People who are injured move differently

Like we have said before, often times when folks are injured they often lose cortical function (afferent input) from a particular area, and their gait becomes more primitive, often taking a broader base, slower movement, increased amplitude of movement and sometimes requiring assistance or something to help them balance, like our post here

"Findings suggest that movement variability in those with a musculo-skeletal injury differs from uninjured individuals. Interestingly, there was an overall trend toward greater movement variability being associated with the injured groups, although it should be noted that this trend was not consistent across all subcategories (eg, injury type). "

Baida SR, Gore SJ, Franklyn-Miller AD, Moran KA. Does the amount of lower extremity movement variability differ between injured and uninjured populations? A systematic review. Scand J Med Sci Sports. 2018 Apr;28(4):1320-1338. doi: 10.1111/sms.13036. Epub 2018 Feb 14. (

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increased cushioning = increased impact forces (GRF)

increased impact forces = increased injuries?

possibly not...

 

footwear can impact injury and biomechanics but may not be the primary factor

a nice recap of the state of what we currently know about shoes, design and cushioning.

http://lermagazine.com/cover_story/running-shoes-and-injury-risk-rethinking-the-importance-of-cushioning-and-pronation

Should you rotate your shoes?

Rotate your shoes more often? Maybe not, if you are concerned about plantar pressures. But do increased plantar pressures actually cause injuries? That is the million dollar question, isn't it?

 

from this paper:

  • Footwear characteristics have been implicated as a cause of foot pain (1)
  • Ill fitting footwear has been associated with foot pain.(2)
  • Individually fitted sport shoes were found to be effective in reducing the incidence of foot fatigue.(3)
  • There is an association between using inappropriate footwear and injuries.(4) 
  • An association between injuries and the age of sport shoes has been reported. (5)
  • The recommendations are that running shoes need to be changed every 500 - 700 kilometres as they lose their shock-absorbing capabilities.(6)
  • Elevated plantar pressures cause increased foot pain in people with cavus feet.(7)

"Walking plantar pressures in running shoes need to be investigated. There are no pedobarographic studies in the literature that compare new with old running shoes. We hypothesized that old running shoes transmitted higher plantar pressures as compared to new running shoes. If so, are old running shoes detrimental to our feet? The purpose of this study was to see whether the mean peak pressures & pressure-time integrals exerted at the plantar surface of feet were higher when using old running shoes as compared to new running shoes.

Plantar pressure measurements in general were higher in new running shoes. This could be due to the lack of flexibility in new running shoes. The risk of injury to the foot and ankle would appear to be higher if running shoes are changed frequently. We recommend breaking into new running shoes slowly using them for mild physical activity.

 Rethnam U, Makwana N. Are old running shoes detrimental to your feet? A pedobarographic study. BMC Research Notes. 2011;4:307. doi:10.1186/1756-0500-4-307. link to FREE FULL TEXThttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3228510/

references:

  1. Grier TL, Knapik JJ, Swedler D. et al. Footwear in the United States Army Band: Injury incidence and risk factors associated with foot pain. Foot (Edinb) 2011;21(2):60–5. [PubMed]
  2. Burns SL, Leese GP, McMurdo ME. Older people and ill fitting shoes. Postgrad Med J.2002;78(920):344–6. doi: 10.1136/pmj.78.920.344. [PMC free article] [PubMed] [Cross Ref]
  3. Torkki M, Malmivaara A, Reivonen N. et al. Individually fitted sports shoes for overuse injuries among newspaper carriers. Scand J Work Environ Health. 2002;28(3):176–83. [PubMed]
  4. Taunton JE, Ryan MB, Clement DB. et al. A prospective study of running injuries: the Vancouver Sun Run "In Training" clinics. Br J Sports Med. 2003;37:239–44. doi: 10.1136/bjsm.37.3.239.[PMC free article] [PubMed] [Cross Ref]
  5. van Mechelen W. Running injuries: A review of the epidemiological literature. Sports Med.1992;14(5):320–35. doi: 10.2165/00007256-199214050-00004. [PubMed] [Cross Ref]
  6. Fredericson M. Common injuries in runners: diagnosis, rehabilitation, prevention. Sports Med.1996;21(1):49–72. doi: 10.2165/00007256-199621010-00005. [PubMed] [Cross Ref]
  7. Wegener C, Burns J, Penkala S. Effect of neutral-cushioned running shoes on plantar pressure loading and comfort in athletes with cavus feet: a crossover randomized controlled trial. Am J Sports Med. 2008;36(11):2139–46. doi: 10.1177/0363546508318191. [PubMed] [Cross Ref]

Concussions and increased risk for musculoskeletal injury.

Concussion Increases Odds of Sustaining a Lower Extremity Musculoskeletal Injury After Return to Play Among Collegiate Athletes. -Brooks et al.

Perhaps we need to be paying far more attention to the musculoskeletal injuries in our contact sport athletes. We need to bring to light some important facts to our athletes (and their parents!).

From the Nauman Purdue football study:
"The worst hit we've seen was almost 300 Gs," Nauman said. A soccer player "heading" a ball experiences an impact of about 20 Gs." 
Here is what we say: now add 20 soccer headers in a week of game and practice. Or take 20 submaximal football tackles, in a week of game and practice. You do the math.

