Here’s to You, Monsignor Tardieu: Guinea Pig, House Cat, and Equinus Contracture

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By Phil Stevens MEd, CPO

When faced with the question of how long you need to stretch a muscle on a daily basis to prevent the development of a contracture, orthotists will give you an interesting collection of responses. Most of these attempt to address the question without actually providing an answer. "As much as possible" and "How long has your doctor recommended?" are two common favorites. However, in my experience, a few venturesome therapists and practitioners have committed to times ranging from six to ten hours. So, where does that magic number come from?

A good deal of what we know about muscle contracture comes from the dedicated work of a French physician, Catherine Tardieu, and his colleagues. To study the topic, we will peruse our way through some preliminary studies in which a number of guinea pigs and house cats gave their all.

The first study was published in 1972 and involved the evaluation of soleus muscle bellies harvested from several groups of cats after several weeks in serial casts1. Cats were assigned to one of five experimental groups. The first acted as a control group with no intervention. The second group had one of their hind limbs immobilized in complete dorsiflexion, such that the soleus muscle was kept in its maximally lengthened position. The hind limbs of a third group were immobilized in complete plantarflexion, with the soleus in its most shortened position. After four weeks of immobilization, the muscle bellies of the second and third groups were examined both physiologically and histologically.

The fourth and fifth groups also were immobilized in full plantarflexion for four weeks. However, upon the removal of the casts, those in the fourth group were allowed four weeks to recover without further interventions, and those in the fifth group were recast in an intermediate range of motion for an additional four weeks. At the conclusions of the second four-week periods, these muscle bellies also were examined.

For those who have a working knowledge of glutaraldehyde fixative and nitric acid baths, the details of the authors' methodology are available in the original publication. For most of us, it's the outcomes that we're interested in. What Tardieu's group found was that striated muscle is very adaptable tissue. More specifically, muscle is able to adjust its length by producing or removing sarcomeres. While lengthened, the dorsiflexed limbs produced 19 percent more sarcomeres in series. In contrast, the plantarflexed or shortened, muscle fibers lost 40 percent of the sarcomeres in series. The significance from a physiologic standpoint was the realization that muscle can ensure maximum functional overlap of actin and myosin filaments at varying lengths. More relevant to our practices was the fact that these significant physiologic changes occurred in a relatively short space of time.

Fortunately, the research found that muscle also was able to adjust its properties back to those of its original length relatively quickly. In the latter two groups, the sarcomere number returned to normal within four weeks of cast removal.

There was one more rather interesting finding. Researchers found a greater abundance of connective tissue when dissecting out the fibers in the muscles that were immobilized in their shortened position. This increase in connective tissue correlated with a reduced extensibility in the same group. The authors speculated that this might be a type of defense mechanism to ensure that a shortened muscle cannot be overstretched to the point that there is no interdigitation of the actin and myosin filaments.

Quantifying Muscle Behavior

Fast-forward nine years to 1981. Having examined the cellular and molecular behavior of muscle when passively shortened, the same research team set out to observe what happens to muscle in the presence of prolonged active shortening (think neurologically induced muscle imbalance). This time around, the authors used guinea pigs to quantify the muscle behavior.2

To do so, they divided the animal subjects into three groups. All three underwent "stimulation" of the sciatic nerve for 12 hours to simulate a neurologic muscle imbalance. This was accomplished through a low-voltage electrical current to the distal sciatic nerve sufficient to obtain a clinically observable, sustained contraction of the soleus. The first group was passively maintained in plantarflexion during the stimulation period. The second group was identical to the first with the addition of a 36- to 48-hour recovery period. The final group also underwent a 12-hour stimulation period. However, in these animals the soleus was held in dorsiflexion throughout the stimulation, maintaining the soleus in a lengthened position.

Following the stimulation period the soleus muscles of groups one and three were analyzed and compared against those of the contralateral leg. Following their recovery period, the same procedures were carried out on the animals in group two. Again, for those who would like to know more about the delivery of square wave pulses of 0.3-msec duration and 20 Hz frequency through the Sachs Electrode, that information is outlined in detail in the original publication. For the rest of us, it is the results that are of interest.

Surprises Found

Clinically, the researchers observed that among those animals in group one, the majority developed significant equinus contractures. Remember, this is after only 12 hours of stimulated muscle contraction! A similar phenomenon was observed among the animals in group two immediately after the nerve stimulation. However, after the 36- to 48-hour recovery period, no significant differences were found between the stimulated and contralateral muscle groups. Of great clinical significance, in the third group, in which the animals were cast in dorsifexion throughout the stimulation of the soleus, there was no noticeable difference in ankle angle between the two sides. In other words, the structural changes in the muscle required both a stimulated contraction and an extreme shortening of the muscle. Furthermore, in the absence of the induced contraction, the muscle could stretch itself back out to its normal range.

