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Related Concept Videos

Cerebral Edema ll: Pathophysiology01:22

Cerebral Edema ll: Pathophysiology

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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...
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Encephalitis ll: Pathophysiology01:26

Encephalitis ll: Pathophysiology

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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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Encephalitis l: Introduction01:19

Encephalitis l: Introduction

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Encephalitis is inflammation of the brain parenchyma, most often due to infections or autoimmune processes. It presents with neuropsychiatric features such as fever, altered mental status, behavioral changes, cognitive dysfunction, seizures, focal deficits, and sometimes autonomic instability. In some cases, the meninges are also involved, resulting in meningoencephalitis.Infectious CausesInfectious encephalitis is most commonly viral but can also result from bacterial, fungal, or parasitic...
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Cerebral Edema l: Introduction01:19

Cerebral Edema l: Introduction

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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...
18
Viral Meningitis01:18

Viral Meningitis

189
Viral meningitis is the most common form of meningitis and is often referred to as aseptic meningitis to indicate the absence of bacterial involvement. It is generally milder than bacterial meningitis, with symptoms including fever, headache, stiff neck, drowsiness, nausea, photophobia, and vomiting. Rarely, more severe manifestations or death may occur. Common causative agents include enteroviruses, particularly coxsackie A and B viruses and echoviruses, all members of the Enterovirus genus...
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Cytomegalovirus Disease01:27

Cytomegalovirus Disease

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Cytomegalovirus (CMV) disease is caused by human cytomegalovirus, a double-stranded DNA virus of the Herpesviridae family. While primary CMV infection is often asymptomatic in immunocompetent individuals, the virus can cause severe disease in neonates and immunocompromised patients. CMV is the most common cause of congenital viral infection in the United States, and a major pathogen in solid organ and hematopoietic stem cell transplant recipients.CMV is transmitted via bodily fluids, sexual...
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Related Experiment Video

Updated: Apr 27, 2026

Isolation and Cannulation of Cerebral Parenchymal Arterioles
09:49

Isolation and Cannulation of Cerebral Parenchymal Arterioles

Published on: May 23, 2016

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[Childhood cerebral vasculitis].

S Chabrier1, S Darteyre1, L Mazzola1

  • 1Pôle Couple-Mère-Enfant, hôpital Bellevue, CHU de Saint-Etienne, 42055 Saint-Etienne cedex 2, France.

Archives De Pediatrie : Organe Officiel De La Societe Francaise De Pediatrie
|July 8, 2014
PubMed
Summary
This summary is machine-generated.

Central nervous system vasculitides in children can be large-vessel or small-vessel. Large-vessel forms often follow infections and are treated with aspirin, while rare primary forms require immunosuppression.

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Area of Science:

  • Neurology
  • Pediatrics
  • Immunology

Context:

  • Central nervous system vasculitides (CNSVs) involve inflammatory cell invasion of CNS blood vessels in children.
  • Classification includes infectious/non-infectious triggers, time course, and vessel size.
  • Distinguishes primary CNSVs from secondary forms linked to systemic conditions.

Purpose:

  • To outline the classification, diagnosis, and management of pediatric central nervous system vasculitides.
  • To differentiate treatment strategies based on vasculitis type and etiology.
  • To highlight the distinct characteristics of childhood-specific vasculitic entities.

Summary:

  • Large-vessel CNSV, common in children, presents with stroke and focal deficits, diagnosed via imaging and history.
  • Small-vessel CNSV manifests insidiously with diverse neurological symptoms; diagnosis relies on clinical/biological signs or biopsy.
  • Transient focal cerebral arteriopathy (post-varicella) is a distinct childhood entity managed with aspirin, unlike primary CNSVs needing immunosuppression.

Impact:

  • Provides a framework for diagnosing and managing pediatric CNS vasculitis.
  • Informs treatment decisions, emphasizing aspirin for post-infectious arteriopathies versus immunosuppression for primary CNSVs.
  • Underscores the importance of a multidisciplinary approach for symptom and adverse effect management.