Concussions have been now shown to cause abnormalities in brain and motor functioning. These issues can last long after perceived clinical recovery. "Recent work suggests subtle deficits in neurocognition may impair neuromuscular control and thus potentially increase risk of lower extremity musculoskeletal injury after concussion."
Do NOT underestimate the impacts of a single concussion, and certainly NEVER in a second impact (Second Impact Syndrome (SIS)). SIS can at worst, lead to death within minutes, so certainly it can lead to impaired neuromuscular control. Our current society continues to ignore the immense long lasting effects of head injuries, even minimal ones. We continue to allow young developing brains to partake in football, soccer, and other jarring sports. Yes, we cannot live in a vacuum, but we can live in awareness and wise choices.

Facts: 
The 2 year Purdue Study of high school football players suggested that concussions are likely caused by many hits over time and not from a single blow to the head, as previously believed. "Over the two seasons we had six concussed players, but 17 of the players showed brain changes even though they did not have concussions," Talavage said. "The most important implication of the new findings is the suggestion that a concussion is not just the result of a single blow, but it's really the totality of blows that took place over the season," said Eric Nauman. "Most clinicians would say that if you don't have any concussion symptoms you have no problems," said Larry Leverenz, an expert in athletic training and a clinical professor of health and kinesiology. "However, we are finding that there is actually a lot of change, even when you don't have symptoms."

"New research into the effects of repeated head impacts on high school football players has shown changes in brain chemistry and metabolism even in players who have not been diagnosed with concussions and suggest the brain may not fully heal during the offseason."-Emil Venere
"We are finding that the more hits you take the more you change your brain chemistry, the more you change your brain's ability to move blood to the right locations," Nauman said.

'Deviant brain metabolism' found in high school football players. 
http://www.purdue.edu/…/deviant-brain-metabolism-found-in-h…

Biomechanical Correlates of Symptomatic and Asymptomatic Neurophysiological Impairment in High School Football
Evan L. Breedlove, BS1,Thomas M. Talavage, PhD2,3,Meghan Robinson, BS2, Katherine E. Morigaki, MS ATC4,Umit Yoruk, BS3, Larry J. Leverenz, PhD ATC4 , Jeffrey W. Gilger, PhD5, Eric A. Nauman, PhD1,2,6

http://www.ncbi.nlm.nih.gov/pubmed/26786903

Take good look at these gals. The gal on the left (in blue) looks like she has a level pelvis, but look at the upper body. She’s leaning to the left and has a great deal of torso rotation backward. One of the clues is the abduction of her left arm. Also note how her right arm crosses across her body. We wonder how she looks in right foot stance.  The gal on the left (in red) has a subtle dip of the right side of her pelvis and also has over rotation of her upper body. Her right on crossing the body is a good reason to believe she will have a crossover gait if viewed from straight on.  While both of these gals may have adequate strength, we question how much endurance they have as well as available rotation in the hips and lumbar spine.  This is an excellent, referenced review of some of the current literature and controversy of strength and injury risk. A good read and certainly worth your time to get caught up on what’s current. We would love to see you study on endurance and injury risk.  “While muscle strength may improve tolerance of loads during running, another reason for inconsistencies in the reported relationships between strength and injury risk may be that strength is typically assessed isometrically. It’s unclear how much of an influence peak isometric strength has on the dynamic task of running, and specifically on prolonged running in the presence of muscular fatigue. Schmitz et al found that, while isometric hip strength values were similar between novice and experienced runners, hip internal rotation motion during running was higher in the novice runners, suggesting isometric strength may not correlate strongly with muscular control and kinematics during running.”      http://lermagazine.com/article/lower-extremity-strength-and-injury-risk-in-runners

Take good look at these gals. The gal on the left (in blue) looks like she has a level pelvis, but look at the upper body. She’s leaning to the left and has a great deal of torso rotation backward. One of the clues is the abduction of her left arm. Also note how her right arm crosses across her body. We wonder how she looks in right foot stance.

The gal on the left (in red) has a subtle dip of the right side of her pelvis and also has over rotation of her upper body. Her right on crossing the body is a good reason to believe she will have a crossover gait if viewed from straight on.

While both of these gals may have adequate strength, we question how much endurance they have as well as available rotation in the hips and lumbar spine.

This is an excellent, referenced review of some of the current literature and controversy of strength and injury risk. A good read and certainly worth your time to get caught up on what’s current. We would love to see you study on endurance and injury risk.

“While muscle strength may improve tolerance of loads during running, another reason for inconsistencies in the reported relationships between strength and injury risk may be that strength is typically assessed isometrically. It’s unclear how much of an influence peak isometric strength has on the dynamic task of running, and specifically on prolonged running in the presence of muscular fatigue. Schmitz et al found that, while isometric hip strength values were similar between novice and experienced runners, hip internal rotation motion during running was higher in the novice runners, suggesting isometric strength may not correlate strongly with muscular control and kinematics during running.”


http://lermagazine.com/article/lower-extremity-strength-and-injury-risk-in-runners

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Got big toe pain? Think it’s gout? Think again!   Things are not always what they appear to be. 

This gent came in with first metatarsophalangeal pain which had begun a few months previous. His uric acid levels were borderline high (6) so he was diagnosed with gout.  It should be noted his other inflammatory markers (SED rate and CRP) were low. Medication did not make the symptoms better, rest was the only thing that helped. 

