Significance of the Crossed Phrenic Phenomenon

Lewis, L. Jerome; Brookhart, John M.

doi:10.1152/ajplegacy.1951.166.2.241

Cited by 66 publications

(40 citation statements)

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“…This type of injury compromises direct (monosynaptic) projections from the ventral respiratory column in the medulla to ipsilateral phrenic motoneurons (Ellenberger and Feldman, 1988; Ellenberger et al, 1990; Keomani et al, 2014; Lane et al, 2009b; Lane et al, 2008; Vinit and Kastner, 2009a), and results in an ipsilateral hemidiaphragm paralysis (Figure 1). Despite the extent of injury, acute partial recovery of phrenic and hemidiaphragm activity after C2Hx can be accomplished by a subsequent contralateral phrenicotomy (Goshgarian, 2003a; Porter, 1895) or by inducing a respiratory stress such as asphyxia, hypoxia or hypercapnia (Golder and Mitchell, 2005; Lewis and Brookhart, 1951). This type of post-injury plasticity - known as the “cross-phrenic phenomenon” (CPP) – is attributed to activation of contralateral (spared), normally latent, bulbospinal pathways that cross the spinal midline below the injury (Figure 1A) (Goshgarian et al, 1991; Moreno et al, 1992).…”

Section: Plasticity After Cervical Scimentioning

confidence: 99%

Enhancing neural activity to drive respiratory plasticity following cervical spinal cord injury

Hormigo

Zholudeva

Spruance

et al. 2017

Experimental Neurology

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Cervical spinal cord injury (SCI) results in permanent life-altering sensorimotor deficits, among which impaired breathing is one of the most devastating and life-threatening. While clinical and experimental research has revealed that some spontaneous respiratory improvement (functional plasticity) can occur post-SCI, the extent of the recovery is limited and significant deficits persist. Thus, increasing effort is being made to develop therapies that harness and enhance this neuroplastic potential to optimize long-term recovery of breathing in injured individuals. One strategy with demonstrated therapeutic potential is the use of treatments that increase neural and muscular activity (e.g. locomotor training, neural and muscular stimulation) and promote plasticity. With a focus on respiratory function post-SCI, this review will discuss advances in the use of neural interfacing strategies and activity-based treatments, and highlights some recent results from our own research.

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Section: Plasticity After Cervical Scimentioning

confidence: 99%

Enhancing neural activity to drive respiratory plasticity following cervical spinal cord injury

Hormigo

Zholudeva

Spruance

et al. 2017

Experimental Neurology

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“…The significant increase in the drive to breathe activated a latent pathway that restored function to the hemidiaphragm paralyzed by hemisection and was later termed the ''crossed phrenic phenomenon'' (37). Further examination revealed that the amount of activity recorded from the previously paralyzed hemidiaphragm was proportional to the intensity of the respiratory drive (38). The presence of the crossed phrenic phenomenon has since been confirmed in dogs (37)(38)(39), cats (37)(38)(39)(40)(41), rabbits (37,(41)(42)(43), guinea pigs (44,45), rats (35,(46)(47)(48), mice (49), and even woodchucks (37).…”

Section: History Of the Crossed Phrenic Phenomenonmentioning

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

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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“…In this model a cervical spinal cord hemisection interrupts the major descending respiratory pathways and paralyzes the hemidiaphragm ipsilateral to hemisection. Subsequent transection of the phrenic nerve contralateral to the hemisection induces asphyxia, which enhances central respiratory drive and, thus, activates the latent respiratory motor pathway, reestablishing function to the hemidiaphragm paralyzed by hemisection [267]. Activation of the latent respiratory motor pathway can also be achieved pharmacologically by the application of antagonist of adenosine receptor type 1 and agonists of adenosine receptor type 2 [268,269] as well as serotonergic agonists [270,271] by a mechanism mediated by the 5-HT2 receptor [272].…”

Section: Spinal Cord Injurymentioning

confidence: 99%

Breathing Generation and Potential Pharmacotherapeutic Approaches to Central Respiratory Disorders

Peña

García²

2006

CMC

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Breathing is generated and controlled by a brainstem neuronal network. Both intrinsic and synaptic interactions are involved in respiratory rhythm generation and their contribution is state-dependent, changing with hypoxia and the neuromodulatory state. Cellular mechanisms involved in acute or chronic pathological conditions are still unknown. A dysfunction in the neuronal network that controls breathing may be involved in several respiratory disorders such as central sleep apnea, sudden infant death syndrome, congenital hypoventilation, and in some clinical conditions that produce breathing dysfunction such as drug-induced respiratory depression, obesity hypoventilation syndrome, etc. Despite the fact that several drugs are currently used to treat these diseases, the probable effects of this pharmacotherapy on the central rhythm generator and on other neuronal networks related with breathing control is poorly understood. Here, we review the current pharmacological approaches in the treatment of respiratory disorders, such as acetazolamide, theophylline, aminophylline, progesterone, nitric oxide. Possible effects of these drugs on the central respiratory network are discussed and putative therapeutic targets for the development of future pharmacological therapies suggested.

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Significance of the Crossed Phrenic Phenomenon

Cited by 66 publications

References 0 publications

Enhancing neural activity to drive respiratory plasticity following cervical spinal cord injury

Enhancing neural activity to drive respiratory plasticity following cervical spinal cord injury

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

Breathing Generation and Potential Pharmacotherapeutic Approaches to Central Respiratory Disorders

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