The Homunculus Group

We all see patients with joint injuries. We know that the joint capsules are blessed with four types of mechanoreceptors, aptly named Type I, II, III, and IV, which when stimulated physically, chemically, or thermally apprise the nervous system of the forces acting on that joint as well as its position in space.

Joint pathology or inflammation will often cause distention of its capsule. The effect of the resulting joint effusion on the actions of the muscles crossing that joint have been examined extensively in the literature. We will look at one of the studies and its implications.

Reflex Actions of Knee Joint Afferents During Contraction of the Human Quadriceps
Iles JF, Stokes M, Young A: Clinical Physiology (10) 1990: 489-500

In this paper, the authors infuse hypotonic saline into the knees of eight asymptomatic individuals (including one of the authors) using a 16 gauge needle (ouch!) and studied its effects on the H reflexes and muscle recruitment. An H reflex is like performing a tendon jerk reflex (the involuntary contraction you would check with a neurological hammer) using an electrical stimulus. The onset time (also called the latency) and its amplitude are recorded. Muscle recruitment is the voluntary contraction of that muscle, measured with electromyography (EMG) by having an electrode either over (surface EMG) or within (needle EMG) the muscle and examining how hard the muscle is working based on the amplitude and frequency of the response.

First of all, no one in the study experienced any pain, only the sensation of pressure in their knees (which was considered activation of only the proprioceptors of the joint). The authors found that any pressure increase within the joint capsule depressed the H reflex and inhibited the action of the quadriceps. They hypothesize that this may contribute to pathological weakness after joint injury.

So how does all this apply to us?

As we all know, lots of patients have joint dysfunction. According to the Kirkaldy-Willis model, this leads to facet joint irritation, which leads to joint effusion. This will inhibit the small intrinsic muscles which cross the joint (remember the multifidus?) as well as the long extrinsic muscles. This causes the patient to become unable to stabilize their spine (through muscular action) under an applied load (not to mention their lack of coordination from aberrant proprioception, like we discussed last time). Next the stress is transferred to the connective tissue structures surrounding the joint which, if the force is sufficient, will fail. Now we have a sprain and some of the protective reflexes may take over. Abnormal forces can now be translated to the cartilage and disc. This can perpetuate degeneration, which causes further joint dysfunction. The cycle repeats and if someone doesn’t intervene and control the effects of inflammation, restore normal joint motion and rehabilitate the surrounding musculature, the patient’s condition will continue its downward spiral, becoming another statistic contributing to the tremendous economic and physical costs of back pain.

All this from joint effusion. Arthrogenic inhibition is yet another way that muscles can test weak.Food for thought on your next patient.