Intracranial Pressure VI Edited by J. D. Miller, G. M. Teasdale, J. O. Rowan, S. L. Galbraith, and A. D. Mendelow
With 361 Figures and 127 Tables
Springer-Verlag Berlin Heidelberg New York Tokyo
Professor J. D. Miller Department of Surgical Neurology, Western General Hospital, University of Edinburgh, Crewe Road, GB-Edinburgh EH4 2XU
Professor G. M. Teasdale Professor J. O. Rowan Professor S. L. Galbraith Professor A. D. Mendelow Department of Neurosurgery, Institute of Neurological Sciences, The Southern General Hospital, University of Glasgow, GB-Glasgow G51 4TF
ISBN-13: 978-3-642-70973-9 e-ISBN-13: 978-3-642-70971-5 DOl: 10.1007/978-3-642-70971-5
Library of Congress Cataloging in Publication Data. Main entry under title: Intracranial pressure VI. "Proceedings of the Sixth International Symposium on Intracranial Pressure held in Glasgow, Scotland, June 9-13, 1985"-P. Includes index. 1. Brain-Diseases-Congresses. 2. Intracranial pressure-Congresses. 3. Head-Wounds and injuries-Congresses. I. Miller, J. Douglas (James Douglas), 1937- . II. International Sympo­ sium on Intracranial Pressure (6th: 1985 : Glasgow, Stratchclyde) III. TItle: Intracranial pres­ sure 6. IV. TItle: Intracranial pressure six. RC 386.2.158 1986 617'.51044 85-23386
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Proceedings of the Sixth International Symposium on Intracranial Pressure Held in Glasgow, Scotland, June 9-13, 1985
Organizing Committee G. M. Teasdale (Secretary) S. L. Galbraith A. D. Mendelow J. D. Miller J.O.Rowan E. M. Teasdale
Advisory Board A. Baethmann, Munich D. P. Becker, Los Angeles J. W. F. Beks, Groningen M. Brock, Berlin S. Ishii, Tokyo B. Jennett, Glasgow T. W. Langfitt, Philadelphia A. Marmarou, Richmond
Preface
A quarter of a century has elapsed since Nils Lundberg published his thesis "Continuous Recording and Control of Ventricular Fluid Pressure In Neurosurgical Practice". This publication, more than any other, propelled continuous monitoring of intracranial pressure from the status of a research tool to become an integral part of neurosurgical intensive care, with wide application in the management of patients with head injuries, intracranial haemorrhage, brain tumours and disorders of the CSF circulation. At the same time, experimental studies by Langfitt and others stimulated investigations of the relationships between intracranial pressure and cerebral blood flow, intracranial pressure volume relationships and studies of the formation and absorption of CSF. By 1972, Mario Brock had realised the extent of the interest in intracranial pressure research and organised the First International Symposium on Intracranial Pressure in Hanover in that year. This was the start of a series of highly successful meetings, subsequently held in Lund (1974), Groningen (1976), Williamsburg (1979) and Tokyo (1982), the proceed­ ings of which have been published as a uniform series of books. In each of these volumes the up to date status of research and clinical application of intracranial pressure measurement has been presented in a concise yet comprehensive way.
The present volume contains the proceedings of the Sixth International Intracranial Pressure Symposium that was held in Glasgow, Scottland, from June 9th to 13th, 1985. Since the last Intracranial Pressure Symposium three years ago much new work has been done and new inSights gained; we hope that the proceedings reflect these advances in understanding of the factors that generate intracranial hypertension, its deleterious effects and the means needed to control it.
