Intracranial Elastance Research Articles

Rate of CSF formation and resistance to reabsorption of CSF during sevoflurane or remifentanil in rabbits.

Information on the effects of sevoflurane on the rate of cerebrospinal fluid (CSF) formation (Vf) and resistance to reabsorption of CSF (Ra) is incomplete, and no such information is available for remifentanil. The present study examined the dose-related effects of sevoflurane and remifentanil on Vf and Ra in rabbits. Eight rabbits were studied during isoflurane 1.4% (baseline) and sevoflurane 1.4%, 2.5%, and 3.7%, and eight were studied during isoflurane 1.4% (baseline) and remifentanil 0.30, 0.67, and 1.00 microg x kg(-1) x min(-1) in randomized order. Ventriculocisternal perfusion at two CSF pressure states for each experimental condition was used to determine Vf and Ra. There was no dose-response relation for Vf (10.4+/-2.5, 9.0+/-2.0, and 10.0+/-3.0 microl x min(-1)) or Ra (0.81+/-0.33, 1.35+/-0.54, and 0.84+/-0.27 cm H2O x microl(-1) x min) between the three sevoflurane concentrations. There also was no dose-response relation for Vf (7.8+/-1.2, 8.8+/-3.0, and 6.5+/-2.3 microl x min(-1)) or Ra (1.07+/-0.54, 1.23+/-0.50, and 1.13+/-0.51 cm H2O x microl(-1) x min) between the three remifentanil doses. Vf and Ra during either sevoflurane or remifentanil were not significantly different from Vf and Ra during the two isoflurane baseline conditions (Vf = 8.5+/-2.5 and 9.8+/-1.3 microl x min(-1), and Ra = 0.97+/-0.36 and 1.38+/-0.55 cm H2O x microl(-1) x min, mean +/- SD). Vf and Ra are of interest because they influence CSF volume, intracranial pressure, and/or intracranial elastance. In our model, sevoflurane or remifentanil did not significantly alter Vf or Ra.

New monitors of neurological functions — part 2

This article is the second of two parts. In this section, techniques for monitoring cerebral oxygenation, cerebral biochemistry, intracranial elastance and spinal cord integrity are described. The developments of certain of the new monitors including near-infrared spectroscopy, brain tissue oxygen tension measurement, intracerebral microdialysis, monitors of compliance and techniques for measuring motor evoked potential are discussed in detail. New applications for some established monitors (jugular bulb venous oximetry, intracranial pressure waveform analysis) are also described.

Evaluation of the pressure transfer system in the intracranial cavity by coherency.

Coherency provides a method to evaluate model linearity. The characteristics of pressure wave transmission in the intracranial cavity were studied by coherency in 16 cats with hydrostatic pressure loading to assess the linearity of the system, which is an assumption for use of the transfer function. Linearity was observed in only the fundamental waves of the respiration-induced component and the cardiac-induced component of intracranial pressure oscillation, and in the second harmonic wave of the latter. Linearity at the other frequencies was close to zero. The pressure transfer system in the intracranial cavity was basically a non-linear system. As intracranial pressure rose, the increase in the pressure transfer efficiency was largest in the low-frequency domain and smallest in the high-frequency domain, indicating that the cerebral blood vessels are characterized by inferior transmission of high frequency due to increased intracranial pressure. In addition, the correlation between the coherencies of the cardiac-induced fundamental wave component and intracranial pressure, and between those of the cardiac-induced second harmonic wave component and intracranial pressure, showed that the slope of the straight line was greater between 45 and 70 mmHg than between 10 and 45 mmHg. This suggests that there is a break point, located between 45 and 70 mmHg, where the increase in the coherency values is accelerated, caused by an increase in the intracranial elastance, as well as an increase in the cerebrovascular compliance due to the reduced vascular transmural pressure.

Modeling cerebral autoregulation and CO2 reactivity in patients with severe head injury.

