A Serious Gait Problem: Pancompartmental Compromise of the Lower Leg.

“Pan” is a prefix (combining form) meaning all, entire, everything, everywhere 

This was a case we discussed during a more recent podcast, perhaps pod 63 or 64? This doctor had fallen asleep with the left leg dangling over the side of his bed. The issue was that the leg not only dangled over the mattress, but also over a wooded side bed frame, so there was a firm upward compression into the posterior/popliteal compartment. He awoke the next day with complete loss of function of the foot and ankle.  This video is 8 weeks after the compressive event and there has been a significant improvement in function, but there are still some deficits here.  Can you see them ?  We will show you come other video clips in a future blog post discussing some other components of his gait but lets get you familiar with the case today.

What you should see here:

1- Left heel shows a staggered drop. He cannot hold heel rise because of compromise to the posterior compartment strength (gastrocsoleus complex). This was a drastic improvement from his complete inability to heel rise at all at on his initial visit. You can easily see the fatiguability of the calf after just a few steps. 

2- There is a pathetic attempt at heel walking; gross function testing of the anterior compartment. What appears to be an attempt at just right heel walking is actually an attempt to do it on both sides, there is just still so much weakness in the left anterior compartment that you cannot even see his attempts to dorsiflex the foot/ankle or toes. But, what we do not show here is that he has non-weight bearing dorsiflexion now, which was completely absent for the first 6 weeks.  

Neuronal regeneration is possible. It takes time.  Depending on your referenced source the numbers vary. But in his case, in 8 weeks there is progressive improvements and he can say for certain that in the last 2 weeks they are exponential.  The time to restoration of neuronal function is said to be directly proportional to the measurable length of nerve damage.  

What is interesting in this case, is that there is anterior and posterior compartment neurologic compromise. This was a case of vascular and mechanical compression to the neurovascular bundle at the popliteal/knee level. 

Wallerian degeneration is a process that results when a nerve is severely damaged. The axon of the nerve which is separated from the neuron cell body degenerates distal to the injury. The part of the axon distal to the injury begins its degeneration within 24-36 hours of the lesioning event and is followed by myelin sheath degradation. Somewhere around 4 days from the time of the injury, the distal end of the portion of the nerve fiber proximal to the lesion begins sprouting in an attempt to regrow and fill the gap along the length of axonal damage. Sources vary, but many seem to indicate a 1mm per day reinnervation. 

More on this case next time, but the stage has been set.

Shawn and Ivo

This is a nice study looking at lateral gastroc activity and changing firing patterns with speed of movement. It also melds nicely with yesterdays Neuromechanics post…
Those darn Ia afferents….
You remember them, large diameter afferent (sens…

This is a nice study looking at lateral gastroc activity and changing firing patterns with speed of movement. It also melds nicely with yesterdays Neuromechanics post…

Those darn 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 leads (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.

We remain, inexplicably….The Gait Guys

 

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.