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It is a well-known phenomenon that muscle inhibition can occur due to changes in, or injury to, joint tissues.  Recently, I found two review articles that discuss this fact.  Furthermore, they delve deeper into the “why” as well as “how to treat” this type of muscle inhibition.  This is a topic that all involved in rehabilitation should all be aware of!

Arthrogenic muscle inhibition (AMI) is the term used to describe the disruption of neurological function following a musculoskeletal injury that interferes with a patient’s ability to fully engage (i.e. fully contract) their muscles during exercise.  The lack of ability to do so interferes with strength recovery.

AMI is hypothesized to be a protective mechanism, one that limits movement and force to safeguard the joint from further damage.  Simply put, failure to address AMI through the rehabilitative process can render even the most well-intentioned therapeutic exercise program ineffective.

To understand this phenomenon from a neurophysiological perspective, we must consider motor neuron behavior as muscle function is dependent on both the availability of motor neurons and the ability to voluntarily recruit them.

Figures 1 and 2 below present the most up to date paradigm that highlight the sequence of events leading up to AMI.

Figure 1

—Theoretical AMI paradigm. Joint injury triggers a cascade of neurological consequences that begin with deafferentation and altered afferent signaling (pain and swelling) and ultimately leads to decreased motor output to the muscles surrounding the injured joint. This cycle of AMI negatively influences clinical outcomes, leading to muscle weakness and biomechanical alterations, which can also contribute to further joint injury. AMI indicates arthrogenic muscle inhibition.

Citation: Journal of Sport Rehabilitation 31, 6; 10.1123/jsr.2020-0479

Figure 2

—Neurological diagram emphasizing the sequential and cumulative nature of AMI while also highlighting the complexity of neurological events that collectively contribute to muscle weakness, impaired proprioception, altered movement patterns, and other clinical impairments following joint injury. AMI indicates arthrogenic muscle inhibition. 

Citation: Journal of Sport Rehabilitation 31, 6; 10.1123/jsr.2020-0479

What does all of this mean?

Firstly, there is a joint injury.  Then,  likely due to changes in joint homeostasis secondary to any combination of tissue damage, joint laxity, effusion, pain, or inflammation,  there is a reduced ability to voluntarily contract muscles associated with that joint.  Some evidence suggests that there is LESS input from the damaged joint mechanoreceptors to the central nervous system (i.e. deafferentation), however experimental pain & inflammation models suggest that excessive neural input from overstimulation of nociceptors results in sensory overload. 

Persons with joint injury often present with fewer motor neurons in a muscle or muscle group available to recruit and a diminished ability to voluntarily recruit motor neurons.  (So, proportionally less muscle fibres react to recruitment stimuli, and the central nervous system is further compromised by failure to adequately signal for a full muscle fibre recruitment.  This phenomenon is reflexive in nature.   

The persistent muscular impairments are commonly reported at the time (human) patients are returning to unrestricted physical activity and for many years thereafter and may contribute to higher reinjury rates.  The proportion of motor neuron available to recruit appears to resolve over time.  However, central activation failure persists, and a decrease in the excitability of neuronal projections from the motor cortex to peripheral musculature develops during chronic phases of recovery.  

Furthermore, individuals recovering from joint injury demonstrate widespread differences in patterns of brain activity indicative of greater cognitive effort, attention, and visual reliance during simple motor tasks.  These findings suggest that persistent muscle inhibition may be influenced by neural plasticity within the brain, highlighting the need to consider supraspinal origins when treating muscle inhibition.

It is therefore apparent that traditional rehabilitation approaches may fail to resolve the underlying pathophysiology of muscle dysfunction.

Stay tuned for part two, where evidence-based interventions for AMI are discussed.

References:

Lepley AS, Lepley LK. Mechanisms of Arthrogenic Muscle Inhibition. J Sport Rehabil. 2021 Sep 1;31(6):707-716. doi: 10.1123/jsr.2020-0479. PMID: 34470911.

Norte G, Rush J, Sherman D. Arthrogenic Muscle Inhibition: Best Evidence, Mechanisms, and Theory for Treating the Unseen in Clinical Rehabilitation. J Sport Rehabil. 2021 Dec 9;31(6):717-735. doi: 10.1123/jsr.2021-0139. PMID: 34883466.