The backstory is a few months ago he was running in the snow and “punched through"the snow, hitting the bottom of his foot on the ground. Pain developed over the next few days and then subsided. The pain would come on whenever he try to run or walk along distances and he noticed a difficult time extending his big toe.

 Examination revealed some redness mild swelling over the 1st metatarsophalangeal joint (see pictures above) and hallux dorsiflexion of 10°.   If we raised the base of the first metatarsal and pushed down on the head of the 1st, he was able to dorsiflex the 1st MTP approximately 50°. He had point tenderness over the medial sesamoid. We shot the x-rays you see above. The films revealed a fracture of the medial sesamoid with some resorption of the bone.

The  sesamoid fracture caused the head of the 1st metatarsal to descend on one side, and remain higher on the other, altering the axis of rotation of the joint and restricting extension. We have talked about the importance of the axis of this joint in may other posts (see here and here).

 He was given exercises to assist in descending the first ray (EHB, toe waving, tripod standing).  He will be reevaluated in a week and if not significantly improved we will consider a wedge under the medial sesamoid. 

A pretty straight forward case of “you need to be looking in the right place to make the diagnosis”. Take the time to examine folks and get a good history.

Do you know your stuff? Would you correct this child’s gait ? Give them orthotics, exercises, force correction, leave them alone ? 

Is he Internal Tibial torsioned ? Is he “pigeon toed” ,if that is the only lingo one knows, :(  Does he have femoral torsion ?  A pronation problem locally at the foot or an internal spin problem through the entire limb ? Or a combination of the above ? 

What’s your solution?

It MUST be based on the knowledge necessary to fix it, not the limits of YOUR knowledge. You can never know what to do for this lad from his gait evaluation, no matter how expensive your digital, multi-sensor, 3D multi-angle, heat sensor, joint angle measuring, beer can opening, gait analysis set up is. You can never know what to do for this lad if you do not know normal gait, normal neuro-developmental windows, normal biomechanics, know about torsions (femoral, tibial, talar etc), foot types etc.  It is a long list.  You cannot know what to do for this kid if you do not know how to accurately and logically examine them. 


Rule number 1. First do no harm.

If your knowledge base is not broad enough, then rule number one can be easily broken ! Hell, if you do not know all of the parameters to check off and evaluate, you might not even know you are breaking rule number one !  If everything looks like a weak muscle, every solution will be to “activate” and strengthen and not look to find the source of that weakness.  Muscles do not “shut down” or become inhibited because it is 10 minutes before practice or because it is the 3rd Monday of the month. You are doing your client a huge disservice if you think  you are smarter than their brain and activate muscles that their brain has inhibited for a reason. What if it were to prevent joint loading because of a deeper problem ?  If every foot looks flat and hyper pronated, and all you know is orthotics or surgery or shoe fit, guess what that client is prescribed ? If all you see is torsions, that is all you will look to treat. If all you see is sloppy “running form” and all you know is “proper running form” forcing your client into that “round peg-square hole” can also lead to injury and stacking of compensation patterns.  

One’s lack of awareness and knowledge, are one’s greatest enemies. If you don’t know something exists, because you’ve never studied or learned it, how can you be aware of it ? If you’re not spending enough time examining a client, you might not be aware of an issue even though you may be knowledgeable about the issue.
One must have both awareness and knowledge. One must also be aware that compensations are the way of the body. What you see is not your client’s problem. It is their strategy to cope.

Are you helping your client ? Hurting them ?  Adding risk to their activity ? Are you stepping beyond your skill set ?  

Rule Number 1: First do no harm. 

Shawn and Ivo

PS: we will get to this case another time, we just wanted to make a point today about the bigger problems out in the world.

the gait guys

How injury and pain reorganize the brain.

Gait, Arm Swing and Reorganizing the Brain

When we injure a body part there is a price to pay, how expensive it will be is entirely up to you. Upon injury, the brain takes note and typically dives into a backup plan of neurologic inhibition, neuro-protective tightness and alteration of motor patterns to protect that injured area and allow it to heal. Moderating and altering the forces and demands upon said tissues is the goal to enable healing, if we as humans, don’t get in the way first (“I have to get that run in, I am behind in my training with all these injuries !” or “Ah, its still not that bad, the pain wasn’t worse on Tuesday’s run, I will be ok.”). The bigger question for most folks is, will you listen to what your body is asking of you? Heed the warnings and messages, and your injury will come and go in a timely manner, ignore the messages and welcome to a chronic festering problem.

These protective mechanisms need to be in place, we just have to listen to them.  Failure to heed their warnings to dial things back and rest, recover and heal, the brain will make alternative changes out of necessity.

In the medpage today article in the references below, the authors discuss several important things.

“Getting a cast or splint causes the brain to rapidly shift its resources to make righties function better as lefties, researchers found.
Right-handed individuals whose dominant arm had to be immobilized after an injury showed a drop in (brain) cortical thickness in the area that controls primary motor and sensory areas for the hand, Nicolas Langer, MSc, of the University of Zurich in Switzerland, and colleagues reported.
Over the same two-week period, white and gray matter increased in the areas that controlled the uninjured left hand, suggesting “skill transfer from the right to the left hand,” the group reported in the Jan. 17 issue of Neurology.
The findings highlight the plasticity of the brain in rapidly adapting to changing demands, but also hold implications for clinical practice, they noted.”

This article highlights the rapid changes in motor programs that occur. It does not take long for the body to begin to develop not only functional adaptations but neurologic changes at the brain level within days and certainly less than 2 weeks.

