Purpose: To prop up for target practice 17 assumed dysfunctions in human movement.  Ideally, each “dysfunction” can be thoroughly critiqued to determine its relevance to ideal or painfree movement.

Why am I so critical?

I am critical of the strong.  There is no point in slamming ridiculous fitness guru’s or fish in the barrel weak-ass chiropractic/rehabilitation theories.  I want to critically evaluate the things that are closest to how I practice and those things that actually seem to dominate big swathes of evidence based practice.  I challenge the strong because the ideas should be able to take it.  If the “dysfunctions” in the post don’t hold up to scrutiny (and some don’t) then we are all the better for it.

Assessing function - the first step of corrective exercise

You can pick out a boatload of assumed dysfunctions.  You can use the FMS, you can use Kinetic Control, you could use Sahrmann’s tests, you can read Kendall and Kendall and test every muscle for strength, you can pull out your goniometer, fire up your 3D motion capture system and assess displacement, velocity, acceleration, summation of velocity across joints during a dynamic task, you can use an Ultrasound machine and determine some muscle thickness that seems aberrant,  you can steal my old EMG equipment (someone actually did this) and test muscle fatigue, muscle timing, muscle activation during functional tests or you can reincarnate Janda and put him to work. Whatever, its easy to find what someone in the world considers to be less than ideal function.  I’ve listed what I consider to be the most common ones that are regularly touted without any special equipment.

Assumed dysfunctions need to be examined in four areas

1. Their relationship to the occurrence of future injury (i.e. if you have one of these dysfunctions are you prone to getting injured in the future?)

2. Their relationship to performance.  If you have one of these assumed dysfunctions does it negatively influence objective performance variables (e.g. speed, power, force, running economy)

3. How do the existence of these dysfunctions relate to the person in pain? Are these dysfunctions defects or defenses? Is it necessary for the dysfunction to be corrected for a decrease in pain to occur? Does the dysfunction have to specifically addressed or is it “cleaned up” with other non-specific interventions?

4. If you think its relevant to correct these dysfunctions by what mechanism are they corrected if they can even be corrected

The most commonly reported “dysfunctions“:

1. Decreased ankle dorsiflexion: perhaps leading to increased pronation, knee valgus, hip IR and dysunction up the chain.  No one every says the decreased dorsiflexion encourages a more vertical tibia during the squat and therefore a greater reliance on the hip musculature and perhaps less knee loading.  Why not? It is just as plausible.

2. Decreased hip extension: perhaps  because of tight hip flexors due to our sedentary lifestyles or hip joint dysfunction

3. Weak gluteus maximus: perhaps causing hamstring, calf and spinal overload (this is often reported to be linked to tight hip flexors via some bastardized and probably wrong interpretation of reciprocal inhibition)

4. Increased pronation: either in terms of absolute amount or the time before pronation is reversed into supination.  We then tie this “dysfunction” into any kinetic chain abnormality we want

5. Altered timing or relative strength of the quadriceps muscle group

6. Tight hamstrings leading to spinal flexion

7. Tight hip flexors: perhaps leading anterior pelvic tilit and I have even heard the oppostie that it can lead to spinal flexion during a squat (this makes no mechancal sense but I hear it all time).

9.  Poor or inhibited activation of the deep trunk muscles with increases in the superficial global muscle’s activity (e.g a high threshold activity)

10.  Poor core strength, control or timing - this is diagnosed by any subtle movement of the spine away from neutral during any movement involving the lower limbs (e.g one leg glut bridge, single leg raise, prone leg extension, side lying hip abduction, side bridges, single leg squat)

11a. Poor pelvic control: perhaps manifesting as a Tredelenberg sign (pelvic drops to side during one leg activity) or as increased anterior tilt (perhaps secondary to weak gluts or tight hip flexors)

11b. Poor femoral control: perhaps manifested as increased knee valgus or increased hip internal rotation.  Rationale may be related to weak hip musculature, tight adductors, restricted ankle dorsiflexors, increased ROM of hip external rotators.

12. Poor breathing: you don’t breath through your belly, your diaghragm will suffer and you will lose core stability.  You might also see greater activity in the secondary muscles of respiration and neck and shoulder pain will result

13. Weak glutes leading to opposite arm movement dysfunction.  You will hear that during running the opposite arm might be abducted for balance or that the arm will be adducted to “cinch down” on the lumbodorsal fascia” to provide stability to the SI joint.

14. Poor scapular control- scapular dyskinesis, flying scapula, winging scapula, scapular malposition, medial border prominence, tight pectoralis minor.

15. Increased thoracic kyphosis or loss of thoracic extension or rotation leading to excessive strain on the lumbar spine, cervical spine or shoulder

16. Glenohumeral internal rotation deficit (GIRD) or loss of 180 degrees of shoulder rotation

17. Inhibited deep neck flexors leading to substitution by the scalenes and SCM

Alrighty, there are a bunch.  I won’t even get into joint arthrokinematics (i.e. stuck SI joint, upslips, loss of fibular head movement, thoracic ring dysfunctions etc).  These are some of the most common ones.  I hope to explore over the course of the year what we should do about these assumed dysfunctions.

Please leave any additions to the comment sections and I can even add them to the post.  Anyone up for writing a blog post about one of the specific dysfunctions.