Article ID Journal Published Year Pages File Type
3044480 Clinical Neurophysiology 2011 6 Pages PDF
Abstract

ObjectiveHyperexcitability of nociceptive pathways has been demonstrated with several musculoskeletal conditions but not anterior cruciate ligament (ACL) injury. The purpose was to investigate flexor withdrawal reflex (FWR) excitability following ACL rupture and determine if painless stretch of knee joint structures enhanced reflexive responses.MethodsTen subjects with and 10 subjects without unilateral ACL rupture were compared. FWRs were induced through sural nerve stimulus in symmetrical stance and recumbent positions, with the knee in relaxed and stressed condition. Latencies and amplitudes of hamstring electromyographic activity were analyzed.ResultsFWR thresholds were significantly diminished (p = 0.05) on the injured limb (11.8 ± 8 mA) compared to non-injured limb (18.6 ± 13 mA) and controls (22.5 ± 3 mA). Anterior tibial translation resulted in increased (p = 0.001) amplitude of EMG hamstring response on the injured limb (70 ± 50%) versus control (−1 ± 20%) and decreased latency (p = 0.01) of hamstring activation (82.0 ± 13 ms).ConclusionsIndividuals with ACL rupture demonstrated increased excitability of FWR responses indicated by decreased FWR threshold and reduced hamstring muscle latency. Responses were enhanced by passive stretch of the knee joint.SignificanceSubjects with ACL rupture demonstrated hyperexcitability of nociceptive pathways on the injured limb which may trigger the FWR more readily and promote the sensation of instability at the knee.

► Individuals with anterior cruciate ligament rupture demonstrated increased excitability of flexor withdrawal responses suggesting central sensitization of nociceptive pathways. ► This hyperexcitability may trigger the flexor withdrawal response more promptly producing the sensation of instability and knee “giving way” in individuals with anterior cruciate ligament deficiency. ► Pain-free passive stretch of the affected joint tissues resulted in a significant increase in flexor withdrawal reflex response (compared to baseline responses), as measured by amplitude of hamstring activation, potentially indicating that non-noxious afferent input may facilitate hyperexcitability of nociceptive pathways.

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