The mathematical model presented in a previous work is used to simulate the time pattern of intracranial pressure (ICP) and of blood velocity in the middle cerebral artery (VMCA) in response to maneuvers simultaneously affecting mean systemic arterial pressure (SAP) and end-tidal CO2 pressure. In the first stage of this study, a sensitivity analysis was performed to clarify the role of some important model parameters [cerebrospinal fluid (CSF) outflow resistance, intracranial elastance coefficient, autoregulation gain, and the position of the regulation curve] during CO2 alteration maneuvers performed at different SAP levels. The results suggest that the dynamic "ICP-VMCA" relationship obtained during changes in CO2 pressure may contain important information on the main factors affecting intracranial dynamics. In the second stage, the model was applied to the reproduction of real ICP and velocity tracings in neurosurgical patients. Ten distinct tracings, taken from six patients during CO2 changes at different mean SAP levels, were reproduced. Best fitting between model and clinical curves was achieved by minimizing a least-squares criterion function and adjusting certain parameters that characterize CSF circulation, intracranial compliance, and the strength of the regulation mechanisms. A satisfactory reproduction was achieved in all cases, with parameter numerical values in the ranges reported in clinical literature. It is concluded that the model may be used to give reliable estimations of the main factors affecting intracranial dynamics in individual patients, starting from routine measurements performed in neurosurgical intensive care units.

Estimation of the main factors affecting ICP dynamics by mathematical analysis of PVI tests.

A simplified model of intracranial dynamics is used to reproduce the intracranial pressure (ICP) time pattern in 20 patients with severe brain damage during PVI tests. A comparison of model responses and clinical tracings was achieved by minimizing a least square criterion function and adjusting just 5 parameters. These are: the CSF outflow resistance, the intracranial elastance coefficient, the autoregulation gain and time constant, and the basal values of arteriolar compliance. Based on the value of the autoregulation gain, the patients were classified into two groups: those with damaged autoregulation (8 out of 12) and those with preserved autoregulation (12 out of 20). Finally, analysis of the correlation between parameter estimates provided suggestions on the combination of a parameter changes which may have the greater impact on ICP in the individual cases. Once these parameters have been identified, they may become possible targets for therapeutic interventions.

Elastance Versus Compliance

Professor of Anesthesiology, University of California, San Diego, Anesthetist-in-Chief, VA Medical Center, San Diego, 3350 La Jolla Village Drive, San Diego, California 92161.To the Editor:—A recent case report [1] suggests that the plea by Lanier and Warner that the anesthesia community discontinue its use of the term “compliance” in connection with the intracranial space has been heard. [2] Others who predicted that the misuse of the term compliance was too “well entrenched” to be changed have been proved wrong. [3] Elastance (elastance Delta P/Delta V) is the correct term when referring to the pressure changes that occur inside the cranium in response to changes in the volume of the intracranial contents, and compliance (compliance Delta V/Delta P), the inverse of elastance, is incorrect. However, the report by Sperry et al. suggests that we are experiencing some growing pains as we evolve toward the more appropriate use of terminology. [1] Sperry et al. begin with the premise that patients with a cerebrospinal fluid leak after dural puncture may coincidentally have intracranial pathology and that they “may have decreased intracranial elastance … and may be at risk for developing increased intracranial pressure when a mass effect is produced in the spinal epidural space during epidural blood patch.” The problem, of course, is one of increased elastance rather than decreased elastance. This may seem like a small matter to present to the correspondence section of an important journal, but the fact that the error passed by three authors, several reviewers, the Editor-in-Chief, and one or two copy editors suggests that our community is not accustomed to the use of this terminology and that a significant potential for miscommunication exists while we adapt to it.John C. Drummond, M.D., Professor of Anesthesiology, University of California, San Diego, Anesthetist-in-Chief, VA Medical Center, San Diego, 3350 La Jolla Village Drive, San Diego, California 92161.(Accepted for publication February 23, 1995.)

Intracranial pressure dynamics in clinical practice: online PC-based ICP monitoring system

Correct patient management involves determining the exact point on the intracranial pressure/volume (P/V) curve that corresponds to the patient; this requires calculating intracranial elastance (IE). Intracranial pressure (ICP) monitoring systems should provide the necessary information for this purpose. An ICP monitoring unit is presented that acquires ICP, systemic arterial pressure (SAP) and airway pressure (AWP). The cerebral perfusion pressure (CPP) and the mean values and the peak-to-peak values of the two of them (ICPmean, SAPmean, ICPp-p, SAPp-p,) are calculated. Graphs display the temporal evolution (TE) of the ICP and SAP, as well as histograms of the ICP (%) and intracranial pulse amplitude (ICPAmP) with respect to the ICP or CPP during the preceding 3, 6, 12 or 24 h of monitoring. By digital filtering the ICP respiratory and cardiac components (RCICP, CCICP) are calculated. Finally, the pulse amplitudes (AmP) of the ICP, CCICP and RCICP are computed, as well as the average pulses per minute of SAP, CCICP, AWP and RCICP. Two off-line pulse-amplitude and pulse-morphology oriented toolkits display the afore-mentioned curves, histograms and average pulses per minute, and other additional ones, in order to achieve a deeper patient monitoring study.

