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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...

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...

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...

Hemorrhagic Stroke l: Introduction

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...

Glaucoma: Overview

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Glaucoma is an eye condition characterized by increased intraocular pressure that damages the retina and optic nerve, leading to irreversible blindness if left untreated. The human eye has various components, including the cornea, iris, pupil, lens, and optic nerve. Aqueous humor is secreted by the epithelium of the ciliary body in the posterior chamber and flows through the trabecular meshwork and canal of Schlemm, maintaining normal intraocular pressure. The trabecular meshwork and the canal...

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...

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Related Experiment Video

Updated: Jun 3, 2026

Translaminar Autonomous System Model for the Modulation of Intraocular and Intracranial Pressure in Human Donor Posterior Segments

Translaminar Autonomous System Model for the Modulation of Intraocular and Intracranial Pressure in Human Donor Posterior Segments

Published on: April 24, 2020

[Intracranial hypertension and lupus].

E Maillart¹, A Gueguen, M Obadia

¹Service de Neurologie, Fondation Ophtalmologique A-de-Rothschild, 25-29 rue Manin, 75940 Paris cedex 9, France. emaillart@fo-rothschild.fr

Revue Neurologique

|March 23, 2011

Summary

Idiopathic intracranial hypertension (IH) can be associated with systemic lupus erythematosus (SLE), particularly in young women with nephritis. Early diagnosis and treatment are crucial for managing this rare complication.

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Intracranial Pressure Monitoring In Nontraumatic Intraventricular Hemorrhage Rodent Model

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Last Updated: Jun 3, 2026

Translaminar Autonomous System Model for the Modulation of Intraocular and Intracranial Pressure in Human Donor Posterior Segments

Translaminar Autonomous System Model for the Modulation of Intraocular and Intracranial Pressure in Human Donor Posterior Segments

Published on: April 24, 2020

Intracranial Pressure Monitoring In Nontraumatic Intraventricular Hemorrhage Rodent Model

Intracranial Pressure Monitoring In Nontraumatic Intraventricular Hemorrhage Rodent Model

Published on: February 8, 2022

Area of Science:

Neurology
Nephrology
Rheumatology

Background:

Idiopathic intracranial hypertension (IH) is more prevalent in women and overweight individuals.
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease that can present with various organ involvements.
A potential association between IH and SLE, especially with nephritis, has been noted in medical literature.

Observation:

A case of a 29-year-old woman with SLE, skin and arthritic manifestations, and subsequent glomerulonephritis is presented.
The patient developed IH with papilledema six weeks after the onset of nephrotic syndrome, despite immunosuppressive therapy.
Cerebral imaging and cerebrospinal fluid analysis ruled out cerebral venous thrombosis and other abnormalities, confirming IH.

Findings:

Twenty-seven cases of IH associated with SLE and nephritis have been documented.
Young women are disproportionately affected, often with diffuse proliferative glomerulonephritis.
Factors like anemia may contribute to the development of IH in SLE patients.

Implications:

SLE should be investigated as a potential cause of IH, especially in non-obese patients presenting with nephritis.
IH can sometimes be an early indicator for diagnosing SLE.
Prompt management, including cerebrospinal fluid evacuation and adjusted immunosuppression, can lead to symptom resolution.