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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...
Encephalitis l: Introduction01:19

Encephalitis l: Introduction

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...
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...
Dementia l: Introduction01:22

Dementia l: Introduction

Dementia is an acquired, progressive syndrome characterized by a decline in multiple cognitive domains severe enough to impair daily functioning and reduce independence. Although memory loss is a central feature, the diagnosis requires additional deficits involving language, executive function, visuospatial skills, judgment, calculation, or abstract reasoning. These cognitive impairments reflect underlying neurodegenerative or vascular processes that gradually disrupt neuronal networks...
Ischemic Stroke ll: Pathophysiology01:15

Ischemic 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...

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Updated: May 28, 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

Delayed radiation-induced vasculitic leukoencephalopathy.

Philipp J Rauch1, Henry S Park, Jonathan P S Knisely

  • 1Departments of Pathology and Neurosurgery, Yale University School of Medicine, New Haven, Connecticut, USA.

International Journal of Radiation Oncology, Biology, Physics
|October 26, 2011
PubMed
Summary

High-dose radiation therapy for brain tumors can cause delayed leukoencephalopathy. This study found evidence of vasculitis in brain tissue, suggesting it may drive the progressive nature of this radiation side effect.

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Isolation and Cannulation of Cerebral Parenchymal Arterioles
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Isolation and Cannulation of Cerebral Parenchymal Arterioles

Published on: May 23, 2016

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Last Updated: May 28, 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

Isolation and Cannulation of Cerebral Parenchymal Arterioles
09:49

Isolation and Cannulation of Cerebral Parenchymal Arterioles

Published on: May 23, 2016

Area of Science:

  • Neurology
  • Radiation Oncology
  • Pathology

Background:

  • Single-fraction, high-dose focused radiation therapy, like Gamma Knife radiosurgery, is increasingly used for metastatic brain cancer.
  • Radiation therapy to the brain can lead to delayed leukoencephalopathy, a condition with significant morbidity and mortality.
  • Pathological differences between radiosurgery-induced and fractionated radiation-induced leukoencephalopathy are not well understood.

Purpose of the Study:

  • To integrate radiographic and histopathologic findings to understand radiosurgery-induced leukoencephalopathy.
  • To characterize the pathological differences in delayed leukoencephalopathy following Gamma Knife radiosurgery.

Main Methods:

  • Retrospective analysis of resected brain tissues from 10 patients treated with Gamma Knife radiosurgery for brain metastases.
  • Examination of clinical and magnetic resonance imaging data.
  • Neuropathologic assessment of tissue samples, focusing on leukoencephalopathic changes and vascular pathology.

Main Results:

  • Radiosurgery-induced leukoencephalopathy can extend beyond the high-dose radiation field.
  • Histopathology revealed demyelination, coagulation necrosis, and vascular sclerosis.
  • Unexpectedly, small and medium-sized vessels showed transmural T-cell infiltration, indicating active vasculitis.

Conclusions:

  • A vasculitic component may contribute to the progressive nature of radiation-induced leukoencephalopathy.
  • Vasculitis could explain the imaging similarities between delayed leukoencephalopathy and tumor recurrence.
  • Understanding these pathological mechanisms is crucial for accurate post-treatment follow-up.