Effects of Fenoldopam on Intracranial Pressure and Hemodynamic Variables at Normal and Elevated Intracranial Pressure in Anesthetized Pigs

Fenoldopam (FE), a dopamine DA1-receptor agonist, has been introduced for treatment of arterial hypertension and heart failure and for preservation of renal function. Vasodilators are generally assumed to affect all vascular beds including the cerebral circulation. We have evaluated effects of FE-induced (4 micrograms.kg-1.min-1) arterial hypotension on intracranial pressure (ICP) and intraocular pressure (IOP) under conditions of normal and increased intracranial elastance. ICP and IOP responses to hypertension were tested by infusion of angiotensin II (15 micrograms.kg-1.min-1), and the response to hypercapnia was tested by elimination and reintegration of soda lime canisters in the breathing circuit. Intracranial elastance was increased by infusing mock cerebrospinal fluid (CSF) into the lateral ventricle (20 +/- 3 ml.h-1). Arterial hypotension induced with FE did not increase ICP. With increased intracranial elastance, the infusion rate of mock CSF had to be reduced while administering FE to avoid a rise in ICP (p < 0.05 compared with preinfusion value); this indicates a shift on the volume-pressure curve to the right. There were no indicators that cerebral autoregulation or CO2 reactivity of the cerebral vasculature were affected by FE in this anesthetized porcine model, as speculated from analysis of the time course of delta ICP. There are, however, indicators of increased intracranial elastance, most likely caused by vasodilation. Caution should hence be exercised when FE is administered to patients with increased intracranial elastance.

Sufentanil Increases Intracranial Pressure in Patients with Head Trauma

Sufentanil is an intravenous opioid often used as a component of anesthesia during neurosurgical procedures. However, the effects of sufentanil on intracranial pressure in patients with diminished intracranial compliance are not well established, and remain controversial. Ten patients with head trauma, in each of whom the trachea was intubated, were studied for the effects of sufentanil on intracranial pressure (ICP) and on cerebral perfusion pressure (CPP). In all patients, ICP monitoring was instituted before the study. Sedation was obtained using a propofol infusion, and paralysis was achieved with vecuronium. After obtaining control of ICP (between 15 and 25 mmHg) hemodynamic values and blood gas tensions (PaCO2 between 30 and 35 mmHg), the level of sedation was deepened with an intravenous injection of sufentanil (1 microgram/kg over 6 min), followed by an infusion of 0.005 microgram.kg-1min-1. Mean arterial pressure (MAP), ICP (fiberoptic intracranial pressure monitor), and end-tidal CO2 were continuously measured and recorded at 1-min intervals throughout the 30-min study period. Sufentanil injection was associated with a statistically significant increase in ICP of 9 +/- 7 mmHg (+ 53%), which peaked at 5 min. Then ICP gradually decreased and returned to baseline after 15 min. This was accompanied by a significant decrease in MAP (24% decrease) and, thus, CPP (38% decrease). After 5 min, MAP and CPP gradually increased, but remained significantly decreased throughout the study. The results of the current study indicate that caution should be exercised in the administration of sufentanil bolus to patients with abnormal intracranial elastance, particularly if ICP is significantly increased.

