The role of higher-level cognitive function in gait: executive dysfunction contributes to fall risk in Alzheimer's disease

Abstract

Alzheimer's disease (AD) is generally understood as primarily affecting cognition while sparing motor function, at least until the later stages of the disease. Studies reported over the past 10 years, however, have documented a prevalence of falls in AD patients significantly higher than in age-matched normal elders; also persons with AD have been observed to have different walking patterns with characteristics that increase gait instability. Recent work in cognitive neuroscience has begun to demonstrate the necessity of intact cognition, particularly executive function, for competent motor control. We put the pieces of this puzzle together and review the current state of knowledge about gait and cognition in general along with an exploration of the association between dementia, gait impairment and falls in AD. We also briefly examine the current treatment of gait instability in AD, mainly exercise, and propose a new approach targeting cognition.

Fig. 1

This is a schematic of the network of intentional and automatic motor behavior. The conscious pathway is represented by continuous, bold arrows; the unconscious by broken arrows. The posterior cortex is involved in sensory integration and memory. The frontal cortex primarily plans, sequences and organizes movement and action. The basal ganglia are involved with long-term storage; the cerebellum controls timing. PFC = Prefrontal cortex; DLPFC = dorso-lateral prefrontal cortex; FC = frontal cortex; SMA = supplementary motor cortex; MC = motor cortex; PMC = premotor cortex; PC = parietal cortex; TL = temporal lobe; STG = superior temporal gyrus; H = hippocampus; PH = parahippocampal regions; OC = occipital cortex; BG = basal ganglia; CB = cerebellum; SC = spinal cord; AHC = anterior horn motor neurons.

Fig. 2

This is an example of the effect of dual task walking from one subject (a stride time, usual walking; b stride time dual-task walking). For this subject, the stride time variability increased from 59 to 141 ms (or from 5.6 to 118%). In general, performance of a dual task markedly decreased (p < 0.002) the ability of patients with AD to regulate the stride-to-stride variations in gait timing ( c ). The standard deviation of the stride time (the gait cycle duration) increased by 52% when subjects were asked to walk and talk at the same time. This increase was associated with impaired executive function (see text). Error bars reflect the standard error of the mean. Mean was obtained from all 28 subjects (adapted from Sheridan et al. [12]).