Related Experiment Video
Updated: May 17, 2026
07:56
Transient Middle Cerebral Artery Occlusion Model of Neonatal Stroke in P10 Rats
Published on: April 21, 2017
Reversible cerebral vasoconstriction syndrome: rare or underrecognized in children?
Rebecca Probert1, Dawn E Saunders, Vijeya Ganesan
1Neurosciences Unit, University College London Institute of Child Health, London, UK. beckyprobert@msn.com
Developmental Medicine and Child Neurology
|October 17, 2012
Summary
Reversible cerebral vasoconstriction syndrome (RCVS) can occur in children, presenting with severe thunderclap headaches and stroke. This case highlights RCVS diagnosis in pediatric patients with evolving cerebrovascular imaging findings.
Area of Science:
- Neurology
- Pediatric Neurology
- Neuroradiology
Background:
- Reversible cerebral vasoconstriction syndrome (RCVS) is characterized by thunderclap headaches and reversible arterial narrowing.
- RCVS can lead to ischemic or hemorrhagic stroke.
Observation:
- A 13-year-old male presented with severe thunderclap headaches and no focal neurological deficits.
- Brain imaging revealed multiple posterior circulation infarcts.
- Cerebral angiography demonstrated multifocal arterial irregularity and narrowing, with evolving changes over time.
Findings:
- Laboratory studies excluded vasculitis.
- The patient's symptoms resolved within 3 weeks.
- Follow-up angiography at 3 months and 2 years showed normal cerebral arteries.
Implications:
- RCVS should be considered in children presenting with thunderclap headaches or stroke syndromes.
- Evolving or discrepant findings on cerebrovascular imaging warrant consideration of RCVS in pediatric patients.
- Early diagnosis and recognition of RCVS in children are crucial for appropriate management and prognosis.
Related Concept Videos
01:22Cerebral 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...
01:15Ischemic 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...
01:26Transient Ischemic Attack l: Introduction
A transient ischemic attack (TIA) is a brief episode of neurological dysfunction caused by a temporary, focal reduction in cerebral blood flow. Although symptoms resemble those of an ischemic stroke, the interruption in perfusion is short-lived and does not cause permanent infarction. TIAs are clinically important because they often serve as early warning events for future stroke.Mechanisms of Transient Cerebral IschemiaTransient cerebral ischemia may arise through several mechanisms. One...
01:14Increased Intracranial Pressure l: Introduction
Intracranial hypertension is a sustained elevation of intracranial pressure (ICP) above 22 mm Hg. In supine adults, normal ICP is ~7–15 mm Hg.The rigid, nonexpandable cranium contains three components—brain tissue, blood, and cerebrospinal fluid (CSF)—that total ~1,700 mL in a typical adult: 1,400 mL brain (~80%), 150 mL blood (~10%), and 150 mL CSF (~10%). According to the Monro–Kellie doctrine, total intracranial volume is effectively fixed. When one component expands, CSF and venous blood...
01:17Hemorrhagic 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...