One way compensations develop   
  We have all had injuries; some acute some chronic. Often times injuries result in damage to the joint or articulation;  when the ligament surrounding a joint becomes injured we call this a “sprain”.   
  Joints are blessed with four types of mechanoreceptors.  We have covered this in many other posts (see  here  and  here ).  These mechanoreceptors apprise the central nervous system of the position (proprioception or kinesthesis) of that body part or joint via the dorsal column system or spinocerebellar tracts. Damage to these receptors can result in a mismatch or inaccuracy of information to the central nervous system (CNS). This can often result in further injury or a new compensation pattern.   
  Joints have another protective mechanism called arthrogenic inhibition (see diagram above). This protective reflex turns off the muscles which cross the joint. This was described in a few great paper by Iles and Stokes in the late 80’s an early 90’s (vide infra). Not only are the muscles inhibited, but it can also lead to muscle wasting; there does not need to be pain and a small joint effusion can cause the reflex to occur.   
  If the muscles are inhibited and cannot provide appropriate afferent (sensory) and efferent (motor) information to the CNS, your brain makes other arrangements to have the movement occur, often recruiting muscles that may not be the best choice for the job. We call this a “compensation” or “compensation pattern”. An example would be that if the glute max is inhibited (a 2 joint muscle, with a larger attachment to the IT band and a smaller to the gluteal tuberosity; it is a hip extender, external rotator and adductor of the thigh), you may use your lumbar erectors (multi joint muscles; extensors and lateral rotators of the lumbar spine) or hamstrings (2 joint muscles; hip extenders, knee flexors, internal and external rotators of the thigh)  to extend the hip on that side, resulting in aberrant mechanics often observable in gait, which may manifest itself as a shortened step length, increased vertical displacement of the pelvis, lateral shift of the pelvis or increase in step height, just to name a few. Keep this up for a while and the new “pattern” becomes ingrained in the CNS and that becomes your  new default  for that motion.   
    Now to fix the problem, you not only need to reactivate the muscle, but you need to retrain the activity.   Alas, the importance of doing a thorough exam and thorough rehab to fix the problem.    
  Often times, the fix is much more involved than figuring out what the problem is (or was). Take your time and do a good job. Your clients and patients will appreciate it!  

Ivo and Shawn, the gait guys

   Young A ,  Stokes M ,  Iles JF  : Effects of joint pathology on muscle.  Clin Orthop Relat Res.  1987 Jun;(219):21-7  

   Iles JF ,  Stokes M ,  Young A .: Reflex actions of knee joint afferents during contraction of the human quadriceps.  Clin Physiol.  1990 Sep;10(5):489-500.  


  image from:  http://chiroeco.com/chiro-blog/results-to-referrals/2013/04/03/neurology-based-simplified-musculoskeletal-assessment/

One way compensations develop

We have all had injuries; some acute some chronic. Often times injuries result in damage to the joint or articulation;  when the ligament surrounding a joint becomes injured we call this a “sprain”. 

Joints are blessed with four types of mechanoreceptors.  We have covered this in many other posts (see here and here).  These mechanoreceptors apprise the central nervous system of the position (proprioception or kinesthesis) of that body part or joint via the dorsal column system or spinocerebellar tracts. Damage to these receptors can result in a mismatch or inaccuracy of information to the central nervous system (CNS). This can often result in further injury or a new compensation pattern. 

Joints have another protective mechanism called arthrogenic inhibition (see diagram above). This protective reflex turns off the muscles which cross the joint. This was described in a few great paper by Iles and Stokes in the late 80’s an early 90’s (vide infra). Not only are the muscles inhibited, but it can also lead to muscle wasting; there does not need to be pain and a small joint effusion can cause the reflex to occur. 

