Evidence map›Paper›PMID 40445402›Full record

ArticleActa neurochirurgica2025

Paroxysmal sympathetic hyperactivity risk modeling based on transients in time series describing the autonomic nervous system and cerebral hemodynamics.

Mikołaj Najda, Cyprian Mataczyński, Małgorzata Burzyńska, Magdalena Kasprowicz, Jarosław Kędziora, Emma Hammarlund, Eric P Thelin, Agnieszka Uryga

Abstract read
In one paragraph

Article in Acta neurochirurgica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Mikołaj NajdaInstitute of Data Science, Maastricht University, Maastricht, Limburg, The Netherlands.
Cyprian MataczyńskiFaculty of Information and Communication Technology, Wroclaw University of Science and Technology, Wroclaw, Poland.
Małgorzata BurzyńskaFaculty of Medicine, Clinical Department of Anesthesiology and Intensive Therapy, Wroclaw Medical University, Wroclaw, Poland.
Magdalena KasprowiczDepartment of Biomedical Engineering, Wroclaw University of Science and Technology, Wybrzeze Wyspianskiego 27, 50-370, Wroclaw, Poland.
Jarosław KędzioraFaculty of Medicine, Clinical Department of Anesthesiology and Intensive Therapy, Wroclaw Medical University, Wroclaw, Poland.
Emma HammarlundMedical Unit Neurology, Karolinska University Hospital, Stockholm, Sweden.
Eric P ThelinMedical Unit Neurology, Karolinska University Hospital, Stockholm, Sweden.
Agnieszka UrygaDepartment of Biomedical Engineering, Wroclaw University of Science and Technology, Wybrzeze Wyspianskiego 27, 50-370, Wroclaw, Poland. agnieszka.uryga@pwr.edu.pl.

Funding

Karolinska Institutet Funds 2022-01576National Science Centre, Poland UMO-2022/47/D/ST7/00229Region Stockholm Clinical Research Appointment FoUI-981490 and FoUI-1001497Research Committee of the Medical University of Wroclaw SUBK.A170.23.048The Swedish Brain Foundation FO2023-0124The Swedish Society of Medicine SLS-985504
6 · The paper itself

Abstract

purposeOverstimulation of the autonomic nervous system (ANS) in the acute phase after traumatic brain injury (TBI) may lead to paroxysmal sympathetic hyperactivity (PSH) syndrome. This study aimed to investigate the impact of the relationship between ANS activity and cerebral hemodynamics on the development of PSH syndrome. MATERIALS AND

methodsThis retrospective study included 41 TBI patients admitted to Wroclaw University Hospital (Poland). Among them, 14 were classified as at risk for PSH based on the probabilistic Paroxysmal Sympathetic Hyperactivity Assessment Measure (PSH-AM), with 10 rated as 'possible' and 4 as 'probable'. High-resolution neuromonitoring data from the first 72 h post-injury included intracranial pressure (ICP), pressure reactivity index (PRx), baroreflex sensitivity (BRS), arterial blood pressure (ABP), and heart rate (HR). The correlation between ANS activity and cerebral hemodynamics was quantified using the mean, standard deviation, and zero-crossing rate (ZCR) across sliding windows of 3, 6, 12, and 24 h. Logistic regression was used to model PSH risk.

resultsThe PSH risk model, including ZCR-based variability of ANS-cerebral hemodynamic correlations within a 3-h sliding window and adjusted by clinical metadata, achieved the highest performance (AUC 0.72 ± 0.27), outperforming the clinical metadata-only model (AUC 0.64 ± 0.18). Aggregated feature importance values indicated that the most predictive relationships were observed between HR-ICP and HR-PRx.

conclusionsIncluding the early post-injury interactions between ANS and cerebral hemodynamics in the clinical characteristics-based PSH risk model may improve its performance. Further studies in larger cohorts are necessary to validate these findings.

Indexed as

Autonomic Nervous System DiseasesBrain Injuries, TraumaticCerebrovascular CirculationHemodynamicsAdultBaroreflexFemaleHeart RateHumansIntracranial PressureMaleMiddle AgedRetrospective StudiesYoung AdultAutonomic nervous systemCerebral hemodynamicsParoxysmal sympathetic hyperactivityTraumatic brain injury

Identifiers

PMID40445402
PMCPMC12125141

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.