When the muscles were examined histologically, there were even more surprises. As might be expected, in the animals in group one, there was a decrease in the number of sarcomeres in series. The authors had predicted this based on their earlier work. However, the rapidity of sarcomere loss was impressive. Within 12 hours the number of sarcomeres reduced by an average of almost 30 percent! Remember, the changes they observed in the first study were observed after four weeks of passive positioning. Thus contracting muscle is at a much greater risk for shortening than idle muscle. The clinical significance of this finding should be immediately apparent when the cerebral palsy population is considered.

So, 27 cats and 37 guinea pigs later, we've learned the following:

  1. Muscle adapts its molecular build-up in response to changes to length, both with respect to sarcomere number and connective tissue content in the case of shortening;
  2. Muscle that is shortened and contracting is at much greater risk for these changes;
  3. Muscle can restore itself to its previous length in the absence of abnormal contractions and external restrictions to motions; and
  4. Passive prevention of muscle shortening can prevent these structural changes, even in the presence of unopposed contraction.

Clinical Study

Realizing the clinical implications of these statements, it was only natural to seek their application in a treatment population. Seven years later, Tardieu's team did just that in their attempt to answer the question, "For how long must the soleus muscle be stretched each day to prevent contracture?3"

At the time of the publications, several treatment modalities had been proposed for the prevention of equinus contracture among children with cerebral palsy. These included serial castings, bracing, and aggressive stretching. Tardieu's group was careful to point out that they were not out to compare the various modalities, but to determine if there was a time threshold that needed to be met, regardless of how the stretching occurred.

To do so, the team identified ten children with cerebral palsy with "clinically observed, persistent, sustained contractions of the triceps surae." The first step in the process was to determine each child's passive range of motion. It sounds straightforward enough, but suffice it to say that great pains were encumbered to standardize how this was done. If the reader has any desire to see the testing apparatus utilized, he or she is referred to the original article. For our purposes, let's just say that Galileo would have been proud.

Each child was stretched until minimal torque or resistance was encountered, and this measurement (think R1) was recorded. Stretching continued until a maximal torque of 5 to 7 Nm was reached, and this measurement (think R2) also was recorded. The difference between the two was the range of passive soleus muscle stretch. This was assessed at the beginning and at the conclusion of an observation period averaging seven months.

In between these two assessments, a 24-hour period was selected for each child in which the researchers continuously monitored the sagittal angle of the ankle. Again, their methods were impressive, and beyond the scope of this review. However, the authors were clear to point out that the measurement equipment did not hinder eversion or inversion, produced "minimal disturbance to the children," and allowed them to wear their usual shoes and participate in their normal day-to-day activities. For each child, the equipment recorded the range of ankle motion experienced in the 24-hour period and the amount of time spent at each angle. The amount of time that the soleus was spent "in stretch" could be determined for each child by summing up the time spent at every dorsiflexion angle in excess of their respective "angle 1," or the angle at which initial resistance was encountered.

Unsurprisingly, over the course of the observation period, some children retained their available range of motion at the ankle, and lost range. However, among the four children who did not experience progressive soleus contracture, the mean soleus stretching time over the 24 hours was about six hours. In other words, these kids spend about six hours in relative dorsiflexion over the course of a given day. Among the six children who lost range in their soleus, the mean time spent in a dorsiflexion angle exceeding "angle 1" was just under two hours.

Now, there are a lot of limitations to this study. The demanding nature of the protocols restricted the number of kids that could be examined. While the observation period between measurements was an average of seven months, the children were only monitored over one 24-hour period which was assumed to be representative of normal life. Also, this evaluation was restricted to the soleus muscle only. However, at the present time, it's the best answer we have. How many hours do you have to stretch the soleus to prevent progressive contractures? According to this study, six hours.

Here's to you, Monsignor Tardieu.

Phil Stevens is the director of Clinical Education at SPOT-Specialized Prosthetic and Orthotic Technologies, in Salt Lake City, Utah. He can be reached at philmstevens@hotmail.com

References

  1. Tabary JC, Tabary C, Tardieu C, Tardieu G, Goldspink G. Physiologic and structural changes in the cat's soleus muscle due to immobilization at different lengths by plaster casts. J Physiol. 1972; 224: 231-244.

  2. Tabary JC, Tabary C, Tardieu C, Tardieu G, Goldspink G. Physiologic and structural changes in the cat's soleus muscle due to immobilization at different lengths by plaster casts. J Physiol. 1972; 224: 231-244.

  3. Tabary JC, Tardieu C, Tardieu G, Tabary C. Experimental rapid sarcomere loss with concomitant hypoextensibility. Muscle Nerve. 1981; 4:198-203.

  4. Tardieu C, Lespargot A, Tabary C, Bret MD. For how long must the soleus muscle be stretched to prevent contracture? Dev Med Child Neurol. 1988; 30:3-10.