CAN COMBINED NEUROPHYSIOLOGICAL AND MRI EVALUATION HELP GAIN NEW INSIGHTS IN ARTHROGENIC MUSCLE INHIBITION AMONG PATIENTS WITH KNEE PAIN? PROOF OF CONCEPT

INTRODUCTION

Arthrogenic muscle inhibition (AMI) is a neuromuscular impairment that is commonly described in patients after knee joint injuries and surgeries. AMI is characterized by profound quadriceps muscle atrophy and persistent muscle weakness secondary to neural inhibition of motor pathways due to altered afferent feedback. While AMI is well-recognized in rehabilitation research, there is a critical lack of standard clinical diagnostic criteria limiting rehabilitation practitioners’ ability to prescribe treatments. In this context, MRI can be a helpful adjunct tool to neurophysiological testing by identifying joint pathology causing AMI and quadriceps muscle inhibition resulting from it.

OBJECTIVE

Describe MRI and neurophysiological findings of the knee joint and thighs among patients with AMI secondary to knee injury or surgery.

MEHTODS

Four patients with marked quadriceps weakness (presumed AMI) following knee joint injury or surgery are presented. All patients had MR imaging data, including two with unilateral thigh MRI (Patients A-B), 1 with unilateral knee and thigh MRI (Patient C), and 1 with bilateral knee and thigh MRIs, as well as neurophysiological testing (Patient D). Neurophysiological testing included muscle activation failure, Hoffman stretch reflex testing, and cortical inhibition using peripheral nerve and transcranial magnetic stimulation techniques. All imaging data was acquired 12-16 weeks post knee injury or surgery.

RESULTS

Patients A-C (each 12-14 weeks status-post ACL reconstruction, uni-compartment arthroplasty, and arthroscopic drilling, respectively) present with marked quadriceps volume loss and diffuse increased T2 signal, resembling denervation edema (Figure 1). Patient C, who underwent arthroscopic drilling, had osteochondral fracture prior to surgery which worsened on the postoperative imaging. Patient D (12-16 weeks post soccer injury) presented with osteochondral fracture of the lateral trochlea with marked atrophy of the quadriceps muscle (Figure 2A-B). Neurophysiological testing revealed volitional quadricep activation failure (51%, Figure 2C), as well as intracortical inhibition (37%, Figure 2D), afferent inhibition (81%, Figure 2E), and Hoffmann reflex facilitation on the involved limb (cf. 29%, Figure 2F vs. 15%, Figure 2G). These findings suggest a cortically mediated muscle activation failure and paradoxical reflex facilitation to preserve strength (spinal cord involvement). The absence of denervation edema could be plausibly explained by the central nervous involvement rather than a peripheral nerve or neuromuscular problem.

CONCLUSION

These cases highlight the value of combined MR imaging and neurophysiological assessment in AMI. The presence of denervation-like edema on MRI, alongside quantifiable neural inhibition patterns, offers potential diagnostic markers for AMI subtypes. Further research incorporating both modalities is needed to develop targeted rehabilitation strategies that address specific inhibitory mechanisms, potentially improving outcomes for patients with persistent post-injury weakness.