So how long have you been in this pain ? If someone has to ask you this question, the process has already begun.

We tell our patients, if pain does not go away fairly quickly, that we need to get on top of the injury quickly. That is not to say you need to reach for the phone every time you have pain but you need to heighten your awareness of the injury’s status and  you need to make sure you are not driving session after session of training into a festering injury. If you do not let something heal and recover, the brain will find a way around it.  And it will imprint that new motor pattern into hard wiring, and into the hard wiring of other patterns, if you do not heed the warning signs.  This new wiring is a compensation pattern. And the longer it is there the more the neurologic pattern becomes embedded by layerings of myelin coating.  Which means that in the future, if you fatigue or injury another local tissue, this old compensation pattern is waiting in the shadows looking for an opening to rear its ugly head for old times sake.

Furthermore, on the topic of asymmetry, the above concept holds strongly true. In our clinics, we recognize asymmetry as a strong clinical finding. Despite the  Lathrop-Lambach study below, mentioning that they feel a 10% baseline asymmetry is the norm, if you do not rehab and correct both an injury and its new neurologic hardwiring changes, you have enabled and welcomed asymmetry. We feel, as many others do, that asymmetry can be a major component and predictor to injury. Logically, restoring as much symmetry as possible, both biomechanically and neurologically, is restorative and protective.

Don’t be a stoic knucklehead. Get your stuff fixed by someone who knows what they are doing. And remember, watching your gait on a treadmill or through some high tech gait analysis software and making recommendations from that information is just plain idiotic. Go see someone smart who can correlated it to examination findings. 

This article pertains to athletes and non-athletes of all walks of life. From 5 to 105 years of age, we are all susceptible to the brain’s overriding mechanisms. 

Shawn and Ivo

references:

1. Broken arm can reorganize the brain.

http://www.medpagetoday.com/Neurology/GeneralNeurology/30686

Gait Posture. 2014 Jul 1. pii: S0966-6362(14)00610-9. doi: 10.1016/j.gaitpost.2014.06.010. [Epub ahead of print]
Evidence for joint moment asymmetry in  healthy populations during gait.
"We found a high amount of asymmetry between the limbs in healthy populations. More than half of our overall population exceeded 10% asymmetry in peak hip and knee flexion and adduction moments. Group medians exceeded 10% asymmetry for all variables in all populations. This may have important implications on gait evaluations, particularly clinical evaluations or research studies where asymmetry is used as an outcome. Additional research is necessary to determine acceptable levels of joint moment asymmetry during gait and to determine whether asymmetrical joint moments influence the development of symptomatic pathology or success of lower extremity rehabilitation.”
Making a list and checking it twice…  
 So you or someone you are treating/coaching/ rehabbing, etc has muscle weakness, either perceived by them or noted by you, by observation or muscle testing. Have you stopped to think what might be causing the weakness? 
 Cross sectional area is directly proportional to strength. With strength, we are talking predominantly about Type II muscle (remember, Type I is predominantly endurance muscle, due to differing histological structure).    Type II muscle fibers are larger, have fewer capillaries, less myoglobin, fewer mitochiondra . They obtain most of their energy by anaerobic glycolysis, rather than aerobic respiration    (ie the Krebs cycle).    All muscles are made of a mixture of Type I and Type II fibers, but most muscles tend to have a predominance of one over the other. Here we are referring to strength. 
 There are many causes of muscle weakness. Here are a few: 
  Injury to the muscle 
 Injury to the joint the muscle crosses 
 Stretch weakness 
 Tight weakness 
 Neurogenic weakness 
 Myopathic weakness 
 Reflexogenic weakness 
 And the list goes on… 
  The 1 st  one on the list is an easy one to understand. If you break the machine, it doesn’t work. Torn contractile proteins with leaky sarcoplasmic reticulum (calcium reservoirs) do not allow for efficient contractions. 
 The second on the list is a bit more complex. 
 We remember that that the joint capsules are blessed with four types of mechanoreceptors, aptly named Type I, II, III, and IV, which when stimulated physically, chemically, or thermally apprise the nervous system of the forces acting on that joint as well as its position in space. For a great video review of mechanoreceptors, click  here  
 Joint pathology or inflammation will often cause distention of its capsule. The effect of the resulting joint effusion on the actions of the muscles crossing that joint have been examined extensively in the literature. Let’s look at one of the studies and its implications. 
  Reflex Actions of Knee Joint Afferents During Contraction of the Human Quadriceps  
  Iles JF, Stokes M, Young A: Clinical Physiology (10) 1990: 489-500  

