Review Article
Volume 4, No.2
October 2000
 Jan-Uwe Müller
 Jürgen Piek
 Joachim Oertel
 Michael R Gaab
 Neurosurgical Department
 Ernst-Moritz-Arndt-Univ.
 Greifswald
 Germany

 Correspondence:
 Prof. Michael R Gaab
 Neurosurgical Department
 Ernst-Moritz-Arndt-Univ.
 Sauerbruchstr.
 D-17487 Greifswald
 Germany
 Tel: (49) 3834 86 61 62
 Fax: (49) 3834 86 61 64
 E-mail:
   gaab@mail.uni-greifswald.de

 
Intracranial pressure (ICP) and cerebrospinal fluid (CSF) dynamics


1. History of ICP monitoring

As early as in 1866, continuous ICP monitoring was introduced by fluid manometry in dogs by Leyden.(59) His research mainly focused on the correlation of clinical symptoms and increased ICP. For the first time, changing of the craniospinal pressure after CSF drainage was reported by Quinke in his description of the spinal puncture technique in 1878.(79) Later around the turn of the century, experimental (mainly animal) research dealing with this topic was intensified and the theory of ICP dynamics was founded. (17,18,46,53,71,84, 92) At this time, Kocher and Cushing performed first studies of the relationship of blood pressure and ICP.(17-19) Based on their results, they recommended several methods of decompressive craniectomy as adaequate treatment. (20,21,54) In contrast, Weed and McKibben demonstrated evidence of ICP decrease by dehydration.(93,94) Unfortunately at this time, a reliable method for ICP assessment was missing. Kocher himself pointed out the problems with lumbar pressure measurement and the risk of cerebellar herniation into the foramen magnum with increased intracranial pressure and spinal puncture.(54) The first systematic investigations of the correlation of changes in the CSF volume and ICP was performed by Ayala.(5)
 


With introduction of the ventricular puncture and catheter insertion for central ICP monitoring by Adson and Lillie in 1927, a reliable assessment was possible without the risk of herniation.(1) Later, Guillaume and Janny employed a mechanic-electrical pressure transducer for this measurement.


More public interest was evoked when Lundberg published his fundamental work on ICP analysis in the 1960’s and almost at the same time Langfitt presented his concept of cerebrospinal compliance.(56,60,68) The breakthrough for the clinical application of ICP monitoring brought the development of reliable and stable pressure sensors.(29)

2. Principles of ICP monitoring

Pressure (P)/ ICP describes the force (F) acting on a defined area (A):

One must distinguish between the absolute pressure and the physiological pressure used in medicine, which is the differential pressure between the measured pressure and the atmospheric pressure. Only in fluids pressure is exactly defined. In inhomogeneous tissues of unfixed shape a high distribution of various force vectors occurs. Therefore, pressure is defined as the force vector which acts homogeneously vertical on a defined measuring area.(30) Taking this into account, the measured data obtained in various locations is of limited value and a comparison might be difficult.

The intracranial space is divided into three large compartments by the falx cerebri and the tentorium cerebelli. The supratentorial space is further divided by the sphenoid wings. These structures are quite resistant to pressure. Therefore, the measured pressure can differ supra- and infratentorially as well as between both cerebral hemispheres. Also, there can occur a difference in intraparenchymal measuring in relation to location and position of the sensors to the main vector of the acting force. Clinically important syndromes are falcine and tentorial herniation of the brain parenchyma across the pressure gradient. The latter can also occur in the opposite direction with infratentorial lesions (inverse tentorial herniation).

3. Definition of ICP and normal values

The ICP is defined as the fluid pressure of the CSF that is measured at the level of the foramen of Monro; the assessment must be performed in supine position for comparison with “normal” references. The normal values are age dependent ( Table 1).

Table 1 - Normal ICP Values (30,36,55,60,62,63,95)
Age Group
ICP normal
Infant
<7.5 mm Hg
Child
<10 mm Hg
Adult
<15 mm Hg

4. Pressure sensors used for ICP monitoring

4.1. External pressure transducer: A typical application for an external pressure transducer is the adaptation of a fluid pressure sensor to a ventricular or spinal catheter. The advantage of this method is its inexpensiveness, but it also possesses several pitfalls. Very important is the exact selection of the neutral level (level of the foramen of Monro). This projects at the level of the external acoustic meatus in supine patient and at the level of the root of the nose in lateral position. Therefore, with each positional change a new calibration is required if the pressure sensor is not head-fixed.

Another problem is present when silicon catheters are used, which remarkably reduce or distort the transmitted wave amplitude by dumping or by resonance. There may be records of inadequate low ICP values with occlusion of the catheter with maintained pulse waves due to the compressible silicon tube. Therefore, with this method, a short transmitting distance and the use of pressure stable (incompressible) tubes are important.

