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Related Concept Videos

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...
Cerebral Edema l: Introduction01:19

Cerebral Edema l: Introduction

Cerebral edema is a pathological increase in brain water content that disrupts intracranial pressure regulation and impairs neurological function. Because the cranial vault is rigid, even modest increases in tissue volume can compromise cerebral perfusion, distort neural structures, and initiate secondary injury. Cerebral edema develops through four principal mechanisms: vasogenic, cytotoxic, interstitial, and ionic.Vasogenic EdemaVasogenic edema arises from disruption of the blood–brain...
Increased Intracranial Pressure ll: Pathophysiology01:29

Increased Intracranial Pressure ll: Pathophysiology

Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins with...
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...
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...
Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

Encephalitis is inflammation of the brain parenchyma caused by direct viral invasion or immune-mediated mechanisms triggered by infections or tumors. Both processes lead to neuronal injury, disrupted neurotransmission, and diverse neurological symptoms, often with overlapping clinical and pathological features.Autoimmune EncephalitisIn autoimmune encephalitis, antibodies target neuronal antigens on cell surfaces, synapses, or within neurons. A key example is anti-NMDAR encephalitis, which can...

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Updated: May 25, 2026

A Volumetric Method for Quantification of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage
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A Volumetric Method for Quantification of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage

Published on: July 28, 2018

[Cerebral vasculitides].

Hubert de Boysson1, Anthony Faivre, Christian Pagnoux

  • 1CHU Côte-de-Nacre, université de Caen, pôle de médecine interne et d'immunologie clinique, avenue de la Côte-de-Nacre, 14033 Caen cedex 9, France.

Presse Medicale (Paris, France : 1983)
|February 14, 2012
PubMed
Summary
This summary is machine-generated.

Diagnosing cerebral vasculitis requires ruling out secondary causes through comprehensive clinical, biological, and radiological evaluation. Definitive diagnosis often necessitates a leptomeningeal biopsy when uncertainty persists.

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Analysis of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage with High Frequency Transcranial Duplex Ultrasound
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Last Updated: May 25, 2026

A Volumetric Method for Quantification of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage
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Analysis of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage with High Frequency Transcranial Duplex Ultrasound
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Quantification of Cerebral Vascular Architecture using Two-photon Microscopy in a Mouse Model of HIV-induced Neuroinflammation
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Quantification of Cerebral Vascular Architecture using Two-photon Microscopy in a Mouse Model of HIV-induced Neuroinflammation

Published on: January 12, 2016

Area of Science:

  • Neurology
  • Immunology
  • Radiology

Background:

  • Cerebral vasculitides encompass primary central nervous system vasculitis and secondary forms linked to systemic diseases, infections, malignancies, or toxic exposures.
  • Suspected cerebral vasculitis mandates an exhaustive diagnostic workup to exclude diverse secondary etiologies.

Purpose of the Study:

  • To outline the diagnostic approach for cerebral vasculitis.
  • To emphasize the importance of differentiating primary from secondary forms and the role of specific investigations.

Main Methods:

  • Diagnosis typically integrates clinical presentation, biological markers, and neuroimaging (MRI).
  • Cerebrospinal fluid examination and MRI can help rule out the condition.
  • Leptomeningeal biopsy is considered definitive, particularly in cases of diagnostic uncertainty or underlying systemic disease.

Main Results:

  • A combination of clinical, biological, and radiological findings often suggests cerebral vasculitis.
  • Normal MRI and cerebrospinal fluid findings may exclude the diagnosis.
  • Leptomeningeal biopsy provides definitive diagnosis when suspicion remains high.

Conclusions:

  • Early diagnosis and prompt treatment of cerebral vasculitis improve prognosis.
  • Treatment for secondary vasculitis targets the underlying cause, often supplemented by corticosteroids and immunosuppressants.
  • Consensus on treatment for primary central nervous system vasculitis is lacking.