On the subject of manual muscle work…

image credit: https://commons.wikimedia.org/wiki/File:Muscle_spindle_model.jpg

Here is an older 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)

• inhibit a muscle

• 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

Yan Lu Synaptic Wiring in the Deep Dorsal Horn. Focus on Local Circuit Connections Between Hamster Laminae III and IV Dorsal Horn Neurons J Neurophys Volume 99 Issue 3

March 2008 Pages 1051-1052 link: http://jn.physiology.org/content/99/3/1051

The Power of Facilitation: How to supercharge your run.

While running intervalsone morning, something dawned on me. My left knee was hurting from some patellar tracking issues, but only on initial contact and toe off. I generally run with a midfoot strike. I began concentrating on my feet, lifted and spread my toes and voila! my knee pain instantly improved. Very cool, and that is why I am writing this today. 

Without getting bogged down in the mire of quad/hamstring facilitation patterns, lets look at what happened.

I contracted the long extensors of the toes: the extensor digitorum longus and the extensor hallicus longus; the short extensors of my toes: the extensor digitorum brevis, the extensor hallucis brevis: as well as the dorsal interossei.the peroneus longus, brevis and tertius were probably involved as well.

Do you note a central theme here? They are all extensors. So what, you say. Hmmm… 

Lets think about this from a neurological perspective:

In the nervous system, we have 2 principles called convergence and divergence. Convergence is when many neurons synapse on one (or a group of fewer) neuron(s). It takes information and “simplifies” it, making information processing easier or more streamlined. Divergence is the opposite, where one(or a few) neurons synapse on a larger group. It takes information and makes it more complicated, or offers it more options.

In the spinal cord, motor neurons are arranged in sections or “pools” as we like to call them in the gray matter of the cord. These pools receive afferent information  and perform segmental processing (all the info coming in at that spinal cord segment) before the information travels up to higher centers (like the cerebellum and cortex). One of these pools fires the extensor muscles and another fires the flexor muscles.. 

If someone in the movie theater keeps kicking the back of our seat, after a while, you will say (or do) something to try and get them to stop. You have reached the threshold of your patience. Neurons also have a threshold for firing.  If they don’t reach threshold, they don’t fire; to them it is black and white. Stimuli applied to the neuron either takes them closer to or farther from threshold.  When a stimulus takes them closer to firing, we say they are “facilitating” the neuron. If it affects a “pool” of neurons, then that neuronal pool is facilitated. If that pool of neurons happens to fire extensor muscles, then that “extensor pool” is facilitated.

When I consciously fired my extensor muscles, two things happened: 1. Through divergence, I sent information from my brain (fewer neurons in the cortico spinal pathway) to the motor neuron pools of my extensor muscles (larger groups of motor neurons) facilitating them and bringing them closer to threshold for firing and 2. When my extensor muscles fired, they sent that information (via muscle spindles, golgi tendon organs, joint mechnoreceptors, etc) back to my cerebellum, brain stem and cortex (convergence) to monitor and modulate the response.

When I fired my extensor muscles, I facilitated ALL the neuronal pools of ALL the extensors of the foot and lower kinetic chain. This was enough to create balance between my flexors and extensors and normalize my knee mechanics.

If you have followed us for any amount of time, you know that it is often “all about the extensors” and this post exemplifies that fact.

 Next time you are running, have a consciousness of your extensors. Think about lifting and spreading our toes, or consciously not clenching them. Attempt to dorsiflex your ankles and engage your glutes. It just may make your knees feel better!

Is Turning off the Quads a good thing?

Especially in light of the Vastis lateralis acting as an internal rotator in closed chain? 

"Foam rolling of the quadriceps muscle is associated with decreased biceps femoris activation, an effect that may be related to pain perception, according to research from the Memorial University of Newfoundland in St. John’s, Canada.

In 18 recreationally active individuals (eight women), the investigators used surface electromyography to assess vastus lateralis, vastus medialis, and biceps femoris activation during a single-leg landing from a hurdle jump under four foam-rolling conditions: application to the hamstrings only, the quadriceps only, both, and neither.

Biceps femoris activation was significantly lower for the conditions in which foam rolling was applied to the quadriceps. However, the reverse was not true: Foam rolling of the hamstrings had no significant effect on activation of either of the quadriceps muscles.

The authors hypothesized that the perceived pain associated with quadriceps foam rolling, which was significantly greater than that associated with hamstrings foam rolling, may trigger the alteration in antagonist muscle function."