4.2. Fibreoptic systems: Common applications of the fibreoptic system are intraparenchymal and intraventricular pressure monitoring. The mode of assessment consists of reflection of a light ray at a pressure sensitive membrane within the catheter tip. The reflected light is transferred via light-wave cable to an external monitor, where the pressure is calculated.(16) This procedure was introduced by Gaab and Dietrich (1975) and is commercially available since 1985 (Camino Laboratories); it has found great acceptance.(22) Most studies dealing with this method report high accuracy with a low complication rate.(32,73,83,87) Others observed a progressive drifting of the measured values with measuring time or a frequent fibreglass breaking.(16,96) The largest published study demonstrated plausible data in only 85% of cases and dysfunction in 11% due to cable breaking or catheter dislocation.(70)

4.3. Piezoresistive systems: This method is based on the phenomenon that some crystals polarise under pressure, resulting in a pressure dependent change of the electric conduction capability. The employment of piezoresistive pressure transducers enabled a far-reaching miniaturisation of the sensors.

Sensors of this type possess a very small drift of the measured values.(76) Most sensors can easily be hooked up to the usual patient ICU monitors.

5. Modes of ICP monitoring

5.1. Measuring localisations: As reported by Unterberg 1995, exclusively epidural, intraventricular and intraparenchymal pressure monitoring systems are used in Germany. Very rarely, there is reference to the application of fontanometry in the literature.

5.1.1. Fontanometry: In infants, there is the possibility of non-invasive pressure measurement through the open frontal fontanel with the "aplanation principle". (31) For this, it is important to take into account that the elastic membrane develops during the 23rd week and the subcutaneous fat layer within the 28th week of pregnancy.(89) The main problem is the inability to measure an exact pressure at the beginning. The procedure is suited for non-invasive screening and trend evaluation, but not for exact evaluation of the ICP.(50)

5.1.2. Epidural pressure monitoring: As early as 1948, Riechert (cited by Gaab) suggested this method of epidural pressure monitoring. It was first performed by Gerlach in 1952.(30,33) The method currently used is based on the fundamental experimental work of Gaab.(30) In his work, he for the first time used an epidural pressure transducer with correct implantation technique (sufficient loosening of the dura mater of 1 cm around the sensor and coplanar implantation of the probe) to exactly measure the ICP. For the exact evaluation of the ICP, the sensor is epidurally implanted through a burr hole or a present craniotomy after loosening the dura. Main mistakes are the insufficient loosening of the dura with consecutive assessment of false high pressures due to dural tension and the disregard of the coplanar measuring principle (roughness or scarring of the dura, tilted implantation of the sensor).

The advantage of this method lies in the integrity of the cerebrospinal space; this allows a consecutive reliable evaluation of the cerebrospinal compliance and of the CSF outflow resistance (Fig. 1).


Figure 1 - Epidural ICP sensor (type Mammendorf Accurate plus)

5.1.3. Subdural pressure monitoring: This method focuses on the evaluation of the superficial CSF pressure in the subdural space without injury to the brain parenchyma. For this method, the measuring probe or a catheter with external pressure transducer is implanted through an opening into the subdural space. A problem remains the small lumen of the subarachnoid space, that is easily and quickly used up with intracranial space occupying lesions.(30) With loss of the fluid adaptation, subdural (”cup”) catheters quickly stop functioning and this explains the high inaccuracy of the assessed data.(67) Subdurally implanted mini-sensors, however, give similar results as epidural transducers.

5.1.4. Parenchymal measuring: This relatively new method has come into increasingly wide use because of its simple implantation technique. A piezoresistive or fibreoptic sensor is implanted through a frontal burr hole or a screw. Signal transduction occurs either simply via the pressure input of the usual patient monitors, or by additional interface boxes.

For the interpretation of the data, it is important to note that vectors and not a “pressure” are measured, and that due to the compartmentalisation of the intracranial space an uneven pressure distribution exists. Nevertheless, there is a good correlation between ventricular and parenchymal “pressure” values.(32)

Infection incidence and post-operative bleeding complications are between 0-5%. This complication rate is less than with ventricular pressure monitoring (Fig. 2).(32,78)

Figure 2 - Intraparenchymal ICP probe

5.1.5. Ventricular pressure monitoring: This method is often referred to as the ”gold standard”. Measurement of ventricular pressure is performed in classic fashion via a catheter in the non-dominant anterior horn which is connected to an external pressure transducer. Another possibility is the formation of a subcutaneous Rickham reservoir and the percutaneous puncture with a cannula. Unfortunately, this method possesses the highest infection rates. Telemetric systems have often been reported but never went into clinical routine.

Advantages of this method are low costs combined with the possibility of permanent or intermittent CSF drainage for ICP reduction and repeated calibration. Disadvantages are the increasing infection rates with time progression, the risk of the ventricular puncture itself, susceptibility to artefacts (distortion, blocking of the catheter, dislocation of the systems; mean rate of dysfunction 3%), and mismeasurement (dislocation, hydrostatic measuring mistakes, pressure suppression by air bubbles, resonance phenomena, slit ventricles with loss of fluid adaptation with massive increased ICP and positioning of the patients).(39) Particularly with small or shifted ventricles, puncture of the lateral ventricles can be difficult.(30,39,58) The rate of missed punctures is around 6%.(39) We ourselves found, in a prospective investigation of 121 patients with ventricular pressure monitoring (traumatic head injury and spontaneous haemorrhage) only in 2 cases a manifest meningitis, and one clinically relevant haemorrhage but a relatively high number of technical dysfunctions due to catheter dislocation (n=7) or occlusion (n=6). There was a particularly high complication rate with regard to bleeding; intracerebral haemorrhages associated with percutaneous needle puncture occurred in up to 40% of patients.(37) The infection rate sharply increases after 5 days, and is especially high (30%) in haemorrhagic CSF (eg. SAH, IVH). The use of a pressure transducer integrated into the catheter tip gives a better measuring quality and reduces the incidence of false low data due to catheter occlusion and dislocation, but also leads to higher costs (Fig. 3).

