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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...
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...
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...
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...

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Related Experiment Video

Updated: May 28, 2026

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

A Piglet Model of Neonatal Hypoxic-Ischemic Encephalopathy

Published on: May 16, 2015

Neonatal encephalopathy in foals.

David Wong1, Pamela A Wilkins, Fairfield T Bain

  • 1Iowa State University.

Compendium (Yardley, PA)
|October 14, 2011
PubMed
Summary
This summary is machine-generated.

Neonatal encephalopathy affects foals and human infants, causing neurological deficits. Research into equine-specific causes and treatments is limited, often relying on human medicine data.

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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

Related Experiment Videos

Last Updated: May 28, 2026

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

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Published on: May 16, 2015

Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
07:36

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

Published on: November 20, 2015

Area of Science:

  • Veterinary Neurology
  • Neonatal Medicine

Background:

  • Neonatal encephalopathy (NE) is a prevalent central nervous system disorder in foals and human infants.
  • Clinical signs include lethargy, abnormal behavior, seizures, and other neurological deficits.
  • Limited veterinary research exists for equine NE, necessitating extrapolation from human medicine.

Purpose of the Study:

  • To review the pathophysiologic mechanisms of neonatal encephalopathy in equids.
  • To highlight the extrapolation of human medical data for equine NE management.
  • To emphasize the importance of understanding NE mechanisms for improved foal care.

Main Methods:

  • Literature review of human and equine medical data on neonatal encephalopathy.
  • Analysis of pathophysiologic mechanisms including energy deprivation, excitotoxicity, and free radical injury.
  • Examination of diagnostic and therapeutic approaches used in equine practice.

Main Results:

  • Pathophysiologic mechanisms in foals are often inferred from human studies.
  • Commonly implicated mechanisms include energy deprivation, excitotoxicity, and oxidative stress.
  • Human-derived diagnostic and therapeutic strategies show reasonable success in foals.

Conclusions:

  • Understanding the pathophysiologic basis of NE is crucial for effective foal management.
  • Further equine-specific research is needed to refine diagnostic and therapeutic protocols.
  • Bridging the knowledge gap between human and equine NE can improve outcomes for affected foals.