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

The Arch of Aorta01:10

The Arch of Aorta

The coronary arteries, originating from the ascending aorta, bifurcate from two sinuses located within the ascending aorta. Positioned just above the aortic semilunar valve, these sinuses house essential aortic baroreceptors and chemoreceptors, crucial for maintaining cardiac function. The left coronary artery and the right coronary artery branch off from the left posterior and anterior aortic sinuses, respectively.
Encircling the heart, the coronary arteries form a ring-like structure before...
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...
Hemorrhagic Stroke l: Introduction01:17

Hemorrhagic Stroke l: Introduction

A hemorrhagic stroke is an acute neurological event that occurs when a weakened cerebral blood vessel ruptures, allowing blood to accumulate within or around the brain. The sudden release of blood forms a focal hematoma that increases intracranial pressure, displaces neural tissue, and can obstruct cerebrospinal fluid pathways. These effects may be compounded by intraventricular extension of the hemorrhage, cerebral edema, or compression of adjacent structures, all of which contribute to...
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 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...
Increased Intracranial Pressure l: Introduction01:14

Increased Intracranial Pressure l: Introduction

Intracranial hypertension is a sustained elevation of intracranial pressure (ICP) above 22 mm Hg. In supine adults, normal ICP is ~7–15 mm Hg.The rigid, nonexpandable cranium contains three components—brain tissue, blood, and cerebrospinal fluid (CSF)—that total ~1,700 mL in a typical adult: 1,400 mL brain (~80%), 150 mL blood (~10%), and 150 mL CSF (~10%). According to the Monro–Kellie doctrine, total intracranial volume is effectively fixed. When one component expands, CSF and venous blood...

You might also read

Related Articles

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

Sort by
Same author

Ozzy Osbourne and Parkinson's disease: from darkness to awareness.

Arquivos de neuro-psiquiatria·2026
Same author

Longitudinally extensive myelitis in neurosarcoidosis.

Practical neurology·2026
Same author

SCA27B in Brazil: frequency, phenotype and genotype-phenotype correlations.

Journal of neurology·2026
Same author

Adult-onset spontaneous periodic hypothermia with hyperhidrosis: three cases of a Shapiro syndrome variant.

Clinical autonomic research : official journal of the Clinical Autonomic Research Society·2026
Same author

Reply to: "Drinking-Induced Orolingual Tremor: Report of Two Cases with a Novel Response to Propranolol".

Movement disorders clinical practice·2026
Same author

Arts Syndrome and Involuntary Eye Movements.

Movement disorders clinical practice·2026

Related Experiment Video

Updated: Jun 23, 2026

Permanent Cerebral Vessel Occlusion via Double Ligature and Transection
08:22

Permanent Cerebral Vessel Occlusion via Double Ligature and Transection

Published on: July 21, 2013

Ondine's curse after brainstem infarction.

Jose Luiz Pedroso1, Robson Fantinato Baiense, Ana Paula Scalzaretto

  • 1Department of Neurology, Federal University of São Paulo, São Paulo, Brazil. zeluizpedroso@yahoo.com.br

Neurology India
|May 15, 2009
PubMed
Summary

This report details a rare case of acquired Ondine's curse, a central sleep apnea syndrome, which developed after a brainstem infarction. The condition results from damage to pathways controlling automatic breathing.

More Related Videos

2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia
09:29

2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia

Published on: June 22, 2013

Establishment of Acute Pontine Infarction in Rats by Electrical Stimulation
05:02

Establishment of Acute Pontine Infarction in Rats by Electrical Stimulation

Published on: August 27, 2020

Related Experiment Videos

Last Updated: Jun 23, 2026

Permanent Cerebral Vessel Occlusion via Double Ligature and Transection
08:22

Permanent Cerebral Vessel Occlusion via Double Ligature and Transection

Published on: July 21, 2013

2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia
09:29

2-Vessel Occlusion/Hypotension: A Rat Model of Global Brain Ischemia

Published on: June 22, 2013

Establishment of Acute Pontine Infarction in Rats by Electrical Stimulation
05:02

Establishment of Acute Pontine Infarction in Rats by Electrical Stimulation

Published on: August 27, 2020

Area of Science:

  • Neurology
  • Sleep Medicine
  • Cardiorespiratory Physiology

Background:

  • Ondine's curse, or congenital central hypoventilation syndrome, is a rare disorder affecting autonomic control of breathing.
  • Acquired forms of Ondine's curse are exceptionally uncommon, with limited documented cases.
  • Understanding the pathophysiology of acquired central sleep apnea is crucial for patient management.

Observation:

  • A patient presented with symptoms consistent with acquired Ondine's curse following a brainstem infarction.
  • The infarction affected specific descending medullocervical pathways essential for regulating spontaneous respiration.
  • Clinical presentation included severe central sleep apnea, highlighting the impact on automatic breathing control.

Findings:

  • The brainstem infarction directly led to the development of central sleep apnea syndrome, mimicking congenital Ondine's curse.
  • Lesions in the medullocervical pathways were identified as the causative factor for the loss of automatic breathing.
  • This case underscores the critical role of brainstem integrity in maintaining cardiorespiratory homeostasis.

Implications:

  • This case highlights a rare etiology of acquired central sleep apnea syndrome.
  • It emphasizes the potential for brainstem lesions to disrupt automatic breathing control, leading to Ondine's curse.
  • Further research into acquired forms of central hypoventilation is warranted for improved diagnostic and therapeutic strategies.