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January/February 2003


A Joint Dilemma

By Christopher D. Ingersoll, PhD, ATC, FACSM; Riann M. Palmieri, MS, ATC; and J. Ty Hopkins, PhD, ATC


Christopher D. Ingersoll, PhD, ATC, FACSM

Jane sustained an injury to her anterior cruciate ligament (ACL). There are four noticeable symptoms. First, there is increased anterior tibial translation (she has laxity). Second, she has intraarticular swelling. Third, she is experiencing pain. Finally, she has lost some ability to contract her quadriceps.

Surgery can resolve the laxity. Compression and elevation can resolve the swelling. Cryotherapy and medication can resolve the pain. Her ability to contract her quadriceps may eventually resolve with time, aided by active exercise.

Is the time course for recovery of muscle function adequate? Until recovery of strength, Jane is susceptible to all of the negative effects of inactivity on various tissues (see Table 1). Should rehabilitative efforts include attempts to restore muscle function more quickly?

Jane did not injure her quadriceps, yet her ability to contract them is inhibited. This is called arthrogenic muscle inhibition (AMI), more specifically defined as a presynaptic, ongoing reflex inhibition of musculature surrounding a joint following distension or damage to structures of that joint.1


Table 1. Secondary effects of arthrogenic muscle inhibition.

Removal of arthrogenic muscle inhibition is not generally a stated goal of rehabilitation. Why? First, it is often considered to be unalterable or is assumed to resolve itself (which it may or may not with time). Second, we do not understand it well enough to formulate effective rehabilitative strategies to remove it. Third, we are concerned that if we remove AMI, a response thought to protect the joint from further injury, we might put patients at risk for reinjury.

So, we are faced with a dilemma: remove inhibition early, diminish the negative effects of inactivity, and risk reinjury due to the patient’s enhanced ability to move the injured joint; or allow AMI to occur, reduce the likelihood of reinjury, and tolerate the secondary conditions caused by inactivity.

The cost of therapeutic interventions needed to resolve conditions caused by AMI is unknown. However, these costs could be minimized if AMI were resolved early in rehabilitation.

We believe the benefits of removing AMI can be realized while protecting patients from reinjury (ie, we can maximize the benefits while minimizing the risks). To do this, we need techniques to remove or minimize AMI while patients are supervised by qualified health care professionals, but still allow AMI to return when patients leave our care. Or we need techniques that remove AMI along with appliances to protect the joint from further injury (eg, braces).

WHAT IS AMI?

AMI is a natural response designed to protect the joint from further damage. Muscle inhibition reduces and discourages use of a damaged joint. AMI has been demonstrated in a knee effusion model2-7 and in injured subjects.8-10 We typically consider arthrogenic muscle inhibition to accompany acute injuries, but it may be present with chronic or long-term conditions as well.

In some cases, the response may be an arthrogenic muscle response (rather than inhibition). In the ankle, for example, we see facilitation of the leg muscles in response to an experimental effusion.11,12 This, too, is likely a protective mechanism. Shunting of the leg muscles may help protect the ankle from further injury. Without other means of protecting a joint, AMI is the body’s method of choice to protect injured extremities. However, it protects the joint at a cost, which must be dealt with throughout the rehabilitation process. AMI is caused by activity from many different joint receptors, which act on inhibitory interneurons synapsing on the motoneuron (MN) pool of joint musculature.13,14 The information from inhibitory interneurons impedes recruitment within the MN pool, decreasing the force of any contraction originating from that MN pool. Free nerve endings and specialized nociceptors may play a role in inhibition, but the primary effect seems to be a result of mechanoreceptor activity.15-18

A patterned response of joint musculature mediated through interneuronal activity following injury may then cause adaptations in movement to allow for function. Mechanoreceptor activity will continue to alter muscle activity surrounding the joint, and to compound the problem, the patient will replace normal muscle patterning with an adapted functional motor program.

Ongoing inhibition of a muscle, with its concomitant decrease in physical activity, can have numerous long-term effects on a number of tissues in the body. In muscle, we may see type I fiber atrophy, decreased cross-sectional area, and decreased oxidative enzyme activity. Periosteal and subperiosteal resorption, decreased strength and stiffness, and diminished load to failure and energy storage capacity may occur in bone. Ligaments may lose tensile strength, experience decreased load to failure, become more elongated, and be less stiff. Negative neural factors include depolarized muscle fiber membrane, decreased potential at motor end plates, and reduced Na+ - K+ transport across membranes. Removal of muscle inhibition, along with maintained activity levels, could eliminate or reduce these negative effects.

