Tackling Arthrogenic Muscle Inhibition: A Vet Rehab Perspective

Arthrogenic muscle inhibition (AMI) occurs following a joint injury or orthopaedic condition and results in inhibited muscle function and activation. If left untreated, it can be a major limiting factor in the success of a rehabilitation programme.

AMI occurs secondarily to joint injury and results in a reflexive inhibition of muscle activation. Inhibition occurs within the motor neuron pool, as well as the central nervous system. During the acute phase of healing, cryotherapy, TENS and NMES can aid in reversing muscle inhibition. During the subacute phase, eccentric exercise and vibration therapy may aid in reversing the inhibition.

In this blog, we summarise the findings from the research article: ‘Arthrogenic muscle inhibition: Best evidence, mechanisms, and theory for treating the unseen in clinical rehabilitation’, by Norte, Rush and Sherman, 2021.

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Arthrogenic muscle inhibition (AMI)

AMI is a neurophysical phenomenon in which healthy muscle tissue becomes reflexively inhibited following an injury to the joint. AMI can occur as a result of injury in any joint, and can significantly impede the recovery of muscle function and ultimate rehabilitation.

As early as 1965, it was established that the stretching of the joint capsule that results from joint effusion led to reflexive inhibition of the surrounding muscle. In the 1980s, this was confirmed, and it was further established that the degree of inhibition was related to the degree of effusion within the joint. Pain may or may not be present in a joint for AMI to occur.

In the 2000s, the role of AMI and its treatment became more widely known, and studies were conducted to try to identify interventions that could successfully treat AMI.

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The clinical relevance of arthrogenic muscle inhibition

To appreciate the broader impact of AMI, we need to consider its clinical manifestations and how they influence the interactions between the patient, their functional activities and their environment.

In patients experiencing AMI following joint injury, surgery or pathology, we will see:

• muscle weakness;
• reduced muscle activation or failure to activate muscle; and
• muscle atrophy

Muscle function is dependent on the availability of motor neurons in the muscle and on the ability to voluntarily recruit them. Patients with joint injury usually present with fewer motor neurons available for recruitment, or a lower motor neuron pool excitability, as well as a reduced ability to voluntarily recruit motor neurons, or a central activation failure. This inhibition is reflexive and involuntary and is controlled by the presynaptic mechanisms within the spinal cord, or a lowered spinal reflexive excitability during acute stages of healing as a result of tissue damage, joint laxity, joint effusion, pain or inflammation within a joint.

Changes within a joint disrupt the normal neural signalling between joint receptors and the central nervous system, changing the sensory feedback transmitted to the spinal cord and brain.

Clinical interventions or modalities that help to restore or augment the sensory information should be incorporated during the acute phases of healing.

Within the human population, persistent muscle impairments are commonly reported at the end of rehabilitation periods, when patients are returning to unrestricted activity. This can last for years and can contribute to high re-injury rates and further dysfunction.

What does and does not change over time:

• Motor neuron pool excitability resolves over time.
• Central activation failure does not resolve without intervention.
• During chronic phases of healing, a decrease in corticospinal excitability occurs – there is silencing in the cortical map.
• Differences in brain activity indicate that functional activities require greater cognitive effort, attention and visual support.

While in the acute phase of injury the cause of muscle inhibition is primarily caused by injury to the joint, over time it will shift to primarily being caused by corticospinal mechanisms.

A failure to address AMI in the initial phases of healing may result in maladaptive neuroplasticity and lead to persistent muscular impairments and compensatory movement patterns.

Evidence-based interventions

The use of any modality or clinical intervention must be linked to a specific goal, and needs to be safe and effective at the specific point of healing in which it is utilised. The individual needs of the patient must always be considered when developing a treatment programme.

Let’s discuss interventions with empirical or theoretic support for reducing the immediate and secondary effects of AMI.

Acute phase of healing

During the acute phase of healing, we want to focus on three areas:

1. Minimise pain, swelling and inflammation.
2. Improve muscle activation.
3. Minimise muscle atrophy.

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Focal joint cooling

Focal joint cooling, or cryotherapy, may reduce AMI by altering the sensory input from nociceptors and thermoreceptors, as well as increasing the motor neuron pool excitability and voluntary activation of muscles.

To achieve focal joint cooling, cryotherapy needs to be applied around the entire affected joint, for 20-30 minutes prior to therapeutic exercise.

Cryotherapy may provide a 60-minute treatment window where there is increased availability of motor neurons, making this modality ideal in the rehabilitation setting prior to therapeutic exercise.

Cryotherapy is commonly used to address and reduce pain perception, thus disinhibiting or masking the inhibition signals originating from the joint.

‘Clinical bottom line: Focal joint cooling has the potential to increase motor neuron pool excitability and voluntary activation among individuals with lower-extremity joint injury. The effects appear to last the duration of a traditional rehabilitation session. Application is most appropriate to apply prior to exercise’ (Norte et al., 2021).

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Transcutaneous electrical nerve stimulation (TENS)

TENS may reduce inhibition by masking the inhibitory signals of AMI.

When positioned over a joint, high-frequency TENS masks type I and II afferent fibres responsible for pre-synaptic spinal-level reflex mechanisms and subsequent inhibition of motor neurons.

High-frequency TENS of 120-150 Hz has the greatest disinhibitory effect for increasing voluntary muscle activation when compared to other modalities.

TENS can effectively increase muscle activation and maximal voluntary contractions.

The most pronounced effects can be achieved when TENS is applied for more than 20 minutes prior to exercise following surgery or joint effusion.

TENS can create a 45-minute therapeutic window where motor unit excitability and strength are temporarily restored, making it the ideal modality to use during therapy, prior to therapeutic exercise.

‘Clinical bottom line: High-frequency TENS applied before and/or during exercise can increase the availability and voluntary recruitment of quadriceps motor neurons in those with quadriceps inhibition. Taking advantage of this therapeutic effect results in retention of gains over four-week training periods, although the effects may not be better than exercise alone’ (Norte et al., 2021).

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Neuromuscular electrical stimulation (NMES)

NMES circumvents inhibited motor neurons through direct stimulation of the muscle, thereby supporting muscle strengthening and preventing atrophy during periods of AMI. When NMES is used during exercise, it may help retain motor neuron recruitment and improve force production.

NMES can be paired with eccentric exercise to improve strength and voluntary muscle contraction.

NMES can be paired with isometric exercise to improve motor neuron pool excitability.

‘Clinical bottom line: The use of NMES in conjunction with therapeutic exercise may help minimise strength and muscle volume loss in the early phases of recovery and improve voluntary recruitment of motor neurons. The use of NMES may be the most beneficial during early phases of recovery but may become less effective as patients’ strength and voluntary muscle activation is restored’ (Norte et al., 2021).

Keep reading about this research and their findings, here