Lower limb muscle strategies in low back pain patients.

When your client comes in with knee or foot/ankle issues do not dismiss the history of intermittent or exercise induced low back issues. It is possible that your client may be coming in with a loss of ankle rocker/dorsiflexion.  And, from your physical exam and screens, you may be at a loss as to why their ankle rocker is impaired. This problem further down the chain may simply be a compensation strategy to maintain function and postural integrity due to lumbar functional/fatigue challenges.

So you have sporadic low back pain and knee pain. Could they be linked ?

It has been a long believed rule that it is “all about the core”.  We have learned in recent years that this should be a very loosely accepted rule. 

In an old blog post (link) we stated some deeper truths:

Dr. McGill discusses the basic tenet that the hips and shoulders are used for power production and that the spine and core are used for creating stiffness and stability for the ultimate power transmission through the limb.  He makes it clear that if power is generated from the spine, it will suffer.  As gait experts, you should never forget this principle, if the spine and lumbopelvic interval is not strong/stiff and stable enough, the limbs can over power them and thus your gait, your running, your sport, could be causing you pain as the forces are poorly managed as they attempt to traverse the spine. 

Here we find a study referenced below that suggests that when the lumbopelvic interval is fatigued, that the lower limb muscles may step up activity.  This is a neat concept, not earth shaking by any means, but it nice to have studies that help solidify knowledge of compensation strategies.

“Individuals with low back pain (LBP) have been shown to demonstrate decreased quadriceps activation following lumbar paraspinal fatigue. The response of other lower extremity muscles is unknown. The purpose of this study was to determine changes in motoneuron pool excitability of the vastus medialis, fibularis longus, and soleus following lumbar paraspinal fatigue in individuals with and without a history of LBP.” 

What this study attempted to do was perform a controlled laboratory study designed to compare motoneuron pool excitability before and after a lumbar paraspinal fatiguing exercise. Twenty individuals (10 with history of low back pain) performed isometric lumbar paraspinal exercise until a 25% shift in paraspinal muscle surface electromyography median frequency occurred. 

What they discovered was that the soleus motoneuron pool excitability increased following lumbar paraspinal fatigue independent of group allocation and occurred in the absence of changes in vastus medialis or fibularis longus muscles. 

The authors propose that “increased soleus motoneuron pool excitability may be a postural response to preserve lower extremity function”.

When your client comes in with knee or foot/ankle issues do not dismiss the history of intermittent or exercise induced low back issues. They very well could be coming in with a loss of ankle rocker/dorsiflexion.  And, from your physical exam and screens, you may be at a loss as to why their ankle rocker is impaired.The problem further down the chain may simply be a compensation strategy to maintain function and postural integrity due to lumbar functional/fatigue challenges. 

Dr. Shawn Allen, one of the gait guys.

Reference:

J Electromyogr Kinesiol. 2011 Jun;21(3):466-70. doi: 10.1016/j.jelekin.2011.02.002. Epub 2011 Mar 8.Effects of paraspinal fatigue on lower extremity motoneuron excitability in individuals with a history of low back pain.Bunn EA1, Grindstaff TL, Hart JM, Hertel J, Ingersoll CD.

http://www.ncbi.nlm.nih.gov/pubmed/21388827

Ankle Plantarflexors as Gait compensators ?

We are always talking about compensations. We have worn out our statement “what you see in someone’s gait is not their problem, ti is their compensation stratetgy(s).”
Here is a study with an interesting thought.
Just remember, try to fix the underlying problems. But, realizing sometimes you cannot, especially in the elderly population, sometimes you have to give a strategy to help them even though it is not the solution you want. And remember also that driving the anterior compartment with appropriate exercises as our “shuffle walk” might stop any loss of ankle dorsiflexion that might be met with the extra calf work that this article seems to suggest.

From the study: “ Of particular importance were the compensatory mechanisms provided by the plantar flexors, which were shown to be able to compensate for many musculoskeletal deficits, including diminished muscle strength in the hip and knee flexors and extensors and increased hip joint stiffness. This importance was further highlighted when a normal walking pattern could not be achieved through compensatory action of other muscle groups when the uniarticular and biarticular plantar flexor strength was decreased as a group. Thus, rehabilitation or preventative exercise programs may consider focusing on increasing or maintaining plantar flexor strength, which appears critical to maintaining normal walking mechanics.”

Gait Posture. 2007 Mar;25(3):360-7. Epub 2006 May 23.
Compensatory strategies during normal walking in response to muscle weakness and increased hip joint stiffness.
Goldberg EJ1, Neptune RR.
http://www.ncbi.nlm.nih.gov/pubmed/16720095

Medial or lateral ankle swelling. Not a unicorn, but perhaps close. 

Photo: note the enlargement of the soft tissue in the left medial achilles area.