Figure 3 - Venticular catheter with integrated ICP sensor (Medtronic)

5.1.6. Lumbar pressure monitoring: Because of the risk of tentorial herniation after spinal puncture (tentorial pressure gradient with infra- and supratentorial space occupying lesions, compartmentalisation of the CSF spaces with non-communicating hydrocephalus) the application of this method should be limited to communicating normal pressure hydrocephalus. It is important to note that exact measuring with good transduction of the wave amplitudes is only possible with rigid transduction media (stainless steel cannulas) but not with the usually employed microcatheters. The latter leads to false low pressure values and wave amplitudes. The measuring via a steel needle (puncture cannula) and a pressure transducer is only acceptable for some hours, eg. during an infusion test. An alternative is the insertion of a fibreoptic sensor through a lumbar catheter introduced by Bolander.(9)

6. Data registration

The base for any analysis consists in the exact and continuous registration of the measured data. A minimum requirement is a paper based registration with a paper speed of 0.5 cm/min. The usual minute registration of the mean ICP values by ICU monitors is only sufficient for the evaluation of the cerebral perfusion pressure and leads to an unfortunate reduction of the data information. More appropriate appears the application of PC-based registration and analysis systems. Therefore, NEUROLAB* was developed by us, which allows a continuous evaluation of the ICP and CPP, as well as pulse, breathing and B-waves (Fig. 4).
Figure 4 - On line ICP analysis with the NEUROLAB monitoring system.

7. Compliance and pressure volume index (PVI)

The compliance (C) describes the volume-dependent increase of the pressure in the craniospinal space and can be used for the assessment of the cerebrospinal space reserves. The inversion is termed elastance (E).


The pressure increase caused by volume substitution or growing of intracranial space occupying lesions occurs exponentially.(56,82) The first part of the function takes a relatively flat course, indicating potential for compensation, while with consumption of the space reserve already small volumes may lead to an enormous pressure increase. In contrast, Friden reported no exponential correlation (Fig. 5).(28)
Fig . 5
As the compliance represents a relatively abstract value, in 1978 Marmarou introduced the pressure volume index (PVI) for clinical use. It describes the theoretical volume, which is required to increase the measured ICP up to 10-fold.(64) The PVI is easily evaluated with either a defined volume load dV (eg. injection of fluids in positioned ventricular catheter, inflating of an epidural balloon) or withdrawal (eg. CSF drainage via ventricular catheter) and simultaneous measuring of the baseline (Po) and maximum pressure (Pp).(77) The PVI (normal value 25-30 cc) is calculated as follows:

Marmarou developed for the description of the compliance a simplified formula(64)::
This formula describes the intracranial pressure graph in the median part of the pressure-volume-diagram but it possesses an unacceptable simplification in the initial flat part of the pressure curve, as well as in the terminal part that is particularly important for the diagnosis of hydrocephalus. Therefore, this method might lead to false results but Gaab and Friden further modified this formula to correct this inaccuracy (Fig. 6).(27,28,30)


Figure 6 - Bolus injection test – clinical examples

Nevertheless, for the usual intensive care of patients the formula by Marmarou is valid; it gives an estimation of the intracranial space reserve of the actual compliance and elastance of the intracranial space.

8. CSF circulation parameters

For the description of the CSF circulation, the CSF formation rate (Iform), the CSF outflow resistance (Rout), and conduction (Cout) (which is the inverse of resistance) are used. For assessing these parameters several methods exist:

8.1. CSF outflow resistance: The calculation of the CSF outflow resistance allows an accurate assessment of resorptional dysfunctions. This investigation depends on several conditions: Any spinal or ventricular puncture in the time period immediately before the examination should be avoided (about two weeks), nor must there be any large bone defect in the skull. Due to the risk of herniation, craniospinal pressure gradients are a contraindication for this procedure.

The CSF resorption can be assessed with isotope cisternography, the bolus test or the constant volume test.(13,14,30,35,38,47,51,64,74,91)

The latter has first been described by Katzman in 1970.(51) It is a time consuming test and a burden for the patients. Subsequent developments include the constant pressure infusion test by Friden and Ekstedt and the constant volume infusion test by Gjerris modified by Gaab (Fig. 7). (11,27,30)


Figure 7 - Constant volume test – clinical examples
Particularly in the upper value level high amplitudic B-waves may occur, that aggravate the test data interpretation. Not infrequently plateau waves are observed, which lead to test break-off. Nevertheless, these investigations enable a reasonable judgement of the CSF resorption with a PC-supported method.(10)

The PVI was aimed to shorten the examination time (Marmarou(64) 1978).

