tendons and it connects the calf muscles (the gastroc in the upper calf and the soleus closer to the ankle) to the heel bone (calcaneus).Â The Achilles tendon and calf muscles are put on stretch when the ankle is flexed up and it is shortened when the toes are pointed.Â A tight Achilles or one that is overstretched can predispose to rupture.
What are the consequences of Achilles rupture?
In addition to the pain and swelling that are expected with any sports injury, disruption of the connection between the calf muscles and the heel results in an inability to contract these muscles; That means that you cannot rise up on your toes or walk with a normal push off when weight-bearing on your injured side. Running and jumping are therefore also out of the question.Â Â However, it may be possible to actively point your toes while you are not bearing weight due to the action of other muscles that help to provide this movement.
Why do Achilles tendons rupture?
There is an area of the Achilles that has less blood flow than the rest and it is thought that this section of the tendon may not be as strong.Â As we age, tendons, as other tissues of the body, become less supple and may degenerate.Â These are some reasons why ruptures generally occur in people over 30 (Beckham is 34), and especially in middle age.Â Younger athletes generally experience a higher tear, well above the ankle, where the muscle joins the tendon (musculo-tendinous junction), though they too can experience a tear closer to the heel.
Some sports are more stressful to the calf muscles and Achilles than others.Â Those that require the powerful push-off needed for running and jumping place the greatest demand, as do those like racquet sports which entail a lot of stutter-steps and quick stops and starts.Â Men are far more likely to suffer Achilles ruptures than women and though it is thought that obesity adds to the stress to the Achilles, increasing risk of rupture, that is clearly not a factor for elite athletes.
Other predisposing factors for weekend warriors like you and me include stepping up activity suddenly and significantlyÂ â€“ either by increasing the intensity, frequency or duration of participation or perhaps beginning a new activity without preparation.Â All of these increase the demand placed on the Achilles. It is thought that weakness of the calf muscles, particularly the soleus, may also be a factor causing the Achilles to rupture; The soleus can be strengthened by pointing the foot — against resistance — while the knee is bent (as in a sitting position).Â A history of multiple steroid injections at the Achilles may be to blame in some cases of rupture.Â Be aware that manufacturers of certain medications, such as the antibiotic Levaquin, name tendon issues as a potential side effect.Â Inform your physician if you begin to feel Achilles symptoms after beginning a new medication.
One exercise I strongly suggest you avoid is strengthening the gastroc muscles of the upper calf by hanging the mid-foot and heel off a step or raised platform and doing heel-raises from this position of maximum stretch. Repeatedly lowering the heel below the level of the step (with your body weight and gravity loading the Achilles tendon), puts the tendon at greater risk of rupture.Â This is an exercise I see so often in the gym.Â Yes, you should strengthen the calf, but it is recommended to do so from the more neutral foot flat position or not fully weight-bearing if on stretch.
How is an Achilles rupture diagnosed?
Physical exam is often pretty conclusive.Â The first test is simply to squeeze the belly of the calf muscles and observe whether the foot points as the muscles are manually shortened. Another obvious sign is when the examiner can move the ankle excessively into a dorsiflexed position (toes toward your nose) with the knee straight. This motion is generally restricted by the tightness of the Achilles and in the case of rupture it is not.Â A third test involves observing the motion of a needle inserted into the tendon as the foot is passively moved up and down.Â An ultrasound exam and/or positive x-ray findings — particularly those in a lateral (side) view â€“ support the diagnosis.
What are the treatment options?
Small tears may do well with immobilzation.Â Casting is generally done with the foot in a pointed position, which shortens the tendon allowing it to heal.Â Bracing that restricts motion is an alternative. Athletes are not good candidates for conservative management, and those who do not undergo surgery should expect a long recovery (up to a year) before returning to sports.
Operative treatment is the gold standard for athletes, younger patients and those with a complete rupture.Â Both treatments are followed by periods of decreased weight-bearing, though the surgical patient progresses at a much faster rate.
