Spastic movement disorder: impaired reflex function and altered muscle mechanics

Dietz, Volker; Sinkjær, Thomas

doi:10.1016/s1474-4422(07)70193-x

Cited by 494 publications

(383 citation statements)

References 131 publications

(133 reference statements)

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“…Among the many physiopathological mechanisms involved in spasticity, we highlight the effective loss of descending inhibitory influences, which increases excitability in gamma fusimotor neurons and alpha motor neurons 5,6 . In accordance with Dietz and Sinkjaer 7 , the hyperexcitability reflex in stroke patients interferes with motor function. This causes restricted and compromised movement control, limitations in standard functional movement necessary for daily activities and difficulties in progressing through rehabilitation.…”

Section: Introductionsupporting

confidence: 72%

Immediate effects of TENS and cryotherapy in the reflex excitability and voluntary activity in hemiparetic subjects: a randomized crossover trial

Martins¹,

Carvalho²,

Silva³

et al. 2012

Rev. bras. fisioter.

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Section: Introductionsupporting

confidence: 72%

Immediate effects of TENS and cryotherapy in the reflex excitability and voluntary activity in hemiparetic subjects: a randomized crossover trial

Martins¹,

Carvalho²,

Silva³

et al. 2012

Rev. bras. fisioter.

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“…Reflex activation is known to be task specific Zehr and Stein 1999;Dietz and Sinkjaer 2007) and our results must be interpreted in that context. Nevertheless, the observed patterns of reflex coupling may provide insight into the mechanisms constraining muscle activation patterns during volitional movements, including gait.…”

Section: Functional Implicationsmentioning

confidence: 88%

Stretch reflex coupling between the hip and knee: implications for impaired gait following stroke

2008

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Individuals with hemiparetic stroke often exhibit an abnormal coupling between the frontal plane of the hip and saggital plane of the knee during gait. The purpose of this study was to determine if stretch sensitive reflexes, which are known to be altered following stroke, exhibit similar coupling between the muscles of the hip and knee in the post-stroke population. Eighteen subjects were recruited for this study including ten with hemiparesis resulting from stroke and eight unimpaired, age-matched controls. A servomotor was used to apply ramp and hold perturbations to both the hip and knee joints in separate sessions and electromyographic activity was recorded in eight muscles of the lower limb. Hip abduction perturbations elicited abnormal activation in rectus femoris (RF) in seven of ten stroke subjects with amplitudes ranging from 3.2 to 12.5% of the maximum voluntary contraction (MVC). Only two of eight control subjects exhibited any activity in RF and these responses were only 2.1 and 2.7% of MVC. To determine if the responses in the stroke group were a result of muscle stretch, a musculoskeletal model was used to simulate the experimental abduction perturbations and estimate muscle length changes. The simulation revealed that RF should be shortened by the perturbations and this suggests that the response was not likely due to direct stretch. Moreover, knee flexion perturbations elicited responses in the hip adductors (AL) with a mean amplitude of 5.1 ± 3.8% of MVC across all stroke subjects while no significant responses were recorded in controls. The presence of a reciprocal, reflex-mediated coupling between RF and AL following stroke suggests

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“…Changes in the mechanical properties of muscle fibers 34 result in spastic muscle tone, which partly compensates for the paresis. 35 In patients with incomplete SCI, these non-neuronal changes allow to keep posture during walking, as seen in the spastic movement disorder.…”

Section: Neuronal Dysfunction After Scimentioning

confidence: 99%

Neuronal dysfunction in chronic spinal cord injury

2010

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This review describes the changes of spinal neuronal function that occur after a motor complete spinal cord injury (cSCI) in humans. In healthy subjects, polysynaptic spinal reflex (SR) evoked by non-noxious tibial nerve stimulation consists of an early SR component and rarely a late SR component. Soon after a cSCI, SR and locomotor activity are absent. After spinal shock; however, an early SR component re-appears associated with the recovery of locomotor activity in response to appropriate peripheral afferent input. Clinical signs of spasticity take place in the following months, largely as a result of nonneuronal changes. After around 1 year, the locomotor and SR activity undergo fundamental changes, that is, the electromyographic amplitude in the leg muscles during assisted locomotion exhaust rapidly, accompanied by a shift from early to dominant late SR components. The exhaustion of locomotor activity is also observed in non-ambulatory patients with an incomplete spinal cord injury (SCI). At about 1 year after injury, in most cSCI subjects the neuronal dysfunction is fully established and remains more or less stable in the following years. It is assumed that in chronic SCI, the patient's immobility resulting in a reduced input from supraspinal and peripheral sources leads to a predominance of inhibitory drive within spinal neuronal circuitries underlying locomotor pattern and SR generation. Training of spinal interneuronal circuits including the enhancement of an appropriate afferent input might serve as an intervention to prevent neuronal dysfunction after an SCI.

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Spastic movement disorder: impaired reflex function and altered muscle mechanics

Cited by 494 publications

References 131 publications

Immediate effects of TENS and cryotherapy in the reflex excitability and voluntary activity in hemiparetic subjects: a randomized crossover trial

Immediate effects of TENS and cryotherapy in the reflex excitability and voluntary activity in hemiparetic subjects: a randomized crossover trial

Stretch reflex coupling between the hip and knee: implications for impaired gait following stroke

Neuronal dysfunction in chronic spinal cord injury

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