Respiratory Training and Plasticity After Cervical Spinal Cord Injury

Randelman, Margo L.; Zholudeva, Lyandysha V.; Vinit, Stéphane; Lane, Megan

doi:10.3389/fncel.2021.700821

Cited by 19 publications

(12 citation statements)

References 229 publications

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“…Current therapeutic modalities aimed at restoring respiratory motor function after injury are largely ineffective. Identification of novel therapies that harness the intrinsic capacity of the CNS for plasticity are of paramount importance (Randelman et al., 2021; Vose et al., 2022). Moreover, when combined with task‐specific respiratory training, AIHH effects may be synergistic (Welch, Sutor et al., 2020), further increasing the potential for recovery.…”

Section: Discussionmentioning

confidence: 99%

Acute intermittent hypercapnic‐hypoxia elicits central neural respiratory motor plasticity in humans

Welch

Nair

Argento

et al. 2022

The Journal of Physiology

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Acute intermittent hypoxia (AIH) elicits long‐term facilitation (LTF) of respiration. Although LTF is observed when CO2 is elevated during AIH in awake humans, the influence of CO2 on corticospinal respiratory motor plasticity is unknown. Thus, we tested the hypotheses that acute intermittent hypercapnic‐hypoxia (AIHH): (1) enhances cortico‐phrenic neurotransmission (reflecting volitional respiratory control); and (2) elicits ventilatory LTF (reflecting automatic respiratory control). Eighteen healthy adults completed four study visits. Day 1 consisted of anthropometry and pulmonary function testing. On Days 2, 3 and 4, in a balanced alternating sequence, participants received: AIHH, poikilocapnic AIH, and normocapnic‐normoxia (Sham). Protocols consisted of 15, 60 s exposures with 90 s normoxic intervals. Transcranial (TMS) and cervical (CMS) magnetic stimulation were used to induce diaphragmatic motor‐evoked potentials and compound muscle action potentials, respectively. Respiratory drive was assessed via mouth occlusion pressure (P0.1), and minute ventilation measured at rest. Dependent variables were assessed at baseline and 30–60 min after exposures. Increases in TMS‐evoked diaphragm potential amplitudes were observed following AIHH vs. Sham (+28 ± 41%, P = 0.003), but not after AIH. No changes were observed in CMS‐evoked diaphragm potential amplitudes. Mouth occlusion pressure also increased after AIHH (+21 ± 34%, P = 0.033), but not after AIH. Ventilatory LTF was not observed after any treatment. We demonstrate that AIHH elicits central neural mechanisms of respiratory motor plasticity and increases resting respiratory drive in awake humans. These findings may have important implications for neurorehabilitation after spinal cord injury and other neuromuscular disorders compromising breathing. Key points The occurrence of respiratory long‐term facilitation following acute exposure to intermittent hypoxia is believed to be dependent upon CO2 regulation – mechanisms governing the critical role of CO2 have seldom been explored. We tested the hypothesis that acute intermittent hypercapnic‐hypoxia (AIHH) enhances cortico‐phrenic neurotransmission in awake healthy humans. The amplitude of diaphragmatic motor‐evoked potentials induced by transcranial magnetic stimulation was increased after AIHH, but not the amplitude of compound muscle action potentials evoked by cervical magnetic stimulation. Mouth occlusion pressure (P0.1, an indicator of neural respiratory drive) was also increased after AIHH, but not tidal volume or minute ventilation. Thus, moderate AIHH elicits central neural mechanisms of respiratory motor plasticity, without measurable ventilatory long‐term facilitation in awake humans.

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Section: Discussionmentioning

confidence: 99%

Acute intermittent hypercapnic‐hypoxia elicits central neural respiratory motor plasticity in humans

Welch

Nair

Argento

et al. 2022

The Journal of Physiology

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“…At the cervical level (C3–C4) originates the phrenic nerve that innervates the diaphragm (responsible for changing respiratory volumes at the ribcage level Hoh et al, 2013). The nerves that innervate the inspiratory and expiratory muscles will additionally be impacted if the upper cervical spinal cord is injured, potentially causing breathing impairment up to apnea and other respiratory complications [ 48 ]. Some functional plasticity is mentioned, but the functional deficit persists for a long time.…”

