Background: Patellofemoral pain (PFP) is a common knee pain condition that affects up to 30% of adolescents and is disproportionately distributed between sexes, affecting females 2-10 times more frequently than male counterparts (Fulkerson, 2002). PFP, characterized by retro- or peripatellar pain, can be debilitating, leading to cessation of physical activity in 74% of adolescents (Fairbank, Pynsent, van Poortvliet, & Phillips, 1984). Aberrant lower-extremity biomechanics for those with PFP has been identified (Souza & Powers, 2009; Willson & Davis, 2008), but the underlying brain activation patterns contributing to pain-disrupted knee motor control is unknown. Patients with knee ligament deficiency demonstrate decreased sensorimotor activity and increased prelimbic activity in response to knee pain, compared with matched controls (Kadowaki, Tadenuma, Kumahashi, & Uchio, 2017), and those with knee ligament reconstruction demonstrate a disrupted sensory-motor brain activation strategy to control the knee (Grooms et al., 2017; Grooms, Page, & Onate, 2015). As PFP has been identified as a contributing factor to knee osteoarthritis later in life (Utting, Davies, & Newman, 2005), identifying the neural mechanisms driving pain-disrupted motor control could guide innovative neural-targeted interventions to treat and reduce knee pain. We hypothesized that patients with PFP, like those with knee ligament deficiencies and reconstruction, would demonstrate decreased sensorimotor brain activation and increased medial pain network brain activation to control the knee. We used our previously established knee motor control neuroimaging paradigm that simulates knee flexion and extension movements (Grooms et al., 2015) to identify altered neural activation patterns for those with PFP and compared those with matched controls. Methods: Four adolescent girls with patellofemoral pain (PFP: n = 4, 15.4 ± 2.2yrs, 158.5 ± 5.4 cm, 61.5 ± 15.6 kg) were matched with four adolescent girls with no history of knee pain (controls) based on age, height, and weight (Con: n =4, 16.4 ± 1.8yrs, 161.8 ± 5.1 cm, 54.9 ± 6.9 kg). Participants were positioned supine in a magnetic resonance imaging (MRI) scanner and completed a series of unilateral 45° knee extension/flexion movements at a velocity of 1.2 Hz (Figure 1; Left Panel). Various torso straps and head packing procedures were utilized to restrict excessive head motion. A second level mixed-effects (FLAME 1+2) independent samples t-test contrasted brain activation between the PFP and controls using a significance level set a priori at p < .05; Gaussian random field cluster corrected and z threshold set at z > 1.5. Results: Results revealed significantly depressed brain activation in the right parietal operculum cortex (z = 5.99, p < .001) and left Heschl’s gyrus (z = 3.83, p < .001) for the PFP compared to the controls (Figure 1; Right Panel). Discussion: The present study revealed significant differences in the neural activation patterns to control the knee between adolescent girls with PFP and those with no knee pain. Patients with PFP demonstrated less activation in sensorimotor cortices, seen in the parietal operculum, and sensory integration, seen in Heschl’s gyrus, when compared to healthy controls (Grooms et al., 2017; Kadowaki et al., 2017). These results indicate that pain may be suppressing sensory integration to control the knee for those with PFP. Congruent with previous neuroimaging investigations assessing those with knee injury (Grooms et al., 2017; Kadowaki et al., 2017), PFP appears to also induce neuroplastic effects identifiable using fMRI. These results provide a potential neural target for interventions that aim to restore sensorimotor integration in those with PFP, reduce pain, and restore an active lifestyle in young females. [Figure: see text]
Read full abstract