If the muscles are inhibited and cannot provide appropriate afferent (sensory) and efferent (motor) information to the CNS, your brain makes other arrangements to have the movement occur, often recruiting muscles that may not be the best choice for the job. We call this a “compensation” or “compensation pattern”. An example would be that if the glute max is inhibited (a 2 joint muscle, with a larger attachment to the IT band and a smaller to the gluteal tuberosity; it is a hip extender, external rotator and adductor of the thigh), you may use your lumbar erectors (multi joint muscles; extensors and lateral rotators of the lumbar spine) or hamstrings (2 joint muscles; hip extenders, knee flexors, internal and external rotators of the thigh)  to extend the hip on that side, resulting in aberrant mechanics often observable in gait, which may manifest itself as a shortened step length, increased vertical displacement of the pelvis, lateral shift of the pelvis or increase in step height, just to name a few. Keep this up for a while and the new “pattern” becomes ingrained in the CNS and that becomes your new default for that motion.

Now to fix the problem, you not only need to reactivate the muscle, but you need to retrain the activity. Alas, the importance of doing a thorough exam and thorough rehab to fix the problem.

Often times, the fix is much more involved than figuring out what the problem is (or was). Take your time and do a good job. Your clients and patients will appreciate it!

Ivo and Shawn, the gait guys

Young A, Stokes M, Iles JF : Effects of joint pathology on muscle. Clin Orthop Relat Res. 1987 Jun;(219):21-7

Iles JF, Stokes M, Young A.: Reflex actions of knee joint afferents during contraction of the human quadriceps. Clin Physiol. 1990 Sep;10(5):489-500.

image from: http://chiroeco.com/chiro-blog/results-to-referrals/2013/04/03/neurology-based-simplified-musculoskeletal-assessment/

Why does it feel so good to stretch?   
 We are sure you have read many articles, some written by us, about the good the bad and the ugly about stretching.    Regardless of how you slice the cake, we think we can all agree that stretching “feels” good. The question of course is “Why?” 
 Like it or not, it all boils down to neurology. Our good old friends, the Ia afferents are at least partially responsible, along with the tactile receptors, like Pacinian corpuscles, Merkel’s discs, Golgi tendon organs, probably all the joint mechanoreceptors and well as a few free nerve endings. We have some reviews we have written of these found   here  , and   here   and   her  e  . 
 What do all of these have in common? Besides being peripheral receptors. They all pass through the thalamus at some point (all sensation EXCEPT smell, pass through the thalamus) and the information all ends up somewhere in the cortex (parietal lobe to tell you where you are stretching, frontal lobe to help you to move things, insular lobe to tell you if it feels good, maybe the temporal lobe so you remember it, and hear all those great pops and noises and possibly the occipital lobe, so you can see what you are stretching. 
 The basic (VERY basic) pathways are:Peripheral receptor-peripheral nerve-spinal cord-brainstem-thalamus-cortex; we will call this the “conscious” pathway:  and peripheral receptor-peripheral nerve-spinal cord-brainstem-cerebellum- cortex; we will call this the “unconscious” pathway. 
 Of course, the two BASIC pathways cross paths and communicate with one another, so not only can you “feel” the stretch with the conscious pathway but also know “how much” you are stretching through the unconscious pathway. The emotional component is related through the insular lobe (with relays from the conscious and unconscious pathways along with collaterals from the temporal lobe to compare it with past stretching experiences) to the cingulate gyrus and limbic cortex,    where stretching is “truly appreciated”.  
 As we can see, there is an interplay between the different pathways and having “all systems go” for us to truly appreciate stretching from all perspectives; dysfunction in one system (due to a problem, compensation, injury, etc) can ruin the “stretching experience”.    
 Hopefully we have stretched your appreciation (and knowledge base) to understand more about the kinesthetic aspect of stretching. We are not telling you to stretch, or not to stretch, merely offering a reason as to why we seem to like it. 

  
   The Gait Guys

Why does it feel so good to stretch? 

