Tackling Arthrogenic Muscle Inhibition: A Vet Rehab Perspective

Mar 21, 2024 | Equine Therapy, General Veterinary Rehabilitation, Small Animal Rehabilitation

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.


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.


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.

Norte G, Rush J & Sherman D. 2021. Arthrogenic muscle inhibition: Best evidence, mechanisms, and theory for treating the unseen in clinical rehabilitation. Journal of Sport Rehabilitation

To learn more about neurodynamics and the changes that occur to the peripheral and central nervous system, watch the series in the Onlinepethealth Small Animal and Equine members portals by Amie Hesbach, where she discusses neurodynamics in depth.


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.

Norte G, Rush J & Sherman D. 2021. Arthrogenic muscle inhibition: Best evidence, mechanisms, and theory for treating the unseen in clinical rehabilitation. Journal of Sport Rehabilitation


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.


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).


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).


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).


Non-thermal ultrasound

The acoustic energy produced by therapeutic ultrasound (TUS) may deliver mechanical stimulation to the joint receptors implicated in AMI and is safe to use in acute phases of healing. Low-intensity non-thermal ultrasound was shown to increase motor neuron pool excitability 20 minutes after treatment in one study. Theoretically, US may

  • mask inhibitory signals from the injured joint;
  • supplement sensory input; and
  • facilitate a muscle response.

This modality warrants further investigation.

‘Clinical bottom line: Very limited evidence suggests that nonthermal ultrasound has the potential to disinhibit quadriceps motor neurons via spinal-reflexive excitation. Theoretically, application prior to therapeutic exercise may induce an “open an exploit” effect’ (Norte et al., 2021).


Eccentric cross-exercise

Eccentric cross-exercise involves exercising the contralateral limb to increase strength in the ipsilateral limb by leveraging a neurological crossover of information between brain hemispheres. Eccentric cross-exercise produces greater strength and neural activity than concentric exercise.

Eccentric cross-exercise interventions can

  • reduce intracortical inhibition;
  • increase the cortical drive to the untrained muscles, from spinal and paraspinal motor pathways;
  • improve motor neuron pool excitability
  • corticospinal excitability
  • motor cortex activation and
  • strength; and
  • Reduce atrophy.

‘Clinical bottom line: By leveraging the uninjured contralateral limb, eccentric cross-exercise can enhance strength and neuromuscular control following joint injury through supraspinal mechanisms. Since traditional eccentric exercise is typically contraindicated in the early phases of recovery, training the uninjured limb may increase communication between motor cortices and translate clinically as improved muscle function’ (Norte et al., 2021).


Subacute recovery phase

In the subacute phase of healing and recovery, the treatment goals shift from treating pain, inflammation and effusion to increasing joint load and strengthening the muscle. Persistent AMI may, however, delay these goals or lead to compensatory movement patterns during the functional activity of the patient.

Treating AMI during this phase could include the following modalities or techniques:


Eccentric exercise

Eccentric exercise increases morphologic and neurological characteristics of muscle function while increasing muscle strength, activation and hypertrophy. While eccentric exercise is an effective way to restore muscle function and volume following injury, its translation to functional movement remains unclear.

Eccentric training produces greater force production than concentric resistance training, as it maintains actin and myosin cross-bridges and increases the excitation of supraspinal pathways, cortical activation and signalling to peripheral musculature – thereby increasing voluntary motor neuron recruitment.

‘Clinical bottom line: In conjunction with traditional rehabilitation, eccentric-based exercise should be used to help restore muscle strength, voluntary activation, and volume after traumatic joint injury’ (Norte et al., 2021).



Vibration therapy may reduce the effects of AMI by altering somatosensory input to articular and cutaneous mechanoreceptors. Following orthopaedic injury, both whole body vibration and local vibration have been shown to enhance aspects of muscle function in individuals with 

  • joint effusion,
  • osteoarthritis,
  • joint pain and
  • chronic joint instability.

Vibration is usually applied in short bursts of 30 to 60 seconds through a whole-body platform, or directly to a muscle-tendon unit during therapeutic exercise.

