Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Ischemic Stroke ll: Pathophysiology

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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

The International League Against Epilepsy's Classification of the Epilepsies Should Incorporate Multilobar Epilepsies.

The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques·2025

Same author

A historical review of consciousness and its disorders.

Handbook of clinical neurology·2025

Same author

Combination Antithrombotic Therapy for Reduction of Recurrent Ischemic Stroke in Intracranial Atherosclerotic Disease.

Stroke·2025

Same author

Wilder Penfield and Herbert Jasper: Epilepsy and the Functional Anatomy of the Human Brain.

The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques·2024

Same author

An Acute Presentation of Marchiafava-Bignami Disease.

Annals of neurology·2023

Same author

Aiming for Burst Suppression in Treating Refractory Status Epilepticus: Probably Not.

Neurology·2023

Search research articles

Related Experiment Video

Updated: Jun 12, 2026

Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model

Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model

Published on: June 18, 2021

Sparing brain damage in severe sepsis: a beginning.

G Bryan Young¹

¹Departments of Clinical Neurological Sciences and Medicine, The University of Western Ontario, London, Ontario, Canada. bryan.young@lhsc.on.ca

Critical Care (London, England)

|June 23, 2010

Summary

Sepsis-associated encephalopathy (SAE) can cause lasting brain damage, unlike typical metabolic encephalopathies. Understanding SAE mechanisms is key to developing brain-protective strategies during sepsis.

Area of Science:

Neurology
Critical Care Medicine
Pathophysiology

Background:

Sepsis-associated encephalopathy (SAE) presents similarly to metabolic encephalopathies but carries a risk of persistent neurological deficits.
The severity of SAE correlates with the overall severity of the septic illness.
Brain microcirculation is likely impaired in SAE, mirroring effects seen in other organs during sepsis.

Discussion:

SAE pathogenesis is multifactorial, involving complex interactions during systemic infection.
While mild SAE is often reversible, severe cases are increasingly linked to long-term neurological consequences.
The impact on cerebral microcirculation is a critical factor in SAE development and severity.

Key Insights:

SAE is distinct from other encephalopathies due to its potential for enduring brain damage.

More Related Videos

A Reproducible Intensive Care Unit-Oriented Endotoxin Model in Rats

A Reproducible Intensive Care Unit-Oriented Endotoxin Model in Rats

Published on: February 20, 2021

Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression

Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression

Published on: June 15, 2019

Related Experiment Videos

Last Updated: Jun 12, 2026

Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model

Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model

Published on: June 18, 2021

A Reproducible Intensive Care Unit-Oriented Endotoxin Model in Rats

A Reproducible Intensive Care Unit-Oriented Endotoxin Model in Rats

Published on: February 20, 2021

Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression

Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression

Published on: June 15, 2019

The parallel between SAE severity and sepsis severity highlights the systemic nature of the condition.

Cerebral microcirculatory dysfunction is a probable key mechanism in SAE.

Outlook:

Further research into SAE mechanisms is crucial for developing effective brain-sparing interventions.
Identifying protective strategies could mitigate long-term neurological sequelae in sepsis survivors.
Enhanced understanding may lead to improved patient outcomes by targeting brain protection during critical illness.