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Related Concept Videos

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...
Decreased Body Temperature01:29

Decreased Body Temperature

A decreased body temperature can occur in patients with hypothermia and frostbite. Heat loss with extended cold exposure overpowers the body's ability to create heat, resulting in hypothermia. Core temperature readings help classify hypothermia. Mild hypothermia is temperatures between 32 °C (89.6 °F) and 35°C (95 °F) and is caused by impaired thermoregulation. Moderate hypothermia is temperatures between 28 C (82.4 °F) and 32 °C (89.6 °F) caused by sustained extreme cold exposure, and severe...
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.
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...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Increased Body Temperature01:25

Increased Body Temperature

A body temperature above  38°C  (100.4 °F) is known as fever or pyrexia, and a person with fever is termed 'febrile.' Typically, the hypothalamus, a part of the brain that acts as the body's thermostat, regulates body temperature through a thermoregulatory setpoint. It receives signals from cold and warm thermal receptors throughout the body and adjusts the body's temperature accordingly. Fever occurs when this hypothalamic setpoint is altered, usually in response to an infection or illness.

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Related Experiment Video

Updated: Jun 25, 2026

Short-Duration Hypothermia Induction in Rats using Models for Studies examining Clinical Relevance and Mechanisms
05:00

Short-Duration Hypothermia Induction in Rats using Models for Studies examining Clinical Relevance and Mechanisms

Published on: March 3, 2021

Hypothermia after acute ischemic stroke.

Thomas M Hemmen1, Patrick D Lyden

  • 1Department of Neuroscience, University of California, San Diego, California 92103-8466, USA. themmen@ucsd.edu

Journal of Neurotrauma
|February 24, 2009
PubMed
Summary
This summary is machine-generated.

Induced hypothermia shows promise for ischemic stroke neuroprotection. Despite past limitations, recent cooling advances and successful trials in other conditions are reviving interest in its clinical use for stroke patients.

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In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model
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In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model

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Last Updated: Jun 25, 2026

Short-Duration Hypothermia Induction in Rats using Models for Studies examining Clinical Relevance and Mechanisms
05:00

Short-Duration Hypothermia Induction in Rats using Models for Studies examining Clinical Relevance and Mechanisms

Published on: March 3, 2021

In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model
08:22

In vitro Assessment of Myocardial Protection following Hypothermia-Preconditioning in a Human Cardiac Myocytes Model

Published on: October 27, 2020

Area of Science:

  • Neuroscience
  • Cardiovascular Medicine
  • Critical Care Medicine

Background:

  • Induced hypothermia is a potent neuroprotective strategy in preclinical stroke models.
  • Clinical application has been hindered by technological challenges and the body's temperature regulation.
  • Recent advancements in intravascular cooling offer new possibilities.

Purpose of the Study:

  • To review the potential of induced hypothermia as a neuroprotective therapy for ischemic stroke.
  • To discuss the limitations and recent advancements in applying hypothermia clinically.
  • To highlight renewed interest in hypothermia for stroke treatment based on recent evidence.

Main Methods:

  • Review of preclinical and clinical studies on induced hypothermia for ischemic stroke.
  • Analysis of technological advancements in cooling methods.
  • Examination of outcomes from hypothermia trials in related conditions like cardiac arrest and neonatal asphyxia.

Main Results:

  • Induced hypothermia demonstrates significant neuroprotection in experimental stroke models.
  • Technological and physiological barriers have limited its widespread clinical adoption.
  • Successful application in global cerebral ischemia cases has spurred renewed investigation for stroke.

Conclusions:

  • Induced hypothermia remains a promising neuroprotective approach for ischemic stroke.
  • Overcoming previous limitations through technological innovation is key for clinical translation.
  • Evidence from other critical care scenarios supports further exploration of hypothermia in stroke management.