The 4 Factors of Heel Rise.

These SHOULD all happen to have appropriate heel rise and forward progression

1. active contraction of the posterior compartment of the calf

2. passive tension in the posterior compartment of the calf

3. knee flexion and anterior translation of the tibia ankle rocker

4. the windlass mechanism

a problem with any one of these (or more collectively) can effect heel rise, usually causing premature heel rise.

ask yourself:

• Do you think the posterior compartment is actively contracting? not enough or too much? Remember the medial gastrocnemius adducts the heel at the end of terminal stance to assist in supination. Don't forget about the tibialis posterior as well as the flexor digitorum longs and flexor hallucinate longus.

• Does there appear to be increased passive tension in the posterior compartment? How visible and prominent are their calf muscles?

• Do they have forward progression of the body mass?

• How is his windlass mechanism? Good but not good enough.

Dr Ivo Waerlop. One of The Gait Guys…

#gait, #gaitanalysis, #continuingeducation, #limp, #casestudy, #gaitparameters, #heelrise, #prematureheelrise, #windlassmechanism

What do you know about the Ia Afferents?

This is a nice study looking at lateral gastroc activity and changing firing patterns with speed of movement. Great if you treat anyone or anything that walks...

Ia afferents

You remember them, large diameter afferent (sensory) fibers coming from muscle spindles and appraising the nervous system of vital information like length and rate of change of length of muscle fibers, so we can be coordinated. They act like volume controls for muscle sensitivity. Turn them up and the muscle becomes more sensitive to ANY input, especially stretch (so they become touchy…maybe like you get if you are hungry and tired and someone asks you to do something); turn them down and they become less or unresponsive.

Their excitability is governed by the sum total (excitatory and inhibitory) of all neurons (like interneuron’s) acting on them (their cell bodies reside in the anterior horn of the spinal cord).

If we slow things down, the rate of change of length slows as well and excitability decreases, like we see in this study (3-6% slower). We also notice that the length of contraction increases; hmmm, why doesn’t it decrease?

Remember these folks are on a treadmill. The treadmill is constantly moving, opposite the direction of travel. With the foot on the ground, this provides a constant rate of change of length of the gastroc/soleus (ie, it is putting it through a slow stretch); so , once the muscle is activated, it contracts for a longer period of time because of the treadmill putting a slow stretch on the gastroc (and soleus).

This article also talks about people with upper motor neuron lesions. An important set of inhibitory neurons come from higher centers of the brain, in the motor cortex. These tend to attenuate the signals affecting the Ia afferents, and keep us stable. When we have an upper motor neuron lesion (like a brain lesion or stroke), we lose this “attenuation” and the stretch reflexes (and muscle tone) becomes much more active (actually hyperactive), making the muscle more sensitive to stretch. This loss of attenuation, along with differing firing patterns of the gastroc are important to remember in gait rehab.

The soleus and medial gastroc begin firing in the first 10% of the gait cycle (at the beginning of loading response) and fire continuously until pre swing (peaking just after midstance). The lateral head begins firing at midstance; both heads (along with soleus) decelerate the forward momentum of the tibia, flex the knee at midstance, and the medial head assists in adducting the calcaneus to assist in supination.

Making sure these muscles fire appropriately is important and needling is just one way of helping them to function better. Don’t overlook the tricep surae on your next patient that has a “hitch in their giddyup”.

Effects of treadmill walking speed on lateral gastrocnemius muscle firing.

by Edward A Clancy, Kevin D Cairns, Patrick O Riley, Melvin Meister, D Casey Kerrigan

American journal of physical medicine rehabilitation Association of Academic Physiatrists (2004) Volume: 83, Issue: 7, Pages: 507-51 PubMed: 15213474

Abstract

OBJECTIVE: To study the electromyographic profile-including ON, OFF, and peak timing locations-of the lateral gastrocnemius muscle over a wide range of walking speeds (0.5-2.1 m/sec) in healthy young adults. DESIGN: We studied gastrocnemius muscle-firing patterns using an electromyographic surface electrode in 15 healthy subjects ambulating on a treadmill at their normal walking speed and at three paced walking speeds (0.5, 1.8, and 2.1 m/sec). Initial heel contact was determined from a force-sensitive switch secured to the skin over the calcaneous. RESULTS: For all speeds, the gastrocnemius firing pattern was characterized by a main peak, occurring 40-45% into the gait cycle, that increased in amplitude with walking speed. Speeds of > or =1.3 m/sec produced a common electromyographic timing profile, when the profile is expressed relative to the stride duration. However, at 0.5 m/sec (a speed typical of individuals with upper-motor neuron lesions), the onset of gastrocnemius firing was significantly delayed by 3-6% of the gait cycle and was prolonged by 8-11% of the gait cycle. CONCLUSION: Many patients with upper motor neuron lesions (e.g., stroke and traumatic brain injury) walk at speeds much slower than those commonly described in the literature for normal gait. At the slow walking speed of 0.5 m/sec, we have measured noticeable changes in the electromyographic timing profile of the gastrocnemius muscle. Given the importance of appropriate plantar flexor firing patterns to maximize walking efficiency, understanding the speed-related changes in gastrocnemius firing patterns may be essential to gait restoration.

