Wednesday, August 7, 2013

The Lumbar Multifidus Muscle & Chronic Low Back Pain


It is well known that within the general population, 60-80% of individuals will experience an episode of low back pain (LBP) during their lifetime, with many experiencing more than one episode.

Spinal stabilization therapy has become very popular for treating LBP, and appears to be more effective over time than minimal intervention and exercise therapy alone. It has also been observed to reduce pain and disability associated with low back pain, as well as medication use and recurrence rates. Increasing our understanding of the mechanics of the low back - specifically with respect to the ability to stabilize the spinal "Neutral Zone" - was critical to the development of this exercise approach. From a rehabilitation and exercise perspective, our focus has shifted to strengthening and reactivating the stabilizing muscles of the spine, while encouraging proper motor control and "grooving" proper movement patterns. The lumbar mutifidus muscle(s) play a key role in stabilizing the spine. Therefore, neuromuscular training directed at 'neutral zone' stabilization is thought to impact these muscles and the outcome of LBP, disability, recurrence and prevention.

To quickly review, the "Neutral Zone", originally proposed by Panjabi, is defined as the part of the range of intervertebral motion, measured from the neutral position, in which spinal motion can occur with minimal non-muscular, passive resistance from spinal structures.

Lumbar multifidus muscles (LMM) are important stabilizers of this neutral zone, and dysfunction in these muscles is consistently associated with low back pain in existing studies. This dysfunction may be the result of reflexive inhibition from the spine leading to atrophic changes in the LMM musculature and fatty replacement that can be visualized on MRI.

This article discusses the role of LMM in recurrent (chronic) low back pain and reviews several literature-based approaches pertaining to the assessment and treatment of LMM dysfunction. The "Additional References" section below can serve as a resource for those interested in more information on this topic.

Multifidus Function:

Multifidus are important stabilizers of the lumbar region, and account for more than two-thirds of the stiffness in the spine when it is in the neutral position.

LMM is divided into deep in superficial fibers: the deep fibers span 2 segments and are tonically innervated; while superficial fibers span 3-5 levels and function physically. This anatomical architecture makes it suitable mechanically as well as anatomically for optimal stabilization.

Multifidus Atrophy and Low Back Pain:

The pathological process that involves the LMM and can accompany LBP closely includes LMM atrophy and replacement of this muscle with fat (this can also occur after low back surgery). This is typically classified as: none, slight and severe in imaging studies. Such changes have been demonstrated in adults with LBP, and do not appear to be correlated with Body Mass Index.

"Dorsal ramus syndrome" (low back pain with referred leg pain) produced by the irritation of structures supplied by the dorsal ramus (i.e. facet joints and LMM) might very well explain atrophic changes observed in the LMM after injury. In turn, abnormalities of the LMM might explain referred leg pain in the absence of other MRI abnormalities such as obvious disc or neural compromise.

Advanced imaging (MRI) of the lumbar multifidus can measure atrophy and fatty replacement with good inter-observer reliability.

Multifidus Atrophy and Reflexive Inhibition:

LMM is divided into five distinct myotomes, each innervated by a single spinal segment - medial branch of the dorsal ramus - which also innervates the zygapophyseal joints. The shared innervation suggests that nociceptive input from the facet joints could result in reflexive inhibition and subsequent atrophy of the LMM at the same level.

LMM atrophy seen in the human spine as a result of reflexive inhibition is caused by afferent feedback from the zygapophyseal joint. This in turn impedes the voluntary activation of the LMM. The inhibitory response might explain (at least in part) the efficacy of manual approaches such as manipulation and mobilization directed at the facet joints.

In animal models, rapid onset of LMM atrophy can occur within as little as three days after experimentally induced nerve root injury.

LMM atrophy tends to be local in studies comparing multifidus size and symmetry between chronic low back patients and healthy asymptomatic subjects.

LMM atrophy is typically associated with reduction in the ability to voluntary contract the muscles.

There is also evidence to suggest that those with LBP and LMM atrophy demonstrate a significantly decreased ability to perform isometric contractions of the multifidus muscle.

Clinical Application & Conclusions: Multifidus Atrophy - Treatment:

In one study a randomized group of patients were allocated into three programs: i) stabilization training, ii) stabilization training combined with dynamic resistance, and iii) stabilization training with dynamic-static resistance. CT scan was used to monitor LMM development over 10 weeks of training. Conclusions indicated that concentric and eccentric contraction phases were critical to induce LMM re-growth.

Exercise specifically designed to increase the ability to contract LMM improves functions and reduces LBP disability.

In general, the research supports the concept that the LMM are critical stabilizers for the lumbar spine neutral zone, and that atrophy in these muscles is strongly correlated with low back pain & dysfunction. It has been suggested that the atrophy perpetuates an inhibitory feedback loop that begins with pain in the spine and can be associated with additional areas sharing the same segmental innervations (i.e. from the dorsal rami of the spinal nerve), which would include the intervertebral disc and facet joints. The sequela to this is mostly likely reflexive inhibition of the multifidus and fatty replacement of that musculature, subsequent weakening of the area, and insidious dysfunction and pain.

It was noted that LMM atrophy can exist in the general population, including highly active and elite athletes. This may be one reason for the high recurrence of low back pain - particularly after traumatic episodes where LMM atrophic changes occur. This would further suggest that conditioning of the LMM is an integral part of low back function - not only from a rehabilitation perspective but also as a prophylactic or preventive measure for promoting general back health...as always, GET YOUR PATIENTS EXERCISING!

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