Disturbances of automatic gait control mechanisms in higher level gait disorder

• The relationship between stride length and cadence is strong in healthy adults.
• The relationship changed in participants with frontal gait disorder.
• Those with milder disease had disruption of stride length regulation only.
• Stride length and cadence control was disturbed in advanced disease.

The underlying mechanisms responsible for the gait changes in frontal gait disorder (FGD), a form of higher level gait disorders, are poorly understood. We investigated the relationship between stride length and cadence (SLCrel) in people with FGD (n = 15) in comparison to healthy older adults (n = 21) to improve our understanding of the changes to gait in FGD.Gait data was captured using an electronic walkway system as participants walked at five self-selected speed conditions: preferred, very slow, slow, fast and very fast. Linear regression was used to determine the strength of the relationship (R2), slope and intercept.In the FGD group 9 participants had a strong SLCrel (linear group) (R2 > 0.8) and 6 a weak relationship (R2 < 0.8) (nonlinear group). The linear FGD group did not differ to healthy control for slope (p > 0.05) but did have a lower intercept (p < 0.001). The linear FGD group modulated gait speed by adjusting stride length and cadence similar to controls whereas the nonlinear FGD participants adjusted stride length but not cadence similar to controls. The non-linear FGD group had greater disturbance to their gait, poorer postural control and greater fear of falling compared to the linear FGD group.Investigation of the SLCrel resulted in new insights into the underlying mechanisms responsible for the gait changes found in FGD. The findings suggest stride length regulation was disrupted in milder FGD but as the disorder worsened, cadence control also became disordered resulting in a break down in the relationship between stride length and cadence.