Key result
Autonomic system imbalance, characterized by sympathetic hyperactivity and vagus nerve inhibition, integrates the existing pathogenesis and explains the progression of neurogenic pulmonary oedema.
This review proposes that autonomic system imbalance is a central mechanism in the development of neurogenic pulmonary oedema following central nervous system injury.
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Autonomic imbalance may underlie NPE after CNS injury; leaves open targeted interventions pending higher-level evidence.
Neurogenic pulmonary oedema (NPE) is a life-threatening complication that develops rapidly and dramatically after an injury to the central nervous system (CNS). The autonomic system imbalance produced by severe brain damage may play an important role in the development of NPE. Activation of the sympathetic nervous system and inhibition of the vagus nerve system are essential prerequisites for autonomic system imbalance. The more severe the damage, the more pronounced the phenomenon. Sympathetic hyperactivity is associated with increased release of catecholamines from peripheral sympathetic nerve endings, which can cause dramatic changes in haemodynamics and cause pulmonary oedema. On the other hand, the abnormal inflammatory response caused by vagus nerve inhibition may also play an important role in the pathogenesis of NPE. The perspective of autonomic system imbalance seems to perfectly integrate the existing pathogenesis of NPE and can explain the entire development progression of NPE.
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Yang et al. (2022) conducted a review in Neurogenic pulmonary oedema. Autonomic system imbalance was evaluated. Autonomic system imbalance, characterized by sympathetic hyperactivity and vagus nerve inhibition, integrates the existing pathogenesis and explains the progression of neurogenic pulmonary oedema.
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