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Arthrogenic Inhibition - Glossary Term Illustration

Arthrogenic Inhibition

Athrogenic inhibition is a neuromuscular reflex that reduces the activity of muscles crossing a joint exhibiting signs of dysfunction following injury, surgery, or inflammation.

Arthrogenic Inhibition

Arthrogenic Inhibition (a.k.a. arthrokinematic inhibition or arthrogenic muscle inhibition (AMI)) is a neuromuscular reflex that reduces the activity of muscles crossing a joint exhibiting signs of dysfunction following injury, surgery, or inflammation. This occurs due to altered afferent signaling from joint mechanoreceptors and nociceptors, resulting in a reflexive inhibition of motor units, altering recruitment, and leading to muscle weakness despite no direct structural damage to the muscle itself.

  • Example: A common and relatively dramatic example can be observed following knee surgery, when the quadriceps will atrophy and become hard to activate, much less recruit for strenuous activity. Generally, some physical rehabilitation and a reduction in swelling will result in a full or near full recovery of quadriceps strength and, presumably, a reduction of the arthrogenic inhibition. Note that athrogenic inhibition is believed to contribute to altered recruitment, movement impairment, increased risk of injury, and reduction in human performance in much subtler ways than the example above. For example, pes planus resulting in ankle dysfunction and a reduction in activity of the tibialis posterior, tibialis anterior, and calves may result in an increased risk of ankle injury and reduction in propulsive force.

For more on autogenic inhibition, check out the course:

Additional neuromuscular reflexes:

Mechanisms of Arthrogenic Inhibition

  • Altered Afferent Input: Joint injury (e.g., swelling, ligament damage, or structural changes) leads to altered sensory signals from joint mechanoreceptors and nociceptors.
  • Reflex Inhibition: Increased activity of group II and III afferents inhibits alpha motor neuron excitability via spinal and supraspinal pathways.
  • Changes in Corticospinal Drive: Decreased cortical excitability and synaptic reorganization can further impair voluntary activation of affected muscles.
  • Pain and Effusion Effects: Joint swelling and pain amplify inhibitory signals, reducing motor output.

Rehabilitation Strategies

  1. Neuromuscular Electrical Stimulation (NMES): May aid in activating inhibited motor units.
  2. Local Vibration: Some research suggests that local vibration may aid in muscle recruitment of deconditioned and/or inhibited muscles, and may be an alternative or an adjunct therapy to NMES.
  3. Cryotherapy & Compression: Reduces joint effusion and inflammatory effects that may be contributing to arthrogenic inhibition.
  4. Reduce Movement Impairment: Reduces excessive stress, inflammation and altered afferentation by improving joint alignment, muscle recruitment, and force distribution.
  5. Joint Mobilizations and Manipulation: Joint mobilizations or manipulations may be beneficial for improving arthrokinematic motion.
  6. Proprioceptive Training: Enhances joint position sense and restores afferent feedback.
  7. Strength Training: Helps promote recruitment of additional motor units and improves intramuscular coordination.
  8. Cortical Activation Techniques: Motor imagery, transcranial stimulation, and biofeedback can aid in re-establishing voluntary muscle activation.

Local Vibration

Joint Mobilization

Joint Manipulation

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