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

Increased Intracranial Pressure ll: Pathophysiology

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: Introduction

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...

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 barrier loses...

Cerebral Edema l: Introduction

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...

Brain Abscess l: Introduction

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,...

Cytotoxic Edema: Pathophysiology

Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...

You might also read

Related Articles

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

Sort by

Same author

Racial and Ethnic Disparities in Severe Ischemic Manifestations and Tocilizumab Use Among Patients With Giant Cell Arteritis: A Nationwide Retrospective Cohort Study Using TriNetX.

Journal of neuro-ophthalmology : the official journal of the North American Neuro-Ophthalmology Society·2026

Same author

Green vessel signal on multicolor imaging as an early sign of ischemic vasculitis in IRVAN Syndrome: A case report.

American journal of ophthalmology case reports·2026

Same author

Fluorescence lifetime imaging ophthalmoscopy adds the retina to cortical pathology for visual dysfunction in neurodegenerative diseases.

Frontiers in neurology·2025

Same author

Predictors of Final Visual Outcome in Patients With Leber Hereditary Optic Neuropathy Treated With Lenadogene Nolparvovec Gene Therapy.

Investigative ophthalmology & visual science·2025

Same author

Future applications of fluorescence lifetime imaging ophthalmoscopy in neuro-ophthalmology, neurology, and neurodegenerative conditions.

Frontiers in neurology·2025

Same author

Five-Year Outcomes of Lenadogene Nolparvovec Gene Therapy in Leber Hereditary Optic Neuropathy.

JAMA ophthalmology·2024

Search research articles

Related Experiment Video

Updated: May 21, 2026

3D-Neuronavigation In Vivo Through a Patient's Brain During a Spontaneous Migraine Headache

3D-Neuronavigation In Vivo Through a Patient's Brain During a Spontaneous Migraine Headache

Published on: June 2, 2014

Headaches associated with papilledema.

Robert C Sergott¹

¹Wills Eye Hospital, Thomas Jefferson University, Philadelphia, PA 19107, USA. rcs220@comcast.net

Current Pain and Headache Reports

|June 7, 2012

Summary

This summary is machine-generated.

Headaches linked to papilledema can threaten life and sight. This review covers headache characteristics, visual symptoms, diagnostic findings, and treatments for papilledema.

More Related Videos

Dural Stimulation and Periorbital von Frey Testing in Mice As a Preclinical Model of Headache

Dural Stimulation and Periorbital von Frey Testing in Mice As a Preclinical Model of Headache

Published on: July 29, 2021

Related Experiment Videos

Last Updated: May 21, 2026

3D-Neuronavigation In Vivo Through a Patient's Brain During a Spontaneous Migraine Headache

3D-Neuronavigation In Vivo Through a Patient's Brain During a Spontaneous Migraine Headache

Published on: June 2, 2014

Dural Stimulation and Periorbital von Frey Testing in Mice As a Preclinical Model of Headache

Dural Stimulation and Periorbital von Frey Testing in Mice As a Preclinical Model of Headache

Published on: July 29, 2021

Area of Science:

Ophthalmology
Neurology
Neuro-Ophthalmology

Background:

Headaches are a common symptom, but when associated with papilledema, they indicate increased intracranial pressure and pose significant health risks.
Papilledema, swelling of the optic disc, can lead to irreversible vision loss if not promptly diagnosed and managed.

Purpose of the Study:

To comprehensively review the clinical features, diagnostic approaches, and management strategies for headaches associated with papilledema.
To differentiate true papilledema from pseudo-papilledema and outline the utility of various diagnostic tests.

Main Methods:

Literature review focusing on clinical presentations, diagnostic imaging, ophthalmological testing, and treatment modalities for papilledema-related headaches.
Analysis of funduscopic findings, visual field testing, spectral domain optical coherence tomography (SD-OCT), and neuro-radiological evaluations.

Main Results:

Detailed characterization of headaches indicative of increased intracranial pressure.
Description of visual symptoms and key funduscopic findings differentiating true papilledema from conditions like optic disc drusen.
Evaluation of the diagnostic accuracy of ancillary tests like visual fields and SD-OCT, alongside neuro-imaging findings.

Conclusions:

Accurate diagnosis of papilledema requires a multi-faceted approach combining clinical assessment, funduscopic examination, and specialized testing.
Timely neuro-radiological evaluation and appropriate management are crucial for preventing vision loss and addressing the underlying cause of increased intracranial pressure.