HOW CAN AMI BE MEASURED?

AMI is simply a reduction in MN pool recruitment. This may be considered indirectly by any measurement that takes into account changes in recruitment. It may include voluntary motor unit recruitment as measured by a dynamometer or through electromyography (EMG). It might also include involuntary measures of MN recruitment through controlled stimulation of sensory fibers and evaluation of the reflexive twitch contraction (eg, Hoffmann reflex, recurrent inhibition, paired reflex depression). It may also be measured combining a voluntary contraction with a superimposed electrical impulse (eg, interpolated twitch techniques). Each method has advantages and disadvantages, and each provides valuable information.

Changes in maximal voluntary contraction (MVC) are a final outcome of neuromuscular alterations following joint injury. However, it can be difficult to reproduce an MVC, and an MVC usually consists of contraction of several muscles. Surface EMG allows for examination of individual muscles, but it is often a difficult measurement to control during a functional exercise. The Hoffmann reflex (H-reflex) is an indirect assessment of the motoneuron pool, and it requires no voluntary effort. This could be an advantage when voluntary movement is painful or contraindicated. The H-reflex relies on controlled stimulation of sensory fibers within a mixed nerve, and evaluation of the reflexive twitch contraction. Variations in the stimulation pattern allow for indirect analysis of other factors that may affect the motoneuron pool. While the H-reflex is a very useful tool, it does not take into consideration supraspinal inputs that may affect the motoneuron pool during voluntary exercise.

HOW CAN AMI BE REMOVED?

Simply put, AMI can be eliminated or diminished by removing, masking, overriding, or otherwise altering inhibitory interneuron activity. The question is: how can this be done?

Often we try to override AMI by stimulating the efferent fibers of the peripheral nervous system (PNS) through electrical muscular stimulation. However, we believe the answer lies with what we can do to the sensory portion of the PNS. Anything that may alter, slow, or compete with mechanoreceptor feedback may be a candidate.

Cryotherapy not only decreases general nerve conduction velocity, synaptic transmission, muscle spasm, and pain, but it has a definite slowing and eventual blocking effect on sensory nerve fibers. The relationship appears to be linear; the cooler the nerve becomes, the slower the impulse is carried.19 An increase in action potential time results in a decreased peak to peak amplitude of depolarization at the interneuron, which could possibly result in decreased firing of the inhibitory interneuron, resulting in increased voluntary activation of the MN pool.

Transcutaneous electrical nerve stimulation (TENS) is another appealing intervention that could reduce AMI. While TENS is indicated mostly as a pain intervention,20,21 it stimulates cutaneous type I nerve endings, which could compete for the same type I afferent fibers that carry information from joint receptors to the spinal cord. This makes it a viable candidate for the treatment of AMI. Arvidsson and Eriksson20 reported a small increase in voluntary activation of the quadriceps following TENS treatment in ACL reconstruction and meniscectomy patients. This could be a result of decreased pain, competition for type I afferent pathways, or some other explanation not yet understood. Iles reported that stimulation of cutaneous nerve branches and the sural nerve reduced presynaptic inhibition of the soleus.22

Our data suggest that cryotherapy and TENS disinhibit the quadriceps MN pool following joint effusion.3 Further, cryotherapy facilitated the resting MN pool above baseline measures during cooling and during the 30-minute postcooling phase. TENS treatment resulted in disinhibition during the treatment, but inhibition was evident post-treatment.

While these treatment interventions show promise as a means to reduce AMI, other modalities or programs should be evaluated. Ideally, we will identify an intervention that will prevent the negative effects of AMI in the rehabilitation setting, while allowing the protective effects of AMI to limit activity.

WHAT ARE THE ADVANTAGES OF REMOVING AMI?

Aside from eliminating or reducing the secondary effects of AMI, there are several benefits to removing it. First, the cost and time of rehabilitation can be reduced. Once healing occurs, the patient should be nearly ready to return to their previous lifestyle. Without removing or reducing AMI, rehabilitation may essentially begin after healing occurs. Further, costs associated with lost time can be reduced. We might also reduce long-term consequences associated with AMI, including susceptibility for further or other injury. A goal would not necessarily be to return an injured patient to activity faster, only to allow a return when healing is complete without neuromuscular deficiencies.

