Related Experiment Video

Updated: May 18, 2026

Double Direct Injection of Blood into the Cisterna Magna as a Model of Subarachnoid Hemorrhage
10:34

Double Direct Injection of Blood into the Cisterna Magna as a Model of Subarachnoid Hemorrhage

Published on: August 30, 2020

Beyond delayed cerebral vasospasm: infarct patterns in patients with subarachnoid hemorrhage

M Wagner1, P Steinbeis, E Güresir

  • 1Institute of Neuroradiology, Goethe University Hospital, Schleusenweg 2-16, 60528, Frankfurt a. M., Germany. marlies.wagner@kgu.de

Clinical Neuroradiology
|September 27, 2012
PubMed

Insights

Delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH) can occur without angiographic vasospasm. Atypical infarcts are often caused by treatment complications or microcirculation disturbances, suggesting broader therapeutic strategies are needed.

Area of Science:

  • Neurology
  • Neurosurgery
  • Radiology

Background:

  • Delayed cerebral ischemia (DCI) is a significant complication following aneurysmal subarachnoid hemorrhage (SAH).
  • Angiographic vasospasm (CVS) is traditionally considered the primary cause of DCI.
  • Current treatments for CVS, including endovascular therapies, have limited success rates.

Purpose of the Study:

  • To analyze patterns of ischemic lesions in SAH patients without angiographic vasospasm.
  • To generate hypotheses regarding the etiology and risk factors of DCI beyond vasospasm.
  • To investigate causes of DCI in the absence of angiographic vasospasm.

Main Methods:

  • Retrospective analysis of 309 SAH patients with cerebral infarcts.
  • Assessment of vasospasm using CT/MR angiography, perfusion imaging, or digital subtraction angiography.
  • Evaluation of clinical and radiological data to determine infarct etiology.

Main Results:

  • 27% of patients exhibited infarcts without angiographic vasospasm.
  • Atypical infarcts were primarily caused by aneurysm therapy complications (73%), hypoxia (7%), or ICP-related herniation (2%).
  • In 17% of cases, the etiology remained unclear, with microcirculation disturbances being the most probable cause.

Conclusions:

  • A significant proportion of DCI in SAH patients is not solely attributable to CVS or treatment complications.
  • Microcirculation disturbances likely play a crucial role in the pathogenesis of infarcts in a subset of SAH patients.
  • Therapeutic strategies focusing solely on vasodilation for CVS may need reevaluation to address other etiological factors.
Abstract

More Related Videos

Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model09:14

Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model

Published on: June 18, 2021

Related Concept Videos

Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Hemorrhagic Stroke l: Introduction01:17

Hemorrhagic Stroke l: Introduction

A hemorrhagic stroke is an acute neurological event that occurs when a weakened cerebral blood vessel ruptures, allowing blood to accumulate within or around the brain. The sudden release of blood forms a focal hematoma that increases intracranial pressure, displaces neural tissue, and can obstruct cerebrospinal fluid pathways. These effects may be compounded by intraventricular extension of the hemorrhage, cerebral edema, or compression of adjacent structures, all of which contribute to...
Ischemic Stroke ll: Pathophysiology01:15

Ischemic Stroke ll: Pathophysiology

An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

Vasogenic edema is a major form of cerebral edema characterized by abnormal accumulation of fluid in the brain’s extracellular space due to disruption of the blood–brain barrier (BBB). The BBB is a specialized structure composed of endothelial cells connected by tight junctions, supported by astrocytic endfeet and a basement membrane. Under normal conditions, it tightly regulates the movement of ions, proteins, and solutes between the bloodstream and brain parenchyma. When this barrier loses...
Ischemic Stroke l: Introduction01:15

Ischemic Stroke l: Introduction

Ischemic stroke is an acute cerebrovascular condition in which blood flow to a brain region is suddenly interrupted, leading to tissue infarction. Neurons depend on continuous oxygen and glucose supply, so even brief reductions in perfusion cause energy failure, ionic imbalance, and irreversible injury. Ischemic strokes are classified into thrombotic and embolic types based on their underlying mechanisms.Thrombotic MechanismsThrombotic stroke develops when a clot forms within a cerebral artery.