However, Sullivan demonstrated that this method leads to an underestimation of the resistance in comparison with the constant volume test, which was confirmed by other authors (Table 2).(88,90)
Table 2 - Normal values for the conductance

Author/Year

Physiologic Cout in ml/min/mm Hg

Method

Ekstedt, 1978 (26)

0.11

Constant pressure test

Sklar, 1980 (86)

0.13

Constant pressure test

Tans &Poortvliet, 1984 (90)

>0.11

Constant volume test

Gjerris (35)

>0.08

Constant volume test

Albeck, 1991(2)

0.11

Constant volume test


Isotope cysternography was introduced by Pappenheimer in 1962 and represented for some time the gold standard for the assessment of CSF absorption.(74) This method was widely used for the description of CSF circulation and the selection of patients for shunting operations.(34,57,61) Nevertheless, the clearance rate describes not only the CSF resorption but is also dependent on the CSF volume.

8.2. CSF formation rate: This parameter for the description of the CSF circulation is difficult to assess in clinical practice. The procedure described by Marmarou suffers from similar restrictions as the method for CSF resorption assessment with the PVI.(64)

More exact, but also more time consuming, is the evaluation with CSF aspiration. Based on the theory that the CSF resorption occurs passively along a pressure gradient between the intracranial space and superior sagittal sinus, the CSF resorption subsides at an ICP of 5 mm Hg, which is identical to the pressure of the superior sagittal sinus. Therefore, the aspirated CSF volume to maintain the ICP <5 mm Hg represents the formation rate Iform (Table 3).(26)

Table 3 - Normal value for CSF formation rate

Author
Ekstedt (25)
0.4 ml/min
Drake (23)
0.15 ml/min (baby, 1 month)
0.25 ml/min (child, 8 years)

9. Wave-like constituents of the ICP-signals

These signals are partly generated extracranially like the pulse and breathing waves. Others like the B- and A- (plateau) - waves are generated within the intracranial vascular system.

9.1. Pulse wave: Under physiological conditions, pulse wave frequency correlated waves occur with an amplitude of 1 to 4 mm Hg or 10-30% of the mean ICP, respectively. A more detailed analysis of the pulse amplitude shows several wave peaks, which are consecutively termed P1-P5. P1-P3 peaks occur regularly and mainly correspond to pulse waves of 2nd class. Cardoso demonstrated a correlation between the P2- wave and the cerebral compliance.(15) Nevertheless, these waves underly multifactorially influences and their analysis cannot provide reliable information on compliance.

With decreasing compliance the pulse wave amplitude increases. This precedes the ICP increase. With hyperventilation and presence of vasospasm, the pulse wave decreases (Fig. 8).


Figure 8 - ICP pulse walve with demonstration of the P1-3 - maxima.

9.2. Breathing wave: The breathing wave is considered as ICP wave of the 2nd class with respect to the terminology known from circulation physiology. It is caused by breathing-synchronous changes of the intracranial blood volume. Under physiological conditions it has an amplitude of 2- 10 mm Hg.(30) With increasing ICP, the amplitude decreases and subsides at 50 mm Hg. Our own analysis showed that critical ICP increases are characterised by an increasing pulse amplitude and a subsidence of the breathing curve (Fig. 9).


Figure 9 - ICP breathing curve.

9.3. Third class ICP-waves: Besides the above mentioned waves, the mean pressure itself has specific wave characteristics of various form and duration. These occur rhythmically (B- and C-waves) or isolated (A- or plateau-waves). Our classification is mainly based on the definitions by Lundberg and Gaab.(30,60)

9.3.1. Plateau-waves: Typical for plateau-waves (synonym: A-waves) are characterised by a quick increase in ICP from a previously slowly increasing mean pressure. Later, the ICP reaches a long persisting plateau of above 40 mm Hg or even more, with a duration between 5 to 30 min. Finally, there is a sudden steep decline of the ICP, much faster than its increase, often reaching a level below the starting pressure. In a decompensating intracranial space-occupying lesion, this decline might be skipped with series of permanently increasing A-waves occurring from higher and higher pressure levels, or there is a sudden terminal ICP-increase within one plateau-wave. Lundberg assumed an acute increase of the intracranial blood volume as the cause of the plateau-wave as early as 1969.(80) This was confirmed by consecutive studies.(45,65,81) First, Rosner introduced the theory that the plateau-wave represents an active reaction in the setting of a far-reaching intact autoregulation with increased ICP and limited CPP.(81) Hayashi demonstrated the induction of plateau-waves in dogs by stimulation of the medulla oblongata.(42-44) Our own results show a positive correlation between the occurrence of plateau-waves and the clinical outcome as an indicator for an intact regulation of the cerebral perfusion.(40)

Also discussed is the compression of parasinal bridging veins as a cause of the A-wave (Fig. 10).(3)


Figure 10 - A (Plateau-) wave after severe head injury.

9.3.2. B-wave: These occur with a frequency of 0.5 to 3 / min and with amplitudes up to 20 mm Hg. According to Gaab, there are two different forms: sinuswave-like and ramp-like B-waves. Sinuswave-like B-waves are independent of changes of the blood pressure, breathing, or CO2-changes. Ramp-like B-waves are produced by snoring and concomitant pCO2 -increases.(30)

Auer demonstrated a correlation of calibre changes of the pial vessels and B-waves.(4) Mautner-Hubert showed a simultaneous occurence of B-waves with changes in the flow velocity within the MCA in healthy volunteers.(66) Other authors supported these findings.(24,72) With the introduction of a continuous automated ICP-analysis, we found a continuous B-activity with small amplitudes also in healthy people.(69) In comparison to this, the lower assessing limit for the paper-supported registration lies at 1.7 mm Hg (Fig. 11).