Christopher D. Ingersoll, PhD, ATC, FACSM, is director, Graduate Programs, and Riann M. Palmieri, MS, ATC, is a doctoral student, in Sports Medicine/Athletic Training, University of Virginia, Charlottesville. J. Ty Hopkins, PhD, ATC, is assistant professor, Illinois State University, Normal.

REFERENCES
  1. Hopkins JT, Ingersoll CD. Arthrogenic muscle inhibition: a limiting factor in knee joint rehabilitation. J Sport Rehabil. 2000;9:135-159.
  2. Baxendale RH, Ferrell WR, Wood L. Knee joint distension and quadriceps maximal voluntary contraction in man. J Physiol. 1985;367:100P.
  3. Hopkins JT, Ingersoll CD, Edwards JE, Klootwyk TE. Cryotherapy and TENS decrease arthrogenic muscle inhibition of the vastus medialis following knee joint effusion. J Athl Train. 2001;37:25-31.
  4. Hopkins JT, Ingersoll CD, Krause BA, Edwards JE, Cordova ML. Effect of knee joint effusion on quadriceps and soleus motoneuron pool excitability. Med Sci Sports Exerc. 2001;33:123-126.
  5. Iles JF, Stokes M, Young A. Reflex actions of knee joint afferents during contraction of the human quadriceps. Clin Physiol. 1990;10:489-500.
  6. Spencer JD, Hayes KC, Alexander IJ. Knee joint effusion and quadriceps reflex inhibition in man. Arch Phys Rehabil. 1984;65:171-177.
  7. Wood L, Ferrell WR, Baxendale RH. Pressures in normal and acutely distended human knee joints and effects on quadriceps maximal voluntary contractions. Q J Exp Physiol. 1988;73:305-314.
  8. Huber A, Suter E, Herzog W. Inhibition of the quadriceps muscles in elite male volleyball players. J Sports Sci. 1998;16:281-289.
  9. Hurley MV, Newham DJ. The influence of arthrogenous muscle inhibition on quadriceps rehabilitation of patients with early, unilateral osteoarthritic knees. British J Rheum. 1993;32:127-131.
  10. Suter E, Herzog W, Bray RC. Quadriceps inhibition following arthroscopy in patients with anterior knee pain. Clin Biomech. 1998;13:314-319.
  11. Palmieri RM, Ingersoll CD, Hoffman MA, et al. Arthrogenic muscle response following artificial ankle joint effusion. J Athl Train. 2002;37:S-25.
  12. Petrik J, Amendola A, Rampersand R, et al. Effects of isolated ankle effusion on H-reflex amplitude, viscoelasticity, and postural control of the ankle [Abstract]. American Orthopaedic Society for Sports Medicine. 1996:63.
  13. Latash M. Neurophysiological Basis of Movement. Champaign, Ill: Human Kinetics; 1998:267.
  14. Leonard CT. The Neuroscience of Human Movement. St Louis: Mosby; 1998:252.
  15. Stokes M, Young A. The contribution of reflex inhibition to arthrogenous muscle weakness. Clin Sci. 1984;67:7-14.
  16. Stokes M, Shakespeare D, Sherman K, Young A. Transcutaneous nerve stimulation and post-meniscectomy quadriceps inhibition. Int J Rehabil Res. 1985;8:248.
  17. Leroux A, Belanger M, Boucher JP. Pain effect on monosynaptic and polysynaptic reflex inhibition. Arch Phys Med Rehabil. 1995;76:576-582.
  18. Young A. Current issues in arthrogenous inhibition. Ann Rheum Dis. 1993;52:829-834.
  19. Knight KL. Cryotherapy in Sport Injury Management. Champaign, Ill: Human Kinetics; 1995:301.
  20. Arvidsson I, Eriksson E. Postoperative TENS pain relief after knee surgery: objective evaluation. Orthopedics. 1986;9:1346-1351.
  21. Foster NE, Baxter F, Walsh DM, Baxter GD, Allen JM. Manipulation of transcutaneous electrical nerve stimulation variables has no effect on two models of experimental pain in humans. Clin J Pain. 1996;12:301-310.
  22. Iles JF. Evidence for cutaneous and corticospinal modulation of presynaptic inhibition of Ia afferents from the human lower limb. J Physiol. 1996;491:197-207.

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