Effect of Cerebral Venous Congestion on the Pressure-Volume Index in the Evaluation of Intracranial Pressure Dynamics

Translocation of cerebrospinal fluid (CSF) between the intracranial and spinal subarachnoid space was blocked by ligating the cervical spinal core in eight cats under pentobarbital and nitrous oxide anesthesia, and the effects of cerebral venous congestion on the pressure-volume index (PVI), a measure relating the change in intracranial volume, and the logarithm of intracranial pressure (ICP) were evaluated. The changes in the volume-pressure response (VPR), a measure of intracranial elastance, were calculated simultaneously. Cerebral venous congestion was induced by lowering the head relative to the level of the heart by tilting the trunk of the animals to 20 degrees below horizontal. The presence of venous congestion was confirmed by an increase in the sagittal sinus pressure (SSP). The body position was shifted from horizontal prone (H1 group) to head-down tilt (D1 group) in four animals (group 1) and from head-down tilt (D2 group) to horizontal prone (H2 group) in the other four animals (group 2), and PVI and VPR were determined in each group. The changes in ICP and SSP with change of body position in group 1 were not significantly different from those in group 2, with both pressures changing by 7-8 mm Hg. PVI showed no significant differences between the H1 group and H2 group or between the D1 group and D2 group. The mean (+/- SEM) PVI for all measurements in the head-down tilt position (D1 and D2 groups) was significantly higher (0.50 +/- 0.02 ml; p < 0.01) than in the horizontal position (H1 and H2 groups; 0.35 +/- 0.02 ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Intracranial Elastance versus Intracranial Compliance

Intracranial Elastance <i>versus</i> Intracranial Compliance

Effect of Sevoflurane on Intracranial Pressure, Sagittal Sinus Pressure, and the Intracranial Volume-Pressure Relation in Cats

The effect of sevoflurane on intracranial pressure (ICP), sagittal sinus pressure (SSP), and the intracranial volume-pressure (V-P) relation was examined in cats. In experiment 1, on nine cats, changes in ICP and SSP were studied for 180 min during anesthesia with 1 MAC sevoflurane (2.6%, inspired) and 50% nitrous oxide (N2O) in oxygen (O2). ICP significantly (p <0.01) increased from 8.4 +/- 3.8 cm H2O (mean +/- SD), the control level to 10.6 +/- 5.1 cm H2O immediately after the administration of sevoflurane. ICP was unchanged for the subsequent 120 min but then increased significantly (p <0.05) 140 min after administration, being 15.5 +/- 9.0 cm H2O at 180 min. There were no changes in SSP or blood gases. In experiment 2, the rapid injection technique of mock cerebrospinal fluid was used to determine the intracranial V-P relation in ten cats. Measures of V-P relationships included (a) ICP before volume injection (Po), (b) peak ICP caused by volume injection (Pp), (c) intracranial compliance (C) calculated as the ratio of change of intracranial volume Delta V) to change of ICP (Delta P), and (d) the pressure volume index (PVI) calculated as the ratio of Delta V to log Pp/Po. The subjects were divided into two groups, one administered 2.6% sevoflurane and 50% N2O in O2 (n = 6) and the other 50% N2O in O2 (n = 4). Each cat in both groups was given two bolus injections into the lateral ventricle at 180 min after the start of anesthesia. Then, C and PVI were calculated. C and PVI in the group treated with sevoflurane were significantly (p <0.05) lower than in the other group. These findings suggest that prolonged use of sevoflurane increases the intracranial elastance.

A mathematical study of human intracranial hydrodynamics. Part 2--Simulation of clinical tests.

The mathematical model of human intracranial hydrodynamics proposed in a previous paper is here used to simulate the results of some dynamical tests of great clinical and physiological value and to analyze the blood flow pattern in the intracranial human basal arteries (especially in the internal carotid artery). Peak to peak amplitude of the blood flow waveform in the intracranial basal arteries, computed through the model, shows a significant increase at intracranial pressure levels above 50-60 mmHg, in accordance with recent experimental data. Moreover, diastolic blood flow appears to be largely sensitive to intracranial pressure changes during severe intracranial hypertension, whereas systolic blood flow is only slightly affected in this condition. The response of intracranial pressure to typical saline injection (volume-pressure response, steady state infusion and bolus injection tests) and to an abrupt obstruction in the extracranial venous drainage pathway is also well reproduced by the model. Finally, alterations in these responses, due to changes in some significant intracranial hydrodynamical parameters (i.e., the intracranial elastance coefficient and CSF outflow resistance) are presented.