 In this paper, the authors infuse hypotonic saline into the knees of eight asymptomatic individuals (including one of the authors) using a 16 gauge needle (ouch!) and studied its effects on the H reflexes and muscle recruitment. An H reflex is like performing a tendon jerk reflex (the  involuntary contraction  you would check with a neurological hammer) using an electrical stimulus. The onset time (also called the latency) and its amplitude are recorded. Muscle recruitment is the  voluntary contraction  of that muscle, measured with electromyography (EMG) by having an electrode either over (surface EMG) or within (needle EMG) the muscle and examining how hard the muscle is working based on the amplitude and frequency of the response. 
 First of all, no one in the study experienced any pain (hmmm, not sure about that) , only the sensation of pressure in their knees (which was considered activation of  only  the proprioceptors of the joint). The authors found that   any   pressure increase within the joint capsule depressed the H reflex and inhibited the action of the quadriceps. They hypothesize that this may contribute to pathological weakness after joint injury. 
 So how does all this apply to us? 
 As we all know, lots of patients have joint dysfunction. Joint dysfunction leads to cartilage irritation, which leads to joint effusion. This will inhibit the muscles that cross the joint. This causes the person to become unable to stabilize that joint and develop a compensation pattern. Next the stress is transferred to the connective tissue structures surrounding the joint which, if the force is sufficient, will fail. Now we have a sprain and some of the protective reflexes can take over. Abnormal forces can now be translated to the cartilage. This, if it goes on long enough,    can perpetuate degeneration, which causes further joint dysfunction. The cycle repeats and if someone doesn’t intervene and control the effects of inflammation, restore normal joint motion and rehabilitate the surrounding musculature, the patient’s condition will continue its downward spiral, becoming another statistic contributing to the tremendous economic and physical costs of an injury. 
  And that, my friends, is  one mechanism  as to how joint effusion disturbs the homeostasis of the musculature surrounding a joint.  
 In future posts, we will examine other causes of muscle weakness. For now, make a list of possible causes before assuming it is just injured or “turned off”. Compensations happen for a reason, and if you remove someone’s compensation pattern, you had better make sure you have another one up your sleeve and that their system is ready for a change. 
   The Gait Guys. Giving you the tools so you can be better. Period. 

Making a list and checking it twice…

So you or someone you are treating/coaching/ rehabbing, etc has muscle weakness, either perceived by them or noted by you, by observation or muscle testing. Have you stopped to think what might be causing the weakness?

Cross sectional area is directly proportional to strength. With strength, we are talking predominantly about Type II muscle (remember, Type I is predominantly endurance muscle, due to differing histological structure).  Type II muscle fibers are larger, have fewer capillaries, less myoglobin, fewer mitochiondra . They obtain most of their energy by anaerobic glycolysis, rather than aerobic respiration  (ie the Krebs cycle).  All muscles are made of a mixture of Type I and Type II fibers, but most muscles tend to have a predominance of one over the other. Here we are referring to strength.

There are many causes of muscle weakness. Here are a few:

  • Injury to the muscle
  • Injury to the joint the muscle crosses
  • Stretch weakness
  • Tight weakness
  • Neurogenic weakness
  • Myopathic weakness
  • Reflexogenic weakness
  • And the list goes on…

The 1st one on the list is an easy one to understand. If you break the machine, it doesn’t work. Torn contractile proteins with leaky sarcoplasmic reticulum (calcium reservoirs) do not allow for efficient contractions.

The second on the list is a bit more complex.

We remember that that the joint capsules are blessed with four types of mechanoreceptors, aptly named Type I, II, III, and IV, which when stimulated physically, chemically, or thermally apprise the nervous system of the forces acting on that joint as well as its position in space. For a great video review of mechanoreceptors, click here

Joint pathology or inflammation will often cause distention of its capsule. The effect of the resulting joint effusion on the actions of the muscles crossing that joint have been examined extensively in the literature. Let’s look at one of the studies and its implications.

Reflex Actions of Knee Joint Afferents During Contraction of the Human Quadriceps

Iles JF, Stokes M, Young A: Clinical Physiology (10) 1990: 489-500

In this paper, the authors infuse hypotonic saline into the knees of eight asymptomatic individuals (including one of the authors) using a 16 gauge needle (ouch!) and studied its effects on the H reflexes and muscle recruitment. An H reflex is like performing a tendon jerk reflex (the involuntary contraction you would check with a neurological hammer) using an electrical stimulus. The onset time (also called the latency) and its amplitude are recorded. Muscle recruitment is the voluntary contraction of that muscle, measured with electromyography (EMG) by having an electrode either over (surface EMG) or within (needle EMG) the muscle and examining how hard the muscle is working based on the amplitude and frequency of the response.

First of all, no one in the study experienced any pain (hmmm, not sure about that) , only the sensation of pressure in their knees (which was considered activation of only the proprioceptors of the joint). The authors found that any pressure increase within the joint capsule depressed the H reflex and inhibited the action of the quadriceps. They hypothesize that this may contribute to pathological weakness after joint injury.

So how does all this apply to us?

As we all know, lots of patients have joint dysfunction. Joint dysfunction leads to cartilage irritation, which leads to joint effusion. This will inhibit the muscles that cross the joint. This causes the person to become unable to stabilize that joint and develop a compensation pattern. Next the stress is transferred to the connective tissue structures surrounding the joint which, if the force is sufficient, will fail. Now we have a sprain and some of the protective reflexes can take over. Abnormal forces can now be translated to the cartilage. This, if it goes on long enough,  can perpetuate degeneration, which causes further joint dysfunction. The cycle repeats and if someone doesn’t intervene and control the effects of inflammation, restore normal joint motion and rehabilitate the surrounding musculature, the patient’s condition will continue its downward spiral, becoming another statistic contributing to the tremendous economic and physical costs of an injury.

And that, my friends, is one mechanism as to how joint effusion disturbs the homeostasis of the musculature surrounding a joint.

In future posts, we will examine other causes of muscle weakness. For now, make a list of possible causes before assuming it is just injured or “turned off”. Compensations happen for a reason, and if you remove someone’s compensation pattern, you had better make sure you have another one up your sleeve and that their system is ready for a change.

