Interlimb reflex activity after spinal cord injury in man: strengthening response patterns are consistent with ongoing synaptic plasticity

Calancie, Blair; Alexeeva, Natalia; Broton, James G.; Molano, Maria R.

doi:10.1016/j.clinph.2004.07.018

Cited by 47 publications

(44 citation statements)

References 61 publications

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“…There is overwhelming evidence that the dramatic consequences of a severe SCI expand beyond these apparent deficits (Hiersemenzel et al, 2000;Dietz and Muller, 2004;Calancie et al, 2005;Courtine et al, 2009;Dietz et al, 2009;Boulenguez et al,electrophysiological studies have suggested that neuronal circuits deprived of supraspinal input undergo a progressive and extensive remodelling (Calancie et al, 1996(Calancie et al, , 2000Maegele et al, 2002;Beres-Jones et al, 2003;Calancie et al, 2005;Harkema, 2008); a process that continues to evolve for years after the SCI (Dietz, 2010). These alterations have been associated with the development of neuronal dysfunction in chronically paralysed individuals.…”

Section: Introductionmentioning

confidence: 99%

Undirected compensatory plasticity contributes to neuronal dysfunction after severe spinal cord injury

Beauparlant

Brand

Barraud

et al. 2013

Brain

115

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Severe spinal cord injury in humans leads to a progressive neuronal dysfunction in the chronic stage of the injury. This dysfunction is characterized by premature exhaustion of muscle activity during assisted locomotion, which is associated with the emergence of abnormal reflex responses. Here, we hypothesize that undirected compensatory plasticity within neural systems caudal to a severe spinal cord injury contributes to the development of neuronal dysfunction in the chronic stage of the injury. We evaluated alterations in functional, electrophysiological and neuromorphological properties of lumbosacral circuitries in adult rats with a staggered thoracic hemisection injury. In the chronic stage of the injury, rats exhibited significant neuronal dysfunction, which was characterized by co-activation of antagonistic muscles, exhaustion of locomotor muscle activity, and deterioration of electrochemically-enabled gait patterns. As observed in humans, neuronal dysfunction was associated with the emergence of abnormal, longlatency reflex responses in leg muscles. Analyses of circuit, fibre and synapse density in segments caudal to the spinal cord injury revealed an extensive, lamina-specific remodelling of neuronal networks in response to the interruption of supraspinal input. These plastic changes restored a near-normal level of synaptic input within denervated spinal segments in the chronic stage of injury. Syndromic analysis uncovered significant correlations between the development of neuronal dysfunction, emergence of abnormal reflexes, and anatomical remodelling of lumbosacral circuitries. Together, these results suggest that spinal neurons deprived of supraspinal input strive to re-establish their synaptic environment. However, this undirected compensatory plasticity forms aberrant neuronal circuits, which may engage inappropriate combinations of sensorimotor networks during gait execution.

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Section: Introductionmentioning

confidence: 99%

Undirected compensatory plasticity contributes to neuronal dysfunction after severe spinal cord injury

Beauparlant

Brand

Barraud

et al. 2013

Brain

115

View full text Add to dashboard Cite

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“…Maladaptive sensory connections may lead to chronic pain 56 or the emergence of interlimb reflexes that provide no functional benefit to the subject. 57 FES training regimens could be used to encourage appropriate adaptive patterns of neural activity that support the recovery of function.…”

Section: Discussionmentioning

confidence: 99%

An animal model of functional electrical stimulation: evidence that the central nervous system modulates the consequences of training

Hook

Grau

2007

Spinal Cord

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Study Design: Review of how spinal neurons can modulate the consequences of functional electrical stimulation (FES) in an animal model. Methods: Spinal effects of FES are examined in male Sprague-Dawley rats transected at the second thoracic vertebra. The rats are exposed to FES training 24-48 h after surgery. Experimental manipulations of stimulation parameters, combined with physiological and pharmacological procedures, are used to examine the potential role of spinal neurons. Results: The isolated spinal cord is inherently capable of learning the response-outcome relations imposed in FES training contingencies. Adaptive behavioral modifications are observed when an outcome (electrical stimulation) is contingent on a behavioral response. In contrast, a lack of correlation between the response and outcome in training produces a learning deficit in the spinal cord, rendering it incapable of adaptive learning for up to 48 h. The N-methyl-D-aspartic acid receptor appears to mediate both the adaptive plasticity and loss of plasticity, seen in this spinal model. Conclusion:The behavioral effects observed with FES therapies are not simply due to the direct (motor) consequences of stimulation elicited by the activation of efferent motor neurons and/or selected muscles. FES training has the capacity to shape inherent spinal circuits and to produce a long-lasting behavioral modification. Further understanding of the spinal mechanisms underlying adaptive behavioral modification will be integral for establishing functional neural connections in a regenerating spinal system.

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“…3 Moreover, structural changes in the cortex and pathways both rostral and caudal to the injury epicenter may provide additional barriers for restoring motor function following SCI. [4][5][6][7] Non-invasive repetitive transcranial magnetic stimulation (rTMS) of the motor cortex, a powerful tool for modulating excitability of the motor cortex, has been used to treat a variety of neurological disorders, including stroke, Parkinson's disease, and multiple sclerosis. days modulated corticospinal excitability and improved hand gross motor skills in persons with injury to the cervical spinal cord.…”

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confidence: 99%

Efficacy of QuadroPulse rTMS for improving motor function after spinal cord injury: Three case studies

Alexeeva

Calancie

2014

The Journal of Spinal Cord Medicine

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Context/objective: To examine the effects of repetitive QuadroPulse transcranial magnetic stimulation (rTMS QP ) on hand/leg function after spinal cord injury (SCI). Design: Interventional proof-of-concept study. Setting: University laboratory. Participants: Three adult subjects with cervical SCI. Interventions: Repeated trains of magnetic stimuli were applied to the motor cortical hand/leg area. Several exploratory single-day rTMS QP protocols were examined. Ultimately we settled on a protocol using three 5-day trials of (1) rTMS QP only; (2) exercise only (targeting hand or leg function); and (3) rTMS QP combined with exercise. Outcome measures: Hand motor function was assessed by Purdue Pegboard and Complete Minnesota Dexterity tests. Walking function was based on treadmill walking and the Timed Up and Go test. Electromyographic recordings were used for neurophysiological testing of cortical (by single-and doublepulse TMS) and spinal (via tendon taps and electrical nerve stimulation) excitability. Results: Single-day rTMS QP application had no clear effect in the 2 subjects whose hand function was targeted, but improved walking speed in the person targeted for walking, accompanied by increased cortical excitability and reduced spinal excitability. All 3 subjects showed functional improvement following the 5-day rTMS QP intervention, an effect being even more pronounced after the five-day combined rTMS QP + exercise sessions. There were no rTMS QP -associated adverse effects. Conclusion: Our findings suggest a functional benefit of motor cortical rTMS QP after SCI. The effect of rTMS QP appears to be augmented when stimulation is accompanied by targeted exercises, warranting expansion of this pilot study to a larger subject population.

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Interlimb reflex activity after spinal cord injury in man: strengthening response patterns are consistent with ongoing synaptic plasticity

Cited by 47 publications

References 61 publications

Undirected compensatory plasticity contributes to neuronal dysfunction after severe spinal cord injury

Undirected compensatory plasticity contributes to neuronal dysfunction after severe spinal cord injury

An animal model of functional electrical stimulation: evidence that the central nervous system modulates the consequences of training

Efficacy of QuadroPulse rTMS for improving motor function after spinal cord injury: Three case studies

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