Figure 11a -Sinus-like B-waves



Figure 11b - Ramp-like B-waves

9.3.3. C-waves: These wave forms with a frequency of 4-8/min and 0.06-0.13-Hz respectively as well as a maximal amplitude of 20 mm Hg represent a transmission of the Hering-Traube-Wave to the intracranial pressure.(30) This is a sign for terminal vasoparalysis.

9.4. Artifacts: Main cause for artifacts are positional changes of the patient (spontaneously or with nursing steps). Particularly susceptible is the external pressure transducer. Others causes are coughing, endotracheal suctioning, changing of the ventilation mode (hyperventilation), etc. Artifacts mostly show typical brief steep pressure increases and decreases. In diagnostics of patients with hydrocephalus, it is recommended to accept only almost artifact free registrations for the calculation of the mean pressure and the wave activity, as typically present during night sleep (Fig. 12).


Figure 12 - Typical artifacts of a restless patient.

9.5. Plausibility control of measured data: Despite technically correct implantation of the probe mismeasuring might occur, so a plausibility control is required. Apart from checking the calibration and the positioning of the probe, simple observation of the wave amplitudes is helpful. The pulse amplitude should be about 20 to 30% of the mean ICP. Exceptions are terminal pressure increases with vasoparalysis, the presence of vasospasm and the use of hyperventilation or the administration of TRIS buffer (THAM), respectively. Simultaneously, there is a decrease in the amplitude of the breathing waves until their complete subsidance with an ICP of about 50 mm Hg.

With uncritical ICP values, unilateral internal jugular vein compression can be employed. Subsequent ICP increase can be used for sensor control.

10. Importance of ICP monitoring

With respect to complications, it is important to take into account that for head injured patients ICP monitoring supplies the decisive parameters for the subsequent treatment decisions. Particularly, these patients benefit from aggressive ICP treatment.(25)

The lowest complication rate is reported with epidural ICP monitoring, the highest with the intraventricular ICP catheter. With the latter, mainly infections are observed, although in the literature there is often no differentiation between positive bacteriological evidence and clinically manifest infection (Table 4).

Table 4 - Complication rate of various ICP monitoring methods.
 
Infection & Bleeding rate in % (Number of Patients)
Author/Reference
Intraventricular
Intraparenchymal
Epidural

Bekar 1998 (6)

5.4 / 2.7 (55)

0 / 0 (20) 20

-

Blei 1993 (7)

 

0 / 4

0 / 1 (262)

Jensen 1997 (49)

-

0 / 7 (98)

-

Pople 1995 (78)

-

0.3 / 0.3 (286)

-

Ivan 1980 (48)

-

0 / 0 (52)

-

Münch 1998 (70)

3.1 / 5.4 (32)

0 / 5.4 (104)

-

Piek 1994 (75)

0 / 4.96 (121)

-

-

Bochicchio 1996 (8)

 

3.3 / 0 (120)

 

Yablon 1993 (96)

 

1.7 / 3.4 (43)

 

Shapiro 1996 (85)

 

0.05 / 0.1 (244)

 

Gaab 1979 (29)

   

0 / 0 (86)

Keays 1993 (52)

   

0 / 2.2 (46)


