*Please note that the following content is solely a brief introduction to arhrogenic muscle inhibition for the purpose of promoting the clarification of chiropractic care.
Significant weakness has been found in healthy uninjured muscles which have shared innervation with an injured or dysfunctional joint which present with or without arthralgia (joint pain). Despite strengthening (rehabilitation) of the weak muscle, no significant improvements were shown. This is due to an ongoing inhibition that prevents the weak muscle from being fully activated in both symptomatic and asymptomatic individuals; a phenomenon known is arthrogenic muscle inhibition (AMI). To the contrary, mobilization and particularly joint manipulation of the dysfunctional joint has been shown to reduce the weak muscle significantly (see scientific support). Joint dysfunction can cause significant weakness of its associated muscle(s) even in the face of the dysfunctional joint not presenting with pain, and through AMI may have significant detrimental impact on the athlete or active individual.
Joint movement can reflexively cause activation or inhibition of the spinal segmentally innervated muscles through spinal reflex arcs known as the arthrokinetic reflex. Type I-III nerve endings are different types of mechanoreceptors which are found in the capsular tissue of a joint; their afferent activity can exert powerful tonic facilitatory (strengthening) and inhibitory (weakening) reflexogenic influences on the homonymous motor neuron pool excitability during postural control and voluntary activity. Thus, when the joint capsule is stretched during joint movement the joint mechanoreceptors will cause activation of the muscles which will reduce stretch on the joint capsular tissue (increase their activity) and cause inhibition of the muscles which will increase the joint capsular stretch (decrease their activity); for the purpose of protecting the joint congruency. The arthrokinetic reflex arc can perform its physiological function by affecting directly the homonymous α motor neuron’s excitability as well as by affecting the homonymous y motor neuron-muscle spindle loop. Any joint dysfunction which can affect its mechanoreceptors and cause alterations in its Aβ-fiber afferent discharge can impair the normal physiological functioning of its arthrokinetic reflex and produce abnormal patterns of spinal reflex arc activity, and lead to neurogenic inhibition and weakness of the homonymous muscles, namely AMI.
An increase in joint mechanoreceptor Aβ-fiber afferent discharge is strongly associated with AMI and it is postulated that joint afferent input has competing excitatory and inhibitory influences on the homonymous motor neuron pool; in a dysfunctional joint, the net effect can be inhibitory. An increased Aβ-fiber afferent input from joint mechanoreceptors can cause inhibition of the homonymous α motor neurons by synapsing on Ib internuncials in lamina VI an VII in the intermediate grey matter of the spinal cord via the joint Ib inhibitory di-synaptic reflex arc. The more recent medical literature has demonstrated that Ib internuncials also receive sensory input from large Aβ-fiber afferent of type I-III nerve endings in joint tissue through several independent spinal reflex arcs. The facilitated joint Ib inhibition can decrease the excitability of the homonymous motor neuron pool at multiple spinal levels and may cause gamma loop dysfunction. Any impaired transmission of Ia afferent signals from the muscle spindles to the homonymous α motor neuron is known as gamma loop dysfunction. Gamma loop dysfunction may contribute to AMI by causing presynaptic inhibition of the Ia afferent axons near their contact points with their homonymous α motor neurons, which may increase the activation threshold and / or cause neurotransmitter depletion of the Ia afferent terminal endings. The result is impaired α motor neuron functioning with subsequent weakness of the homonymous muscles.
It is important to note that a weak correlation has been found between pain and AMI; arhtrogenic muscle inhibition has been demonstrated in the absence of pain. Several studies have found that articular swelling can cause significant AMI even in the absence of pain, inflammation or structural damage of a joint, by infusing fluid into an undamaged joint. Direct recordings from articular nerves have shown that swelling can significantly increase the frequency of discharge and recruitment of both mechanoreceptors and nociceptors (pain receptors) joint afferent. Moderate levels of joint swelling rarely evoke pain, making it unlikely that swelling alone stimulates a significant number of joint nociceptors. An increase in Aβ-fiber afferent discharge from joints can solely occur in minor to moderate joint swelling, whereas nociceptors are more likely to be mechanically stimulated at higher intra-articular pressures or depolarized in the presence of inflammation. It has been demonstrated that as little as 10 ml of fluid infused into joints can cause notable muscle inhibition, whereas infusions of between 20 ml and 60 ml can cause maximum muscle inhibition. There is a close relationship between intra-articular pressure and the discharge of joint mechanoreceptor Aβ-fiber afferents. Articular swelling can increase the intra-articular pressure even at resting joint position; a joint effusion as small as 5 ml has been demonstrated to raise the intra-articular pressure above atmospheric pressure and induce AMI. Swelling has a strong inhibitory effect on the homonymous motor pool and even small, clinically undetectable joint effusions can cause significant AMI.