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Related Concept Videos

Hepatic Encephalopathy01:29

Hepatic Encephalopathy

DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic shunting—including...
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...
Transient Ischemic Attack l: Introduction01:26

Transient 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...
Encephalitis ll: Pathophysiology01:26

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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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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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Related Experiment Video

Updated: May 18, 2026

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
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Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats

Published on: November 20, 2015

[Delayed posthypoxic leukoencephalopathy: case reports].

Shiho Okuda1, Masao Ueno, Michiko Hayakawa

  • 1Department of Neurology, Hyogo Rehabilitation Center Hospital.

Rinsho Shinkeigaku = Clinical Neurology
|September 20, 2012
PubMed
Summary
This summary is machine-generated.

Delayed posthypoxic leukoencephalopathy (DPL) is a rare brain condition. Benzodiazepine overdose can cause DPL, presenting with neurological symptoms days after recovery, highlighting the need for prompt diagnosis.

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A Piglet Model of Neonatal Hypoxic-Ischemic Encephalopathy
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Last Updated: May 18, 2026

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
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Published on: November 20, 2015

A Piglet Model of Neonatal Hypoxic-Ischemic Encephalopathy
10:30

A Piglet Model of Neonatal Hypoxic-Ischemic Encephalopathy

Published on: May 16, 2015

Area of Science:

  • Neurology
  • Toxicology

Background:

  • Delayed posthypoxic leukoencephalopathy (DPL) is a rare neurological complication following hypoxic brain injury.
  • It typically manifests days to weeks after initial recovery, presenting with cognitive impairment, parkinsonism, or psychosis.

Observation:

  • This report details two cases of DPL following hypoxia induced by benzodiazepine overdose.
  • Both patients exhibited normal arylsulfatase A activity, differentiating from other causes.

Findings:

  • Benzodiazepine overdose is an under-recognized cause of DPL, distinct from common causes like carbon monoxide poisoning.
  • MRI reveals characteristic deep white matter abnormalities in DPL patients.

Implications:

  • Recognizing DPL's unique clinical course and MRI findings is crucial to avoid misdiagnosis and inappropriate treatments.
  • Increased awareness may lead to more diagnoses of DPL associated with common benzodiazepine overdoses.