Importance of Attenuating Quadriceps Activation Deficits After Total Knee Arthroplasty

Abbey C. Thomas; Jennifer E. Stevens-Lapsley, M.P.T., Ph.D.

Disclosures

Exerc Sport Sci Rev. 2012;40(2):95-101. 

In This Article

Central Activation Deficits

Origins

The neurophysiologic mechanisms underlying CAD are not understood fully, although CAD at least in part may be due to altered afferent feedback after joint damage. Altered afference may lead to reduced quadriceps alpha motoneuron excitability, ultimately decreasing volitional force output. Cortical pathways also may contribute to reduced alpha motoneuron excitability, although how these pathways are involved is not well understood.

In addition to joint damage, the presence of joint effusion and pain may contribute further to CAD.[29] Pain-free, experimental knee joint effusions with as little as 20–30 mL of saline have been shown to produce quadriceps CAD.[29] The presence of joint effusion may activate several gating mechanisms within the central nervous system, including both presynaptic and postsynaptic inhibition, ultimately reducing excitatory input to the muscles surrounding the effused joint. Furthermore, the presence of joint effusion may activate Ruffini endings, which contribute to the regulation of muscle tone and movement by their influence on the Golgi tendon organ to regulate joint stiffness and stability.[9] Then, Ruffini endings may activate inhibitory interneurons, thereby reducing alpha motoneuron excitability. Experimental muscle pain also has been found to reduce voluntary muscle activation because of central mechanisms.[13] Inhibition of spinal neurons receiving nociceptive, afferent inflow through descending pathways is well established in feline experiments and may be a potential source of quadriceps CAD with OA and early after TKA. Although these investigations do not completely explain the underlying neurophysiologic mechanisms for CAD, collectively, they do suggest the involvement of a central mechanism in regulating the excitability of the motoneuron pool responsible for CAD.

Assessment Techniques

Quadriceps CAD are measured by superimposing percutaneous electrical stimuli on a maximal voluntary isometric contraction. There are two common methods by which CAD are assessed. The burst superimposition technique uses a train of electrical stimuli superimposed on a maximal voluntary muscle contraction (Fig. 1A). In the presence of CAD, an increase in torque is observed when the train of stimuli is delivered. A common alternative is the interpolation technique. This technique involves the superimposition of an electrical stimulus, most commonly a single pulse, both at rest and during a maximal voluntary contraction. In the presence of CAD, an increase in torque is observed when the stimulus is delivered. With the interpolation technique, the increased torque is normalized to the torque produced when the stimulus is delivered to the muscle at rest to account for differences in tissue impedance (Fig. 1B).

Figure 1.

Schematic of how central activation deficits (CAD) are calculated. A. Using the burst superimposition technique, CAD are determined by the equation: (a/b)*100. B. Using the interpolation technique, CAD are determined by the equation (1− (c/d))*100. The arrows indicate delivery of the electrical stimulus.

Comments

3090D553-9492-4563-8681-AD288FA52ACE
Comments on Medscape are moderated and should be professional in tone and on topic. You must declare any conflicts of interest related to your comments and responses. Please see our Commenting Guide for further information. We reserve the right to remove posts at our sole discretion.
Post as:

processing....