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Coordination of Locomotion and Respiration
Published in Alan D. Miller, Armand L. Bianchi, Beverly P. Bishop, Neural Control of the Respiratory Muscles, 2019
Two different mechanisms have been proposed to account for LRC. Passive inertial displacements of the visceral mass drive pulmonary ventilation, independent of diaphragmatic contractions. Different converging data support an active neurogenic control of LRC. Passive periodic motion of hindlimbs is not able to drive the respiratory rate at the imposed frequencies of passive motions. A central 1:1 locomotor-respiratory coupling is induced in different experimental situations. This coupling is achieved through interactions between the spinal locomotion generators and the medullary respiratory ones. Spinal cervical respiratory generators likely play a key role in this central link because of their relationships with the spinal locomotion generators on the one hand, and with the medullary respiratory generator on the other.
Mesolimbic Interactions with Mesopontine Modulation of Locomotion
Published in Peter W. Kalivas, Charles D. Barnes, Limbic Motor Circuits and Neuropsychiatry, 2019
Robert D. Skinner, E. Garcia-Rill
The motivation-motor systems interaction model (Figure 1) is composed of elements of both the limbic and motor systems. However, only those limbic structures in the pathway beginning with mesolimbic cells in the ventral tegmental area (VTA) and most directly related to modulation of the spinal locomotion-pattern generators are represented. These are the VTA, nucleus accumbens (NAc), the subpallidal region (SubP), the pedunculopontine nucleus (PPN; an element common to both systems), and the medial medullary reticular formation (MED; a brain stem region which projects to the spinal cord locomotion-pattern generators); these comprise a system which interfaces with the motor system. This model is expanded somewhat over Mogenson’s system1–3 to include the MED and spinal locomotor pattern generators. It will be referred to as the motivation system because it appears to induce or motivate the more well-known motor system to action via interactions at several sites between these two systems. The classical motor system is here defined as the motor cortex, caudate nucleus, globus pallidus (GP), substantia nigra (SN), subthalamic nucleus, and the reticular formation. It is conceivable, however, that the motor system could activate or inhibit the motivation system via the same interaction sites to provide an appropriate emotional content for actions initiated by the motor system. Included in the model are only the portions of the motor system which compose an analogous system: the substantia nigra pars compacta (SNc), striatum, and GP. The nucleus reticularis gigantocellularis (NRG) represents an inhibitory motor system which parallels the MED region.
Kinematics associated with treadmill walking in Rett syndrome
Published in Disability and Rehabilitation, 2021
Charles S. Layne, David R. Young, Beom-Chan Lee, Daniel G. Glaze, Aloysia Schwabe, Bernhard Suter
Despite the minimal range of slow walking speeds, our participants did decrease their stride times such that they were able to maintain pace with the increasing treadmill speeds. This finding strongly suggests that our participants were able to both adequately detect sensory information indicating the treadmill speed was increasing as well as integrate that information and increase their lower limb velocities in response (thereby significantly decreasing stride times). This is consistent with Aoi et al.’s [21] assertion that foot contact information and muscle spindle input can activate the CPG and adjust the locomotor pattern to meet the lower limb movement demands associated with increasing treadmill speed. Consistent with the decrease in stride times, there are the significant increases in knee and hip ROMs and angular velocities associated with increases in treadmill speed. This has also been reported for a large range of typical individuals [36–38]. These significant main effects and the highly significant correlations between knee and hip ROMs and their associated angular velocities (see Figure 5) also reflect our participants’ ability to modify their lower limb kinematic motion to adapt to increasing treadmill speed. Our data thereby suggest that participants have intact spinal locomotion circuity that can be regulated by sensory input and stimulated by walking within a narrow range of walking speeds. We speculate that our participants inability to increase their walking speed beyond 0.5 m/s may be primarily related to their failure to maintain attention on the walking task as well as their inability to preserve postural stability despite the safety that the harness provided. Although the spinal CPG may be able to produce the fundamental alternating lower limb motion necessary to walk, associated kinematics display a large amount of variance and the relationship between the two limbs is asymmetric. These features contribute to our participants’ lack of postural stability, which prevents them from being able to further increase their walking speed.