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.

Independent Regulation of the Cycle and Acceleration in Parkinsonian Gait Analyzed by a Long-Term Daily Monitoring System

“…Stepping cycle is regulated by spinal rhythm generators, which are assumed to be regulated under 2 separate descending pathways: (1) the basal ganglia-midbrain locomotion region-reticulospinal pathways and (2) noradrenergic descending pathways [15]. Consistent with this theory, freezing of gait, a prominent deficit in rhythm generation, could be improved not only by dopaminergic medications but also by noradrenergic medications [16,17].…”

Aspects of speech rate and regularity in Parkinson's disease

“…The resulting instability of motor sequences involves aspects of abnormal scaling and amplitude of movement, abnormal sensory processing and deficits in internal cueing. These abnormalities can be observed in PD related to the execution of repetitive movements within different modalities [58][59][60] and can partially be improved by voluntary attention or the use of external cues [61,62] as a kind of compensation for the impairment of automaticity [63]. Specifically, correlations have been found between speech abnormalities and some aspects of gait disturbance in PD [64][65][66].…”

Endoscopic third ventriculotomy improves Parkinsonism following a ventriculo-peritoneal shunt in a patient with non communicating hydrocephalus secondary to idiopathic aqueduct stenosis

“…Excessive inhibition upon thalamocortical neurons due to reduced dopaminergic neurons is assumed to decrease the velocity and amount of movement in Parkinson's disease. [10][11][12][13] In this model, cortical dysfunction without loss of nigrostriatal dopaminergic neurons can also result in movement or muscle tone abnormality such as bradykinesia and cogwheel like rigidity. In our case, the Parkinsonism was probably related to the dysfunction of the 'cortico-basal ganglia loop' resulting from the reduction of cerebral cortical flow without loss of nigrostriatal dopaminergic neurons.…”