Related Experiment Video
Updated: Jun 21, 2026
14:08
Automated Midline Shift and Intracranial Pressure Estimation based on Brain CT Images
Published on: April 13, 2013
Elevated intracranial pressure and pseudotumor cerebri.
1Mayo School of Medicine, Mayo Clinic Jacksonville, FL 32224, USA.
Current Opinion in Ophthalmology
|July 1, 1999
Summary
Papilledema, linked to pseudotumor cerebri (PTC), involves increased intracranial pressure. While optic nerve sheath fenestration and lumboperitoneal shunting can help, the best surgical approach for PTC remains undetermined.
Area of Science:
- Neuro-ophthalmology
- Neurology
- Neurosurgery
Background:
- Papilledema results from elevated cerebrospinal fluid (CSF) pressure, central retinal vein pressure, and impaired optic nerve perfusion.
- Pseudotumor cerebri (PTC) is characterized by increased intracranial pressure (ICP) with normal neuroimaging and CSF composition.
- Elevated intracranial venous pressure is a proposed universal mechanism for PTC, with obesity potentially contributing via increased intra-abdominal and cardiac pressures impeding venous return.
Purpose of the Study:
- To review the pathophysiology of papilledema and pseudotumor cerebri (PTC).
- To discuss the proposed mechanisms linking obesity to idiopathic PTC.
- To compare the surgical interventions of optic nerve sheath fenestration (ONSF) and lumboperitoneal shunting (LPS) for PTC management.
Main Methods:
- Literature review of papilledema and pseudotumor cerebri (PTC) pathophysiology.
- Analysis of proposed mechanisms for obesity-related PTC.
- Comparative discussion of optic nerve sheath fenestration (ONSF) and lumboperitoneal shunting (LPS) based on existing literature.
Main Results:
- Papilledema development requires elevated CSF pressure, central retinal vein pressure, and impaired optic nerve perfusion.
- Obesity may increase PTC risk by raising intra-abdominal and cardiac pressures, impeding cerebral venous return and elevating ICP.
- Both ONSF and LPS show potential for improving vision in PTC patients.
Conclusions:
- The exact mechanism of obesity's role in idiopathic PTC requires further elucidation.
- Optic nerve sheath fenestration (ONSF) and lumboperitoneal shunting (LPS) are viable surgical options for PTC.
- A definitive comparison between ONSF and LPS for PTC treatment awaits prospective, randomized trials.
Related Concept Videos
01:26Brain 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,...
01:14Increased 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...
01:29Increased 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...
01:19Cerebral 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...
01:22Cerebral 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...
01:21Cytotoxic 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...