The Gait Guys. Giving you the tools so you can be better. Period. 

Just because a muscle tests weak doesnt mean it needs activated.

To Activate or Not Activate: That is the question…

Just because a muscle tests weak does not mean it can, should or needs to be activated.

Muscles become inhibited for many reasons.  Perhaps it is being forced into a substitution or compensation pattern because the primary motor pattern is not accessible.  Perhaps it is because there is a local inflammatory response (ie injury) near by or within the muscle. Perhaps the muscle is lacking in one or several of its primary tenants, S.E.S. (Skill, Endurance, or Strength). Perhaps the joint(s) that muscle crosses are arthritic, inflamed, damaged, remember that an inflamed joint does not like compression/loading. When a muscle contracts it will increase compression across the joint surfaces. Maybe it is being reciprocally inhibited by it’s antagonist, or does not have appropriate sensory feedback from its mechanoreceptors and is neurologically inhibited. The nervous system is wired with many “faults”, which shut things down. Often times, you need to explore the reason why.

So…What happens if you decide to “activate” the muscle regardless of any of the above, which should have been clearly determined by a clinical examination ?

You very well could be forcing that muscle back on the grid encouraging the muscle to perform in an unsafe or undesirable environment. You may be forcing compressive loading across a joint that is inflamed. You could be forcing compression and shear across a damaged cartilage interface, an osteochondral defect, a ligamentous tear or a combination of the above.  You will also be over riding the nervous systems inherent neuro-protective mechanism and by forcing the muscle to once again activate and work in a faulty movement pattern.  You very likely are reprogramming an unsafe and potentially damaging motor pattern.

Remember, when you “mess around” and over ride neuro-protective inhibition of a motor pattern you reteach a potentially dangerous sensory response telling the joint that the nervous system has been mistaken, that it is actually safe to place load and shear across the joint when in fact it is dangerous. Protective reflexes are there for a reason, to protect you!

We have seen the results of well intentioned or sometimes untrained individuals implementing activation into their clinical practices, coaching, or training.  Without a sound clinical examination to determine the reason for muscle inhibition one is taking a whole pile of warning signs and throwing them to the wind.  Remember, if you force a muscle back into activation despite all of the warning signs and reasons for inhibition, you will get a temporarily stronger muscle. This is not necessarily success.

In fact, what you have done, is enabled your client the ability to once again impart load and shear across a joint(s) and motor chain that was getting clear central nervous system signals to avoid the loading response.  You are essentially forcing a  compensation pattern and we all know where that leads to. 

As clinicians, we take an oath that states: “Primo Non Nocere”, which means “first, do not injure”. Know what you are doing. If you don’t, then get the training or don’t do it.

The Gait Guys. Were are here to help. We are watching. Do us proud and do the right thing.

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Since the world did not end, you should probably think twice about those motion control shoes….

WE can all agree that there is a time and a place for motion control shoes. For people with chronic ankle sprains or lateral instability (ie, an incompetent lateral compartment; peroneus longus, brevis or tertius), it is neither the time, nor the place.

The lateral ankle is stabilized by both static (ligaments: above lower left) and dynamic (muscles above, lower right) elements. This is often called “the lateral stabilizing complex” The lateral ankle (ie the lateral malleolus) also projects more inferiorly than the medial. This means that when push comes to shove, the ankle is more likely to invert (or go medially) than evert (or go laterally). What protects it? The static component consist of three main ligaments (seen above) the posterior and anterior talofibular ligaments and the calcaneofibular ligaments. The dynamic components are the peroneii muscles. These muscles not only stabilize but also exert an eversion (brings the bottom of the foot to the outside) force on the ankle.

So what you say?

according to one study we found “Using an in-shoe plantar pressure system, chronic ankle instability subjects had greater plantar pressures and forces in the lateral foot compared to controls during jogging.”

Hmmm. Remember the midsole? (If not click here and here for a review) Motion control shoes are medially posted. That means they provide more support medially or  have a tendency to tip the foot laterally. SO, motion control shoes shift forces laterally.

A person with chronic ankle instability has weakness of either the static, dynamic, or both components of the lateral stabilizing complex.

bottom line? make sure folks have a competent lateral stabilizing complex and if they don’t, you may want to think twice about using a motion control shoe.

Ivo and Shawn. Increasing your shoe geekiness coefficient on daily basis!                                                                                                                                                      

Foot Ankle Int. 2011 Nov;32(11):1075-80. Increased in-shoe lateral plantar pressures with chronic ankle instability. Schmidt H, Sauer LD, Lee SY, Saliba S, Hertel J. Source

University of Virginia, 2270 Ivy Road, Box 800232, Charlottesville, VA 22903, USA.

Abstract BACKGROUND:

Previous plantar pressure research found increased loads and slower loading response on the lateral aspect of the foot during gait with chronic ankle instability compared to healthy controls. The studies had subjects walking barefoot over a pressure mat and results have not been confirmed with an in-shoe plantar pressure system. Our purpose was to report in-shoe plantar pressure measures for chronic ankle instability subjects compared to healthy controls.

METHODS:

Forty-nine subjects volunteered (25 healthy controls, 24 chronic ankle instability) for this case-control study. Subjects jogged continuously on a treadmill at 2.68 m/s (6.0 mph) while three trials of ten consecutive steps were recorded. Peak pressure, time-to-peak pressure, pressure-time integral, maximum force, time-to-maximum force, and force-time integral were assessed in nine regions of the foot with the Pedar-x in-shoe plantar pressure system (Novel, Munich, Germany).

