The length–tension relationship of human dorsiflexor and plantarflexor muscles after spinal cord injury

Pelletier, Chelsea; Hicks, Audrey L.

doi:10.1038/sc.2009.106

Cited by 12 publications

(9 citation statements)

References 19 publications

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“…Moreover, the proportion of type I to type II fibers was similar to age-matched control rats (Harris et al, 2007), although the muscles were more fatigable (Harris et al, 2006). In agreement with the rat results, participants with motor incomplete [ASIA Impairment Scale (AIS) C&D] or motor complete (AIS A&B) injuries having marked spasticity exhibited stimulus-torque responses characteristic of plantarflexor muscles with slow contractile properties (Hidler et al, 2002; Pelletier and Hicks, 2010). Additionally, in participants with motor complete and incomplete SCI (AIS B&C), muscle cross-sectional area was positively correlated to modified Ashworth scores (Gorgey and Dudley, 2008).…”

Section: Changes In Tissue Properties After Scisupporting

confidence: 78%

“…There are also changes in the joint angle-torque relationship of some muscles that may accompany reductions in the range of joint motion. For example, in plantarflexors (but not dorsiflexors) peak twitch torque occurs at more plantarflexed joint angles in SCI participants compared to non-injured controls (McDonald et al, 2005; Pelletier and Hicks, 2010). The shift in the joint angle-torque relationship has been attributed to shortening of the muscle as a result of sarcomere loss and increases in connective tissue, but this has not been directly proven.…”

Section: Changes In Tissue Properties After Scimentioning

confidence: 99%

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Recovery of neuronal and network excitability after spinal cord injury and implications for spasticity

D’Amico

Condliffe

Martins

et al. 2014

Front. Integr. Neurosci.

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The state of areflexia and muscle weakness that immediately follows a spinal cord injury (SCI) is gradually replaced by the recovery of neuronal and network excitability, leading to both improvements in residual motor function and the development of spasticity. In this review we summarize recent animal and human studies that describe how motoneurons and their activation by sensory pathways become hyperexcitable to compensate for the reduction of functional activation of the spinal cord and the eventual impact on the muscle. Specifically, decreases in the inhibitory control of sensory transmission and increases in intrinsic motoneuron excitability are described. We present the idea that replacing lost patterned activation of the spinal cord by activating synaptic inputs via assisted movements, pharmacology or electrical stimulation may help to recover lost spinal inhibition. This may lead to a reduction of uncontrolled activation of the spinal cord and thus, improve its controlled activation by synaptic inputs to ultimately normalize circuit function. Increasing the excitation of the spinal cord with spared descending and/or peripheral inputs by facilitating movement, instead of suppressing it pharmacologically, may provide the best avenue to improve residual motor function and manage spasticity after SCI.

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Section: Changes In Tissue Properties After Scisupporting

confidence: 78%

Section: Changes In Tissue Properties After Scimentioning

confidence: 99%

Recovery of neuronal and network excitability after spinal cord injury and implications for spasticity

D’Amico

Condliffe

Martins

et al. 2014

Front. Integr. Neurosci.

View full text Add to dashboard Cite

show abstract

“…These findings are similar to earlier work that has shown changes in M-wave characteristics to be disassociated with changes in muscle torque during fatigue in the paralyzed soleus muscle. 7 M-wave amplitude was greater in the AB group at baseline, which supports earlier findings 13 and is likely a reflection of the significant muscle atrophy after SCI. The fact that M-wave amplitude and area stayed relatively constant over the course of fatigue in the SCI group suggests that the previously reported decrease in Na þ /K þ pump concentration after SCI does not contribute to muscle fatiguability.…”

Section: Discussionsupporting

confidence: 88%

“…This angle has been previously determined as optimal for evoked dorsiflexor torque in the SCI and AB populations. 13 The common peroneal nerve was stimulated with rubber-stimulating electrodes (3 cm diameter). Muscle electrical activity was collected using two surface electromyogram electrodes (Kendall Medi-Trace 133, Mansfield, MA, USA) placed 5 cm apart on the muscle belly of the tibialis anterior.…”

