Neurogenic organ dysfunction syndrome after acute brain injury.

Systemic complications are common after acute brain injury (ABI) and may trigger coagulation cascades, systemic inflammation, as well as dysfunction of the cardiovascular, respiratory, and gastrointestinal systems, etc. The pathogenesis of these systemic manifestations is multifactorial but not yet fully elucidated. This paper introduces the novel term neurogenic organ dysfunction syndrome (NODS) to characterize systemic instability arising from internal and external perturbations of the neuronal center following ABI. Elucidating the central neurogenic mechanisms of NODS is critical for early detection and prevention of complications, thereby reducing mortality and improving patient outcomes following ABI. In this paper, we explore the potential central neurogenic mechanisms of NODS from the perspective of complex brain network theory, focusing on the structural network of the central autonomic system (CAS) that maintains systemic stability, and the functional network governed by the central stress system (CSS). The CAS can be divided into the cortical autonomic network, which involves higher cortical regions, and the subcortical autonomic network, which is relatively conserved, with its main connections located in deep brain structures. The CSS is a large-scale complex network characterized by hierarchy, hubs, and modularity, which together enable the competitive optimization of functional segregation and integration. Under physiological conditions, modules (mediating functional segregation) and hubs (functional integration) within the CSS dynamically trade-off with each other to maintain the overall homeostasis. However, this balance is disrupted following pathological insults or injury, resulting in weakened functional integrity of the CSS following ABI, impaired module activity, and disturbed hub integration. This paper also demonstrates the distinct pathological manifestations arising from disturbances at different levels of the homeostatic system. Finally, this study proposes potential clinical interventions, including analgesia and sedation, neuromodulation, and receptor regulation, for early interventions and potential treatment of NODS, aiming to improve patient outcomes.