Knee Effusion and Neural Inhibition
Abstract & Commentary
Synopsis: Knee joint effusion has an inhibitory effect on the vastus medialis and a facilitatory effect on the soleus.
Source: Hopkins JT, et al. Effect of knee joint effusion on quadriceps and soleus motoneuron pool excitability. Med Sci Sports Exerc. 2001;33(1):123-126.
The effusion associated with knee joint injury results in muscle weakness, atrophy, and deficits in neuromuscular control. This study sought to create an experimental model in which the effect of knee effusion on motoneuron pool recruitment could be measured. For this purpose, the quadriceps and soleus Hoffman reflexes (H-reflex) were measured before and after the inducement of an artificial knee effusion.
The H-reflex was elicited by applying a percutaneous stimulus to the femoral nerve in the femoral triangle for the quadriceps and the tibial nerve in the popliteal fossa for the soleus. Surface electromyography over the belly of the medial soleus and vastus medialis (superomedial to the patella) measured the response to the percutaneous stimulation. Seven to 12 stimuli were delivered at 20-second intervals at varying intensities to find the maximum H-reflex. The H-reflex measurements were obtained before inducement of the effusion and at 30- 90- 150- and 210-minute intervals following the effusion.
For the knee effusion procedure, 2 mL of lidocaine was first injected for anesthetic purposes. Next, 30 mL of sterile saline was injected into the superolateral knee joint capsule. Effusion wave and ballotable patella tests confirmed the presence of an effusion within the knee joint.
Two, one-way repeated measures analysis of variance found that the soleus H-reflex increased and the quadriceps H-reflex decreased after the effusion. All posteffusion soleus and quadriceps measures were significantly higher and lower, respectively, in comparison to the preeffusion measures.
Comment by David H. Perrin, PhD, ATC
Most clinicians surmise that inhibition of the quadriceps causes strength loss, atrophy, and deficits in neuromuscular control, and that knee joint effusion is a likely precursor to this process. This and several other studies have demonstrated a quadriceps inhibition following effusion. This study further found that the inhibition lasts for at least 120 minutes following inducement of the artificial effusion.
Perhaps the most interesting findings were the increased activity in the soleus motoneuron pool, and the moderate inverse relationship between the soleus and vastus medialis H-reflexes after inducement of the knee effusion. Hopkins and colleagues postulated that facilitation of the soleus could be a compensatory mechanism in response to the inhibited quadriceps.
As with all research, this study’s design has some strengths and weaknesses. A strength is that the effects of effusion on neural inhibition could be measured in the absence of associated pain. The amount of the effusion could also be quantified. The weaknesses are that the composition of the effusion was saline and only the acute effect of an effusion was measured. In the injury model, swelling may consist of synovial fluid and blood, and the chronic effects of an effusion may have greater relevance to neuromuscular function in rehabilitation.
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