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CONTEXT The etiology of patellofemoral pain has remained elusive, potentially due to an incomplete understanding of how pain, motor control, and kinesiophobia disrupt central nervous system functioning. OBJECTIVE To directly evaluate brain activity during experimental knee pain and its relationship to kinesiophobia in patients with patellofemoral pain. DESIGN Cross-sectional. METHODS Young females clinically diagnosed with patellofemoral pain (n = 14; 14.4 [3.3] y; body mass index = 22.4 [3.8]; height = 1.61 [0.1] m; body mass = 58.4 [12.7] kg). A modified Clarke test (experimental pain condition with noxious induction via patella pressure and quadriceps contraction) was administered to the nondominant knee (to minimize limb dominance confounds) of patients during brain functional magnetic resonance imaging (fMRI) acquisition. Patients also completed a quadriceps contraction without application of external pressure (control contraction). Kinesiophobia was measured using the Tampa Scale of Kinesiophobia. The fMRI analyses assessed brain activation during the modified Clarke test and control contraction and assessed relationships between task-induced brain activity and kinesiophobia. Standard processing for neuroimaging and appropriate cluster-wise statistical thresholds to determine significance were applied to the fMRI data (z > 3.1, P < .05). RESULTS The fMRI revealed widespread neural activation in the frontal, parietal, and occipital lobes, and cerebellum during the modified Clarke test (all zs > 4.4, all Ps < .04), whereas neural activation was localized primarily to frontal and cerebellar regions during the control contraction test (all zs > 4.4, all Ps < .01). Greater kinesiophobia was positively associated with greater activity in the cerebello-frontal network for the modified Clarke test (all zs > 5.0, all Ps < .01), but no relationships between kinesiophobia and brain activity were observed for the control contraction test (all zs < 3.1, all Ps > .05). CONCLUSIONS Our novel experimental knee pain condition was associated with alterations in central nociceptive processing. These findings may provide novel complementary pathways for targeted restoration of patient function.