Does McKenzie’s derangement syndrome fit into a traditional patho-anatomical model? And if not, does it matter anyways?

With the derangement syndrome, we witness lasting changes in movement characteristics, strength, reflexes, and dural signs after the performance of directional preference movements. Mechanical and symptomatic responses to mechanical loading strategies, consistent with the operational definitions of McKenzie’s derangement syndrome, exist throughout the musculoskeletal system. The problem lies in providing a clear and consistent systemic or anatomical foundation to explain the phenomenon.

It is my proposal that the central nervous system may in fact provide the basis for McKenzie’s derangement syndrome, and may also provide yet another reason for MDT as a systems-based approach to musculoskeletal care.

Over the past 5 decades, a great deal of scientific research has been done on reflex inhibition. This is a neurophysiological feedback loop. One of the most common clinical scenarios is quadriceps reflex inhibition. A trauma or change in the movement characteristics of the knee (either by swelling, injury, or otherwise) elicits and/or disrupts afferent stimuli from nociceptors, proprioceptors, and mechanoreceptors. This afferent input travels to the central nervous system where it then contributes to an altered efferent output and impaired neuromuscular function of the quadriceps. We also know that neuronal plasticity exists in which the structure, function, and organization of neurons can be altered via this afferent input.

Reflex inhibition of the quadriceps will persist until the afferent stimuli are normalized.

This type of afferent-efferent feedback loop exists throughout the neuro-musculo-skeletal system. As computer scientists have noted, “Garbage In, Garbage Out”. Impaired afferent input (“garbage in”) will lead to impaired efferent output (“garbage out”).

The central nervous system will respond very readily to changes in afferent stimuli. Mechanical loading provides a significant influx of afferent stimuli. The tissues – muscular and nervous, connective and epithelial - will adapt to the imposed demands given an environment in which to do so over time.

Now, we have a rationale for the derangement syndrome and it’s treatment. Our lives are full of repeated movements and sustained postures. Can there be a disruption of afferent input to the central nervous system? Yes. This can occur in a variety of ways. Could this produce central sensitization over time? Absolutely.

The treatment goal then becomes one of normalizing afferent input to the central nervous system. Within the current paradigm, repeated movements and/or sustained postures – changes in mechanical loading – will normalize (or provide a barrage of normalized) afferent input to the central nervous system. This normalized afferent input would then immediately alter the potential for improved efferent output. Immediate lasting changes would be witnessed, including changes in strength and reflexes. These changes would occur far more rapidly than actual changes related to tissue repair and remodeling. If unresolved, or if impaired afferent input persists, the patient could then develop disuse atrophy, diminished EMG of various muscles, and tissue changes.

Take low back pain as an example. If the patient has a lumbar derangement, there is typically a directional preference. But what happens if the patient does not receive treatment addressing the directional preference? Impaired afferent input and reflex inhibition would persist. This inhibition could be reflected in decreased EMG function of the muscles that support the lumbar spine, along with long-term central sensitization. Neuromuscular inhibition could also explain why specific stabilization exercises have not proven to be any more effective in low back pain than other more general exercise programs. If there is a reflex inhibition present, all the strengthening in the world would not necessarily reduce it. This would be much like trying to strengthen the quadriceps without diminishing the reflex inhibition first.

A neurophysiological model would explain how any joint can derange without necessarily having some form of intra-articular pathology (i.e. meniscus, disc, etc). It also avoids the traditional use of a patho-anatomical, tissue-based model as such without altering the dynamics of the understanding of the behavior of the system itself (via repeated movements and sustained postures).

Neuromuscular inhibition (and facilitation) may in fact be the key to understanding McKenzie's derangement syndrome. With further research, we may find that McKenzie’s definition of derangement - “anatomical disruption or displacement within the motion segment” – may require adjustment. Perhaps we may find that the derangement is, more accurately, a “neurological disruption within the motion segment(s)”. But I digress.

To my knowledge, this is the first proposal of a neurologically-based foundation for McKenzie’s derangement syndrome that provides sound anatomical and physiological principles to explain the derangement (and the systems-based approach to care) for all regions of the musculoskeletal system.

Photo credits: pfly