According to Wheeless Textbook of Orthopaedics, non-operative patients have an average re-rupture rate of 18% and can expect a decrease in strength and muscle endurance of 30%. 83% of surgical patients and 69 % of immobilization patients can expect to resume their pre-injury level of activity. Wheeless also reported that 93 % of surgical patients were satisfied with the results of treatment, while only 66% of conservatively managed patients felt likewise. Because of the positioning of the foot with the tendon in a shortened position while casted or braced, non-operative treatment generally does not restore the Achilles tendon to its full length. In contrast, if immobilized with the ankle in a neutral position, the tendon is generally lengthened, leading to a poor outcome.
The Spartans of Michigan State will meet up with Cinderella Northern Iowa, a ninth seed, this Friday. Tom Izzo is a great guy and a great coach.Â His team has stepped up under pressure before, just as they did on Sunday. Kalin Lucas will either be with them in spirit or cheerleading from he bench. Maybe they can pull this one out in his honor.
Sam Bradford, 2008 Heisman winner and Oklahoma Sooner star quarterback, was virtually a sure thing to be the number one pick in this yearâ€™s NFL draft â€“ At least that was the prevailing opinion until he sprained his right AC joint in Septemberâ€™s home opener.Â Optimism reigned when Bradford missed only three games, until he fell hard, re-injuring the same area, on the first play of the teamâ€™s second possession against Texas only six weeks later.Â Hopes for Bradfordâ€™s senior season came to a screeching halt with reconstructive surgery, performed by Dr. James Andrews on October 28th.
What is the difference between the AC joint and the shoulder joint?
The AC joint and the shoulder joint are not one and the same, though they are often referred to interchangeably in the sports pages.Â Both are a part of the shoulder girdle. The AC joint, or acromio-clavicular joint, is the connection between the outer end of the collarbone (clavicle) and the hood over the shoulder joint called the acromion.Â The acromion is an extension of the shoulder blade (scapula).
The shoulder joint (also called the gleno-humeral joint) is the interface between the upper arm bone (humerus) and its socket (the glenoid fossa), which is also an extension of the shoulder blade. Though the shoulder is the more complex joint, and can therefore suffer a more extensive variety of injuries, the AC joint is also important to the overall mechanics of the shoulder girdle.Â An unstable (too loose) or restricted (too tight) AC joint can be a precursor to pain, a decline in function, abnormal movement and a number
of shoulder pathologies.
FYI: There is one more joint in the shoulder girdle, and that is where the inner end of the clavicle is attached to the breastbone (sternum).Â It is called the sternoclavicular (SC) joint.Â The SC joint is more protected because of its central position; it is also less mobile and is rarely injured.
Â What is an AC sprain?
Ligaments connect one bone to another, providing stability at joints.Â In the case of any sprain, a ligament is stretched, sometimes to the point of tearing it completely.Â There are two sets of ligaments that stabilize the AC joint â€“ one set securing the clavicle to the acromion (which is next to it and above the shoulder joint) and another securing it to a small bone below called the coracoid process.Â The coracoid is yet another (though smaller) extension of the shoulder blade.
Trauma, generally resulting from a fall onto the involved shoulder with the arm at the side, can sprain the clavicular ligaments. Â AC sprains come in several varieties â€“ those that tear both sets of ligaments outright are the most dramatic and the clavicle becomes elevated because its anchors are ruptured.Â These are called AC separations.Â In Grade I AC sprains the ligaments are injured but remain essentially intact, while Grade II sprains result in tears of some but not all of the ligaments.Â That is why in a Grade II sprain there is no obvious deformity. Both Grade I and II sprains are treated conservatively, meaning that they do not require surgery.Â In Grade III sprains both sets of ligaments are ruptured and the stability of the AC joint is significantly compromised; the greater the instability, the more likely the need for surgery.Â AC injuries that are even more severe may result in the clavicle being displaced into the soft tissue behind it.Â These are Grade IV sprains (though in some rating systems Grades V and VI describe the most severe injuries).Â
Why didnâ€™t Sam Bradford have surgery after his initial injury?
It was reported that Bradfordâ€™s opening game AC sprain was a Grade II or III.Â He returned to play faster than you or I might have (not that Iâ€™ve played football lately), but this course of action was not out of the ordinary for a serious athlete.Â Had a hard tackle to his midsection not forced him to land on that shoulder so soon afterward, Bradford would likely have recovered sufficiently to make it through the balance of the season relatively unscathed.Â Re-injury evidently exacerbated his condition so much so that surgery was the best option to move forward with confidence.
