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Related Concept Videos

Ischemic Stroke l: Introduction01:15

Ischemic Stroke l: Introduction

Ischemic stroke is an acute cerebrovascular condition in which blood flow to a brain region is suddenly interrupted, leading to tissue infarction. Neurons depend on continuous oxygen and glucose supply, so even brief reductions in perfusion cause energy failure, ionic imbalance, and irreversible injury. Ischemic strokes are classified into thrombotic and embolic types based on their underlying mechanisms.Thrombotic MechanismsThrombotic stroke develops when a clot forms within a cerebral artery.
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...
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...
Cytotoxic Edema: Pathophysiology01:21

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Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...
Hepatic Encephalopathy01:29

Hepatic Encephalopathy

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Related Experiment Video

Updated: May 27, 2026

The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia
08:47

The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia

Published on: November 19, 2008

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Hypoxic-Ischemic Encephalopathy: Pathogenesis and Promising Therapies.

Mingming Yang1, Kexin Wang2, Boya Liu2

  • 1Department of Pediatrics, Binhai County People's Hospital, Yancheng, Jiangsu Province, 224500, P. R. China.

Molecular Neurobiology
|July 29, 2024
PubMed
Summary

Hypoxic-ischemic encephalopathy (HIE) involves brain damage from oxygen deprivation in newborns. This review details HIE mechanisms and explores adjunctive therapies to improve outcomes.

Keywords:
Drug therapyHIEHypothermia therapyPathogenesisStem cell therapy

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Early Pathological and Magnetic Resonance Detection of Cerebral Injury Using a Rat Model of Neonatal Hypoxic Ischemic Encephalopathy
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Last Updated: May 27, 2026

The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia
08:47

The Hypoxic Ischemic Encephalopathy Model of Perinatal Ischemia

Published on: November 19, 2008

35.7K
A Piglet Model of Neonatal Hypoxic-Ischemic Encephalopathy
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Early Pathological and Magnetic Resonance Detection of Cerebral Injury Using a Rat Model of Neonatal Hypoxic Ischemic Encephalopathy
05:52

Early Pathological and Magnetic Resonance Detection of Cerebral Injury Using a Rat Model of Neonatal Hypoxic Ischemic Encephalopathy

Published on: October 28, 2022

761

Area of Science:

  • Neuroscience
  • Neonatal Medicine
  • Pathophysiology

Background:

  • Hypoxic-ischemic encephalopathy (HIE) is a critical neonatal condition resulting from impaired blood and oxygen supply.
  • It is a significant cause of chronic neurological deficits in newborns following birth asphyxia.
  • The exact molecular and cellular pathways driving HIE pathogenesis remain incompletely understood.

Purpose of the Study:

  • To systematically review the multifaceted pathophysiological mechanisms contributing to HIE.
  • To elucidate the roles of hypoxia-ischemia, reperfusion, inflammation, oxidative stress, and other key pathways.
  • To evaluate current and emerging therapeutic strategies for HIE management.

Main Methods:

  • Systematic literature review of HIE pathogenesis.
  • Analysis of contributing factors including cellular stress pathways and cell death mechanisms.
  • Review of therapeutic interventions, including hypothermia, drug therapy, and stem cell therapy.

Main Results:

  • HIE involves complex interactions between initial ischemia, reperfusion injury, and secondary cellular insults.
  • Multiple pathways such as oxidative stress, excitotoxicity, ferroptosis, ER stress, and apoptosis are implicated.
  • Hypothermia offers partial neuroprotection, but adjunctive therapies are needed.

Conclusions:

  • A comprehensive understanding of HIE's complex pathogenesis is crucial for developing effective treatments.
  • Combining hypothermia with targeted drug or stem cell therapies shows promise for enhanced neuroprotection.
  • Further research into these combined strategies is essential to improve long-term outcomes for HIE patients.