DOES FEAR OF MOVEMENT ALTER BRAIN ACTIVITY? INVESTIGATING THE NEURAL MARKERS OF KINESIOPHOBIA IN PEDIATRIC PATIENTS WITH PATELLOFEMORAL PAIN

Abstract

Background: Patellofemoral pain (PFP) is a chronic knee condition that inhibits movement quality and can cascade into kinesiophobia (i.e., fear of pain/movement). Despite its high prevalence in adolescent girls, PFP etiology has remained elusive, potentially due to an incomplete understanding of how pain, motor control, and kinesiophobia interact with central nervous system (CNS) functioning. Discovering linkages between motor control, kinesiophobia, and the CNS for patients with PFP could provide novel opportunities to refine neural therapeutic strategies for enhanced, personalized treatment approaches. Hypothesis/Purpose: To identify neural markers of kinesiophobia in pediatric patients with PFP. Methods: Adolescent girls clinically diagnosed with PFP (n = 14; 14.3 ± 3.2 yrs) were positioned supine in a magnetic resonance imaging (MRI) scanner. A modified Clarke’s test (patellofemoral grind test) was administered to the left knee of patients during brain functional MRI (fMRI) acquisition. The experimenter placed a hand at the superior patellar border applying intermittent distal pressure while the patient contracted her quadriceps. Patients also completed a quadriceps contraction test without application of external pressure (control). Kinesiophobia was measured using the Tampa Scale of Kinesiophobia. fMRI analyses compared brain activation between the two tasks, and correlation analyses were performed to assess relationships between task-induced brain activity and kinesiophobia. Statistical corrections were made to account for multiple, voxel-wise comparisons. Results: Evidenced in Table 1 and Figure 1A, neuroimaging analyses revealed distinct bidirectional activation during the Clarke’s test compared to the control (all p corrected < .05, all z max > 3.1). Table 1 and Figure 1B further highlight that greater kinesiophobia was associated with increased brain activity during the Clarke’s test in two clusters (both p corrected < .05, both z max > 3.1), but no relationships between kinesiophobia and brain activity during the control test were observed (all p corrected > .05, all z max < 3.1). Conclusion: The current results indicate that the Clarke’s test induced differential pain-related brain activity relative to the control (e.g., paracingulate gyrus). The patients’ degree of kinesiophobia was also related to brain activity in regions important for sensorimotor control, attention, and pain. Collectively, these data indicate that PFP may be due to alterations in nociceptive processing throughout the CNS, providing novel complementary pathways for targeted restoration of patellofemoral joint dysfunction. Future research should consider combined mechanistic pain profiling, sensorimotor, psychometric, and CNS assessments to identify patients most susceptible to kinesiophobia to refine treatment approaches that work towards a goal of disease prevention. Tables/Figures:Figure 1: A:. Greater activation during the modified Clarke’s test compared to the control test is colored red and less activation during the Clarke’s test compared to the control test colored blue. B: Green indicates regions for which higher kinesiophobia was positively associated with increased activity during the Clarke’s test. All image slices are shown in neurological convention and identified by the respective Z coordinate in Montreal neurological institute space. Cluster and anatomical details are provided in Table 1.