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Intracranial Hypertension Condition Monitoring By Time Domain Analysis

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Conference

1998 Annual Conference

Location

Seattle, Washington

Publication Date

June 28, 1998

Start Date

June 28, 1998

End Date

July 1, 1998

ISSN

2153-5965

Page Count

9

Page Numbers

3.371.1 - 3.371.9

Permanent URL

https://peer.asee.org/7238

Download Count

22

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Paper Authors

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Robert Allen

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Richard Penson

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Abstract
NOTE: The first page of text has been automatically extracted and included below in lieu of an abstract

Session 1559

Intracranial Hypertension - Condition Monitoring by Time Domain Analysis

Professor Richard Penson, Dr Robert Allen Southampton Institute/Southampton University UK

Abstract This paper discusses the developments in the assessment of intracranial hypertension in humans and recent research carried out by the authors on the techniques for the non-invasive measurement of intracranial pressure. A brief historical review sets the scene with regard to clinical and invasive

pressure can be predicted. Although a simulation and a frequency domain analysis of the dynamics of the human brain has been carried out, due to space constraints, this paper concentrates only on the time domain experiments and analysis that were used in developing a non-invasive approach to the measurement of intracranial pressure. The time domain analysis uses the cross- correlation of the non-invasive blood flow of the middle cerebral artery with blood pressure measurements and their varying phase shift with trauma characteristics to make predictions of intracranial pressure trends that lead to pathologically dangerous conditions. The paper concludes with a section concerning the development of software and associated graphical displays that could inform the nursing staff of trends in intracranial pressure and life threatening conditions so that immediate action can be taken.

1 Introduction Intracranial hypertension is caused by raised intracranial pressure (ICP) which is the pressure that can be measured within the cranial cavity between the outer membrane (dura) and the brain tissue including the ventricles within the brain and the spinal compartments. These ventricles and interconnecting passages contain a lubricating or damping fluid known as the cerebrospinal fluid (CSF). The CSF circulates over the surface of the brain, brain stem and the spinal cord at a rate of about 500 ml/day and has a rate of formation of about 0.4 ml/mm. This means that the CSF is renewed 4-5 times every day. Normal ICP is about 10 mmHg average with dynamic components due to blood pressure and respiration at the same frequencies as heartbeat and respiration respectively. Raised ICP, caused by a pathological condition when the balance of production and absorption of CSF has broken down can go up to 70 mmHg or even higher. Raised ICP can lead to death and therefore monitoring and patient management is very important for any pathological condition leading to intracranial hypertension. Monitoring changes to ICP is particularly important and the anticipation of changes very helpful to clinicians and nursing staff involved in patient management. Intracranial hypertension and craniospinal volume-pressure relationships started back in 1783 by Monro and Kellie in 1824. Munro who was President of the Royal College of surgeons and Professor of Physics, Anatomy and Surgery at the University of Edinburgh made a number of observations in his book entitled “Observations on the Structure and Function of the Nervous System”[l].The original Monro-Kellie doctrine or hypothesis proposed a rigid and extensible cranial cavity, filled to capacity with incompressible brain tissue and blood, from which it was concluded that the volume of the latter must at all times be constant. The doctrine was extremely simple and did not take into account the CSF nor the spinal portion of the craniospinal compartment. Various researchers gradually modified this original Monro-Kellie paradigm

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Allen, R., & Penson, R. (1998, June), Intracranial Hypertension Condition Monitoring By Time Domain Analysis Paper presented at 1998 Annual Conference, Seattle, Washington. https://peer.asee.org/7238

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