We are sure you have read many articles, some written by us, about the good the bad and the ugly about stretching.  Regardless of how you slice the cake, we think we can all agree that stretching “feels” good. The question of course is “Why?”

Like it or not, it all boils down to neurology. Our good old friends, the Ia afferents are at least partially responsible, along with the tactile receptors, like Pacinian corpuscles, Merkel’s discs, Golgi tendon organs, probably all the joint mechanoreceptors and well as a few free nerve endings. We have some reviews we have written of these found here, and here and here.

What do all of these have in common? Besides being peripheral receptors. They all pass through the thalamus at some point (all sensation EXCEPT smell, pass through the thalamus) and the information all ends up somewhere in the cortex (parietal lobe to tell you where you are stretching, frontal lobe to help you to move things, insular lobe to tell you if it feels good, maybe the temporal lobe so you remember it, and hear all those great pops and noises and possibly the occipital lobe, so you can see what you are stretching.

The basic (VERY basic) pathways are:Peripheral receptor-peripheral nerve-spinal cord-brainstem-thalamus-cortex; we will call this the “conscious” pathway:  and peripheral receptor-peripheral nerve-spinal cord-brainstem-cerebellum- cortex; we will call this the “unconscious” pathway.

Of course, the two BASIC pathways cross paths and communicate with one another, so not only can you “feel” the stretch with the conscious pathway but also know “how much” you are stretching through the unconscious pathway. The emotional component is related through the insular lobe (with relays from the conscious and unconscious pathways along with collaterals from the temporal lobe to compare it with past stretching experiences) to the cingulate gyrus and limbic cortex,  where stretching is “truly appreciated”. 

As we can see, there is an interplay between the different pathways and having “all systems go” for us to truly appreciate stretching from all perspectives; dysfunction in one system (due to a problem, compensation, injury, etc) can ruin the “stretching experience”. 

Hopefully we have stretched your appreciation (and knowledge base) to understand more about the kinesthetic aspect of stretching. We are not telling you to stretch, or not to stretch, merely offering a reason as to why we seem to like it.

The Gait Guys

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On the subject of manual muscle work…There is more to it than meets the eye….

Following with our last few posts, here is an article that may seem verbose, but has interesting implications for practitioners who do manual muscle work with their clients. We would invite you to work your way through the entire article, a little at a time, to fully grasp it’s implications.

Plowing through the neurophysiology, here is a synopsis for you:

Tactile and muscle afferent (or sensory) information travels into the dorsal (or posterior) part of the spinal cord called the “dorsal horn”. This “dorsal horn” is divided into 4 layers; 2 superficial and 2 deep. The superficial layers get their info from the A delta and C fibers (cold, warm, light touch and pain) and the deeper layers get their info from the A alpha and A beta fibers (ie: joint, skin and muscle mechanoreceptors).

So what you may say.

The superficial layers are involved with pain and tissue damage modulation, both at the spinal cord level and from descending inhibition from the brain. The deeper layers are involved with apprising the central nervous system about information relating directly to movement (of the skin, joints and muscles).

Information in this deeper layer is much more specific that that entering the more superficial layers. This happens because of 3 reasons:

  1. there are more one to one connections of neurons (30% as opposed to 10%) with the information distributed to many pathways in the CNS, instead of just a dedicated few in the more superficial layers
  2. the connections in the deeper layers are largely unidirectional and 69% are inhibitory connections (ie they modulate output, rather than input)
  3. the connections in the deeper layers use both GABA and Glycine as neurotransmitters (Glycine is a more specific neurotransmitter).

Ok, this is getting long and complex, tell me something useful...

This supports that much of what we do when we do manual therapy on a patient or client is we stimulate inhibitory neurons or interneurons which can either (directly or indirectly)

  1. inhibit a muscle
  2. excite a muscle because we inhibited the inhibitory neuron or interneuron acting on it (you see, 2 negatives can be positive)

So, much of what we do is inhibit muscle function, even though the muscle may be testing stronger. Are we inhibiting the antagonist and thus strengthening the agonist? Are we removing the inhibition of the agonist by inhibiting the inhibitory action on it? Whichever it may be, keep in mind we are probably modulating inhibition, rather than creating excitation.

