Interaction between central programs and afferent input in the control of posture and locomotion

Dietz, Volker

doi:10.1016/0021-9290(95)00175-1

Cited by 51 publications

(33 citation statements)

References 14 publications

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“…The basic motor pattern for stepping is generated in the spinal cord, while fine control of walking involves various brain regions, including motor cortex, cerebellum, and brain stem (Dietz, 1996). Human infants exhibit the stepping pattern even before birth and this primitive ability continues throughout life to enhance mobility (Yang and Gorassini, 2006).…”

Section: Neurophysiology Of Gaitmentioning

confidence: 99%

Understanding gait control in post-stroke: Implications for management

Verma

Arya

Sharma

et al. 2012

Journal of Bodywork and Movement Therapies

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Section: Neurophysiology Of Gaitmentioning

confidence: 99%

Understanding gait control in post-stroke: Implications for management

Verma

Arya

Sharma

et al. 2012

Journal of Bodywork and Movement Therapies

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“…[19][20][21][22] Fine control of walking involves several brain regions, including the sensorimotor cortex, supplementary motor area (SMA), cerebellum, and brainstem. 23 Several studies suggest that upper-limb brain activity is mainly lateralized over the contralateral sensorimotor regions during unilateral motor task in healthy individuals, with differences pointing to a less-lateralized activation related to aging or complexity of the motor task. [24][25][26] However, a transfer of findings from arm to leg seems unjustified.…”

Section: Neural Control Of Lower-limb Motor Function and Normal Walkingmentioning

confidence: 99%

Noninvasive Neuromodulation in Poststroke Gait Disorders

Chieffo¹,

Comi²,

Leocani³

2015

Neurorehabil Neural Repair

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Walking rehabilitation is one of the primary goals in stroke survivors because of its great potential for recovery and its functional relevance in daily living activities. Although 70% to 80% of people in the chronic poststroke phases are able to walk, impairment of gait often persists, involving speed, endurance, and stability. Walking involves several brain regions, such as the sensorimotor cortex, supplementary motor area, cerebellum, and brainstem, which are approachable by the application of noninvasive brain stimulation (NIBS). NIBS techniques, such as repetitive transcranial magnetic stimulation and transcranial direct current stimulation, have been reported to modulate neural activity beyond the period of stimulation, facilitating neuroplasticity. NIBS methods have been largely applied for improving paretic hand motor function and strokeassociated cognitive deficits. Recent studies suggest a possible effectiveness of these techniques also in the recovery of poststroke gait disturbance. This article is a selective review about functional investigations addressing the mechanisms of lower-limb motor system reorganization after stroke and the application of NIBS for neurorehabilitation.

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“…Observations in patients with spinal cord lesions suggest that there is a network in the human spinal cord that has the capacity of generating rhythmic alternating muscle activity similar to that seen during walking (Calancie et al 1994;Dimitrijevic et al 1998), but there is still no strong evidence regarding the potential role of this network during walking in intact human subjects. Several groups have studied the modulation of cutaneous and muscular reflexes during the gait cycle (reviewed in Dietz 1996;Zehr and Stein 1999), and recently Sinkjaer et al (2000) have provided evidence that feedback in muscle afferents via spinal interneurons contributes to the activation of soleus motoneurons in the stance phase of walking. Corticospinal function has been investigated by transcranial magnetic stimulation (TMS) of the motor cortex during treadmill walking by several groups (Capaday et al 1999;Petersen et al 1998Petersen et al , 2001Schubert et al 1997Schubert et al , 1999.…”

Section: Introductionmentioning

confidence: 99%

Modulation of Transmission in the Corticospinal and Group Ia Afferent Pathways to Soleus Motoneurons During Bicycling

Pyndt

Nielsen

2003

Journal of Neurophysiology

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Pyndt, H. S. and J. B. Nielsen. Modulation of transmission in the corticospinal and group Ia afferent pathways to soleus motoneurons during bicycling. J Neurophysiol 89: 304 -314, 2003. 10.1152/jn.00386.2002. Transmission in the corticospinal and Ia pathways to soleus motoneurons was investigated in healthy human subjects during bicycling. Soleus H reflexes and motor evoked potentials (MEPs) after transcranial magnetic stimulation (TMS) were modulated similarly during the crank cycle being large during downstroke [concomitant with soleus background electromyographic (EMG) activity] and small during upstroke. Tibialis anterior MEPs were in contrast large during upstroke and small during downstroke. The soleus H reflexes and MEPs were also recorded during tonic plantarflexion at a similar ankle joint position, corresponding ankle angle, and matched background EMG activity as during the different phases of bicycling. Relative to their size during tonic plantarflexion, the MEPs were found to be facilitated in the early part of downstroke during bicycling, whereas the H reflexes were depressed in the late part of downstroke. The intensity of TMS was decreased below MEP threshold and used to condition the soleus H reflex. At short intervals (conditioning-test intervals of Ϫ3 to Ϫ1 ms), TMS produced a facilitation of the H reflex that is in all likelihood caused by activation of the fast monosynaptic corticospinal pathway. This facilitation was significantly larger in the early part of downstroke during bicycling than during tonic plantarflexion. This suggests that the increased MEP during downstroke was caused by changes in transmission in the fast monosynaptic corticospinal pathway. To investigate whether the depression of H reflexes in the late part of downstroke was caused by increased presynaptic inhibition of Ia afferents, the soleus H reflex was conditioned by stimulation of the femoral nerve. At a short interval (conditioning-test interval: Ϫ7 to Ϫ5 ms), the femoral nerve stimulation produced a facilitation of the H reflex that is mediated by the heteronymous monosynaptic Ia pathway from the femoral nerve to soleus motoneurons. Within the initial 0.5 ms after its onset, the size of this facilitation depends on the level of presynaptic inhibition of the Ia afferents, which mediate the facilitation. The size of the facilitation was strongly depressed in the late part of downstroke, compared with the early part of downstroke, suggesting that increased presynaptic inhibition was indeed responsible for the depression of the H reflex. These findings suggest that there is a selectively increased transmission in the fast monosynaptic corticospinal pathway to soleus motoneurons in early downstroke during bicycling. It would seem likely that one cause of this is increased excitability of the involved cortical neurons. The increased presynaptic inhibition of Ia afferents in late downstroke may be of importance for depression of stretch reflex activity before and during upstroke.

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Interaction between central programs and afferent input in the control of posture and locomotion

Cited by 51 publications

References 14 publications

Understanding gait control in post-stroke: Implications for management

Understanding gait control in post-stroke: Implications for management

Noninvasive Neuromodulation in Poststroke Gait Disorders

Modulation of Transmission in the Corticospinal and Group Ia Afferent Pathways to Soleus Motoneurons During Bicycling

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