According to published reports, Bradford was cleared to throw only five weeks before his Pro Day earlier this week.Â General Managers and coaches were out in force to see if he could still put on a show, and that is exactly what Bradford did.Â Known for his passing accuracy, velocity and high completion to interception ratio, the consensus appeared to be that Bradford hadnâ€™t lost a thing.Â The recycled and hard-working Bradford is also said to have added between 12 and 20 pounds of muscle to his upper body (accounts have varied) since his injury and with his rehab. Bill Devaney, GM of the soon-to-pick-first St. Louis Rams, was reportedly very impressed.Â The rest of us will have to wait and see if he was impressed enough.
oot and ankle injuries predominate in the NBA and Joakim Noah, the Chicago Bulls big man who is currently out with plantar fasciitis, is one of the latest high profile players to suffer from this nagging problem.Â Noah missed his first game on January 23rd, returned intermittently for limited minutes and has been out of action since February 27th, a relatively long absence for a non-traumatic injury.Â Athletes are prone to plantar fasciitis, particularly those who do a lot of sprinting and jumping, but even quarterbacks, just like the rest of us, are susceptible.Â Eli Manning, who was diagnosed during the 2009 season, is a case in point.
What is fascia?
Fascia is a fibrous connective tissue that occurs throughout the body and overlays the muscles, organs, nerves and blood vessels.Â It acts as a restraint to keep our tissues and structures in place. If you have ever prepared chicken you have seen the filmy white tissue between the skin and the meat â€“ that is fascia.Â At the bottom of the foot, (the plantar surface), the fascia is particularly fibrous and connects the heel bone to the toes.Â It is prone to stresses or small tears that can result in an inflammatory (â€œitisâ€) response.
Common causes of Plantar Fasciitis
Fasciitis usually develops over time rather than from trauma and the problem is often stubborn, especially if left untreated. Tightness of the calf muscles and Achilles tendon can predispose to plantar fasciitis, as can tightness of the fascia itself.Â A loss of mobility at the ankle or the big toe (not being able to flex up/back sufficiently) can also lead to fasciitis by changing our movement patterns, reducing the shock absorbency of the joints, and limiting the ability of the calf and fascia to stretch to their fullest, resulting in tightness.Â Additionally, weakness of the muscles of the calf or foot/ankle impact function and lead to injury by placing more stress on all the related tissues.Â Other typical pieces of the cause and effect puzzle may include structural malalignment (such as a high or low arched foot) or the presence of a heel (bone) spur.
Women who wear high heels much of the time are prone to fasciitis because the calf muscles and fascia become tight due to the positioning of the foot and ankle.Â People whose work requires that they spend an inordinate amount of time standing or walking (particularly on hard surfaces) and those who are significantly overweight are also more prone to plantar fasciitis.
Symptoms of Plantar Fasciitis
Swelling and tenderness to pressure or touch are generally complaints of those with fasciitis, as is a sharp pain in the heel area or arch of the foot.Â One of the most common complaints is morning pain, particularly with the first steps from bed. During a prolonged period of rest, where the foot and ankle are relaxed (with the toes pointed downward), the plantar fascia and muscles of the calf are on slack.Â The sudden stretch imposed by putting the foot on the floor and walking can trigger significant pain.Â The same might occur after sitting for an extended period.Â In very mild cases, after walking a bit and warming up the tissues, pain subsides. Taj Gibson, another Chicago Bull suffering from plantar fasciitis has been receiving treatment but has been able to play through it, an obvious sign that his condition is not as severe as Joakim Noahâ€™s.
Prolonged walking and especially running, which requires a more forceful push-off, are likely to increase the pain and inflammation associated with fasciitis.Â Jumping will do likewise.Â Not the best scenario for Joakim Noah who, when he began his medical leave, was the NBAâ€™s second leading rebounder.
Treatment of plantar fasciitis requires a multifaceted approach to reduce inflammation, stimulate healing, stretch tight tissues, strengthen weak musculature and minimize additional stresses.Â Here are some tried and true methods of care as well as some of the emerging techniques:
Rest â€“ time off from offending activities is an important part of treatment.