RESULTS:

Chronic ankle instability subjects demonstrated a slower loading response in the lateral rearfoot indicated by a longer time-to-peak pressure (16.5% +/- 10.1, p = 0.001) and time-to-maximum force (16.8% +/- 11.3, p = 0.001) compared to controls (6.5% +/- 3.7 and 6.6% +/- 5.5, respectively). In the lateral midfoot, ankle instability subjects demonstrated significantly greater maximum force (318.8 N +/- 174.5, p = 0.008) and peak pressure (211.4 kPa +/- 57.7, p = 0.008) compared to controls (191.6 N +/- 74.5 and 161.3 kPa +/- 54.7). Additionally, ankle instability subjects demonstrated significantly higher force-time integral (44.1 N/s +/- 27.3, p = 0.005) and pressure-time integral (35.0 kPa/s +/- 12.0, p = 0.005) compared to controls (23.3 N/s +/- 10.9 and 24.5 kPa/s +/- 9.5). In the lateral forefoot, ankle instability subjects demonstrated significantly greater maximum force (239.9N +/- 81.2, p = 0.004), force-time integral (37.0 N/s +/- 14.9, p = 0.003), and time-to-peak pressure (51.1% +/- 10.9, p = 0.007) compared to controls (170.6 N +/- 49.3, 24.3 N/s +/- 7.2 and 43.8% +/- 4.3).

CONCLUSION:

Using an in-shoe plantar pressure system, chronic ankle instability subjects had greater plantar pressures and forces in the lateral foot compared to controls during jogging.

CLINICAL RELEVANCE:

These findings may have implications in the etiology and treatment of chronic ankle instability.


all material copyright 2012 The Homunculus Group/ The Gait Guys. Don’t rip off our stuff. PLEASE ASK 1st!

Runners . . . On Your Mark, Ready, Set.....Swim.

For many of the years of my youth I watched just about every NBA basketball game I could get my eyes on.  When I wasn’t dreaming of playing ball in the big time I was at the local YMCA in my small town shooting jump shots, working on my fading jumper (because i was a small guard with no vertical, the worst of combinations), and working on my ball handling techniques. I was not a great player, not by any means, but I could play in pretty competitive pick up games and at least be somewhat respectable (note that ‘somewhat’ is highlighted).  But I still dreamed big about the NBA until I became old enough to realize that I was just too short and not blessed with the natural talent for the game that others obviously had been blessed. No matter how much I dreamed, being 5 foot 8 inches wasn’t going to ever get me to the big dance.  Body type, form, physiology and your anatomy have a big part in what sport you will be good at. There just are not too many 5'8" NBA guards, there never were minus Mugsy and Spud. They were an exception, obvious outliers. 

Are you a runner with runner’s anatomy ?  Do you have bowed legs ? Forefoot varus flat feet ? Anteverted hips ? Excessive tibial torsion ?  These are not great traits for runners. They tend to lead to many biomechanical issues that provoke injury at a much higher incidence than someone like my friend Charlie Kern , the USA masters mile champion.  Charlie is like Tiger Woods. Charlie has straight lower limb bones, no bony versions or torsions, great feet, he is slender, excellent muscle structure, and has tons of natural ability.  If you have ever seen him run it is like watching water flow. Charlie is as a runner just like Tiger is as a golfing Ferrari. They both happened to pick a sport that their body’s were perfectly suited for, then they had the passion for that sport, were lucky to have found it at a young age, and they worked harder than anyone else at their sport.  Anatomy, a bit of luck in sport choice early on, a physiology that paired well with the anatomy, and a work ethic to trump anyone. Being the best is a combination of things. You can have all the desire in the world as a runner or athlete but if you do not have the magic mixture of all things necessary you might just be average instead of extraordinary. 

Do you get injured all the time when you run ? How are your feet, are they competent or are they flat ? Do your tibias bow like a weathered piece of lumber ?  Are your knees kinked inwards (genu valgum) ? Are you tall and thin or are you build like a line backer ?  In other words, are you suited to be a distance runner or marathoner ? Or should you be happy with three to four 5k runs a week and be happy you can run those smaller distances rather than spend every 2 weeks in the therapists office getting a foot fixed, an orthotic tweaked, kinesiotape on a knee, more rehab. Do you spend more time icing your injuries and doing pre-run theapeutic exercises and foam rolling than you do running ? 

If this is you. God bless your dedicated heart. But maybe you should put on your Speedo and go for a swim.  I put my NBA dreams on hold long ago after realizing that at 5'8" it just wasnt going to happen. I picked up golf and did much better at that game in a shorter period of time than all the work on my hoop dreams.  I would fathom to say I should have picked up ping-pong long ago as a child. Perhaps I would be world champ by this time.

Run, bike, swim, hoops, golf…..whatever your passion. There is nothing wrong with having heart and grinding it out daily to be a runner or do whatever your sport happens to be.  Just never lose sight of the obvious. Maybe you need to look past your heart and look in the mirror and your mounting therapy bills and make some adjustments to your running dreams. Some of my best Triathletes were awesome runners at one time … .  when we could get them healthy to a start line line.  The problem was that they had more unused race bibs than completed races. They were in my office regularly pleading me to fix them up so they could get their training in so they could get to race day. However, after much psychoanalysis and reality talking we finally got through to some of the best athletes. Once we switched them to triathlons where they could moderate the runs and hit some alternative sports that did not play up their challenged race anatomy, they rose to the top and rarely had to hand off a race bib to a friend who was healthy.  And they are happier.  I see them far less in my office and far more at the finish lines with a huge smile.