REFERENCES
1. Adson AW, Lillie WL: The relationship of intracerebral pressure, choked disc, and intraocular tension. Trans Amer Acad Ophth Otoloaryng 1927, 30: 138-154
2. Albeck M, Borgesen SE, Gjerris F, et al: Intracranial pressure and cerebrospinal fluid outflow conductance in healthy subjects. J Neurosurg 1991, 74: 597-600
3. Arnold H, Laas R: Plateau waves; production in the rat and simulation by means of a mechanical model. In Intracranial Pressure IV. Heidelberg, Springer-Verlag 1980, 525-529
4. Auer LM, Sayama I: Intracranial pressure oscillations (B-waves) caused by oscillations in cerebrovascular volume. Acta Neurochir (Wien) 1983, 68: 93-100
5. Ayala G: Die Physiopathologie der Mechanik des Liquor cerebrospinalis und der Rachidealquotient. Monatschr Psych Neurol 1925, 58: 65-104
6. Bekar A, Goren S, Korfali E, et al: Complications of brain tissue pressure monitoring with a fiberoptic device. Neurosurg Rev 1998, 21: 254-259
7. Blei AT, Olafsson S, Webster S, et al: Complications of intracranial pressure monitoring in fulminant hepatic failure. Lancet 1993, 341: 157-158
8. Bochicchio M, Latronico N, Zappa S, et al: Bedside burr hole for intracranial pressure monitoring performed by intensive care physicians. A 5-year experience. Intensive Care Med 1996, 22: 1070-1074
9. Bolander HG: A new method for long-term lumbar pressure monitoring with a fiber optic catheter. Acta Neurochir (Wien) 1990, 105: 135-139
10. Borgesen SE, Albeck MJ, Gjerris F, et al: Computerized infusion test compared to steady pressure constant infusion test in measurement of resistance to CSF outflow. Acta Neurochir (Wien) 1992, 119: 12-16
11. Borgesen SE, Gjerris F, Sorensen SC: Intracranial pressure and conductance to outflow of cerebrospinal fluid in normal-pressure hydrocephalus. J Neurosurg 1979, 50: 489-493
12. Borgesen SE, Gjerris F: The predictive value of conductance to outflow of CSF in normal pressure hydrocephalus. Brain 1982, 105: 65-86
13. Borgesen SE, Gjerris F, Sorensen SC: Cerebrospinal fluid conductance and compliance of the craniospinal space in normal-pressure hydrocephalus. A comparison between two methods for measuring conductance to outflow. J Neurosurg 1979, 51: 521-525
14. Borgesen SE, Westergard L, Gjerris F: Isotope cisternography and conductance to outflow of CSF in normal pressure hydrocephalus. Acta Neurochir (Wien) 1981, 57: 67-73
15. Cardoso ER, Rowan JO, Galbraith S: Analysis of the cerebrospinal fluid pulse wave in intracranial pressure. J Neurosurg 1983, 59: 817-821
16. Crutchfield JS, Narayan RK, Robertson CS, et al: Evaluation of a fiberoptic intracranial pressure monitor. J Neurosurg 1990, 72:482-487
17. Cushing H: Concerning a definitive regulatory mechanism of the vasomotor centre which controls blood pressure during cerebral compression. Bull Johns Hopk Hosp 1901, 290-292
18. Cushing H: Some experimental and clinical observations concerning states of increased intracranial tension. Am J Med Sci 1902, 124: 375-400
19. Cushing H: Physiologische und anatomische Beobachtungen über den Einfluß von Hirnkompression auf den intrakraniellen Kreislauf und über einige hiermit verwandte Erscheinungen. Mitt Grenzgeb Med Chir 1902, 9: 773-808
20. Cushing H: Subtemporal decompressive operations for the intracranial complications associated with bursting fractures of the skull. Ann Surg 1908, 47: 641-644
21. Cushing H: Surgery of the head, in Keen W (Ed): Surgery-Its Principles and Practice, Pa: WB Saunders, 1980, 3: 17-276
22. Dietrich K, Gaab MR, Knoblich OF et al: A new miniaturized system for monitoring the intracranial pressure in children and adults. Neuropäd 1977, 8: 21-28
23. Drake JM, Sainte-Rose C, DaSilva M, et al: CSF Flow Dynamics in External Ventricular Drains, in Matsumoto S, Tamaki N (Eds): Hydrocephalus Pathogenesis and Treatment. Tokyo, Springer-Verlag 1991, 195-206
24. Droste DW, Berger W, Schuler E, et al: Middle cerebral artery blood flow velocity in healthy persons during wakefulness and sleep: a transcranial Doppler study. Sleep 1993, 16: 603-609
25. Eddy VA, Vitsky JL, Rutherford EJ, et al: Aggressive use of ICP monitoring is safe and alters patient care. Am Surg 1995, 61: 24-29
26. Ekstedt J: CSF hydrodynamic studies in man. J Neurol Neurosurg Psych 1978, 41: 345-353
27. Friden H, Ekstedt J: Instrumentation for cerebrospinal fluid hydrodynamics in man. Medical & Biological Engineering & Computing 1982, 20: 167-180
28. Friden HG, Ekstedt J: Volume / pressure relationship of the cerebrospinal space in humans. Neurosurg 1983, 13: 351-366
29. Gaab M, Knoblich OE, Dietrich K: Miniaturisierte Methoden zur Überwachung des intrakraniellen Druckes. Techniken und klinische Ergebnisse. Langenbecks Arch Chir 1979, 350: 13-31
30. Gaab MR: Die Registrierung des intrakraniellen Druckes. Grundlagen, Techniken, Ergebnisse und Möglichkeiten. Habilitationschrift, J.-Maximilians- Universität Würzburg 1980
31. Gaab MR, Ungersbock K, Hufenbeck B: Evaluation of ICP by computerized bedside monitoring: Methods and clinical significance. Neurol Res 1986, 8: 44-52
