Central sympathetic nerve activation in subarachnoid hemorrhage

Abstract

Subarachnoid hemorrhage (SAH) is a life-threatening condition, and although its two main complications-cerebral vasospasm (CVS)/delayed cerebral ischemia (DCI) and early brain injury (EBI)-have been widely studied, prognosis has not improved over time. The sympathetic nerve (SN) system is important for the regulation of cardiovascular function and is closely associated with cerebral vessels and the regulation of cerebral blood flow and cerebrovascular function; thus, excessive SN activation leads to a rapid breakdown of homeostasis in the brain. In the hyperacute phase, patients with SAH can experience possibly lethal conditions that are thought to be associated with SN activation (catecholamine surge)-related arrhythmia, neurogenic pulmonary edema, and irreversible injury to the hypothalamus and brainstem. Although the role of the SN system in SAH has long been investigated and considerable evidence has been collected, the exact pathophysiology remains undetermined, mainly because the relationships between the SN system and SAH are complicated, and many SNmodulating factors are involved. Thus, research concerning these relationships needs to explore novel findings that correlate with the relevant concepts based on past reliable evidence. Here, we explore the role of the central SN (CSN) system in SAH pathophysiology and provide a comprehensive review of the functional CSN network; brain injury in hyperacute phase involving the CSN system; pathophysiological overlap between the CSN system and the two major SAH complications, CVS/DCI and EBI; CSN-modulating factors; and SAH-related extracerebral organ injury. Further studies are warranted to determine the specific roles of the CSN system in the brain injuries associated with SAH.

Trimethylamine N-oxide (TMAO) in patients with subarachnoid hemorrhage: a prospective observational study

“…Patients with SAH typically experience sympathetic activation and a so-called catecholamine surge which could lead to downregulation of the immune system in the gut. Thereupon, the composition of the microbiome changes [18,20]. Beneficial microbiota become increasingly deficient.…”

Plasma Amino Acids May Improve Prediction Accuracy of Cerebral Vasospasm after Aneurysmal Subarachnoid Haemorrhage

“…Minegishi et al (1987) demonstrated that plasma norepinephrine metabolite levels can serve as a prognostic discriminator for patients after aSAH [39]. Catecholamine surge causes activation of the sympathetic nervous system and may induce arrhythmias, neurogenic pulmonary edema, injury to the hypothalamus and brainstem, and is probably associated with the development of CVS [40]. We observed significantly higher levels of phenylalanine on day one post-operation in patients who later developed CVS (p = 0.049), what is consistent with the literature cited above.…”

Percutaneous cervical sympathetic block to treat cerebral vasospasm and delayed cerebral ischemia: a review of the evidence

“…20 The cerebral arteries have rich sympathetic innervation in the large cerebral arteries as well as within the smaller arteries and arterioles, 19 which raises the possibility that sympathetic stimulation in aSAH patients may directly cause vasospasm that impacts the macro-and microcirculation of the brain. 21 It also follows that sympathetic nerve blockade may release the vasoconstricting stimulus and improve CBF and cerebral perfusion (figure 2).…”