Section: Sci-associated Complicationsmentioning

confidence: 99%

The Outcomes of Robotic Rehabilitation Assisted Devices Following Spinal Cord Injury and the Prevention of Secondary Associated Complications

Nistor-Cseppentö¹,

Gherle²,

Negruț³

et al. 2022

Medicina

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Spinal cord injuries (SCIs) have major consequences on the patient’s health and life. Voluntary muscle paralysis caused by spinal cord damage affects the patient’s independence. Following SCI, an irreversible motor and sensory deficit occurs (spasticity, muscle paralysis, atrophy, pain, gait disorders, pain). This pathology has implications on the whole organism: on the osteoarticular, muscular, cardiovascular, respiratory, gastrointestinal, genito-urinary, skin, metabolic disorders, and neuro-psychic systems. The rehabilitation process for a subject having SCIs can be considered complex, since the pathophysiological mechanism and biochemical modifications occurring at the level of spinal cord are not yet fully elucidated. This review aims at evaluating the impact of robotic-assisted rehabilitation in subjects who have suffered SCI, both in terms of regaining mobility as a major dysfunction in patients with SCI, but also in terms of improving overall fitness and cardiovascular function, respiratory function, as well as the gastrointestinal system, bone density and finally the psychosocial issues, based on multiple clinical trials, and pilot studies. The researched literature in the topic revealed that in order to increase the chances of neuro-motor recovery and to obtain satisfactory results, the combination of robotic therapy, a complex recovery treatment and specific medication is one of the best decisions. Furthermore, the use of these exoskeletons facilitates better/greater autonomy for patients, as well as optimal social integration.

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“…Moreover, in this mini-review, we consider only CSH and CIH models which might resemble chronic hypoxic conditions in humans. Intriguing reports of the effects of intermittent hypoxia on neuroplasticity with low-frequency hypoxic episodes lasting several minutes ( Gonzalez-Rothi et al, 2015 ; Navarrete-Opazo et al, 2015 ) are subjects of other expert reviews ( Randelman et al, 2021 ). Finally, we note that our intention is to cover significant breadth of understanding of the topic of cardio-metabolic consequences of chronic hypoxia in animal models, sacrificing some depth of specific models and outcomes.…”

Section: Introductionmentioning

confidence: 99%

The Cardiovascular and Metabolic Effects of Chronic Hypoxia in Animal Models: A Mini-Review

2022

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Animal models are useful to understand the myriad physiological effects of hypoxia. Such models attempt to recapitulate the hypoxemia of human disease in various ways. In this mini-review, we consider the various animal models which have been deployed to understand the effects of chronic hypoxia on pulmonary and systemic blood pressure, glucose and lipid metabolism, atherosclerosis, and stroke. Chronic sustained hypoxia (CSH)—a model of chronic lung or heart diseases in which hypoxemia may be longstanding and persistent, or of high altitude, in which effective atmospheric oxygen concentration is low—reliably induces pulmonary hypertension in rodents, and appears to have protective effects on glucose metabolism. Chronic intermittent hypoxia (CIH) has long been used as a model of obstructive sleep apnea (OSA), in which recurrent airway occlusion results in intermittent reductions in oxyhemoglobin saturations throughout the night. CIH was first shown to increase systemic blood pressure, but has also been associated with other maladaptive physiological changes, including glucose dysregulation, atherosclerosis, progression of nonalcoholic fatty liver disease, and endothelial dysfunction. However, models of CIH have generally been implemented so as to mimic severe human OSA, with comparatively less focus on milder hypoxic regimens. Here we discuss CSH and CIH conceptually, the effects of these stimuli, and limitations of the available data.

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Respiratory Training and Plasticity After Cervical Spinal Cord Injury

Cited by 19 publications

References 229 publications

Acute intermittent hypercapnic‐hypoxia elicits central neural respiratory motor plasticity in humans

Acute intermittent hypercapnic‐hypoxia elicits central neural respiratory motor plasticity in humans

The Outcomes of Robotic Rehabilitation Assisted Devices Following Spinal Cord Injury and the Prevention of Secondary Associated Complications

The Cardiovascular and Metabolic Effects of Chronic Hypoxia in Animal Models: A Mini-Review

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