32. Gambardella G, d‘Avella D, Tomasello F: Monitoring of brain tissue pressure with a fiberoptic device. Neurosurg 1992, 31: 918-921
33. Gerlach J: Zerebraler Grenzdruck und Hirnpuls. Acta Neurochirurg 1952, 2: 120-158
34. Gjerris F, Borgesen SE: Current concepts of measurement of cerebrospinal fluid absorption and biomechanics of hydrocephalus. In Symon L (Ed): Advances and Technical Standards in Neurosurgery. Wien, New York, Springer-Verlag 1992, 246-277
35. Gjerris F, Borgesen SE, Sorensen PS, et al: Resistance to cerebrospinal fluid outflow and intracranial pressure in patients with hydrocephalus after subarachnoid haemorrhage. Acta Neurochir (Wien) 1987, 88: 79-86
36. Gilland O, Tourtelotte WW, OTouma L: Normal cerebrospinal fluid pressure. J Neurosurg 1976, 40: 587- 593
37. Gilsbach J, Schumacher M: Diagnostic and therapeutic value of percutaneous twist-drill puncture and needle exploration. Neurochirurg 1978, 21: 128-131
38. Gilsbach J, Schumacher M: Diagnostic and therapeutic value of percutaneous twist-drill puncture and needle exploration. Neurochirurg 1978, 21: 128-131
39. Grumme TH, Kolodziejczyk D: Komplikationen in der Neurochirurgie. Berlin, Blackwell 1995, 43-48
40. Kleist-Welch Guerra W, Gaab MR, Dietz H, et al: Surgical decompression for traumatic brain swelling: indications and results. J Neurosurg 1999, 90: 187-196
41. Guillaume J, Janny P: Manométrie intra-cranienne continue: Intéret physio-pathologique et clinique de la méthode. Presse Med (Paris) 1951, 59: 953-955
42. Hayashi M, Handa Y, Kobayashi H, et al: Plateau-wave phenomenon (I). Correlation between the appearance of plateau waves and CSF circulation in patients with intracranial hypertension. Brain 1991, 114: 2681-2691
43. Hayashi M, Ishii H, Handa Y, et al: Role of the medulla oblongata in plateau-wave development in dogs. J Neurosurg 1987, 67: 97-101
44. Hayashi M, Kobayashi H, Handa Y, et al: Plateau-wave phenomen (II). Occurence of brain herniation in patients with and without plateau waves. Brain 1991, 114: 2693- 2699
45. Hayashi M, Kobayashi H, Handa Y, et al: Brain blood volume and blood flow in patients with plateau waves. J Neurosurg 1985, 63: 556-561
46. Hill L: The physiology and pathology of the cerebral circulation: an experimental research. London, J & A Churchill 1896
47. Hussey F, Schanzer B, Katzman R: A simple constant- infusion manometric test for measurement of CSF absorption. II. Clinical studies. Neurol 1970, 20: 665-680
48. Ivan LP, Choo SH, Ventureyra EC: Intracranial pressure monitoring with the fiberoptic transducer in children. Childs Brain 1980, 7: 303-313
49. Jensen RL, Hahn YS, Ciro E: Risk factors of intracranial pressure monitoring in children with fiberoptic devices: a critical review. Surg Neurol 1977, 47: 16-22
50. Kaiser G, Minikus H: Simultaneous measurement of ventricular fluid and fontanelle pressure in neonates and infants with hydrocephalus. Z Kinderchir 1985, 40: 3-6
51. Katzman R, Hussey F: A simple constant-infusion manometric test for measurement of CSF absorption. I. Rationale and method. Neurol 1970, 20: 534-544
52. Keays RT, Alexander GJ, Williams R: The safety and value of extradural intracranial pressure monitors in fulminant hepatic failure. J Hepatol 1993, 18: 205-209
53. Key A, Retzius G: Studien in der Anatomie des Nervensystems und des Bindegewebes. Stockholm, Nordstedt und Söhner 1875
54. Kocher T: Text-Book of Operative Surgery. Third English Edition. Authorised translation from the Fifth German Edition by Heraold J. Stiles and C. Balfour Paul. New York, NY: Macmillan 1911
55. Langfitt TW, Weinstein JD, Kassell NF: Transmission of increased intracranial pressure. II: Within the supratentorial space. J Neurosurg 1964, 21: 998-1005
56. Langfitt TW, Weinstein JD, and Kassell NF: Cerebral vasomotor paralysis produced by intracranial hypertension. Caveness WF, Walker AE. Philadelphia, Lippincot. Head Injury 1966, 172-194.
57. Larsson A, Moonen M, Bergh AC, et al: Predictive value of quantitative cisternography in normal pressure hydrocephalus. Acta Neurol Scand 1990, 81: 327-332
58. Levin AB, Braun SR, Grossman JE: Physiological monitoring of the head injured patient, in Clinical Neurosurgery. Williams and Wilkins, Baltimore 1982, 240-287
59. Leyden E: Beiträge und Untersuchungen zur Physiologie und Pathologie des Gehirns. 1. Über Hirndruck und Hirnbewegungen. Virchows Arch Pathol Anat 1866, 37: 519-559
60. Lundberg N: Continuous recording and control of ventricular fluid pressure in neurosurgical practice. Acta Psych Neurol Scand Suppl 1960, 149: 30
61. Lying TU: Quantitative cisternography. Acta Radiol Diagn Stockh 1978, 19: 905-917
62. Magnaes B: Body position and cerebrospinal fluid pressure. Part 1: clinical studies on the effect of rapid postural changes. J Neurosurg 1976, 44: 687-697
63. Magnaes B: Body position and cerebrospinal fluid pressure. Part 2: clinical studies on orthostatic pressure and the hydrostatic indifferent point. J Neurosurg 1976, 44: 698-705
64. Marmarou A, Shulman K, Rosende RM: A nonlinear analysis of the cerebrospinal fluid system and intracranial pressure dynamics. J Neurosurg 1978, 48: 332-344
