Quadriceps Arthrogenic Muscle Inhibition: Neural Mechanisms and Treatment Perspectives

• Published in: Seminars in arthritis and rheumatism Vol. 40; no. 3; pp. 250 - 266
• Main Authors: Rice, David Andrew, BHSc, McNair, Peter John, PhD
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01.12.2010; Elsevier
• Subjects: Adrenal Cortex Hormones - therapeutic use; Anti-Inflammatory Agents, Non-Steroidal - therapeutic use; Arthritis - complications; Arthritis - rehabilitation; arthrogenic; Biological and medical sciences; Cryotherapy; Diseases of the osteoarticular system; Electric Stimulation Therapy; Humans; Injuries of the limb. Injuries of the spine; Knee Injuries - complications; Knee Injuries - rehabilitation; Knee Injuries - surgery; knee trauma; Medical sciences; muscle inhibition; Muscle Weakness - physiopathology; Muscle Weakness - therapy; quadriceps; Quadriceps Muscle - innervation; Quadriceps Muscle - physiopathology; Rheumatology; Traumas. Diseases due to physical agents; voluntary activation; quadriceps; knee trauma; arthrogenic; voluntary activation; muscle inhibition; Knee; Treatment; Rheumatology; Quadriceps muscle; Activation; Trauma; Mechanism
• ISSN: 0049-0172; 1532-866X
• DOI: 10.1016/j.semarthrit.2009.10.001

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.