We used functional magnetic resonance imaging (fMRI) to record human brain activity during slow (30 RPM), fast (60 RPM), passive (30 RPM), and variable rate pedaling. Ten healthy adults participated. After identifying regions of interest, the intensity and volume of brain activation in each region was calculated and compared across conditions (p < .05). Results showed that the primary sensory and motor cortices (S1, M1), supplementary motor area (SMA), and cerebellum (Cb) were active during pedaling. The intensity of activity in these areas increased with increasing pedaling rate and complexity. The Cb was the only brain region that showed significantly lower activity during passive as compared with active pedaling. We conclude that M1, S1, SMA, and Cb have a role in modifying continuous, bilateral, multijoint lower extremity movements. Much of this brain activity may be driven by sensory signals from the moving limbs.
Jay P. Mehta, Matthew D. Verber, Jon A. Wieser, Brian D. Schmit and Sheila M. Schindler-Ivens
Sunghoon Shin and Jacob J. Sosnoff
point [IEP]) or zero horizontal force point for movement, whereas the TM component is defined as the oscillation of the COP around the reference point. It is assumed that the RM component reflects supraspinal processes, whereas the TM component reflects peripheral mechanisms, such as the action of
Mark L. Latash
primitives involving coactivation of agonist–antagonist groups are likely to be of a supraspinal origin, but they can also receive contribution from spinal mechanisms. Coactivation is commonly considered as a competitive mechanism to reciprocal inhibition (reviewed in Nielsen, 2016 ). In particular, during
Harriet G. Williams and Jeanmarie R. Burke
A conditioned patellar tendon reflex paradigm was used to study the contributions of crossed spinal and supraspinal inputs to the output of the alpha motoneuron pool in children with and without developmental coordination disorders. The basic patellar tendon reflex response was exaggerated in children with developmental coordination disorders. Crossed spinal and supraspinal influences on the excitability of the alpha motoneuron pool were similar in both groups of children. However, there was evidence of exaggerated crossed spinal and supraspinal inputs onto the alpha motoneuron pool in individual children with developmental coordination disorder.
David B. Copithorne, Davis A. Forman and Kevin E. Power
The purpose of this study was to determine if supraspinal and/or spinal motoneuron excitability of the biceps brachii were differentially modulated before: 1) arm cycling and 2) an intensity-matched tonic contraction. Surface EMG recordings of motor evoked potentials (MEPs) and cervicomedullary motor evoked potentials (CMEPs) were used to assess supraspinal and spinal motoneuron excitability, respectively. MEP amplitudes were larger and onset latencies shorter, before arm cycling and tonic contraction when compared with rest with no intent to move, but with no difference between motor outputs. CMEP amplitudes and onset latencies remained unchanged before cycling and tonic contraction compared with rest. Premovement enhancement of corticospinal excitability was due to an increase in supraspinal excitability that was not task-dependent. This suggests that a common neural drive is used to initiate both motor outputs with task-dependent changes in neural excitability only being evident once the motor outputs have begun.
Sunghoon Shin, Robert W. Motl and Jacob J. Sosnoff
The rambling-trembling analysis of postural control maintains that the center of pressure (COP) trajectory can be decomposed into deviations resulting from supraspinal (i.e., rambling; RM) and spinal processes (i.e., trembling; TM). The purpose of this investigation was to test the rambling and trembling hypothesis by comparing persons with multiple sclerosis (MS) who had either elevated or normal spinal reflexes to healthy controls. 16 subjects with MS and 16 age and gender matched control subjects completed a postural control task. The persons with MS were divided into groups with high (MShigh) or low (MSlow) H-reflex amplitude. The MShigh group had an elevated ratio of TM to COP compared with healthy controls, but no differences in the ratio between RM and COP. The findings are congruent with the assumptions of the rambling-trembling hypothesis. Further work is needed to determine if RM and TM represent distinct spinal and supraspinal mechanisms to postural control.
Erik A. Wikstrom and Robert B. Anderson
The purpose of this investigation was to determine if stereotypical patterns of gait initiation are altered in those with posttraumatic ankle osteoarthritis. Ten subjects, five with unilateral ankle osteoarthritis and five uninjured controls, participated. Subjects completed the SF-36 and Ankle Osteoarthritis Scale to quantify self-reported disability as well as 10 dual-limb static stance trials and 10 gait initiation trials with each leg. Center of pressure outcomes were calculated for static balance trials while the peak center of pressure excursions were calculated for each phase of gait initiation. The results indicate greater self-reported disability (P < .05) and worse static postural control (P < .05) in the ankle osteoarthritis group. Nonstereotypical patterns were also observed during the first and third phases of gait initiation in those with ankle osteoarthritis. The results of this pilot study suggest that supraspinal motor control mechanisms may have changed in those with posttraumatic ankle osteoarthritis.
Robert L. Sainburg
The purpose of this commentary is to discuss factors that limit consideration of the equilibrium point hypothesis as a scientific theory. The EPH describes control of motor neuron threshold through the variable lambda, which corresponds to a unique referent configuration for a muscle, joint, or combination of joints. One of the most compelling features of the equilibrium point hypothesis is the integration of posture and movement control into a single mechanism. While the essential core of the hypothesis is based upon spinal circuitry interacting with peripheral mechanics, the proponents have extended the theory to include the higher-level processes that generate lambda, and in doing so, imposed an injunction against the supraspinal nervous system modeling, computing, or predicting dynamics. This limitation contradicts evidence that humans take account of body and environmental dynamics in motor selection, motor control, and motor adaptation processes. A number of unresolved limitations to the EPH have been debated in the literature for many years, including whether muscle resistance to displacement, measured during movement, is adequate to support this form of control, violations in equifinality predictions, spinal circuits that alter the proposed invariant characteristic for muscles, and limitations in the description of how the complexity of spinal circuitry might be integrated to yield a unique and stable equilibrium position for a given motor neuron threshold. In addition, an important empirical limitation of EPH is the measurement of the invariant characteristic, which needs to be done under a constant central state. While there is no question that the EPH is an elegant and generative hypothesis for motor control research, the claim that this hypothesis has reached the status of a scientific theory is premature.
Paulo H.C. Mesquita, Emerson Franchini, Marco A. Romano-Silva, Guilherme M. Lage and Maicon R. Albuquerque
supraspinal fatigue. 4 Supraspinal fatigue is related to changes in motor cortex excitability, and together with peripheral mechanisms, participates in muscle fatigue. For this reason, interventions that increase M1 excitability might increase the output from M1, consequently delaying the development of
Mark Holten Mora-Jensen, Pascal Madeleine and Ernst Albin Hansen
)-mediated movement frequency output ( Hansen & Ohnstad, 2008 ; Shima et al., 2011 ). An increased CPG-mediated movement frequency output might be caused by increased supraspinal descending central drive ( Prochazka & Yakovenko, 2007 ). Such an increase might be due to a net excitation of supraspinal centers ( De