Cavanaugh MT, Aboodarda SJ, Hodgson D, Behm DG. Foam rolling of quadriceps decreases biceps femoris activation. J Strength Cond Res 2016 Sep 6. [Epub ahead of print]

Gaining Anterior Length, Through Posterior Strength. A Lesson in Reciprocal Inhibition

Gaining Anterior Length, Through Posterior Strength and vice versa….A Lesson in Reciprocal Inhibition

I found a really cool article, quite by accident. I was leafing through an older copy of one of, if not my favorite Journals “Lower Extremity Review” and there it was. An article entitled “Athletes with hip flexor tightness have reduced gluteus maximus activation”. Wow, I thought! Now there is a great article on reciprocal inhibition! This reminded me of a piece we wrote some time ago

What is reciprocal inhibition, also called “reciprocal innervation” you ask? The concept, was 1st observed as early as 1626 by Rene Descartes though observed in the 19th century, was not fully understood and accepted until it earned a Nobel prize for its creditor, Sir Charles Sherrington, in 1932.

Simply put, when a muscle contracts, its antagonist is neurologically inhibited (see the diagram above) When your hip flexors contract, your hip extensors are inhibited. This holds true whether you actively contract the muscle or if the muscle is irritated in some manner, causing contraction. The reflex has to do with muscle spindles and Type I and Type II afferents which I have covered in an article I wrote some time ago.

We can (and often do) take advantage of this concept with treating the bellies of hip flexors (iliopsoas, tensor fascia lata, rectus femoris, iliacus, iliocapsularis) and extensors (gluteus maximus, posterior fibers of gluteus medius). This is especially important in folks with low back pain, as they often have increased psoas activity and cross sectional area, especially in the presence of degenerative changes.

There also appears to be a correlation between decreased hip extension and low back pain, with a difference of as little as 10 degrees being significant. Take the time to do a thorough history and exam and pay attention to hip extension and ankle dorsiflexion as they should be the same, with at least 10 degrees seeming to be the “clinical” minimum. Since the psoas should only fire at the end of terminal stance/preswing and into early swing, problems begin to arise when it fires for longer periods.

Can you see now how taking advantage of reciprocal inhibition can improve your outcomes? Even something as simple as taping the gluteus can have a positive effect! Try this today or this week in the clinic, not only with your patients hip flexors, but with all muscle groups, always thinking about agonist/antagonist relationships.

In the moment: Sports medicine  Jordana Bieze Foster: Athletes with hip flexor tightness have reduced gluteus maximus activation  Lower Extremity review Vol 6, Number 7 2014

https://tmblr.co/ZrRYjx1VG3KYy

Mills M, Frank B, Blackburn T, et al. Effect of limited hip flexor length on gluteal activation during an overhead squat in female soccer players. J Athl Train 2014;49(3 Suppl):S-83.

Ciuffreda KJ, Stark L.  Descartes’ law of reciprocal innervation. Am J Optom Physiol Opt. 1975 Oct;52(10):663-73.
Jacobson M Foundations of Neuroscience Springer Science and Business Media, Plenum Press, NY 1993 p 277

http://www.nobelprize.org/nobel_prizes/medicine/laureates/1932/sherrington-bio.html

https://thegaitguys.tumblr.com/post/9708399904/ah-yes-the-ia-and-type-ii-afferents-one-of-our

Arbanas J, Pavlovic I, Marijancic V, et al MRI features of the psoas major muscle in patients with low back pain. Eur Spine J. 2013 Sep;22(9):1965-71. doi: 10.1007/s00586-013-2749-x. Epub 2013 Mar 31.

Roach SM, San Juan JG, Suprak DN, Lyda M, Bies AJ, Boydston CR. Passive hip range of motion is reduced in active subjects with chronic low back pain compared to controls. Int J Sports Phys Ther. 2015 Feb;10(1):13-20. Erratum in: Int J Sports Phys Ther. 2015 Aug;10(4):572.

Paatelma M Karvonen E Heiskanen J Clinical perspective: how do clinical test results differentiate chronic and subacute low back pain patients from “non‐patients”? J Man Manip Ther. 2009;17(1):11‐19.[PMC free article] [PubMed]

Evans K Refshauge KM Adams R Aliprandi L Predictors of low back pain in young adult golfers: a preliminary study. Phys Ther Sports. 2005;6:122‐130.

Mellin G Correlations of hip mobility with degree of back pain and lumbar spinal mobility in chronic low‐back pain patients. Spine. June 1988;13(6):668‐670. [PubMed]

Lewis CL, Ferris DP. Walking with Increased Ankle Pushoff Decreases Hip Muscle Moments. Journal of biomechanics. 2008;41(10):2082-2089. doi:10.1016/j.jbiomech.2008.05.013.

Nodehi-Moghadam A, Taghipour M, Goghatin Alibazi R, Baharlouei H. The comparison of spinal curves and hip and ankle range of motions between old and young persons. Medical Journal of the Islamic Republic of Iran. 2014;28:74.

