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Related Concept Videos

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...
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...
Multiple Sclerosis l: Introduction01:19

Multiple Sclerosis l: Introduction

Multiple sclerosis is a chronic autoimmune disease of the central nervous system (CNS) that affects the brain, spinal cord, and optic nerves. It is an inflammatory demyelinating disorder and a leading cause of neurological disability in young adults.EpidemiologyMS commonly begins between 20 and 40 years of age and is twice as common in women. Its exact cause remains unclear, but genetic susceptibility contributes, with higher risk in first-degree relatives and identical twins. A greater...
Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

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...
Bacterial Meningitis II: Pathophysiology01:26

Bacterial Meningitis II: Pathophysiology

Bacterial meningitis typically begins when pathogens such as Neisseria meningitidis and Streptococcus pneumoniae colonize the nasopharynx and invade the bloodstream. This process is facilitated by bacterial virulence factors, such as polysaccharide capsules, which resist phagocytosis and complement-mediated killing. Less commonly, bacteria reach the central nervous system via contiguous spread from infections like otitis media or sinusitis, through congenital or acquired dural defects, or...
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...

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Related Experiment Video

Updated: Jun 7, 2026

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo
10:50

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo

Published on: March 26, 2019

Rapidly progressive primary central nervous system vasculitis.

Carlo Salvarani1, Robert D Brown, Kenneth T Calamia

  • 1Department of Neurology, Mayo Clinic, , Rochester, MN 55905, USA.

Rheumatology (Oxford, England)
|October 21, 2010
PubMed
Summary
This summary is machine-generated.

Rapidly progressive primary CNS vasculitis (PCNSV) is a severe subset characterized by bilateral large vessel lesions and multiple brain infarctions. This subset indicates a worse clinical outcome for PCNSV patients.

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Reliable Isolation of Central Nervous System Microvessels Across Five Vertebrate Groups
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Reliable Isolation of Central Nervous System Microvessels Across Five Vertebrate Groups

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Related Experiment Videos

Last Updated: Jun 7, 2026

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo
10:50

Visualizing Impairment of the Endothelial and Glial Barriers of the Neurovascular Unit during Experimental Autoimmune Encephalomyelitis In Vivo

Published on: March 26, 2019

Reliable Isolation of Central Nervous System Microvessels Across Five Vertebrate Groups
10:35

Reliable Isolation of Central Nervous System Microvessels Across Five Vertebrate Groups

Published on: January 12, 2020

Area of Science:

  • Neurology
  • Vascular Neurology
  • Neuroimmunology

Background:

  • Primary CNS vasculitis (PCNSV) is a rare condition affecting blood vessels in the brain and spinal cord.
  • Understanding distinct clinical courses of PCNSV is crucial for patient management.
  • A rapidly progressive subset of PCNSV may represent a more severe disease phenotype.

Purpose of the Study:

  • To identify and describe the clinical characteristics of patients with a rapidly progressive course of primary CNS vasculitis (PCNSV).
  • To compare the features of rapidly progressive PCNSV with non-rapidly progressive cases within a large cohort.

Main Methods:

  • Retrospective analysis of 131 consecutive PCNSV patients diagnosed between 1983-2007.
  • Diagnosis confirmed by brain/spinal cord biopsy or cerebral angiography.
  • Rapidly progressive disease defined by modified Rankin scale scores indicating severe disability or death within 6 months of diagnosis.

Main Results:

  • Eleven patients (8.4%) exhibited rapidly progressive PCNSV.
  • Rapidly progressive cases more frequently presented with paraparesis/quadriparesis.
  • Angiography revealed bilateral, large-vessel vasculitis; MRI showed multiple, bilateral cortical and subcortical infarctions.

Conclusions:

  • Rapidly progressive PCNSV represents a distinct, severe subset of the disease.
  • Characterized by bilateral large cerebral vessel lesions and multiple CNS infarctions.
  • This subset signifies the worst clinical spectrum of primary CNS vasculitis.