Abstract

While spinal cord injuries (SCIs) result in a vast array of functional deficits, many of which are life threatening, the majority of SCIs are anatomically incomplete. Spared neural pathways contribute to functional and anatomical neuroplasticity that can occur spontaneously, or can be harnessed using rehabilitative, electrophysiological, or pharmacological strategies. With a focus on respiratory networks that are affected by cervical level SCI, the present review summarizes how non-invasive respiratory treatments can be used to harness this neuroplastic potential and enhance long-term recovery. Specific attention is given to “respiratory training” strategies currently used clinically (e.g., strength training) and those being developed through pre-clinical and early clinical testing [e.g., intermittent chemical stimulation via altering inhaled oxygen (hypoxia) or carbon dioxide stimulation]. Consideration is also given to the effect of training on non-respiratory (e.g., locomotor) networks. This review highlights advances in this area of pre-clinical and translational research, with insight into future directions for enhancing plasticity and improving functional outcomes after SCI.

Highlights

  • Respiratory dysfunction is one of the leading causes of morbidity and mortality for individuals with spinal cord injury (SCI) (DeVivo et al, 1993; Winslow and Rozovsky, 2003; Garshick et al, 2005; Hoh et al, 2013)

  • Experimental and clinical studies have demonstrated that these Activity based therapy (ABT) strategies can strengthen existing neuronal networks, stimulate synaptic and dendritic growth/plasticity, and increase baseline neuronal activity (Harkema, 2001; Dunlop, 2008; Lynskey et al, 2008; Dale-Nagle et al, 2010a; Singh et al, 2011a,b; Houle and Cote, 2013; Martinez et al, 2013; Hormigo et al, 2017)

  • Increased phrenic plasticity from intermittent hypoxia or hypercapnia led to using these strategies as an alternative method of “respiratory training.”

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Summary

Introduction

Respiratory dysfunction is one of the leading causes of morbidity and mortality for individuals with spinal cord injury (SCI) (DeVivo et al, 1993; Winslow and Rozovsky, 2003; Garshick et al, 2005; Hoh et al, 2013). One prominent example of neuroplasticity after spinal cord injury (SCI) has been documented in the respiratory system with spontaneous functional improvement.

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