Stretching out Plantar Fasciitis→

Neuromechanics Weekly: Look to the hammy’s???

“These findings show that while we always consider the tightness of the gastrocnemius/soleus complex and the subsequent restricted ankle motion from this equinus, we also need to consider the role of the hamstrings,” said Jonathan Labovitz, DPM, lead author and associate professor at Western University of Health Sciences, Pomona, CA.

this article from Lower Extremity Review, concludes “After controlling for covariates, participants (86 of 210 feet) with hamstring tightness were 8.7 times as likely to experience plantar fasciitis (p < .0001) as participants without hamstring tightness. Patients with a BMI >35 were 2.4 times as likely as those with a BMI <35 to have plantar fasciitis.”

The question is why?

They go on to say “ If you can’t get dorsiflexion at your talo-crural joint, this often drives dorsiflexion at other joints and that is going to cause collapse of the longitudinal arch of the foot, loading the plantar fascia with increased tensile stress.”

So, loss of ankle rocker leads to increased midfoot pronation, which loads the plantar fascia. That sounds pretty logical to us. We are sure you are thinking a loss of hip extension may do the same thing. Correct. Or you may say ” The calves may be tight so the medial gastroc can invert the rearfoot to correct for too much midfoot pronation and the foot can be supinated"…and you would be correct again.

So why are the tight hammys driving the bus? Or are they?

We remember the hams are a 2 joint muscle, and with the foot in a closed chain position (ie, on the ground); they flex the thigh on the lower leg and tilt the pelvis posteriorly (ie reduce the lordosis). They are FLEXORS which are active from late swing phase, just prior to heelstrike (initial contact) and a little nudge just prior to toe off (preswing) to help extend the thigh. 

The tricep surae are FLEXORS and are supposed to be active from loading response till almost pre swing, with a burst of activity at heel lift (terminal stance). 

So they take turns, and are not firing (normally) at the same time (or maybe have a small overlap). Going from heel strike to heel strike, the hammys fire 1st.

So IF the two are related, it could be a neurological sequencing issue. How often does that happen? The literature says (and there aren’t many studies) that you can change the order of recruitment of motor units ( the nerve and the muscle fibers it innervates), but not (usually) individual muscles. So probably not.

OK, how about plan B?

The hams and tricep surae are all flexors, correct? What is the innervation to the hamstrings and tricep surae? Hmm….Hamstrings, mostly tibial branch of the sciatic nerve, short head of biceps femoris is the common peroneal: L5-S2. How about the tricep surae? Tibial nerve, mostly S1-S2. I think I see a trend here. Common neurological overlap of FLEXOR muscles.

So are the hams driving the bus? Probably not, but neither are the gastroc/ soleus. The FLEXORS are driving the bus, and excitation of that common neuronal pool is probably causing the tightness

Ivo and Shawn….Uber footgeeks of the web. Dicing and slicing through the literature so you don’t have to.

Kicking gait?

And now… A question from a reader….

 Dr Allen- There are a few questions troubling me. The first one concerns the loss of the ankle rocker phase of gait which can have implications further up the kinetic chain. It concerns the interplay of gastroc and soleus. Is it possible for gastrocnemius to work as a knee extensor when the foot is in the closed chain position - especially if the bodies centre of mass has advanced in front of the knee joint ? Thanks - RB

Hi RB_____,

yes it is possible…….it is a retrograde movement as you have described.
it is not commonly seen, but can be, and usually manifests itself, in one of 2 ways.

Typically the client is more ligamentously lax than others……..and they tend to have a “kicking” type gait, where they thrust the leg out in front, like kicking a ball, with each step forward. This causes a heavy heel strike and locks the knee in preparation for midstance, and then follows your thinking. By the way, this client also seems to like standing in a hyperextended knee position at rest.

We remember that the gastroc soleus group begins to fire in the first 10% of stance phase (it is acting as a knee extensor here); to promote eccentric deceleration of the forward moving tibia, and continues to fire until terminal swing. It is believed the soleus provides much of the deceleration force and the gastroc assists in inverting the ankle at midstance and primarily flexes the knee at pre swing, just prior to toe off (Nordin, Frankel 2001). If the gastroc /soleus group fires prematurely, or excessively, particularly in prior to midstance, then we see the action you describe, and it manifests itself as premature heel rise and loss of ankle rocker.

A sudden hyperextesion at midstance or later, in a neurologically competent individual, is unlikely, as he force is too abrupt at this point and there is too much of a mechanical disadvantage.

We hope this helps explain things a bit. Please email us back if it doesn’t!

Uber Geeks, Shawn and Ivo