Muscle
Quadriceps Arthrogenic Muscle Inhibition: Neural Mechanisms and Treatment Perspectives

https://doi.org/10.1016/j.semarthrit.2009.10.001Get rights and content

Objectives

Arthritis, surgery, and traumatic injury of the knee joint are associated with long-lasting inability to fully activate the quadriceps muscle, a process known as arthrogenic muscle inhibition (AMI). The goal of this review is to provide a contemporary view of the neural mechanisms responsible for AMI as well as to highlight therapeutic interventions that may help clinicians overcome AMI.

Methods

An extensive literature search of electronic databases was conducted including AMED, CINAHL, MEDLINE, OVID, SPORTDiscus, and Scopus.

Results

While AMI is ubiquitous across knee joint pathologies, its severity may vary according to the degree of joint damage, time since injury, and knee joint angle. AMI is caused by a change in the discharge of articular sensory receptors due to factors such as swelling, inflammation, joint laxity, and damage to joint afferents. Spinal reflex pathways that likely contribute to AMI include the group I nonreciprocal (Ib) inhibitory pathway, the flexion reflex, and the gamma-loop. Preliminary evidence suggests that supraspinal pathways may also play an important role. Some of the most promising interventions to counter the effects of AMI include cryotherapy, transcutaneous electrical nerve stimulation, and neuromuscular electrical stimulation. Nonsteroidal anti-inflammatory drugs and intra-articular corticosteroids may also be effective when a strong inflammatory component is present with articular pathology.

Conclusions

AMI remains a significant barrier to effective rehabilitation in patients with arthritis and following knee injury and surgery. Gaining a better understanding of AMI's underlying mechanisms will allow the development of improved therapeutic strategies, enhancing the rehabilitation of patients with knee joint pathology.

Section snippets

Methods

To implement the review, an initial search of the literature was undertaken using a variety of sources including experimental papers, review papers, and conference proceedings, as well as a general internet search. From this initial search an extensive keyword list was developed (eg, quadriceps, knee extensors, muscle inhibition, voluntary activation, arthrogenic, arthrogenous, knee injury, knee trauma, OA, gonarthrosis, rheumatoid arthritis, knee surgery, joint receptors, articular receptors,

The Presentation of AMI

AMI occurs across a wide range of knee joint pathologies, with significant quadriceps activation deficits observed in patients with OA (11, 28, 29), rheumatoid arthritis (RA) (9), anterior knee pain (30), patella contusion (31), following anterior cruciate ligament (ACL) rupture (10, 32) and reconstruction (33), after meniscal damage (34) and menisectomy (35, 36), and in patients who have undergone knee joint arthroplasty (17, 37, 38).

AMI has been quantified using electromyography (EMG),

Discussion

AMI remains a significant barrier to effective rehabilitation in patients with arthritis and following knee injury and surgery. AMI contributes to quadriceps atrophy and prevents full activation of the muscle, playing a major role in the marked quadriceps weakness that is commonly observed in these patients. Moreover, AMI may delay or prevent effective quadriceps strengthening. This is particularly apparent in the first few months after trauma or in the case of extensive joint damage when AMI

Acknowledgments

The authors thank Dr Gwyn Lewis for helpful comments on an earlier version of the manuscript. Support from the Accident Compensation Corporation and Health Research Council of New Zealand is gratefully acknowledged.

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    Mr. Rice receives financial support from the Accident Compensation Corporation and Health Research Council of New Zealand in the form of a PhD Career Development Award.

    The authors have no conflicts of interests to disclose.

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