Daniel Moon , MD, MS; Alberto Esquenazi , MD Instrumented Gait Analysis: A Tool in the Treatment of Spastic Gait Dysfunction JBJS Reviews, 2016 Jun; 4 (6): e1. http://dx.doi.org/10.2106/JBJS.RVW.15.00076

Kilbreath SL, Perkins S, Crosbie J, McConnell J. Gluteal taping improves hip extension during stance phase of walking following stroke. Aust J Physiother. 2006;52(1):53-6.

Taking advantage of the stretch reflex and reciprocal inhibition; or the “reverse stretch”

Reciprocal inhibition is a topic we have spoken about before on the blog (see here). The diagram above sums it up nicely. Note the direct connection from the spindle to the alpha motor neuron, which is via a Ia afferent fiber.  When the spindle is stretched, and the pathway is intact, the uscle will contract. What kind of stimulus affects the spindle? A simple “stretch” is all it takes. Remember spindles respond to changes in length. So what happens when you do a nice, slow stretch? You activate the spindle, which activates the alpha motor neuron. If you stretch long enough, you may fatigue the reflex. So why do we give folks long, slow stretches to perform? Certainly not to “relax” the muscle!

How can we “use” this reflex? How about to activate a weak or lengthened muscle? Good call.

Did you notice the other neuron in the picture? There is an axon collateral coming off the Ia afferent that goes to an inhibitory interneuron, which, in turn, inhibits the antagonist of what you just stretched or activated. So if you acitvate one muscle, you inhibit its antagonist, provided there are not too many other things acting on that inhibitory interneuron that may be inhibiting its activity. Yes, you can inhibit something that inhibits, which means you would essentially be exciting it. This is probably one of the many mechanisms that explain spasticity/hypertonicity

How can we use this? How about to inhibit a hypertonic muscle?

Lets take a common example: You have hypertonic hip flexors. You are reciprocally inhibiting your glute max. You stretch the hypertonic hip flexors, they become more hypertonic (but it feels so good, doesn’t it?) and subsequently inhibit the glute max more. Hmm. Not the clinical result you were hoping for?

How about this: you apply slow stretch to the glutes (ie “reverse stretch”) and apply pressure to the perimeter, both of which activate the spindle and make the glutes contract more. This causes the reciprocal inhibition of the hip flexors. Cool, eh? Now lightly contract the glutes while you are applying a slow stretch to them; even MORE slow stretch; even MORE activation. Double cool, eh?

Try this on yourself. Now go try it on your clients and patients. Teach others. Spread the word.

Reciprocal Inhibition anyone? Thanks to The Manual Therapist (Erson Religioso) for this great post.

What they are doing here is taking advantage of what Sherrington know many years ago. Activating a muscle (agonist for a movement) will inhibit the muscle with the opposite action (antagonist for a movement), through a disynaptic, post synaptic pathway. It is a great way to gain additional movement and remove or reduce muscular inhibition. Try it!

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/

Do you do manual muscle testing?

Following up on yesterdays post…

We all like to evaluate our patients; hopefully on the table as well as observation while weight bearing. Here is some food for thought.

When your patient or client is lying on the table, do you pay attention to where there head is in space (ie the position of their head)? Why should you care?

Remember our post on facilitation (if not, click here)? That has something to do with it.

Here is the short story. Make sure the head is neutral and midline (lined up between the shoulders), there is good preservation of the cervical curve , with a small pillow supporting the neck, but not altering it’s angle.

The long story involves the vestibular system. It is a part of the nervous system that lives between your ears (literally) and monitors position and velocity of movement of the head. There are three hula hoop type structures called “semicircular canals” (see picture above) that monitor rotational and tilt position and angular acceleration, as well as two other structures, the utricle and saccule, which monitor tilt and linear acceleration. I think you can see where this is going….

The vestibular apparatus (the canals and the utricle and saccule) feed into a part of the brain called the floccular nodular lobe of the cerebellum, which as we are sure you can imagine, have something to do with balance and coordination. This area of the cerebellum feeds back to the vestibular system (actually the vestibular nucleii); which then feed back up to the brain as well as (you guessed it) down the spinal cord and to predominantly the extensor muscles.

So, what do you think happens if we facilitate (or defaciltate) a neuronal pool? We alter outcomes and don’t see a clear picture.

Look at the picture above. Notice the lateral semicicular canals are 30 degrees to the horizontal? If you are lying flat, they are now at 60 degrees. If the head is resting on a pillow and flexed forward 30 degrees, the canals are vertical and rendered inoperable. This could be good (or bad) depending on what muscle groups you are testing.

OK. HEAVY CONCEPT APPROACHING

So if we defacilitate the extensors, what happens to the flexors? Remember reciprocal inhibition (If not click here)? According to the law of reciprocal innervation, the flexors will be MORE FACILITATED. If the extensors are faciltated, they will appear MORE ACTIVE and the flexors LESS ACTIVE.