Section: Apparatusmentioning

confidence: 99%

Muscle fatigue characteristics in paralyzed muscle after spinal cord injury

Pelletier

Hicks

2010

Spinal Cord

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Study design: The study design used is cross-sectional. Objectives: The aim of this study is to examine muscle contractile and excitability characteristics during fatigue of the tibialis anterior in six individuals with chronic spinal cord injury (SCI) and matched able-bodied (AB) controls. Setting: McMaster University, Hamilton, ON, Canada. Methods: Muscle compound action potential (M-wave) characteristics, muscle twitch properties, and summated force were examined during a 2 min fatigue protocol of intermittent bursts at 30 Hz (4 s tetanus, 2 s rest) or maximal voluntary contraction (MVC). Evoked twitch responses were followed during a recovery period. Results: M-wave amplitude was smaller in SCI (2.5±1.6 mV in SCI, 5.7±3.2 mV in AB) at baseline, but there was no change in M-wave amplitude or area during fatigue in either group. There was an increase in M-wave duration toward the end of recovery in the SCI group. Peak torque (PT) was not different between groups at baseline (3.8 ± 1.8 Nm in SCI, 3.7 ± 0.6 Nm in AB); PT potentiated significantly during fatigue in the AB, but not SCI group. There was significantly greater fatigue of both PT (43% decline) and summated force (57% decline) in the SCI group compared with the AB group (13% increase and 22% decline for PT and MVC, respectively). Conclusion: The dorsiflexor muscles in people with SCI are significantly more fatiguable than those in AB controls, but decreases in muscle excitability do not seem to be an important contributor to the increased fatiguability. The mechanisms behind the increased fatigue must lie distal to the muscle membrane.

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“…Plantar-flexor changes after spinal cord injury K Yaeshima et al participants than in the age-matched healthy control participants, [38][39][40][41][42][43][44] presumably because of the changes in proprioceptor function or muscle atrophy. In these studies, the time-dependent decline in Mmax may be caused by muscle atrophy, but because we did not measure Mmax in our study, we cannot conclude that the spinal reflex excitability in chronic SCI is maintained.…”

Section: Discussionmentioning

confidence: 99%

Mechanical and neural changes in plantar-flexor muscles after spinal cord injury in humans

et al. 2015

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Study design: Cross-sectional study. Objectives: To determine the effect of injury duration on plantar-flexor elastic properties in individuals with chronic spinal cord injury (SCI) and spasticity. Setting: National Rehabilitation Center for Persons with Disabilities, Japan. Methods: A total of 16 chronic SCI patients (age, 33 ± 9.3 years; injury localization, C6-T12; injury duration, 11-371 months) participated. Spasticity of the ankle plantar-flexors was assessed using the Modified Ashworth Scale (MAS). The calf circumference and muscle thickness of the medial gastrocnemius (MG), lateral gastrocnemius and soleus were assessed using tape measure and ultrasonography. In addition, the ankle was rotated from 10°plantar-flexion to 20°dorsiflexion at 5 deg s −1 with a dynamometer, and the ankle angle and torque were recorded. After normalizing the data (the initial points of angle and torque were set to zero), we calculated the peak torque and energy. Furthermore, angle-torque data (before and after normalization) were fitted with a second-and fourth-order polynomial, and exponential (Sten-Knudsen) models, and stiffness indices (SI SOP, SI FOP, SI SK ) and Angle SLACK (the angle at which plantar-flexor passive torque equals zero) were calculated. The stretch reflex gain and offset were determined from 0-10°d orsiflexion at 50, 90, 120 and 150 deg s −1 . After logarithmic transformation, Pearson's correlation coefficients were calculated. Results: MAS, calf circumference, MG thickness, peak torque and SI FOP significantly decreased with injury duration (r loglog = − 0.63, − 0.69, − 0.63, − 0.53 and − 0.55, respectively, Po0.05). The peak torque and SI FOP maintained significant relationships even after excluding impacts from muscle morphology. Conclusion: Plantar-flexor elasticity in chronic SCI patients decreased with increased injury duration.

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The length–tension relationship of human dorsiflexor and plantarflexor muscles after spinal cord injury

Cited by 12 publications

References 19 publications

Recovery of neuronal and network excitability after spinal cord injury and implications for spasticity

Recovery of neuronal and network excitability after spinal cord injury and implications for spasticity

Muscle fatigue characteristics in paralyzed muscle after spinal cord injury

Mechanical and neural changes in plantar-flexor muscles after spinal cord injury in humans

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