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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...

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...

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...

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Updated: Jul 9, 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

The brain is hyperexcitable in migraine.

S K Aurora¹, F Wilkinson

¹Centre for Vision Research, York University, Toronto, Canada. sheena.aurora@swedish.org

Cephalalgia : an International Journal of Headache

|November 24, 2007

Summary

Migraine, a common neurological disorder, may stem from central neuronal hyperexcitability. Neurophysiological studies support this theory, offering insights into migraine pathogenesis.

Area of Science:

Neurology
Neuroscience

Background:

Migraine affects 20% of women and 6% of men.
No consistent structural abnormalities are found in migraine patients.
Central neuronal hyperexcitability is a proposed mechanism for migraine.

Purpose of the Study:

To review neurophysiological studies on migraine pathogenesis.
To evaluate the evidence supporting the central neuronal hyperexcitability theory of migraine.

Main Methods:

Review of existing neurophysiological and psychophysical studies.
Analysis of data from physiological and psychophysical investigations.

Main Results:

Neurophysiological studies provide insights into migraine mechanisms.

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Published on: June 2, 2014

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Evidence supports the theory of neuronal hyperexcitability in migraine.

Conclusions:

Central neuronal hyperexcitability is a key factor in migraine pathogenesis.
Further neurophysiological research is crucial for understanding migraine.