Wow. All this from head position…The key herer is to know what you are doing, This gait stuff can get pretty complex; but don’t worry. We aren’t going anywhere and are here to teach you.

The Gait Guys . Gait Geeks are the new cool….

Functional Ankle Instability and the Peroneals 

Lots of links available here with today’s blog post. please make sure to take your time and check out each one (underlined below) 

As you remember, the peroneii (3 heads) are on the outside of the lower leg (in a nice, easy to remember order of longus, brevis and tertius, from top to bottom) and help to stabilize the lateral ankle. The peroneus brevis and tertius dorsiflex and evert the foot while the peroneus longus plantarflexes and everts the foot. We discuss the peroneii more in depth here in this post. It then is probably no surprise to you that people with ankle issues, probably have some degree of peroneal dysfunction. Over the years the literature has supported notable peroneal dysfunction following even a single inversion sprain event. 

Functional ankle instability (FAI) is defined as “ the subjective feeling of ankle instability or recurrent, symptomatic ankle sprains (or both) due to proprioceptive and neuromuscular deficits." 

Arthrogenic muscle inhibition (AMI) is a neurological phenomenon where the muscles crossing a joint become "inhibited”, sometimes due to effusion (swelling) of the joint (as seen here) and that may or may not be the case with the ankle (see here), or it could be due to nociceptive input altering spindle output or possibly higher centers causing the decreased muscle activity. 

This paper (see abstract below) merely exemplifies both the peroneals and FAI as well as AMI.

Take home message?

Keep the peroneals strong with lots of balance work!

The Gait Guys: bringing you the meat, without the filler!                                                                         

Am J Sports Med. 2009 May;37(5):982-8. doi: 10.1177/0363546508330147. Epub 2009 Mar 6.

Peroneal activation deficits in persons with functional ankle instability.

Palmieri-Smith RM, Hopkins JT, Brown TN.

Source

School of Kinesiology, University of Michigan, 401 Washtenaw Avenue, Ann Arbor, MI 48109, USA. riannp@umich.edu

Abstract

BACKGROUND:

Functional ankle instability (FAI) may be prevalent in as many as 40% of patients after acute lateral ankle sprain. Altered afference resulting from damaged mechanoreceptors after an ankle sprain may lead to reflex inhibition of surrounding joint musculature. This activation deficit, referred to as arthrogenic muscle inhibition (AMI), may be the underlying cause of FAI. Incomplete activation could prevent adequate control of the ankle joint, leading to repeated episodes of instability.

HYPOTHESIS:

Arthrogenic muscle inhibition is present in the peroneal musculature of functionally unstable ankles and is related to dynamic peroneal muscle activity.

STUDY DESIGN:

Cross-sectional study; Level of evidence, 3.

METHODS:

Twenty-one (18 female, 3 male) patients with unilateral FAI and 21 (18 female, 3 male) uninjured, matched controls participated in this study. Peroneal maximum H-reflexes and M-waves were recorded bilaterally to establish the presence or absence of AMI, while electromyography (EMG) recorded as patients underwent a sudden ankle inversion perturbation during walking was used to quantify dynamic activation. The H:M ratio and average EMG amplitudes were calculated and used in data analyses. Two-way analyses of variance were used to compare limbs and groups. A regression analysis was conducted to examine the association between the H:M ratio and the EMG amplitudes.

RESULTS:

The FAI patients had larger peroneal H:M ratios in their nonpathological ankle (0.399 +/- 0.185) than in their pathological ankle (0.323 +/- 0.161) (P = .036), while no differences were noted between the ankles of the controls (0.442 +/- 0.176 and 0.425 +/- 0.180). The FAI patients also exhibited lower EMG after inversion perturbation in their pathological ankle (1.7 +/- 1.3) than in their uninjured ankle (EMG, 3.3 +/- 3.1) (P < .001), while no differences between legs were noted for controls (P > .05). No significant relationship was found between the peroneal H:M ratio and peroneal EMG (P > .05).

CONCLUSION:

Arthrogenic muscle inhibition is present in the peroneal musculature of persons with FAI but is not related to dynamic muscle activation as measured by peroneal EMG amplitude. Reversing AMI may not assist in protecting the ankle from further episodes of instability; however dynamic muscle activation (as measured by peroneal EMG amplitude) should be restored to maximize ankle stabilization. Dynamic peroneal activity is impaired in functionally unstable ankles, which may contribute to recurrent joint instability and may leave the ankle vulnerable to injurious loads.

all material (except for the study); copyright 2013 The Gait Guys/ The Homunculus Group. All rights reserved. Please ask before you lift our stuff. If you are nice and give us credit, we will probably let you use it!