Risk factors for intracerebral hemorrhage in small-vessel disease and non-small-vessel disease etiologies-an observational proof-of-concept study.

brain tumor cerebral amyloid angiopathy cerebral small-vessel disease hypertension hypertensive arteriopathy intracerebral hemorrhage trauma vascular malformation

Journal

Frontiers in neurology
ISSN: 1664-2295
Titre abrégé: Front Neurol
Pays: Switzerland
ID NLM: 101546899

Informations de publication

Date de publication:
2024
Historique:
received: 16 10 2023
accepted: 19 02 2024
medline: 22 3 2024
pubmed: 22 3 2024
entrez: 22 3 2024
Statut: epublish

Résumé

Sporadic cerebral small-vessel disease (CSVD), i.e., hypertensive arteriopathy (HA) and cerebral amyloid angiopathy (CAA), is the main cause of spontaneous intracerebral hemorrhage (ICH). Nevertheless, a substantial portion of ICH cases arises from non-CSVD etiologies, such as trauma, vascular malformations, and brain tumors. While studies compared HA- and CAA-related ICH, non-CSVD etiologies were excluded from these comparisons and are consequently underexamined with regard to additional factors contributing to increased bleeding risk beyond their main pathology. As a proof of concept, we conducted a retrospective observational study in 922 patients to compare HA, CAA, and non-CSVD-related ICH with regard to factors that are known to contribute to spontaneous ICH onset. Medical records (available for In 922 patients with ICH (median age of 71 years), HA and CAA caused the majority of cases ( Risk factors for spontaneous ICH are less common in non-CSVD ICH etiologies than in HA- and CAA-related ICH, but are still frequent. Future studies should incorporate these factors, in addition to the main pathology, to stratify an individual's risk of bleeding.

Sections du résumé

Background UNASSIGNED
Sporadic cerebral small-vessel disease (CSVD), i.e., hypertensive arteriopathy (HA) and cerebral amyloid angiopathy (CAA), is the main cause of spontaneous intracerebral hemorrhage (ICH). Nevertheless, a substantial portion of ICH cases arises from non-CSVD etiologies, such as trauma, vascular malformations, and brain tumors. While studies compared HA- and CAA-related ICH, non-CSVD etiologies were excluded from these comparisons and are consequently underexamined with regard to additional factors contributing to increased bleeding risk beyond their main pathology.
Methods UNASSIGNED
As a proof of concept, we conducted a retrospective observational study in 922 patients to compare HA, CAA, and non-CSVD-related ICH with regard to factors that are known to contribute to spontaneous ICH onset. Medical records (available for
Results UNASSIGNED
In 922 patients with ICH (median age of 71 years), HA and CAA caused the majority of cases (
Conclusion UNASSIGNED
Risk factors for spontaneous ICH are less common in non-CSVD ICH etiologies than in HA- and CAA-related ICH, but are still frequent. Future studies should incorporate these factors, in addition to the main pathology, to stratify an individual's risk of bleeding.

Identifiants

pubmed: 38515448
doi: 10.3389/fneur.2024.1322442
pmc: PMC10954881
doi:

Types de publication

Journal Article

Langues

eng

Pagination

1322442

Informations de copyright

Copyright © 2024 Arndt, Chahem, Luchtmann, Kuschel, Behme, Pfister, Neumann, Görtler, Dörner, Pawlitzki, Jansen, Meuth, Vielhaber, Henneicke and Schreiber.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Auteurs

Philipp Arndt (P)

Department of Neurology, Otto-von-Guericke University, Magdeburg, Germany.
German Center for Neurodegenerative Diseases (DZNE) within the Helmholtz Association, Magdeburg, Germany.

Christian Chahem (C)

Department of Neurology, Otto-von-Guericke University, Magdeburg, Germany.

Michael Luchtmann (M)

Department of Neurosurgery, Paracelsus-Klinik, Zwickau, Germany.
Department of Neurosurgery, Otto-von-Guericke University, Magdeburg, Germany.

Jan-Niklas Kuschel (JN)

Department of Neurology, Otto-von-Guericke University, Magdeburg, Germany.

Daniel Behme (D)

Department of Neuroradiology, Otto-von-Guericke University, Magdeburg, Germany.

Malte Pfister (M)

Department of Neurology, Otto-von-Guericke University, Magdeburg, Germany.

Jens Neumann (J)

Department of Neurology, Otto-von-Guericke University, Magdeburg, Germany.

Michael Görtler (M)

Department of Neurology, Otto-von-Guericke University, Magdeburg, Germany.

Marc Dörner (M)

German Center for Neurodegenerative Diseases (DZNE) within the Helmholtz Association, Magdeburg, Germany.
Department of Consultation-Liaison-Psychiatry and Psychosomatic Medicine, University Hospital Zurich, University of Zurich, Zurich, Switzerland.

Marc Pawlitzki (M)

Department of Neurology, Heinrich-Heine-University, Düsseldorf, Germany.

Robin Jansen (R)

Department of Neurology, Heinrich-Heine-University, Düsseldorf, Germany.

Sven G Meuth (SG)

Department of Neurology, Heinrich-Heine-University, Düsseldorf, Germany.

Stefan Vielhaber (S)

Department of Neurology, Otto-von-Guericke University, Magdeburg, Germany.
Center for Behavioral Brain Sciences (CBBS), Magdeburg, Germany.

Solveig Henneicke (S)

Department of Neurology, Otto-von-Guericke University, Magdeburg, Germany.
German Center for Neurodegenerative Diseases (DZNE) within the Helmholtz Association, Magdeburg, Germany.

Stefanie Schreiber (S)

Department of Neurology, Otto-von-Guericke University, Magdeburg, Germany.
German Center for Neurodegenerative Diseases (DZNE) within the Helmholtz Association, Magdeburg, Germany.
Center for Behavioral Brain Sciences (CBBS), Magdeburg, Germany.

Classifications MeSH