Contralateral Neurodynamic Mobilisation Improves Hamstring Flexibility.

This study investigates whether unilateral neurodynamic mobilisation produces measurable changes in active knee extension (AKE) range of motion (ROM) in the contralateral limb. Neurodynamic mobilisation techniques are commonly used to influence the mechanical and physiological behaviour of the peripheral nervous system, and previous research has demonstrated that neurodynamic "slider" techniques can acutely increase ipsilateral hamstring flexibility in asymptomatic individuals. However, the potential for contralateral effects, where treatment applied to one limb results in changes in the opposite limb, has not been directly evaluated using this specific mobilisation approach. The present study addresses this gap by examining whether a single session of unilateral neurodynamic mobilisation alters contralateral AKE performance.

The study was conducted using a counterbalanced crossover design consisting of two separate laboratory sessions: a neurodynamic mobilisation session and a control session. Each participant completed both sessions in a randomised order, with a one-week washout period implemented to minimise potential carry-over effects. All sessions were conducted at the same time of day to reduce variability related to diurnal fluctuations in neuromuscular performance.

During the neurodynamic mobilisation session, participants performed an active neurodynamic sliding technique adapted from previously published protocols. The technique was designed to promote excursion of the sciatic nerve without increasing tensile load. Participants were seated at the edge of a plinth in a flexed spinal posture with the hip and knee flexed and the ankle plantarflexed. From this position, they actively extended the cervical spine, extended the knee, and dorsiflexed the foot before returning to the starting position. Movements were paced using a metronome set at 60 beats per minute, with one full cycle of movement performed per beat. The mobilisation consisted of six sets of 30 seconds, separated by 10-second rest intervals, totalling 90 repetitions. The technique was applied only to the right lower limb.

The control session matched the duration of the mobilisation session but involved no movement. Participants remained seated quietly for four minutes following baseline measurement. This allowed comparison between the effects of the neurodynamic intervention and the passage of time alone.

AKE testing was performed immediately before and after each condition. The test was conducted with the participant lying supine, with the hip and knee of the test limb positioned at 90 degrees using a standardised support. Participants were instructed to actively extend the knee as far as possible while maintaining the hip position. Knee angle was measured using a bubble inclinometer placed on the anterior tibial border. Three measurements were taken at each time point, and the average value was used for analysis. All AKE measurements were performed on the contralateral (left) limb, as the mobilisation was applied to the right limb.

Statistical analysis involved a two-by-two repeated measures analysis of variance to examine the interaction between condition (mobilisation vs control) and time (pre vs post). Normality was assessed using the Shapiro-Wilk test. Post-hoc pairwise comparisons were conducted to explore the direction of significant interactions. Effect sizes were calculated using partial eta squared and Cohen's d. Test-retest reliability of the AKE test was assessed using data from the control condition collected one week apart, enabling calculation of the standard error of measurement (SEM) and minimal detectable change (MDC). These values were used to determine whether observed changes exceeded measurement error at both group and individual levels.