title: Substrates for normal gait and pathophysiology of gait disturbances with respect to the basal ganglia dysfunction.
abstract: In this review, we have tried to elucidate substrates for the execution of normal gait and to understand pathophysiological mechanisms of gait failure in basal ganglia dysfunctions. In Parkinson's disease, volitional and emotional expressions of movement processes are seriously affected in addition to the disturbance of automatic movement processes, such as adjustment of postural muscle tone before gait initiation and rhythmic limb movements during walking. These patients also suffer from muscle tone rigidity and postural instability, which may also cause reduced walking capabilities in adapting to various environments. Neurophysiological and clinical studies have suggested the importance of basal ganglia connections with the cerebral cortex and limbic system in the expression of volitional and emotional behaviors. Here we hypothesize a crucial role played by the basal ganglia-brainstem system in the integrative control of muscle tone and locomotion. The hypothetical model may provide a rational explanation for the role of the basal ganglia in the control of volitional and automatic aspects of movements. Moreover, it might also be beneficial for understanding pathophysiological mechanisms of basal ganglia movement disorders. A part of this hypothesis has been supported by studies utilizing a constructive simulation engineering technique that clearly shows that an appropriate level of postural muscle tone and proper acquisition and utilization of sensory information are essential to maintain adaptable bodily functions for the full execution of bipedal gait. In conclusion, we suggest that the major substrates for supporting bipedal posture and executing bipedal gait are 1) fine neural networks such as the cortico-basal ganglia loop and basal ganglia-brainstem system, 2) fine musculoskeletal structures with adequately developed (postural) muscle tone, and 3) proper sensory processing. It follows that any dysfunction of the above sensorimotor integration processes would result in gait disturbance.
authors.affiliation: Dept. of Physiology, Division of Neural Function, Asahikawa Medical College, Asahikawa, 078-8510, Japan. kusaki@asahikawa-med.ac.jp
authors.forename: Kaoru
authors.initials: K
authors.lastname: Takakusaki
authors.forename: Nozomi
authors.initials: N
authors.lastname: Tomita
authors.forename: Masafumi
authors.initials: M
authors.lastname: Yano
mesh_terms: D001479:Basal Ganglia / Q000503:physiopathology*; D001933:Brain Stem / Q000503:physiopathology; D005684:Gait / Q000502:physiology*; D006801:Humans; D008954:Models, Biological; D009129:Muscle Tonus / Q000502:physiology; D009434:Neural Pathways / Q000503:physiopathology*; D010300:Parkinson Disease / Q000175:diagnosis / Q000503:physiopathology*; D011187:Posture / Q000502:physiology; D011597:Psychomotor Performance / Q000502:physiology