NEURAL ACTIVITY AND LANDING BIOMECHANICS: EXPLORING THE RELATIONSHIPS BETWEEN THE BRAIN, BODY, AND ACL INJURY-RISK

BACKGROUND: Anterior cruciate ligament (ACL) injuries predominantly occur via non-contact mechanisms, secondary to motor coordination errors resulting in aberrant frontal plane knee loads that exceed the thresholds of ligament integrity. However, central nervous system processing underlying high injury-risk motor coordination errors remain unknown, limiting the optimization of current injury reduction strategies. PURPOSE: To evaluate the relationships between brain activity during motor tasks with injury-risk loading during a drop vertical jump. METHODS: Thirty female high school soccer players (16.10 ± 0.87 years, 165.10 ± 4.64 cm, 63.43 ± 8.80 kg) were evaluated with 3D biomechanics during a standardized drop vertical jump from a 30 cm box and peak knee abduction moment was extracted as the injury-risk variable of interest. A neuroimaging session to capture neural activity (via blood-oxygen-level-dependent signal) was then completed which consisted of 4 blocks of 30 seconds of repeated bilateral leg press action paced to a metronome beat of 1.2 Hz with 30 seconds rest between blocks. Knee abduction moment was evaluated relative to neural activity to identify potential neural contributors to injury-risk. RESULTS: There was a direct relationship between increased landing knee abduction moment and increased neural activation within regions corresponding to the lingual gyrus, intracalcarine cortex, posterior cingulate cortex, and precuneus (r(2)= 0.68, p (corrected) < .05, z (max) > 3.1; Table 1 & Figure 1). CONCLUSION: Elevated activity in regions that integrate sensory, spatial, and attentional information may contribute to elevated frontal plane knee loads during landing. Interestingly, a similar activation pattern related to high-risk landing mechanics has been found in those following injury, indicating that predisposing factors to injury may be accentuated by injury or that modern rehabilitation does not recover prospective neural control deficits. These data uncover a potentially novel brain marker that could guide the discovery of neural-therapeutic targets that reduce injury risk beyond current prevention methods.