Cerebellar and Subcortical Connectivity Associated with Arthrogenic Muscle Inhibition After Acute ACL Rupture in Males: A Clinical and fMRI Study.

BACKGROUND

Arthrogenic muscle inhibition (AMI) is a neurally mediated impairment of quadriceps activation following knee injury. Peripheral and spinal mechanisms are well described, but supraspinal contributions to AMI in the acute phase after injury remain underexplored.

OBJECTIVE

To investigate sensorimotor brain network connectivity changes associated with clinically classified AMI with task-based and resting-state functional magnetic resonance imaging (fMRI) in male patients with acute anterior cruciate ligament (ACL) rupture.

METHODS

In this prospective comparative cohort study, 40 male patients (mean age 24.1 ± 2.9 years) with acute ACL injuries underwent resting-state and a motor imagery task-based functional magnetic resonance imaging (fMRI). Patients were classified into AMI (n = 20) and non-AMI (n = 20) groups based on clinical assessment using the SANTI classification system.

RESULTS

The average time from injury to scanning was 22.7 ± 7 days. Clinically, the AMI group presented with qualitative vastus medialis obliquus inhibition and more frequent extension deficit. Compared with the non-AMI group, the AMI group demonstrated significantly greater functional connectivity of the right cerebellar Crus 1 with several sensory and cognitive brain regions. Exploratory (not corrected for multiple comparisons) task-based analyses revealed greater activation in the right caudate nucleus and right thalamus during motor imagery of the involved limb in the AMI group.

CONCLUSION

Male patients with acute ACL rupture and clinically classified AMI using the SANTI classification presented more frequently with knee extension deficits and consistent vastus medialis obliquus inhibition than those without AMI. In these patients, AMI was associated with altered cerebellar connectivity and, on exploratory analysis, greater subcortical activation during motor imagery. These findings support a central neural contribution to AMI and identify cerebellar-subcortical pathways as candidate targets for future mechanistic and rehabilitation studies. Trial registration NCT03950024 (ClinicalTrials.gov) registered on May 9th, 2019.