Does The Central Nervous System Contribute To Weakness In Those After Anterior Cruciate Ligament Reconstruction?

Abstract

Anterior cruciate ligament (ACL) injury is common among adolescents and physically active adults. Despite surgical reconstruction and rehabilitation, quadriceps weakness is a persistent hallmark of injury and a challenging clinical limitation during the recovery process. While other clinical populations have identified the central nervous system as a critical determinant for weakness, few studies have explored this relationship in those after ACL injury. PURPOSE: To determine the relationship between brain activity for knee movement and quadriceps weakness in those after ACL reconstruction (ACL-R). METHODS: 22 patients with unilateral ACL-R (8 females; age 22.1 ± 2.6 years; BMI 23.8 ± 3.1; Tegner 8.4 ± 1.0; time from surgery 4.6 ± 2.6 years) participated. Quadriceps weakness was quantified using limb symmetry index (LSI) of peak isokinetic knee extensor torque assessed at 60°/s for each participant. Neural activation patterns were measured using blood-oxygen-level-dependent (BOLD) signals, cluster corrected z-threshold>3.1, p < .05, during repeated cycles of knee flexion/extension in the fMRI scanner. Percent BOLD signal change was calculated for regions selected within the sensorimotor network using the Juelich Histological Atlas. Pearson product-moment correlations were used to determine the relationship between regional BOLD signal and LSI scores. False-discovery rate correction using the Benjamini-Hochberg procedure was applied to adjust for multiple comparisons. RESULTS: Weak adults with ACL-R displayed greater levels of contralateral premotor cortex (r = -.465, p = 0.03), cerebellum (r = -.485, p = 0.02) and lingual gyrus (r = -.519, p = 0.01) activity for knee flexion/extension. CONCLUSIONS: Our data suggest weaker adults with prior ACL-R require greater levels of descending cortical input during a repeated quadriceps contraction compared to those with no persistent strength deficits. Increased neural activity requirements in regions responsible for motor planning and visual-attention may reflect compensatory motor strategies to mitigate losses in function attributable to weakness.