Effects of high-frequency jet ventilation on intracranial pressure and cerebral elastance in dogs

In order to assess the effect of high-frequency jet ventilation (HFJV) on intracranial pressure (ICP) and cerebral elastance (CE), a model of progressive intracranial hypertension was developed. Six healthy dogs were ventilated using HFJV and another six with conventional mechanical ventilation. ICP and its pulse amplitude (Amp) were measured by means of an epidural transducer, and CE was assessed by analysis of the relationship between the Amp and the mean ICP. The mean ICP, under basal conditions, did not differ between the two forms of ventilation, the Amp and the slope of the relationship Amp/ICP being lower with HFJV (p less than .001). Since the lower airway pressure created with HFJV was the only difference, it is suggested that the differences found in this study are related to these pressures.

Cerebrospinal fluid pulse pressure and the pulsatile variation in cerebral blood volume: an experimental study in dogs.

The cerebrospinal fluid pulse pressure (CSFPP) has found application as a measure of intracranial elastance. However, CSFPP is also dependent on the magnitude of the pulsatile variation in cerebral blood volume (delta Vb). The purpose of the present study was to assess the effect on delta Vb of changes in systemic arterial pressure (SAP) and arterial carbon dioxide tension (PaCO2) as well as elevation of intracranial pressure (ICP). Therefore, delta Vb was computed from the electromagnetically measured flow profile in the vertebral artery of the dog on the assumption of a nonpulsatile cerebral venous outflow. During arterial hypotension, delta Vb was increased due to a shift of flow from diastole to systole, whereas mean flow was not affected. The reverse phenomenon was observed when SAP was raised. Changes in PaCO2 had little effect on pulsatile blood flow. The changes in total blood flow that occurred were evenly distributed over the cardiac cycle. Consequently, delta Vb was not significantly affected, although CSFPP was considerably changed. When ICP was raised, a breakpoint pressure was observed above which cerebral blood flow (CBF) decreased and CSFPP and delta Vb increased. This contradiction was explained by the finding of a decrease in diastolic flow, causing the fall in CBF, whereas systolic flow relative to mean flow was increased, resulting in an increased delta Vb. The underlying mechanisms of the pulsatile flow changes are extensively discussed. It is argued that the arterial inflow profile is largely determined by the compliance of the inflow section of the cerebral vascular bed. Vascular compliance is significantly altered by changes in SAP and ICP because they affect the transmural pressure of the vessels, whereas this is not the case during changes in PaCO2.

Clinical observations on the relationship between cerebrospinal fluid pulse pressure and intracranial pressure.

A method is described for monitoring the relationship between CSF pulse pressure and ICP in clinical patients. Highly significant linear relationships were found during 65 continuous ICP recordings in 58 patients. The slope value of this relationship showed a positive correlation with the elastance coefficient, a volume-pressure parameter assessed by bolus injection. However, the correlation was too weak to allow for a confident prediction of the elastance coefficient on the basis of CSF pulse pressure in the individual patient. This was attributed to the variable magnitude of the volume change underlying the CSF pulse pressure: the pulsatile variation in cerebral blood volume. This quantity was calculated on the basis of a mathematical model from the slope value and the elastance coefficient and was found to vary between 0.36 and 4.38 ml. During plateau waves a disproportionate increase in pulse pressure with the ICP was observed in contrast with a relative decrease in intracranial elastance. This phenomenon was ascribed to an increase in the pulsatile variation in cerebral blood volume. It is concluded that, under certain conditions, the intracranial volume-pressure relationship can be continuously monitored by means of CSF pulse pressure analysis. The findings during plateau waves suggest that the pulse pressure also reflects the state of the cerebral vasomotor tone.

Hydraulic model of the cerebrovascular bed: an aid to understanding the volume-pressure test.

A hydraulic model of the cerebrovascular bed is presented. The model consists of a Starling resistor in series with an upstream resistance. Volume-pressure tests were performed on the model by injecting fluid into the rigid shell of the Starling resistor. An exponential pressure response to the increase in fluid volume was observed, which supports the hypothesis that the origin of the in vivo exponential pressure response to a transient increase in cerebrospinal fluid (CSF) volume can be attributed to compression of the cerebral vessels, most probably the veins. Mathematical expressions for the dependence of pressure on volume change were derived from the model and applied to in vivo volume-pressure data. The correlation between the model and in vivo experiments suggests that the CSF pressure is coupled to cerebral venous pressure and that the volume-pressure test is an indirect measure of the cerebral venous volume and is not a measure of intracranial elastance. The physical basis for the volume-pressure test is clarified, and expressions are derived to improve the utility of the test.