Semantics? Maybe…But we constantly talk about being specific for a fix, not just cover up the compensation. Is it easier to keep filling up the tire (facilitating) or patching the hole (inhibiting). It’s your call

The Gait Guys. Telling it like it is and shedding light on complex ideas, so you can be all you can be.

link: http://jn.physiology.org/content/99/3/1051

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. 

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More on Gait and Vision:  Along the lines of Binocular Parallax….

Yesterdays post talked about vision and parallax. Today’s explores some adaptations we have to poor visual quality. (Note 3 pictures today, toggle amongst them.)

In the attached study, we see people with poorer vision quality had 3 particular gait parameters (although probably had many more parameters) which changed with vision quality:

1. shorter step length

2. less trunk flexion

3. earlier heel contact with the ground (which goes along with shorter step length.)

If we think about what we know about the nervous system, this all makes sense. There are 3 systems that keep us upright in the gravitational plane: vision, the vestibular system and the proprioceptive system. If we remove one of the systems, the other 2 become enhanced (or better said, they had better become enhanced).

In this study they took away (or impaired) vision. This left the vestibular and proprioceptive systems to take over. The vestibular system affects position of the HEAD ONLY and measures linear and angular acceleration.  It makes sense to say that a more upright posture would do wonders for the stability of the system. The semicircular canals found in the inner ear measure angular motion, or rotation. Placing the body upright shifts the position of the semicircular canals in a different posture (particularly the LATERAL semicircular canal, which sits at 30 degrees to the horizontal; ) and places the utricle and saccule (which measure tilt and linear acceleration) in a better position to appreciate these. Translation, correct upright posture and neutral head positioning are critical for their contribution to detecting and maintaining balance and spacial stability.

The study also suggests that earlier heel contact in gait creates an “exploration” of the ground. This is quite important because the foot has so much cortical representation (see bottom picture) and is important for proprioception owing to its 31 articulations LOADED with joint mechanoreceptors, not to mention 4 LAYERS of muscles, LOADED with spindles and Golgi Tendon Organs.  The foot is a highly dense sensory receptor, the problem is we have had it hibernating in shoes for far too long. Imagine the advantage to balance, gait and posture we might have if we hadn’t dampened the mechano-sensory receptors for the better part of our lives. 

So, bringing this all full circle with the study; If you have poor vision, you had better make up for it with good upright posture and a sensory system that is unimpaired.  Most of us could have better posture and could use some retraining of foot function and sensory reception. Blind people generally have good postural and environmental awareness. They are not slouched over leading their gait head first while wearing oven mits on their hands and rigid steel-toed work boots. They take advantage of these systems and optimize them.

Sometimes the simple answers are not as simple as we like, but it is nice to know there is a reason.

The Gait Guys….Providing both simple answers to complex problems and complex answers to apparently simple ones.

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Study: Low vision affects dynamic stability of gait

Gait Posture. 2010 Oct;32(4):547-51. Low vision affects dynamic stability of gait. Hallemans A, Ortibus E, Meire F, Aerts P. Source

Research group of Functional Morphology, Department of Biology, University of Antwerp, Belgium. ann.hallemans@ua.ac.be

