Sensorimotor Cortical Plasticity During Recovery Following Spinal Cord Injury: A Longitudinal fMRI Study

Jurkiewicz, Michael T.; Mikulis, David J.; McIlroy, William E.; Fehlings, Michael G.; Verrier, Mary C.

doi:10.1177/1545968307301872

Cited by 168 publications

(138 citation statements)

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“…Spontaneous recovery primarily appears to depend on the extent of tissue sparing at the injury site, allowing compensatory axonal sprouting and systems reorganization at levels ranging from the spinal cord to the cerebral cortex [3][4][5][6][7][8][9][10]. However, in cases of more severe injuries, means of enhancing endogenous levels of axonal sprouting and inducing true axonal regeneration are required to enhance functional outcomes.…”

Section: Human Spinal Cord Injurymentioning

confidence: 99%

Neurotrophins: Potential Therapeutic Tools for the Treatment of Spinal Cord Injury

Hollis

Tuszynski

2011

Neurotherapeutics

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Spinal cord injury permanently disrupts neuroanatomical circuitry and can result in severe functional deficits. These functional deficits, however, are not immutable and spontaneous recovery occurs in some patients. It is highly likely that this recovery is dependent upon spared tissue and the endogenous plasticity of the central nervous system. Neurotrophic factors are mediators of neuronal plasticity throughout development and into adulthood, affecting proliferation of neuronal precursors, neuronal survival, axonal growth, dendritic arborization and synapse formation. Neurotrophic factors are therefore excellent candidates for enhancing axonal plasticity and regeneration after spinal cord injury. Understanding growth factor effects on axonal growth and utilizing them to alter the intrinsic limitations on regenerative growth will provide potent tools for the development of translational therapeutic interventions for spinal cord injury.Keywords Neurotrophin . spinal cord injury . regeneration . axon plasticity . functional recovery Human Spinal Cord InjuryTraumatic injury of the spinal cord can produce a range of debilitating effects and permanently alter the capabilities and quality of life of its surviving victims. Damage to the central nervous system (CNS) in general results in destruction of neuronal circuitry. Contusion, compression, and penetration injuries of the spinal cord can interrupt the flow of sensory and motor information between the brain and periphery [1]. Depending on the location and severity of the injury, deficits can range from weakness of limb movement to total paralysis and ventilator-assisted respiration. Spontaneous functional recovery is limited, but can and often does occur in patients with initial sparing of sensorimotor function [2]. This recovery, which plateaus between 12 to 18 months, is very likely due to sparing and sprouting of axons within the zone of partial preservation, an area where some motor function remains intact, immediately adjacent to the lesion site [2].Approximately 40% of humans that sustain spinal cord injury (SCI) exhibit improvement from their early postinjury baseline, and this spontaneous recovery can range from modest to extensive [2]. Spontaneous recovery primarily appears to depend on the extent of tissue sparing at the injury site, allowing compensatory axonal sprouting and systems reorganization at levels ranging from the spinal cord to the cerebral cortex [3][4][5][6][7][8][9][10]. However, in cases of more severe injuries, means of enhancing endogenous levels of axonal sprouting and inducing true axonal regeneration are required to enhance functional outcomes.Electronic supplementary material The online version of this article

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Section: Human Spinal Cord Injurymentioning

confidence: 99%

Neurotrophins: Potential Therapeutic Tools for the Treatment of Spinal Cord Injury

Hollis

Tuszynski

2011

Neurotherapeutics

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“…Until now, only two Maximum t-value 11.2 ± 3.9 12.3 ± 4.5 9.9 ± 3.0 10.3 ± 3.7 10.3 ± 4.4 studies have been performed to report the temporal evolution of cortical sensorimotor activity after TSCI. 3,4 In their first study, where TSCI patients with motor recovery were studied, a progressive enlargement in the primary motor cortex and decreased activation in associated cortical areas was detected. 3 When they studied four tetraplegic individuals whose paralysis persisted, the activation was extensive in associated areas early post injury, but progressed towards no activation by the end of the first year.…”

Section: Discussionmentioning

confidence: 99%

“…3,4 In their first study, where TSCI patients with motor recovery were studied, a progressive enlargement in the primary motor cortex and decreased activation in associated cortical areas was detected. 3 When they studied four tetraplegic individuals whose paralysis persisted, the activation was extensive in associated areas early post injury, but progressed towards no activation by the end of the first year. 4 Our results differ slightly from these earlier findings.…”

Section: Discussionmentioning

confidence: 99%

“…Only a few studies have investigated cortical reorganisation after cervical TSCI. [2][3][4][5] However, there is still little evidence on the temporal changes in reorganisation of the sensorimotor cortex. 3,4 Functional magnetic resonance imaging (fMRI) could be used as a surrogate marker of functional outcome after TSCI.…”

Section: Introductionmentioning

confidence: 99%

“…[2][3][4][5] However, there is still little evidence on the temporal changes in reorganisation of the sensorimotor cortex. 3,4 Functional magnetic resonance imaging (fMRI) could be used as a surrogate marker of functional outcome after TSCI. 6,7 The aim of our study was to test the cortical activations in patients with cervical TSCI in acute and sub-acute phase after TSCI.…”

Section: Introductionmentioning

confidence: 99%

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Brain activation in the acute phase of traumatic spinal cord injury

et al. 2013

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Study design: Prospective clinical study. Background: The aim of the study was to investigate cortical reorganisation after traumatic spinal cord injury (TSCI) using functional magnetic resonance imaging (fMRI). Setting: Tartu University Hospital, Tartu, Estonia. Methods: We studied six right-handed tetraplegic TSCI patients at 1, 3 and 12 months after the injury and 12 age-and gender-matched healthy controls. Individuals performed simple test-rest cycles of flexion/extension of the right-hand fingers and flexion/extension of the right ankle during fMRI. The volumes of activation (VOA), maximum t-values, centres of gravity (COG) and weighted laterality indexes were calculated. Results: There was no recovery of neurologic function in three patients and, according to the American Spinal Injury Association (ASIA) Impairment Scale the remaining three recovered. A positive correlation between the VOA in the primary motor cortex and the ASIA Impairment Scale (1 month: r ¼ 0.82, P ¼ 0.002; 3 Month: r ¼ 0.63, P ¼ 0.03; 12 Month: r ¼ 0.23, P ¼ 0.52) was found. The study also revealed a pattern of cortical activation that was increased among the patients who recovered (in Brodmann area 4 (BA 4), P ¼ 0.06; BA 1-2-3-5, P ¼ 0.08; BA 6, P ¼ 0.05). During the hand task there was an expansion of COG laterally, anteriorly and inferiorly among the patients who recovered. During the hand movement the cortical activation was less lateralised among the patients compared with the controls (Po0.05). Conclusion: Our study has found broadening of cortical activation and shift of COG during the first year after TSCI, depending on the recovery.

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Research Methods in Neuropsychology

Bauer

Dunn

2012

Handbook of Psychology, Second Edition

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Sensorimotor Cortical Plasticity During Recovery Following Spinal Cord Injury: A Longitudinal fMRI Study

Cited by 168 publications

References 43 publications

Neurotrophins: Potential Therapeutic Tools for the Treatment of Spinal Cord Injury

Neurotrophins: Potential Therapeutic Tools for the Treatment of Spinal Cord Injury

Brain activation in the acute phase of traumatic spinal cord injury

Research Methods in Neuropsychology

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