Night Splint â€“ wearing a night boot to keep the ankle at a 90-degree angle maintains some stretch of the calf and fascia and significantly reduces early morning pain.Â By helping to lightly stretch tight structures over a prolonged period, resolution of plantar fasciitis is accelerated.
Deep tissue massage â€“ performed manually and also by rolling the foot on massagers or things such as a tennis ball or frozen can of soda can be very helpful.Â Deep massage with the ankle held at 90 degrees and the big toe held gently in a backwards-bent position can help to ease fascial pain and tightness.
Stretching â€“ tight calf muscles and fascia must become more flexible to limit recurrence.
Range of motion â€“ treatment to restore motion where it is limited may be necessary to allow for more flexibility of the attached structures.
Cushioned heel lifts â€“ by slightly elevating the heel, stress on the tight structures is minimized during walking or prolonged standing, and the increased shock absorption of a heel lift also decreases the stress from impact.Â Choice of footwear factors in here as well (notice that many surgeons and chefs wear clogs).
Ice and electric stimulation â€“ both help to reduce inflammation and swelling
Iontophoreses â€“ another very helpful tool used in physical therapy.Â For plantar fasciitis, â€œiontoâ€ involves the use of a corticosteroid medication that is driven through the skin in the region of the inflammation with a transistor size electric stimulator.Â It is painfree, entails only localized use of the drug and does not entail an injection.
Taping â€“ even after returning to competition, taping techniques are used to support the arch.Â Taping can be very helpful and enable a player to compete without aggravating a condition as well as reduce the chance for recurrence after a problem resolves.
Strengthening weak muscles throughout the lower body and especially those of the calf and foot is crucial, as is building muscular endurance.Â For example weak toe flexors (muscles that let you grip with your toes) are a common problem resulting in fatigue in the foot and strain on the fascia due to poor push-off.Â Even the toes must be strengthened when treating foot and ankle conditions.
Balance training is vital as well, working to stabilize while standing on one foot and challenged to reach or bend.Â Balance training should be progressed from stable to unstable surfaces to increase the difficulty of the tasks.
Arch supports â€“ if flattened or high arches or other malalignment issues are part of the problem, over-the- counter or custom orthotics (shoe inserts) may be recommended.Â It is generally suggested to wait until you have increased your flexibility (if it is one of the causative factors) before getting a custom orthotic because the resting position of the foot may change once greater flexibility is achieved.
Prolotherapy â€“ Prolotherapy treatment involves injecting a sugar water solution into the involved ligament or tendon where it attaches to the bone. This is intended to cause a localized inflammation in these affected areas in order to then increase the blood supply and flow of nutrients.Â It is thought to stimulate the tissue to repair itself.Â Iâ€™m not sold.
Plasma Rich Platelet Therapy (PRP)â€“ Joakim Noah recently underwent PRP and shock wave treatments. Both are relatively new.Â Some recent studies on PRP were not as favorable as the original clinical impressions, showing that it was no more effective than injecting saline. Platelets are one of the four components of blood.Â The others are red and white blood cells and plasma. The procedure involves taking a patientâ€™s own blood, spinning it down to the platelets, which are said to release proteins called growth factors, then injecting that back into the injured area.Â The treatment is thought to accelerate tissue and wound healing.
Shock Wave Therapy â€“ Another emerging treatment, shock waves are said to work by inducing microtrauma to the affected tissue, which then stimulates a healing response. This healing response causes a repair process during which small blood vessels form to increase delivery of nutrients to the affected area.
Injections â€“ Not on my go-to list of treatments for plantar fasciitis, they are still in the arsenal so are included here.Â The cortisone injection is occasionally needed to jump start the rehab process by reducing inflammation and pain sufficiently so that the active treatments (such as stretching and strengthening) can be progressed without exacerbating symptoms.Â With the potential side effects of injection always at issue, it should not be a first line of defense or used repeatedly in one area of the body.Â Nor should cortisone be the entire treatment even if it brings relief.Â That is dangerous because it gives a false sense of order when in fact the underlying causes of the problem have yet to be addressed.Â Cortisone by injection at the foot is even riskier because of the more fragile nature of the tendons there and their predisposition to rupture.
Surgery â€“ A very last and infrequently relied upon resort, surgery to lengthen the fascia is sometimes the final step when all else has failed