Delayed Cerebral Vasospasm
Delayed Cerebral Vasospasm - Related Videos
07:03
A Low Mortality Rat Model to Assess Delayed Cerebral Vasospasm After Experimental Subarachnoid Hemorrhage
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Cited by 22 •
2013
Aneurysmal subarachnoid hemorrhage (SAH) is bleeding that occurs into the subarachnoid space when an aneurysm ruptures. While the morbidity and mortality from this event has been on a decline due to improved treatment approaches, the risk of vasospasm after subarachnoid hemorrhage continues to be the same as it was several years ago. The importance of establishing a comprehensive and reproducible animal model to identify initiating events of cerebral vasospasm has been the focus of research...
08:12
A Volumetric Method for Quantification of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage
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Cited by 4 •
2018
The goal of this article is to present a method that allows a 3-dimensional reconstruction of the cerebrovascular tree in mice after micro computed tomography and determination of volumes of entire vessel segments that can be used to quantify cerebral vasospasm in murine models of subarachnoid hemorrhage.
10:41
Analysis of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage with High Frequency Transcranial Duplex Ultrasound
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2021
The aim of this manuscript is to present a sonography-based method that allows in vivo imaging of blood flow in cerebral arteries in mice. We demonstrate its application to determine changes in blood flow velocities associated with vasospasm in murine models of subarachnoid hemorrhage (SAH).
07:05
The Precision of Visual Working Memory with Delayed Estimation
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2023
Source: Laboratory of Jonathan Flombaum—Johns Hopkins University Human memory is limited. Throughout most of its history, experimental psychology has focused on investigating the discrete, quantitative limits of memory—how many individual pieces of information a person can remember. Recently, experimental psychologists have also become interested in more qualitative limits—how precisely is information stored? The concept of memory precision can be both intuitive and elusive at once. It is...
07:47
Measuring Delay Discounting in Humans Using an Adjusting Amount Task
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Cited by 55 •
2016
Delay discounting refers to a decline in the value of a reward when it is delayed relative to when it is immediately available. We outline a computer-based delay discounting task that is easy to implement and allows for the quantification of the degree of delay discounting in human participants.
FAQs
The process is driven by several linked changes rather than by arterial narrowing alone. As blood in the subarachnoid space breaks down, hemoglobin products and inflammation contribute to endothelial dysfunction, meaning impaired function of the vessel lining. These changes can interfere with arterial relaxation and sustain vascular smooth-muscle contraction, creating conditions for reduced cerebral blood flow.
The delayed timing reflects the period during which blood in the subarachnoid space breaks down and vascular effects develop. Hemoglobin products, inflammation, endothelial dysfunction, and sustained smooth-muscle contraction can progressively impair arterial relaxation. Consequently, a patient may develop reduced cerebral perfusion or new neurological deficits after the initial hemorrhagic event, creating a risk of secondary brain ischemia.
Narrowed intracranial arteries can restrict the amount of blood reaching brain tissue. If cerebral blood flow falls sufficiently, oxygen and nutrient delivery may become inadequate, producing secondary ischemia. This makes perfusion assessment clinically important: the severity of the vascular change matters because its consequences depend on whether the brain continues receiving enough blood to support normal neurological function.
Clinical teams monitor for new neurological deficits and signs of reduced cerebral perfusion. These findings can indicate that arterial narrowing is affecting brain function rather than remaining an isolated vascular change. Ongoing observation supports early detection, allowing clinicians to recognize possible secondary ischemia and reassess risk during the vulnerable period following subarachnoid hemorrhage.
Management may include nimodipine, careful hemodynamic management, and endovascular therapy. These approaches address the complication through medication, controlled support of circulation, or an intervention directed at the affected vessels. Treatment decisions occur in the context of neurological findings and cerebral perfusion, with the overall aim of limiting reduced blood flow and subsequent brain injury.
Delayed cerebral vasospasm adds a potentially preventable source of brain injury after hemorrhagic stroke. Recognizing its mechanisms and clinical warning signs helps teams perform risk assessment, monitor patients during the delayed period, and respond when perfusion or neurological status worsens. This clinical focus supports earlier intervention and may contribute to improved outcomes following subarachnoid hemorrhage.