As we’ve explored The Brain over the last few weeks through the perspectives of different professionals, one concept has continued to find its way into my thoughts, raising new questions and potential implications for clinical practice.
So, of course, let’s explore some of the questions I’ve had about arthrogenic muscle inhibition (AMI) and see whether the research can point us towards some answers.
Let’s dive in.
Understanding Arthrogenic Muscle Inhibition
Arthrogenic muscle inhibition (AMI) is an involuntary neurological response to joint injury or pathology that reduces the nervous system’s ability to activate the muscles surrounding an affected joint.
Changes within the joint, including swelling, inflammation, pain and altered sensory feedback, can interfere with muscle activation through both spinal and higher nervous-system pathways (Rice and McNair, 2010).
Clinically, this means that the weakness and atrophy we see following joint injury or surgery may not be caused by disuse alone. The muscles may be capable of contracting, but the nervous system is limiting their activation.
Importantly, AMI can occur even in the absence of pain, and inhibition may persist long after the initial injury. This means that restoring joint function and muscle strength isn’t necessarily as simple as controlling pain and prescribing strengthening exercises.
And this raises an interesting question: What happens when we provide external stability to a joint whose surrounding muscles are being inhibited?
For a deeper exploration of AMI and its treatment, read our previous blog on the subject.
Joint Stabilization and the Effect on Muscle Activity
When it comes to braces and external joint support, we’re often cautioned that a brace may reduce the need for muscular support, potentially contributing to muscle atrophy and increased joint instability over time.
Now, I’m not contesting this advice, but I do want to ask: What else might be true?
During our preliminary interview with Ben Blecha from MediVet Products, we discussed a potentially very different scenario.
When a joint is injured, inflamed and swollen, AMI may occur. Let’s imagine that the joint is also unstable, as we might see following a CCL injury. As a protective response, the patient offloads the affected limb, reducing weight-bearing during locomotion.
We often attribute the rapid muscle atrophy that follows to disuse. But what if AMI is contributing too?
Joint instability may contribute to ongoing inflammation and effusion, potentially perpetuating muscle inhibition. As muscle activation decreases, weakness and atrophy develop, further compromising muscular support around the joint.
We could find ourselves in a downward spiral of instability, effusion, inhibition and weakness.
And importantly, pain control alone may not be enough to interrupt this cycle, because AMI can occur even in the absence of pain.
Now, what if we stabilise that joint with a brace?
Instead of the brace ‘taking over’ the work of the muscular system and allowing further atrophy, could it provide an opportunity to interrupt this downward spiral?
By improving joint stability, could we reduce some of the factors contributing to inhibition, creating an opportunity for better muscle activation and, ultimately, strengthening?
Ben also highlighted the importance of allowing muscles to work through controlled, functional ranges of motion. When joint instability results in excessive or uncontrolled movement, the surrounding musculature may struggle to provide effective support.
Could an orthosis help create a more mechanically favourable environment for muscle activation and strengthening?
Carpal hyperextension comes to mind as another example. External support may help limit excessive movement while allowing the muscles to function within a more controlled range, reducing mechanical demands and creating opportunities for strengthening.
Perhaps the goal isn’t simply to restrict movement, but to create an environment in which movement can occur more effectively.
But while this reasoning feels plausible, is there any research to support it?
Callaghan, Parkes and Felson (2016) investigated the effects of flexible knee bracing on quadriceps strength and AMI in people with patellofemoral osteoarthritis.
After six weeks, participants wearing a brace demonstrated significantly less AMI than those without a brace, without a significant between-group difference in muscle strength. By 12 weeks, the bracing group also demonstrated improvements in strength alongside reduced inhibition.
Although the study cannot tell us precisely why these changes occurred, or whether the same effects would be seen in veterinary patients, the findings challenge the assumption that external support necessarily reduces muscular function.
Conclusion
Perhaps the question isn’t simply whether a brace reduces the work a muscle needs to do, but whether it creates the conditions in which that muscle can work more effectively.
I’m looking forward to exploring this and many other concepts related to the nervous system this weekend at the Vet Rehab Summit.
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References
Rice DA, McNair PJ. Quadriceps arthrogenic muscle inhibition: neural mechanisms and treatment perspectives. Semin Arthritis Rheum. 2010 Dec;40(3):250-66. doi: 10.1016/j.semarthrit.2009.10.001. Epub 2009 Dec 2. PMID: 19954822.
Callaghan MJ, Parkes MJ, Felson DT. The Effect of Knee Braces on Quadriceps Strength and Inhibition in Subjects With Patellofemoral Osteoarthritis. J Orthop Sports Phys Ther. 2016 Jan;46(1):19-25. doi: 10.2519/jospt.2016.5093. Epub 2015 Nov 10. PMID: 26556391.
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