Do some honest inventory of your body.  Sometimes a Speedo just makes sense, well, sort of. If you catch our drift.

Dr. Shawn Allen, The Gait Guys

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Case of the Week: Rib Pain while Running: Part 2

Welcome back. Glad you picked choice d (or maybe you had a pint anyway)

Assessment: This patient has a significant difference in the length of her legs; her left leg being short, right leg being longer. The right ilia is rotated posteriorly (thus the tissue fold) in an attempt to shorten the extremity and the left ilia is rotated anteriorly, in an attempt to lengthen the leg. This is putting the abdominal external obliques in a  lengthened and shortened position, respectively. The right is short weak and the left is long (stretch).  The obliques attach to the lower ribs 5-12 (for external) and ribs 10-12 (for the internals).

The psoas muscle takes its origin form the lumbar vertebral bodies and inserts on the lesser trochanter of the femur. Due to the poterior rotation of the right ilia, it has been lengthened over time (thus the difference in hip extension) and is stretch weak on the right.

So why only on the right and during running?

due to the anatomical leg length difference, the right oblique has shortened over time. Running (forced inspiration and expiration) causes us to use some of our accessory muscles of respiration (obliques, intercostals, serratus posterior superior and inferior, sternocleidomastoid, scalenes. Remember that for quiet respiration, only the diaphragm is used for inspiration; passive tension in muscles for expiration).

Also, the stride length will be increased on the longer leg side (ie when the L leg is in swing and R in stance); this put additional stretch on the R iliopsoas and R abdominal obliques.

iliopsoasthe

Treatment Plan: We placed a 3 mm lift in her left shoe. We treated with manipulative therapy of the lumbar spine.  She was given the nontripod, side bridge, cross/crawl quadruped and hip flexor stretch with side bending exercises to perform on a daily basis.  She felt better post treatment.

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Case of the Week: Rib Pain while Running: Part 1

This 39 year old woman presents with with rib pain, pointing to right ribs. First time it “went out” 1 ½ year ago, second time a year ago and recently two weeks ago. It is usually related to running with pain the day of and day after it is acute; it hurts to lie on her back or roll onto that side or breathe deep. She seems to do best when she is semiflexed on her knees.  Stretching can take the edge off.  When she has an acute episode, it usually lasts about a day.

She is very physically active and works out almost everyday. She runs triathlons and Ironman’s (or Ironwoman’s in this case), and generally is in good shape.

Above is what you see physically (hover mouse over each picture) and here are her exam findings:

She is 5’ and weighs approx. 105 pounds. BP 100/72 left, pulse ox 94, pulse 52. Lungs auscultate clearly, normal heart sounds, abdomen non tender and normal to percussion and auscultation.

Viewed from posterior in a standing position, she had increased tibial varum bi-lat., right greater than left, right hip had posterior rotation, less space between iliac crest and rib margin right hand side. No tenderness noted over the obliques or lower ribs left hand side. She had a loss of lateral bending to the left L2 through L4 negative theta-z stress.

She has a L  left short leg (tibial) 5 mm, bi-lat. external tibial torsion left greater than right. There is weakness of the abdominal internal and external obliques bi-lat. as well as iliopsoas, R > L. There was point tenderness at the R lesser trochanter; active and passive hip extensoin was 10 degrees right, 15 degrees left.

Question: What is your assessment and what are you going to do?

a. do not know, go have a beer

b. do not know, go have 2 beers

c. do not know, do not drink beer, have a double latte after reading Fridays post and try not to spill it

d. reply to this post,  think about it and check back later to see what The Gait Guys have to say

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Injury and Repair?

It appears injury and repair are the yin and yang of healing. Injury may be necessary for nerve regeneration to occur, at least in mice. Talk about neural learning! So injuries (from a neurological perspective) may be a good thing!  Perhaps this is why acupuncture, dry needling and intramuscular therapy work so well for these conditions. ( Watch for a Live Gait Guys course in dry needling and intramuscular stimulation this fall in Chicago and Denver!)    
A protein abbreviated DLK (which stands for dual leucine zipper kinase) apparently is necessary to activate nerve regeneration after an injury.    
“DLK is a key molecule linking an injury to the nerve’s response to that injury, allowing the nerve to regenerate,” says Aaron DiAntonio, MD, PhD, professor of developmental biology. “How does an injured nerve know that it is injured? How does it take that information and turn on a regenerative program and regrow connections? And why does only the peripheral nervous system respond this way, while the central nervous system does not? We think DLK is part of the answer.”    
Most injuries have a neurological component, whether it be the inflammatory process, a change in muscle tone or activity, the perception of pain or proprioceptive abnormality. If this mechanism is not triggered, the nervous system may not heal. This may provide clues as to why nerve injuries heal so slowly or are less responsive. Learning more about this protein may provide clues and answers to this commonly encountered dilemma.    
The original paper was published in Neuron and a nice summary can be found here.    
The Gait Guys: sorting out the literature and giving you the latest information so you can make more informed clinical decisions.