Many times over the last 5 years we have written about the concept that you have to know something exists to even make it a clinical consideration when trying to troubleshoot a clients pain or problem. Without knowing something even exists, you will move onto another diagnostic assumption and perhaps be treating the wrong problem.  This is a big problem in medicine because there is no way any of us knows everything. But this is why we all read, we study, we ask questions and we learn from our mistakes and depend on lateral and higher pay-grade referrals.  

Look at the photos above. Do you or your client have a posterior mass or swelling along side the achilles, medially or laterally ? Are you a rare bipedal mammal or do you have a lipoma, hemagioma or even sarcoma ?  Perhaps it is a swollen achilles ? Are there nodular densities in the achilles tendon proper that might suggest micro tears ? Are the regional busae swollen ? Those are all logical first steps, but maybe it is just a rarity, a more common unicorn of lower limb anomalies (10% incidence), the “accessory soleus”.

When an accessory soleus muscle is present a soft-tissue mass appears bulging medially between the distal part of the tibia and the Achilles tendon. This apparent “swelling”, may be entirely symptom free because it is merely an anatomic variant.  However, variants can become a problem when they impair stability or mobility or when they become irritated because of the same issues elsewhere.  This muscle has its own individual tendon slip onto the calcaneus anteromedial to the Achilles insertion.  This entity is not always painful or symptomatic but it can be expressive during exercise in some clients.  When they present clinically symptomatic one must rule out pathomechanics of the foot, ankle or lower kinetic chain.  The appearance of the assessory soleus is easily diagnostic on CT and MRI imaging. Some sources recommend fasciotomy or excision of the accessory muscle, clearly radical initial measures, but most of the time they can be quieted by resolving the pathomechanics that have allowed this previously quite clinical entity to become symptomatic. If the problem is just recently symptomatic, it is likely not the problem, rather the environment (workout changes, shoe changes, tissue length-tension relationship changes, mobility or stability changes etc) has changed and put a demand on the area and created once quiet tissues to complain.

First one must rule out the nasties, as we eluded to earlier (lipoma, hemagioma, synovial sarcoma etc) and then rule out the complainers (busae, tendonopathies etc) and then look at mobility and stability deficits/challenges. Once all of the more likely suspects have been ruled out, it is time for considering unicorns.

Here are some thoughts. On heel rise does the soft tissue mass become firm as in a muscular contraction would become firm ? After all, it is a soleus component and can act as an ankle plantarflexor of the ankle. Or it is merely firm on forced dorsiflexion because the achilles is drawn firm and tight against the posterior tibia thus medially displacing the soft tissue into a smaller more compacted area? Is the area painful on running ? Jumping? Starts and stops ? Only painful during rest, going up stairs, down stairs, only biking, swimming ? One can see that an understanding the mechanics of an area and how to challenge that area to your diagnostic advantage can help you tease out many of the considerations above.  In this day and age, we always have imaging to fall back on, but remember, imaging is a static picture in a moment of time in an unloaded unfunctional posturing. You will treat your client and their problem, not the imaging. If they in fact do turn out to have an accessory soleus that is inflamed on imaging, you still have to figure out why it has suddenly become cranky and painful. The bottom line is that many people with a painful accessory soleus are coming to you because something they have done, or are doing, or are  compensating around is causing a change in mechanics that is bothering the tissue.  This is where your knowledge of the kinetic chain and foot types, shoe types (see our National Shoe Fit program review here) and gait biomechanics can be invaluable.  Figuring out these issues should be your first line of intervention, and then confirmation on imaging can truly be valuable. 

The accessory soleus, is a more common entity in primates. Is this further proof we used to have tails and swing from trees ? Maybe not, but it is still fun to think about though. 

Shawn and Ivo, the gait guys

So what do we see here?

a limp on the left?
a short leg on the right?
a weak gluteus medius on the left?
a shortened step length on the right?
increased arm swing on the left?

watch the push off (terminal stance/pre swing) on the right and then the left. Note how the left is weaker?
now watch the heel strike. Notice how it is shorter when the right strikes the ground than the left?
did you note the pelvic shift to the left on L stance phase? How about the subtle increased knee flexion on the left?

This gentleman has an atrophied gastroc/soleus on the left from an injury. He compensates by increasing thigh flexion on the left to clear the leg. Because he has lost gastroc/soleus strength on the left (the lateral gastrocis an important inverter of the heel after midstance and important component of rearfoot supination), the rearfoot everts more. allowing more midfoot pronation. This collapse of the midfoot brings his weight more medially, so he shifts his pelvis laterally (to the left) to keep his center of gravity over the foot.

Fix?

  • Make client aware of what is going on.
  • make sure gastroc/soleus complex strength and function is maximized through muscle work, acupuncture, muscle activation, functional gait exercise

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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