Vibration therapy is thought to provide a 60-minute window where voluntary motor neuron recruitment is enhanced in previously inhibited motor neurons. Strength gains following a training regimen that included vibration therapy appeared to last longer than strength gains from therapeutic exercise alone.

‘Clinical bottom line: Vibration therapy applied in conjunction with exercise or static muscle contraction has the potential to enhance muscle function more than control conditions, allowing for a sufficient therapeutic window. Vibration appears to be appropriate for use once the patient can adequately load the injured limb and has regained enough neuromuscular control to perform repeated or prolonged muscle contractions’ (Norte et al., 2021).


Antagonist fatigue

Antagonist fatigue exercise is a novel, clinically relevant intervention that may improve muscular impairment resulting from reciprocal inhibition.

After a joint injury, the antagonist muscle may be facilitated by supraspinal influence to stabilise the joint and prevent further damage to the intra-articular tissue. Fatiguing the antagonist musculature may

  • improve neuromuscular function of the agonist by reducing neural drive to the antagonist and mediating coactivation after injury;
  • decrease motor neuron firing rates and recruitment from the antagonist motor neuron pool, allowing for greater activation of the agonist; and
  • reduce coactivation and enhance agonist muscle function.

Clinical bottom line: Antagonist fatigue may serve to reduce antagonist-agonist coactivation. Reducing the facilitation of the antagonist muscles leverages reciprocal inhibition and allows for more optimal agonist muscle training’ (Norte et al., 2021).


Chronic recovery phase

As joint health is restored and the functional capacity of the patient improves, our clinical goals will again shift towards achieving long-term joint health and a return to sport or competition. During this phase of recovery, we will focus on

  • improving neurocognitive function
  • re-developing motor skills
  • integrating patients back into competition.

In the article, many experimental and emerging interventions are discussed, many of which are not relevant within the veterinary rehabilitation field. We will discuss only those emerging interventions that may be translated to our patients.


Motor skill training

When structuring rehabilitation, retention and transfer of motor skills can be promoted by prioritising implicit learning and feedback, promoting differential learning by manipulating the environment, utilising random practice schedules, and ensuring patient motivation and autonomy. Skill retention and transfer over time can be improved by adding variability to the task and the environment, and performing random practice.

‘Clinical bottom line: Principles of motor learning should be applied to address neural plasticity underlying motor impairments induced by joint injury’ (Norte et al., 2021).


Neurocognitive training

Neurocognitive training may prepare the patient to return to uncontrolled athletic environments where cognitive demands are increased. This includes dual task training, reaction time, visual attention and self-monitoring. Poor or prolonged cognitive processing in an uncontrolled environment may put the patient at greater risk of re-injury.

Dual task training is commonly implemented in rehabilitation in patients with a history of neurological impairment, as well as in the elderly to improve postural stability.

‘Clinical bottom line: Implementing a neurocognitive training protocol may improve patients’ ability to react and process unanticipated sensory information from their sporting environment and reduce risk of secondary injury(Norte et al., 2021).



AMI contributes to muscle weakness, activation failure and atrophy in patients recovering from joint injury or surgery. Without a return of normal muscle function and activation, rehabilitation outcomes will remain poor and the patient will maintain a high risk of reinjury or secondary injury and dysfunction. During the acute and subacute phases of healing and rehabilitation from joint injury, it is essential that AMI be considered and treated with effective and evidence-based methods. AMI interventions should always be patient-specific, and should focus on treating and resolving pain, inflammation and oedema as soon as possible.  




Norte G, Rush J & Sherman D. 2021. Arthrogenic muscle inhibition: Best evidence, mechanisms, and theory for treating the unseen in clinical rehabilitation. Journal of Sport Rehabilitation http://dx.doi.org/10.1123/jsr.2021-0139




Capitalising on Canine Cognition during Hydrotherapy, Ansi van der Walt

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Neurodynamics series, with Gillian Tabor and Amie Hesbach

Putting Neuroplasticity into Practice, Part 1 and 2, with Amie Hesbach

Neurodynamic Mobilisation in Animal Physical Therapy, with Sabine Hárrer


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