65. Matsuda M, Yoneda S, Handa H, et al: Cerebral hemodynamic changes during plateau waves in brain-tumor patients. J Neurosurg 1979, 50: 483-488
66. Mautner Huppert D, Haberl RL, Dirnagl U, et al: B-waves in healthy persons. Neurol Res 1989, 11: 194-196
67. Mendelow AD, Rowan JO, Murray L, et al: A clinical comparison of subdural screw pressure measurements with ventricular pressure. J Neurosurg 1983, 58: 45-50
68. Miller D, Adams H: Physiopathology and managment of increased intracranial pressure, in Critchley M, O’Leary JL. Jennet B (Eds): Scientific foundations of neurology. London: Williams Heinemann Medical, 308-324
69. Müller JU, Junge HM, Tschiltschke W, et al: B-waves in the intracranial pressure - a physiological phenomenon and monitoring of severely head injured patients. Zentralbl Neurochir (Suppl 15) 1998, (Abstr)
70. Münch E, Weigel R, Schmiedek P, et al: The CAMINO Intracranial Pressure Device in Clinical Practice: Reliability, Handling Characteristics and Complications. Acta Neurochir (Wien) 1998, 140: 1113-1120
71. Naunyn B, Schreiber J: Über Gehirndruck. Naunyn-Schmiedebergs Arch Exp Pathol Pharmakol XIV, 1881
72. Newell DW, Aaslid R, Stooss R, et al: The relationship of blood flow velocity fluctuations to intracranial pressure B waves. J Neurosurg 1992, 76: 415-421
73. Ostrup RC, Luerssen TG, Marshall LF, et al: Continuous monitoring of intracranial pressure with a miniaturized fiberoptic device. J Neurosurg 1987, 67: 206-209
74. Pappenheimer JR, Heisey SR, Jordan EF: Perfusion of the cerebral ventricular system in unanaesthetized goats. Am J Physiol 1962, 203: 774
75. Piek J: Complications in measuring ventricular pressure in patients with craniocerebral trauma and spontaneous intracranial hemorrhage - a prospective study. Zentralbl Neurochir 1994, 55: 48-53
76. Piek J, Bock WJ: Continuous monitoring of supratentorial tissue pressure in neurosurgical routine. Experience with 125 patients. In Avezaat, C. J. J. (Ed) Intracranial Pressure VIII. 11-16, Springer 1993
77. Piper IR, Miller JD, Whittle IR, et al: Automated time-averaged analysis of craniospinal compliance (short pulse response). Acta Neurochir (Wien) (Suppl) 1990, 51: 387-390
78. Pople IK, Muhlbauer MS, Sanford RA, et al: Results and complications of intracranial pressure monitoring in 303 children. Ped Neurosurg 1995, 23: 64-67
79. Quinke H: Über den Druck in Transsudaten. Dtsch Arch Klin Med 1878, 21: 454-458
80. Risberg J, Lundberg N, Ingvar DH: Regional cerebral blood volume during acute transient rises of the intracranial pressure (plateau waves). J Neurosurg 1969, 31: 303-310
81. Rosner MJ, Becker DP: Origin and evolution of plateau waves. Experimental observations and a theoretical model. J Neurosurg 1984, 60: 312-324
82. Ryder HW: The mechanism of the change in cerebrospinal fluid pressure following an induced change in the volume of the fluid space. J Lab Clin Med 1953, 41: 428-435
83. Schickner DJ, Young RF: Intracranial pressure monitoring: fiberoptic monitor compared with the ventricular catheter. Surg Neurol 1992, 37: 251-254
84. Schulten MW: Untersuchungen über den Hirndruck mit besonderer Rücksicht auf seine Einwirkung auf die Circulationsverhältnisse des Auges. Arch Klin Chir1885, 32: 733-762
85. Shapiro S, Bowman R, Callahan J, et al: The fiberoptic intraparenchymal cerebral pressure monitor in 244 patients. Surg Neurol 1996, 45: 278-282
86. Sklar FH: Non-steady-state measurement of cerebrospinal fluid dynamics. Laboratory and clinical applications. In Wood JH (Ed): Neurobiology of Cerebrospinal Fluid. New York, Plenum Press 1980, 365-379
87. Statham PF, Midgley S, Dearden NM, et al: A clinical evaluation of an intraparenchymal intracranial pressure transducer. In Avezaat CJ, Eijndhofen JHM (Eds): Intracranial Pressure. Berlin, Springer 1993, 8: 7-10
88. Sullivan HG, Miller JD, Griffith RL, et al: Bolous versus steady-state infusion for determination of CSF outflow resistance. Ann Neurol 1979, 5: 228-238
89. Sundaresan M, Wright M, Price AB: Anatomy and development of the fontanelle. Arch Dis Child 1990, 65: 386- 387
90. Tans JTJ, Poortvliet DCJ: Comparison of ventricular steady-state infusion with bolus infusion and pressure recording for differentiating between arrested and non- arrested hydrocephalus. Acta Neurochir (Wien) 1984, 72: 15-29
91. Vastola EF: CSF formation and absorption estimates by constant flow infusion method. Arch Neurol 1980, 37: 150-154
92. von Bergmann E: Über den Hirndruck. Langenbecks Arch Klin Chir 1885, 32: 705-732
93. Weed LH, McKibben PS: Pressure changes in the cerebrospinal fluid following intravenous injections of solutions in various concentrations. Am J Physiol 1919, 48: 512-530
94. Weed LH, McKibben PS: Experimental alteration of brain bulk. Am J Physiol 1919, 48: 531-555
95. Welch K: The intracranial pressure in infants. J Neurosurg 1980, 52: 693-699
96. Yablon JS, Lantner HJ, McCormack TM, et al: Clinical experience with a fiberoptic intracranial pressure monitor. J Clin Monit 1993, 9: 171-175
 


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