Rehabilitation of Arthrogenic Muscle Inhibition in Patients with Knee Osteoarthritis and after Knee Arthroplasty.
Level 5 - mechanism / opinion, no new human data
Narrative review proposing mechanism-based reasoning without systematic methodology or primary human data.
PubMed 42249256 · doi:10.1007/s12178-026-10038-7
What was done
This review synthesized literature on the neurophysiological mechanisms driving arthrogenic muscle inhibition (AMI) in patients with knee osteoarthritis and following total knee arthroplasty (TKA). Based on these mechanisms, the authors developed a proposed framework for targeted rehabilitation strategies.
What was found
The abstract reports no quantitative data or effect sizes. It describes AMI as a multilevel sensorimotor deficit driven by altered joint afferents that alter spinal reflex excitability, increase presynaptic inhibition, decrease alpha-motoneuron excitability, disrupt gamma-loop function, and impair motor unit firing. The review proposes addressing these mechanisms via joint effusion control, neuromuscular electrical stimulation, blood flow restriction training, and sensorimotor retraining.
Why it matters
Persistent quadriceps weakness post-TKA often resists standard strength training because neural inhibition prevents full voluntary muscle activation. Framing AMI as a multilevel neurological deficit helps clinicians select targeted interventions rather than relying solely on traditional progressive overload.
Limits
This is a narrative review with no primary data, systematic search criteria, or meta-analytic pooling. The proposed rehabilitation strategies reflect theoretical and mechanistic models rather than comparative outcome data evaluated directly within this paper.
Cited by
- supports Pain and structural damage inhibit the central nervous system from maximally activating and recruiting muscles.