Abstract

The objective of this study was to demonstrate specific differences in gait patterns between those with and without a visual impairment… .  Adults with a visual impairment walked with a shorter stride length (1.14 ± 0.21m), less trunk flexion (4.55 ± 5.14°) and an earlier plantar foot contact at heel strike (1.83 ± 3.49°) than sighted individuals (1.39 ± 0.08 m; 11.07 ± 4.01°; 5.10 ± 3.53°). When sighted individuals were blindfolded (no vision condition) they showed similar gait adaptations as well as a slower walking speed (0.84 ± 0.28 ms(-1)), a lower cadence (96.88 ± 13.71 steps min(-1)) and limited movements of the hip (38.24 ± 6.27°) and the ankle in the saggital plane (-5.60 ± 5.07°) compared to a full vision condition (1.27 ± 0.13 ms(-1); 110.55 ± 7.09 steps min(-1); 45.32 ± 4.57°; -16.51 ± .59°). Results showed that even in an uncluttered environment vision is important for locomotion control. The differences between those with and without a visual impairment, and between the full vision and no vision conditions, may reflect a more cautious walking strategy and adaptive changes employed to use the foot to probe the ground for haptic exploration.

homunculus photo courtesy of : http://joecicinelli.com/homunculus-training/

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And now, some light reading for a Saturday….

Review of knee proprioception and the relation to extremity function after an anterior cruciate ligament rupture.

J Orthop Sports Phys Ther. 2001 Oct;31(10):567-7

http://www.ncbi.nlm.nih.gov/pubmed/11665744

What the Gait Guys say about this article:

Aren’t you glad you have mechanoreceptors?

As we have discussed in other posts, proprioception is subserved by cutaneous receptors in the skin (pacinian corpuscles, Ruffini endings, etc.), joint mechanoreceptors (types I,II,III and IV) and muscle spindles (nuclear bag and nuclear chain fibers) . It is both conscious and unconscious and travels in two  main pathways in the nervous system.

Conscious proprioception (awareness of where a joint or body part is in space or action) arises from the peripheral mechanoreceptors in the skin and joints and travels in the dorsal column system (an ascending spinal cord information highway) to ultimately end in the thalamus of the brain, where the information is relayed to the cerebral cortex.

Unconscious proprioception arises from joint mechanoreceptors and muscle spindles and travels in the spino-cerebellar pathways to end in the midline vermis and flocculonodular lobes of the cerebellum.

Conscious proprioceptive information is relayed to other areas of the cortex and the cerebellum. Unconscious proprioceptive information is relayed from the cerebellum to the red nucleus to the thalamus and back to the cortex, to get integrated with the conscious proprioceptive information. This information is then sent down the spinal cord to effect a response in the periphery. As you can see, there is a constant feed back loop between the proprioceptors, the cerebellum and the cerebral cortex. This is what allow us to be balanced and coordinated in our movements and actions.

The ACL is blessed with type I, II and IV mechanoreceptors (Knee Surgery, Sports Traumatology, Arthroscopy Volume 9, Number 6)   We remember that type I mechanoreceptors exist in the periphery of a joint capsule (or in this case, the periphery of the ACL) and are largely tonic in function (ie: they fire all the time) and type II are located deeper in the joint (or deeper in the ACL) and are largely phasic (ie they fire with movement). Type IV mechanoreceptors are largely pain receptors and anyone who has injured his knee can tell you all about them.

The article does a great job reviewing the importance of proprioception and how it relates to knee function and concludes A higher physiological sensitivity to detecting a passive joint motion closer to full extension has been found both experimentally and clinically, which may protect the joint due to the close proximity to the limit of joint motion. Proprioception has been found to have a relation to subjective knee function, and patients with symptomatic ACL deficiency seem to have larger deficits than asymptomatic individuals.”  Bottom line, never quit on the rehab and training of an ACL deficient knee until the absolute best outcome has unequivocally been achieved with certainty that no further improvement can be achieved…… absolute certainty.  Too many stop shy of certainty, and your brain will know it.  And it will show it in small gait, running and athletic skills.

Yup, this is some heavy stuff, but hey…you’re reading it, right?  If we didn’t explain it in detail you might not believe that WE are The Gait Guys ……. more than just foot and shoe guys. After all, there is a brain attached to the other end calling the shots.

Sorting it out so you don’t have to…We remain…The Gait Guys