Quantitative Assessment of Respiratory Function Following Contusion Injury of the Cervical Spinal Cord

El-Bohy, Ashraf A.; Schrimsher, Gregory W.; Reier, Paul J.; Goshgarian, Harry G.

doi:10.1006/exnr.1997.6757

Cited by 61 publications

(58 citation statements)

References 32 publications

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“…10 This hypothesis was supported by findings from el-Bohy and colleagues that demonstrated an increase in phrenic neurogram activity ipsilateral to contusion. 5 In our previous study, we found an increase in hemidiaphragm EMG activity ipsilateral to the cervical injury site, 2 supporting the notion of increased drive from supraspinal circuitry. Local changes in spinal circuits or reorganization of suprapinal pathways have been extensively described following C2 hemisection; [19][20][21] however, at present we are uncertain of the effect of a midcervical contusion injury on these mechanisms.…”

Section: Discussionsupporting

confidence: 68%

“…Nevertheless, experimental data are lacking regarding the timing of early PhMN loss and the consequent role of gray matter sparing on global breathing function during the initial stages following midcervical spinal contusion. 5,6 Detailed characterization of the time course of PhMN loss post-injury will provide valuable information for determining the therapeutic window for targeting secondary PhMN degeneration. We therefore focused our study on the analysis of PhMNs during the first 2 weeks following midcervical C4 contusion SCI, including PhMN loss, anterograde degeneration along the phrenic nerve, and innervation changes at the diaphragm neuromuscular junctions.…”

Section: Introductionmentioning

confidence: 99%

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Early Phrenic Motor Neuron Loss and Transient Respiratory Abnormalities after Unilateral Cervical Spinal Cord Contusion

Nicaise

Frank

Hala

et al. 2013

Journal of Neurotrauma

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Contusion-type cervical spinal cord injury (SCI) is one of the most common forms of SCI observed in patients. In particular, injuries targeting the C3-C5 region affect the pool of phrenic motor neurons (PhMNs) that innervates the diaphragm, resulting in significant and often chronic respiratory dysfunction. Using a previously described rat model of unilateral midcervical C4 contusion with the Infinite Horizon Impactor, we have characterized the early time course of PhMN degeneration and consequent respiratory deficits following injury, as this knowledge is important for designing relevant treatment strategies targeting protection and plasticity of PhMN circuitry. PhMN loss (48% of the ipsilateral pool) occurred almost entirely during the first 24 h post-injury, resulting in persistent phrenic nerve axonal degeneration and denervation at the diaphragm neuromuscular junction (NMJ). Reduced diaphragm compound muscle action potential amplitudes following phrenic nerve stimulation were observed as early as the first day post-injury (30% of pre-injury maximum amplitude), with slow functional improvement over time that was associated with partial reinnervation at the diaphragm NMJ. Consistent with ipsilateral diaphragmatic compromise, the injury resulted in rapid, yet only transient, changes in overall ventilatory parameters measured via whole-body plethysmography, including increased respiratory rate, decreased tidal volume, and decreased peak inspiratory flow. Despite significant ipsilateral PhMN loss, the respiratory system has the capacity to quickly compensate for partially impaired hemidiaphragm function, suggesting that C4 hemicontusion in rats is a model of SCI that manifests subacute respiratory abnormalities. Collectively, these findings demonstrate significant and persistent diaphragm compromise in a clinically relevant model of midcervical contusion SCI; however, the therapeutic window for PhMN protection is restricted to early time points post-injury. On the contrary, preventing loss of innervation by PhMNs and/or inducing plasticity in spared PhMN axons at the diaphragm NMJ are relevant long-term targets.

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Section: Discussionsupporting

confidence: 68%

Section: Introductionmentioning

confidence: 99%

Early Phrenic Motor Neuron Loss and Transient Respiratory Abnormalities after Unilateral Cervical Spinal Cord Contusion

Nicaise

Frank

Hala

et al. 2013

Journal of Neurotrauma

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“…Previous reports examining respiratory dysfunction after SCI examined pathophysiology in either thoracic models or anesthetized rats (El-Bohy et al, 1998;Teng et al, 1999Teng et al, , 2003Golder et al, 2001). These studies were pivotal but showed only transient dysfunction or were necessarily terminal.…”

Section: Discussionmentioning

confidence: 99%

Respiratory Abnormalities Resulting from Midcervical Spinal Cord Injury and their Reversal by Serotonin 1A Agonists in Conscious Rats

Choi

Liao²,

Newton³

et al. 2005

J. Neurosci.

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“…Recently, contusion models have been used to examine the effect of high SCI on respiration (33)(34)(35). Baussart et al (35) developed a C2-contusion injury that displays respiratory patterns similar to a C2-hemisection injury and allows one to examine the activation and neuroplasticity of latent respiratory pathways similar to the hemisection model.…”

Section: Neural Circuitry Underlying Respirationmentioning

confidence: 99%

Effect of Spinal Cord Injury on the Respiratory System: Basic Research and Current Clinical Treatment Options

Zimmer

Nantwi

Goshgarian

2007

The Journal of Spinal Cord Medicine

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154

126

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Summary: Spinal cord injury (SCI) often leads to an impairment of the respiratory system. The more rostral the level of injury, the more likely the injury will affect ventilation. In fact, respiratory insufficiency is the number one cause of mortality and morbidity after SCI. This review highlights the progress that has been made in basic and clinical research, while noting the gaps in our knowledge. Basic research has focused on a hemisection injury model to examine methods aimed at improving respiratory function after SCI, but contusion injury models have also been used. Increasing synaptic plasticity, strengthening spared axonal pathways, and the disinhibition of phrenic motor neurons all result in the activation of a latent respiratory motor pathway that restores function to a previously paralyzed hemidiaphragm in animal models. Human clinical studies have revealed that respiratory function is negatively impacted by SCI. Respiratory muscle training regimens may improve inspiratory function after SCI, but more thorough and carefully designed studies are needed to adequately address this issue. Phrenic nerve and diaphragm pacing are options available to wean patients from standard mechanical ventilation. The techniques aimed at improving respiratory function in humans with SCI have both pros and cons, but having more options available to the clinician allows for more individualized treatment, resulting in better patient care. Despite significant progress in both basic and clinical research, there is still a significant gap in our understanding of the effect of SCI on the respiratory system.

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Quantitative Assessment of Respiratory Function Following Contusion Injury of the Cervical Spinal Cord

Cited by 61 publications

References 32 publications

Early Phrenic Motor Neuron Loss and Transient Respiratory Abnormalities after Unilateral Cervical Spinal Cord Contusion

Early Phrenic Motor Neuron Loss and Transient Respiratory Abnormalities after Unilateral Cervical Spinal Cord Contusion

Respiratory Abnormalities Resulting from Midcervical Spinal Cord Injury and their Reversal by Serotonin 1A Agonists in Conscious Rats

Effect of Spinal Cord Injury on the Respiratory System: Basic Research and Current Clinical Treatment Options

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