Related Experiment Video

Updated: Aug 26, 2026

A Bedside, Single Burr Hole Approach to Multimodality Monitoring in Severe Brain Injury
06:18

A Bedside, Single Burr Hole Approach to Multimodality Monitoring in Severe Brain Injury

Published on: March 26, 2019

Intracranial hypertension: what additional information can be derived from ICP waveform after head injury?

M Balestreri1, M Czosnyka, L A Steiner

  • 1Department of Neurosurgery, Addenbrooke's Hospital, Cambridge, UK.

Acta Neurochirurgica
|February 14, 2004
PubMed

Insights

Analyzing intracranial pressure (ICP) waveforms reveals key indicators of cerebrovascular pressure-reactivity and compensatory reserve. These advanced metrics improve prognostication in patients with traumatic brain injury and intracranial hypertension.

Area of Science:

  • Neuroscience
  • Critical Care Medicine
  • Biomedical Engineering

Background:

  • Intracranial hypertension (ICH) is a critical prognostic factor following head trauma.
  • Increased intracranial pressure (ICP) can occur even in patients with favorable outcomes, complicating prognostication.
  • Standard ICP monitoring may not fully capture the nuances of cerebrovascular dynamics.

Purpose of the Study:

  • To investigate if cerebrovascular pressure-reactivity and pressure-volume compensatory reserve indices, derived from ICP and arterial blood pressure (ABP) waveforms, can enhance the prognostic value of ICP monitoring.
  • To explore the relationship between waveform-derived indices and patient outcomes after head injury.

Main Methods:

  • Retrospective analysis of 96 patients with intracranial hypertension (57 fatal, 39 favorable outcome).
  • Recorded arterial blood pressure (ABP) and intracranial pressure (ICP) waveforms.
  • Calculated cerebrovascular reactivity (PRx) and pressure-volume compensatory reserve (RAP) using moving correlation coefficients of slow waves in ABP, ICP, and ICP pulse amplitude, with slow wave magnitude derived from low-pass spectral filtration.

Main Results:

  • Patients with favorable outcomes exhibited persistently higher magnitudes of ICP slow waves (p<0.00004).
  • Died patients had significantly higher ICP (p<0.0001) and compromised cerebrovascular pressure-reactivity (PRx, p<0.024).
  • Pressure-volume compensatory reserve (RAP) deteriorated over time in non-survivors, dropping sharply as ICP rose, indicating disrupted vasomotor response.

Conclusions:

  • Indices derived from ICP waveform analysis offer valuable insights beyond standard ICP monitoring.
  • These advanced metrics can aid in interpreting progressive intracranial hypertension and improving prognostication in traumatic brain injury patients.
Abstract

More Related Videos

A Detailed Protocol for Physiological Parameters Acquisition and Analysis in Neurosurgical Critical Patients05:01

A Detailed Protocol for Physiological Parameters Acquisition and Analysis in Neurosurgical Critical Patients

Published on: October 17, 2017

Automated Midline Shift and Intracranial Pressure Estimation based on Brain CT Images14:08

Automated Midline Shift and Intracranial Pressure Estimation based on Brain CT Images

Published on: April 13, 2013

Related Concept Videos

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...
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...
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...
Cerebral Edema l: Introduction01:19

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...
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...
Cytotoxic Edema: Pathophysiology01:21

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...