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

Hepatic Encephalopathy

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...

Cerebral Edema ll: Pathophysiology

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...

Encephalitis ll: Pathophysiology

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...

Acute Respiratory Failure-III

Acute Respiratory Failure-III

Hypercapnic respiratory failure, also known as Type 2 or ventilatory respiratory failure, is a severe condition characterized by the body's inability to effectively remove carbon dioxide (CO2) from the bloodstream. It leads to an arterial CO2 pressure (PaCO2) exceeding 45 mmHg and a blood pH above 7.35. This situation indicates that the body's ventilatory demand, or the ventilation needed to maintain normal PaCO2 levels, surpasses its supply or the maximum gas flow achievable without...

Secondary Spinal Cord Injury llI: Pathophysiology

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...

Encephalitis l: Introduction

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...

You might also read

Related Articles

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

Sort by

Same author

Epilepsy and vascular risk: Evaluation of the influence of antiseizure medications on atherosclerotic disease.

Epileptic disorders : international epilepsy journal with videotape·2026

Same author

Breast Sensation After Abdominal Free Flap Reconstruction With or Without Neurotization: A Systematic Review and Meta-analysis.

Plastic and reconstructive surgery. Global open·2026

Same author

Fetal Dural Sinus Malformation: Prenatal Diagnosis and Follow-up With Thrombus Resolution and Associated Developmental Venous Anomalies.

Journal of child neurology·2026

Same author

Pipeline evaluation of a state-of-the-art AI algorithm for detection of focal cortical dysplasia: insights into potential failure sources.

Brain informatics·2026

Same author

ESR Essentials: neuroimaging of pediatric headaches in the emergent and non-emergent setting-practice recommendations by the European Society of Neuroradiology.

European radiology·2026

Same author

Microcephaly with Simplified Gyral Pattern in Children: Quantitative Morphometric Assessment on Brain MRI and Correlation with Clinical Outcome.

AJNR. American journal of neuroradiology·2026

Search research articles

Related Experiment Video

Updated: Apr 20, 2026

Experimental Models to Study the Neuroprotection of Acidic Postconditioning Against Cerebral Ischemia

Experimental Models to Study the Neuroprotection of Acidic Postconditioning Against Cerebral Ischemia

Published on: July 31, 2017

Delayed leukoencephalopathy after acute carbon monoxide intoxication.

Ana Filipa Geraldo¹, Cristiana Silva², Dulce Neutel³

¹Department of Neuroradiology, Hospital de Santa Maria (CHLN, EPE), Lisbon, Portugal ; Lisbon School of Medicine, Lisbon, Portugal.

Journal of Radiology Case Reports

|November 27, 2014

Summary

Carbon monoxide (CO) intoxication can cause delayed leukoencephalopathy, a rare brain condition. This case highlights a patient who recovered from CO exposure but later developed neurological deficits, emphasizing the importance of recognizing this delayed complication.

Keywords:

Carbon monoxide poisoning delayed post-ischemic encephalopathy diffusion magnetic resonance imaging heroin inhalation syndrome magnetic resonance spectroscopy neurotoxicity syndromes

More Related Videos

Optimization of the Longa Middle Cerebral Artery Occlusion Method for Complete Reperfusion

Optimization of the Longa Middle Cerebral Artery Occlusion Method for Complete Reperfusion

Published on: November 22, 2024

Author Spotlight: Enhancing Cerebral Ischemia Research with a Simplified Rat Model

Author Spotlight: Enhancing Cerebral Ischemia Research with a Simplified Rat Model

Published on: July 5, 2024

Related Experiment Videos

Last Updated: Apr 20, 2026

Experimental Models to Study the Neuroprotection of Acidic Postconditioning Against Cerebral Ischemia

Experimental Models to Study the Neuroprotection of Acidic Postconditioning Against Cerebral Ischemia

Published on: July 31, 2017

Optimization of the Longa Middle Cerebral Artery Occlusion Method for Complete Reperfusion

Optimization of the Longa Middle Cerebral Artery Occlusion Method for Complete Reperfusion

Published on: November 22, 2024

Author Spotlight: Enhancing Cerebral Ischemia Research with a Simplified Rat Model

Author Spotlight: Enhancing Cerebral Ischemia Research with a Simplified Rat Model

Published on: July 5, 2024

Area of Science:

Neurology
Toxicology
Neuroimaging

Background:

Delayed leukoencephalopathy is an uncommon neurological sequela following hypoxic-ischemic events.
Carbon monoxide (CO) intoxication is a recognized, though infrequent, cause of this delayed complication.
Early diagnosis and management are crucial for favorable outcomes.

Observation:

A 40-year-old male presented with acute neurocognitive and behavioral decline one month after accidental CO intoxication.
Initial CO exposure resulted in loss of consciousness and hospitalization, followed by apparent full recovery.
Delayed neuroimaging revealed confluent, symmetric white matter lesions consistent with demyelination.

Findings:

Magnetic resonance imaging (MRI) demonstrated restricted diffusion and spectroscopic abnormalities in the affected white matter.
The clinical presentation and imaging findings led to a diagnosis of CO-mediated delayed post-hypoxic leukoencephalopathy.
Other potential causes of leukoencephalopathy were systematically excluded.

Implications:

This case underscores the potential for delayed neurological sequelae after seemingly resolved CO poisoning.
Early recognition of delayed leukoencephalopathy is critical for timely intervention.
Hyperbaric oxygen therapy may be a beneficial treatment option, as suggested by the patient's favorable response.