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.
An extensive literature search of electronic databases was conducted including AMED,
CINAHL, MEDLINE, OVID, SPORTDiscus, and Scopus.
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.
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.
Copyright © 2010 Elsevier Inc. All rights reserved.