| Literature DB >> 33280491 |
Marta Fedriga1,2, Andras Czigler1,3, Nathalie Nasr4, Frederick A Zeiler5,6,7,8, Soojin Park9, Joseph Donnelly10, Vasilios Papaioannou11, Shirin K Frisvold12, Stephan Wolf13, Frank Rasulo2, Marek Sykora14, Peter Smielewski1, Marek Czosnyka1.
Abstract
Refractory intracranial hypertension (RIH) is a dramatic increase in intracranial pressure (ICP) that cannot be controlled by treatment. Recent reports suggest that the autonomic nervous system (ANS) activity may be altered during changes in ICP. Our study aimed to assess ANS activity during RIH and the causal relationship between rising in ICP and autonomic activity. We reviewed retrospectively 24 multicenter (Cambridge, Tromso, Berlin) patients in whom RIH developed as a pre-terminal event after acute brain injury (ABI). They were monitored with ICP, arterial blood pressure (ABP), and electrocardiography (ECG) using ICM+ software. Parameters reflecting autonomic activity were computed in time and frequency domain through the measurement of heart rate variability (HRV) and baroreflex sensitivity (BRS). Our results demonstrated that a rise in ICP was associated to a significant rise in HRV and BRS with a higher significance level in the high-frequency HRV (p < 0.001). This increase was followed by a significant decrease in HRV and BRS above the upper-breakpoint of ICP where ICP pulse-amplitude starts to decrease whereas the mean ICP continues to rise. Temporality measured with a Granger test suggests a causal relationship from ICP to ANS. The above results suggest that a rise in ICP interacts with ANS activity, mainly interfacing with the parasympathetic-system. The ANS seems to react to the rise in ICP with a response possibly focused on maintaining the cerebrovascular homeostasis. This happens until the critical threshold of ICP is reached above which the ANS variables collapse, probably because of low perfusion of the brain and the central autonomic network.Entities:
Keywords: Granger causality; autonomic nervous system; refractory intracranial hypertension; upper breakpoint of ICP
Mesh:
Year: 2021 PMID: 33280491 PMCID: PMC8336253 DOI: 10.1089/neu.2020.7091
Source DB: PubMed Journal: J Neurotrauma ISSN: 0897-7151 Impact factor: 4.869