Related Experiment Video
Updated: May 5, 2026

09:14
Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model
Published on: June 18, 2021
2.3K
Delayed neurological deterioration after subarachnoid haemorrhage
1Division of Neurosurgery, St Michael's Hospital, 30 Bond Street, Toronto, ON M5B 1W8, Canada.
Nature Reviews. Neurology
|December 11, 2013
Summary
Subarachnoid haemorrhage (SAH) can lead to delayed cerebral ischaemia (DCI), a major cause of poor outcomes. This review explores DCI pathophysiology and treatments, including novel strategies.
Area of Science:
- Neurology
- Neurosurgery
- Critical Care Medicine
Background:
- Subarachnoid haemorrhage (SAH) causes early brain injury (EBI) and secondary complications.
- Delayed cerebral ischaemia (DCI) significantly contributes to poor outcomes in up to 30% of SAH patients.
- DCI pathophysiology involves vasospasm, thrombosis, and processes triggered by EBI.
Purpose of the Study:
- To review the pathophysiology of DCI following SAH.
- To discuss established and novel treatment strategies for DCI.
- To highlight the importance of prompt DCI recognition and management.
Main Methods:
- Literature review of SAH and DCI pathophysiology.
- Summary of current neurointensive care and DCI treatments.
- Discussion of emerging therapeutic agents and delivery methods.
Main Results:
- SAH-induced EBI and subarachnoid blood contribute to secondary brain injury.
- DCI is a complex process involving multiple ischemic and inflammatory pathways.
- Established treatments include nimodipine and supportive neurocritical care; evidence for induced hypertension and angioplasty is limited.
Conclusions:
- Understanding DCI pathophysiology is crucial for effective management.
- Novel therapeutic strategies show promise for improving DCI outcomes.
- Further research is needed to validate new treatments for DCI after SAH.
More Related Videos
Related Concept Videos
Hemorrhagic Stroke ll: Pathophysiology
30
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...
30
Hemorrhagic Stroke l: Introduction
20
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...
20
Secondary Spinal Cord Injury llI: Pathophysiology
52
Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...
52
Ischemic Stroke ll: Pathophysiology
54
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...
54
Cerebral Edema ll: Pathophysiology
19
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...
19
Dementia l: Introduction
35
Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...
35