Analysis of the ICP pulse-pressure relationship as a function of arterial blood pressure. Clinical validation of a mathematical model.

The influence of arterial blood pressure (ABP) on the intracranial pulse pressure relationship (PPR) was studied in 17 patients in 29 recordings, with a total period of registration of 71.5 hours. The relationship between ICP and ABP was analysed by sampling the data every 15 seconds during spontaneous fluctuations of both these variables, and the analysis was performed on the basis of a mathematical model which includes pulsatory components. MABP and ABP amplitude had an opposite effect on the slope of PPR. Flattening of the PPR slope was caused by a MABP increase or an ABP amplitude decrease. The slope became steeper with decreasing MABP or increasing ABP amplitude. In accordance with the theoretical assumptions the quotient MABP/ABP-AMP was found to be suitable to express these opposite effects on PPR. Qualitatively, the same pattern of reaction was found in all patients. Rapid changes in PPR occurring during monitoring can be explained by a change in MABP/ABP-AMP relationship, regardless whether ABP changes influence intracranial elastance or not. The breakpoint of the PPR was recorded only on two occasions and could be explained in one by the influence of ABP. Monitoring of PPR as a measure of intracranial elastance and correlation of PPR with the patient's condition it not permitted unless at least the influence of ABP is analysed in each individual case.

Acute therapeutic modalities for experimental vasogenic edema

Experimental vasogenic cerebral edema was created in rabbits with a cold-induced left occipital cortical lesion. Intracranial pressure (ICP), intracranial elastance (Em), water content, hemispheric brain tissue volume, electrolytes, electroencephalograms, behavior, and gross pathology were studied. Various therapeutic modalities were employed alone or in combination to reduce ICP acutely: acetazolamide, furosemide, mannitol, pentobarbital, lorazepam, and dexamethasone. All therapies except dexamethasone were effective in reducing ICP. Peak ICP reduction occurred at 27 ± 9.8 (SD) minutes with mannitol and at 71.4 ± 15.5 minutes with acetazolamide, with the remaining agents and combinations falling between these two extreme values. Em improved by 31.7 ± 17.02% in all therapeutic trials except those employing acetazolamide and lorazepam. With therapy, there was a reduction in the water content of the hemispheres, but the difference from that in the untreated, lesioned animals was not statistically significant. In the lesioned left hemisphere, sodium content was increased by acetazolamide (p < 0.005), furosemide (p < 0.025), pentobarbital (p < 0.05), and the combination of dexamethasone, pentobarbital, and mannitol (p < 0.005), Significant reduction was noted in the lesioned group for the potassium content of the left hemisphere in the dexamethasone (p < 0.05), pentobarbital (p < 0.025), and combination groups containing these agents (p < 0.005 to 0.025), (Neurosurgery, 5: 656-665, 1979)

Acute Therapeutic Modalities for Experimental Vasogenic Edema

Experimental vasogenic cerebral edema was created in rabbits with a cold-induced left occipital cortical lesions. Intracranial pressure (ICP), intracranial elastance (Em), water content, hemispheric brain tissue volume, electrolytes, electroencephalograms, behavior, and gross pathology were studied. Various therapeutic modalities were employed alone or in combination to reduce ICP acutely: acetazolamide, furosemide, mannitol, pentobarbital, lorazepam, and dexamethasone. All therapies except dexamethasone were effective in reducing ICP. Peak ICP reduction occurred at 27 +/- 9.8 (SD) minutes with mannitol and at 71.4 +/- 15.5 minutes with acetazolamide, with the remaining agents and combinations falling between these two extreme values. Em improved by 31.7 +/- 17.02% in all therapuetic trials except those employing acetazolamide and lorazepam. With therapy, there was a reduction in the water content of the hemispheres, but the difference from that in the untreated, lesioned animals was not statistically significant. In the lesioned left hemisphere, sodium content was increased by acetazolamide (p less than 0.005), furosemide (p less than 0.025), pentobarbital (p less than 0.05), and the combination of dexamethasone, pentobarbital, and mannitol (p less than 0.005). Significant reduction was noted in the lesioned group for the potassium content of the left hemisphere in the dexamethasone (p less than 0.05), pentobarbital (p less than 0.025), and combination groups containing these agents (p less than 0.005 to 0.025). (Neurosurgery, 5: 656--665, 1979).