Neural Substrates of Cognitive Motor Interference During Walking; Peripheral and Central Mechanisms

We investigated changes of regional activation in the frontal cortices as assessed by changes of hemoglobin oxygenation during walking at 3 and 5 km/h and running at 9 km/h on a treadmill using a near-infrared spectroscopic (NIRS) imaging technique. During the acceleration periods immediately preceded reaching the steady walking or running speed, the levels of oxygenated hemoglobin (oxyHb) increased, but those of deoxygenated hemoglobin (deoxyHb) did not in the frontal cortices. The changes were greater at the higher locomotor speed in the bilateral prefrontal cortex and the premotor cortex, but there were less speed-associated changes in the sensorimotor cortices. The medial prefrontal activation was most prominent during the running task. These results indicate that the prefrontal and premotor cortices are involved in adapting to locomotor speed on the treadmill. These areas might predominantly participate in the control of running rather than walking.

The cortical, cerebellar and brainstem BOLD-signal changes have been identified with fMRI in humans during mental imagery of walking. In this study the whole brain activation and deactivation pattern during real locomotion was investigated by [(18)F]-FDG-PET and compared to BOLD-signal changes during imagined locomotion in the same subjects using fMRI. Sixteen healthy subjects were scanned at locomotion and rest with [(18)F]-FDG-PET. In the locomotion paradigm subjects walked at constant velocity for 10 min. Then [(18)F]-FDG was injected intravenously while subjects continued walking for another 10 min. For comparison fMRI was performed in the same subjects during imagined walking. During real and imagined locomotion a basic locomotion network including activations in the frontal cortex, cerebellum, pontomesencephalic tegmentum, parahippocampal, fusiform and occipital gyri, and deactivations in the multisensory vestibular cortices (esp. superior temporal gyrus, inferior parietal lobule) was shown. As a difference, the primary motor and somatosensory cortices were activated during real locomotion as distinct to the supplementary motor cortex and basal ganglia during imagined locomotion. Activations of the brainstem locomotor centers were more prominent in imagined locomotion. In conclusion, basic activation and deactivation patterns of real locomotion correspond to that of imagined locomotion. The differences may be due to distinct patterns of locomotion tested. Contrary to constant velocity real locomotion (10 min) in [(18)F]-FDG-PET, mental imagery of locomotion over repeated 20-s periods includes gait initiation and velocity changes. Real steady-state locomotion seems to use a direct pathway via the primary motor cortex, whereas imagined modulatory locomotion an indirect pathway via a supplementary motor cortex and basal ganglia loop. 2009 Elsevier Inc. All rights reserved.

Automaticity is a hallmark feature of walking in adults who are healthy and well-functioning. In the context of walking, “automaticity” refers to the ability of the nervous system to successfully control typical steady state walking with minimal use of attention-demanding executive control resources. Converging lines of evidence indicate that walking deficits and disorders are characterized in part by a shift in the locomotor control strategy from healthy automaticity to compensatory executive control. This is potentially detrimental to walking performance, as an executive control strategy is not optimized for locomotor control. Furthermore, it places excessive demands on a limited pool of executive reserves. The result is compromised ability to perform basic and complex walking tasks and heightened risk for adverse mobility outcomes including falls. Strategies for rehabilitation of automaticity are not well defined, which is due to both a lack of systematic research into the causes of impaired automaticity and to a lack of robust neurophysiological assessments by which to gauge automaticity. These gaps in knowledge are concerning given the serious functional implications of compromised automaticity. Therefore, the objective of this article is to advance the science of automaticity of walking by consolidating evidence and identifying gaps in knowledge regarding: (a) functional significance of automaticity; (b) neurophysiology of automaticity; (c) measurement of automaticity; (d) mechanistic factors that compromise automaticity; and (e) strategies for rehabilitation of automaticity.