Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Traumatic Brain Injury l: Introduction01:28

Traumatic Brain Injury l: Introduction

DefinitionTraumatic brain injury, or TBI, is a disturbance of normal brain function induced by an external mechanical force, such as a direct blow to the head or a penetrating injury. It can affect both brain structure and function, producing a wide range of clinical outcomes. TBI is a heterogeneous condition, meaning its effects may differ based on the type, location, and severity of the injury.Basis of ClassificationTBI is classified based on severity, injury mechanism, or pathophysiology. In...
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...
Brain Abscess l: Introduction01:26

Brain Abscess l: Introduction

A brain abscess is a focal, intracerebral infection characterized by a localized collection of pus within the brain parenchyma, resulting from microbial invasion and the body’s inflammatory response. It progresses through stages: early and late cerebritis, followed by early and late capsule formation, reflecting tissue destruction, immune response, and eventual encapsulation.Etiology and PathogenesisCausative organisms vary with source and host factors, often involving polymicrobial infections,...
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 l: Introduction01:19

Cerebral Edema l: Introduction

Cerebral edema is a pathological increase in brain water content that disrupts intracranial pressure regulation and impairs neurological function. Because the cranial vault is rigid, even modest increases in tissue volume can compromise cerebral perfusion, distort neural structures, and initiate secondary injury. Cerebral edema develops through four principal mechanisms: vasogenic, cytotoxic, interstitial, and ionic.Vasogenic EdemaVasogenic edema arises from disruption of the blood–brain...
Increased Intracranial Pressure ll: Pathophysiology01:29

Increased Intracranial Pressure ll: Pathophysiology

Increased intracranial pressure (ICP) refers to a potentially life-threatening rise in pressure inside the skull. This usually happens when there is a major change in the volume of brain tissue, blood, or cerebrospinal fluid (CSF) — the three components inside the skull. According to the Monro-Kellie doctrine, if the volume of one component increases, the volumes of the other components must decrease to maintain normal pressure. If this does not happen, ICP rises.The process often begins with...

You might also read

Related Articles

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

Sort by
Same author

Longitudinal Analysis of Sleep-Disordered Breathing and Cognitive Outcomes in Children Living With Sickle Cell Anaemia.

Clinical otolaryngology : official journal of ENT-UK ; official journal of Netherlands Society for Oto-Rhino-Laryngology & Cervico-Facial Surgery·2026
Same author

Identifying strokes in Nigerian children with sickle cell disease as part of clinical trials: training curriculum for healthcare professionals in low-income settings.

Frontiers in stroke·2026
Same author

Cerebral Blood Flow Decline in Adults With Sickle Cell Anemia: What Does It Mean and Is Treatment Required?

Neurology·2025
Same author

Airborne injustice: a preliminary exploration of the associations between pollutants and hospitalizations, sleep, and cognition in children and young adults living with sickle cell disease.

Journal of pediatric psychology·2025
Same author

Prevalence of Antiplatelet and Anticoagulation Therapy in Children with Sickle Cell Anemia and Stroke.

Pediatric stroke·2025
Same author

Sleep Behaviour in Sickle Cell Disease: A Systematic Review and Meta-Analysis.

Children (Basel, Switzerland)·2025
Same journal

Preface.

Handbook of clinical neurology·2026
Same journal

Foreword.

Handbook of clinical neurology·2026
Same journal

Fundus autofluorescence imaging.

Handbook of clinical neurology·2026
Same journal

The electroretinogram as a means to study the physiology of the retina.

Handbook of clinical neurology·2026
Same journal

Adaptive optics scanning light ophthalmoscopy.

Handbook of clinical neurology·2026
Same journal

Modeling the human retina in a dish: Advances and future directions.

Handbook of clinical neurology·2026
See all related articles

Related Experiment Video

Updated: May 11, 2026

Brain Death Induction in Mice Using Intra-Arterial Blood Pressure Monitoring and Ventilation via Tracheostomy
05:03

Brain Death Induction in Mice Using Intra-Arterial Blood Pressure Monitoring and Ventilation via Tracheostomy

Published on: April 17, 2020

Coma and brain death.

Fenella J Kirkham1, Stephen Ashwal

  • 1Neurosciences Unit, University College London Institute of Child Health, London, UK.

Handbook of Clinical Neurology
|April 30, 2013
PubMed
Summary
This summary is machine-generated.

Pediatric coma, lasting over an hour, requires prompt neuroimaging to identify serious conditions like hemorrhage or thrombosis. Early diagnosis and management are crucial for improving outcomes in critically ill children.

More Related Videos

Study of Experimental Organ Donation Models for Lung Transplantation
08:56

Study of Experimental Organ Donation Models for Lung Transplantation

Published on: March 15, 2024

Cerebral Ischemic Coma Model Induced by Modified Four-Vessel Occlusion
03:37

Cerebral Ischemic Coma Model Induced by Modified Four-Vessel Occlusion

Published on: July 5, 2024

Related Experiment Videos

Last Updated: May 11, 2026

Brain Death Induction in Mice Using Intra-Arterial Blood Pressure Monitoring and Ventilation via Tracheostomy
05:03

Brain Death Induction in Mice Using Intra-Arterial Blood Pressure Monitoring and Ventilation via Tracheostomy

Published on: April 17, 2020

Study of Experimental Organ Donation Models for Lung Transplantation
08:56

Study of Experimental Organ Donation Models for Lung Transplantation

Published on: March 15, 2024

Cerebral Ischemic Coma Model Induced by Modified Four-Vessel Occlusion
03:37

Cerebral Ischemic Coma Model Induced by Modified Four-Vessel Occlusion

Published on: July 5, 2024

Area of Science:

  • Pediatric Neurology
  • Emergency Medicine
  • Neurocritical Care

Background:

  • Coma in children, both traumatic and nontraumatic, presents significant mortality and morbidity risks.
  • Distinguishing coma from transient unconsciousness requires a minimum duration of 1 hour.
  • Pediatric coma often stems from diverse etiologies, necessitating rapid diagnostic approaches.

Purpose of the Study:

  • To outline the importance of emergency neuroimaging in pediatric coma, even with known etiologies.
  • To highlight key diagnostic tools and presumptive treatments for pediatric coma.
  • To emphasize the role of the modified Child's Glasgow Coma Scale (CGCS) and signs of brain herniation.

Main Methods:

  • Review of evidence-based guidelines for investigating and managing decreased consciousness in children.
  • Utilizing neuroimaging and laboratory testing for emergency diagnosis.
  • Application of the modified Child's Glasgow Coma Scale (CGCS) and assessment for brain herniation signs.

Main Results:

  • Emergency neuroimaging frequently diagnoses treatable complications like venous sinus thrombosis and hemorrhages.
  • A wide range of etiologies in previously healthy children can be identified via emergency diagnostics.
  • Antimicrobials may be used for presumptive treatment of infections.

Conclusions:

  • Prompt neuroimaging and laboratory testing are vital for diagnosing and managing pediatric coma.
  • The modified Child's Glasgow Coma Scale (CGCS) and herniation signs aid in assessing neurological status.
  • Long-term outcomes depend on etiology, coma depth/duration, and serial monitoring, requiring cautious interpretation.