Recent discoveries indicate neurophysiological mechanisms might underlie pain symptoms and knee extension strength deficits in patellar tendinopathy. Specifically, reduced spinal excitability could underlie strength deficits, while a proportion of individuals exhibit altered endogenous pain modulation. Parallels can be drawn to other persistent knee conditions where links between pain and motor neurophysiological mechanisms have been established. Whether similar neural mechanism interplay occurs in patellar tendinopathy has not yet been investigated. We aimed to determine whether endogenous pain modulation was associated with motor neurophysiological outcomes in patellar tendinopathy. We included n = 19 athletes with patellar tendinopathy who participated in two cross-sectional studies; one assessing endogenous pain modulation, and the other motor neurophysiological function. We quantified pain inhibition as pressure pain threshold change immediately following 120-seconds hand immersion in painful cold-water, while pain facilitation was calculated as hand-pain change from five to 20 s. Following knee extension MVIF assessment, we used transcranial magnetic stimulation (TMS) to measure corticospinal excitability and inhibition via production of motor evoked potentials and their silent period. Additionally, we collected lumbar-evoked potentials (LEPs) to quantify spinal excitability. We could only collect TMS and LEP outcomes in n = 15 and n = 17 participants, respectively. Greater pain facilitation predicted higher LEP (indicating lower spinal excitability) (β = 38.4 95%CI 10.3–77.0) and reduced strength (β=-7.9 95%CI − 15.1 to − 2.6). Pain inhibition was not associated with motor neurophysiological outcomes (p > 0.05). Our findings provide preliminary evidence of interplay between the neurophysiological mechanisms underlying pain facilitation and knee extension strength deficits in patellar tendinopathy.
Vallance et al. (2026) studied this question.