The Editors
Chairmen: T.w. Langfitt and G.M. Teasdale
Causes and Consequences of Raised Intracranial Pressure in Head Injuries G.M. Teasdale, A.D. Mendelow, and S. Galbraith. . . . . . . . . . . . . . . . . . . .. 3
Dynamics of Intracranial Pressure Rise in Severely Head Injured Patients A. Marmarou, A.L Maset, J.D. Ward, R.I. Moulton, H.A. Lutz, G.L. Clifton, and D.P. Becker. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 9
ICP After Experimental Diffuse Head Injuries T. Gennarelli, M. Pastuszko, T. Sakamoto, G. Tomei, A. Duhaine, R. Wiser, and L. Thibault. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 15
The Value of CT Scan Density Measurements After Human Head Injury: A Com­ parative Study Using Microgravimetric Measurement of Brain Specific Gravity
R. Bullock, G. Blake, M. du Trevou, and J. Favier . . . . . . . . . . . . . . . . . . .. 20 Causal Factors in the Development of Brain Lactic Acidosis: Relationship Between Intracranial Pressure, CSF Lactate and CSF-CKBB After Severe Head Injury
L. Rabow, A.A.F. DeSalles, M. Yang, A.L. Maset, H. Kontos, H.A. Lutz, J.D. Ward, R.Y. Moulton, G.L. Clifton, P. Muizelaar, A. Marmarou, and D.P. Becker. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 25
Changes in Brain Phosphorus Metabolism in Rats Following Fluid Percussion Injury T. Hashimoto, L.H. Pitts, L. Pogliani, and H.M. Bartkowski. . . . . . . . . . . . .. 30
Brain Damage in Non-Missile Head Injury Secondary to High Intracranial Pressure D.1. Graham, A.E. Lawrence, J.H. Adams, D. Doyle, and D.R. McLellan ..... 35
Session II: Pressure Volume Relationships
Chairmen: J.D. Miller and K. Shapiro
Variations in Pressure Volume Index and CSF Outflow Resistance Measured at Different Places in the Craniospinal Axis
H. Takizawa, T. Gabra-Sanders, and J.D. Miller ...................... 43
IX
The Constant Pressure Term (Po) of the Volume-Pressure Relationship. Comparison Between Results of Infusion Test and Pulse Pressure Analysis
J.H.M. Van Eijndhoven, S. Sliwka, and C.J.J. Avezaat ................. 48 Volume Accounting: A Method for the Study of CSF-Hydrodynamics. An Aid for Parameter Estimation and Validation of Pressure/Flow Models
H. Fridenand J. Ekstedt. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 54 Brain Elastic Behavior and CSF Dynamics During Progressive Epidural Balloon Expansion
E.K. Walsh, A. Schettini, J. Beck, and R.A. Salton. . . . . . . . . . . . . . . . . . .. 62 Brain Elastic Behavior and CSF Dynamics in Cold Induced Edema
A. Schettini E.K. Walsh, J.Beck, and R.A. Salton ..................... 68 Independence of Compliance and CSF Hydrodynamics as an Explanation for Volume Preservation in the Neural Axis
K. Shapiro, F. Takei, A. Fried, and I. Kohn . . . . . . . . . . . . . . . . . . . . . . .. 74 Comparison of Pressure Volume Indices Obtained with Constant Rate and Bolus Infusions
J.T.J. Tans and D.C.J. Poortvliet . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 79 Static and Dynamic Cerebrospinal Elastance - Clinical Verification
S. Sliwka . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. 84 Elastic Properties of the Cerebrospinal System and Hydrodynamic of the CSF in Patients with Intracranial Hypertension
A.R. Shakhnovich, A.E. Razumovsky, S.S. Gasparian, and A.Ja. Rakier ..... 89
Session III: Resistance to CSF Outflow
Chairmen: A. Marmarou and H. Portnoy
How Does the Craniospinal System Cope with a Disturbance of Its Volume? C.J.J. Avezaat and J.H.M. Van Eijndhoven ......................... 99
Validity of Measurements of CSF Outflow Resistance Estimated by the Bolus Injection Method
J.D. Miller and H. Takizawa ................................... 105 Comparison of CSF Formation and Outflow Resistance Measured by Ventriculo­ Cisternal Perfusion and Volume Manipulation Techniques
H. Sakamoto, T. Nakamura, A. Marmarou, and D.P. Becker .............. 108 CSF Outflow Resistance: No Current Model is Satisfactory
J. Gyring, F. Gjerris, H.E. Br~ndsted, and N.E.O Andersen .............. 111 Shunt Dependent Hydrocephalus: Pressure Volume Characterization and Altered CSF Outflow Resistance
K. Shapiro and A. Fried ..................................... 118 Resistance to Outflow of Cerebrospinal Fluid as a Determinant of the Intracranial Pressure
M. Kosteljanetz. . . . . . ..................................... 123
x
Radioisotopic Observations on Volume Changes in Cranial Versus Spinal CSF in Response to Intracranial Pressure Changes. A Clinical Study
M. Taneda, N. Shimada, Y. Kinoshita, J. Taguchi, and K. Kuboyama ........ 128 Labile Sagittal Sinus Pressures in the Cat
J.A. Love, J. Ekstedt, and H. Friden ............................. 132
Session IV: Causes of Increased ICP: Autonomic, Vascular
Chairmen: A.D. Mendelow and J.T. Hoff
The Vasodilatory Cascade and Intracranial Pressure M.J. Rosner ............................................. 137
Clinical Evidence of Compressed Lacunar Veins Causing Plateau Waves I. Nyary and J. Vajda ....................................... 142
Cerebral Blood Volume as Another Cause ofIntracranial Hypertension Following Cold-Induced Edema
O. Hirai, H. Handa, and M. Ishikawa ............................. 146 The Role of the Central Monoamine System and the Cholinoceptive Pontine Area on the Oscillation of ICP 'Pressure Waves'
M. Maeda, K. Takahashi, M. Miyazaki, and S. Ishii .................... 151 Pressure Wave-Like Changes in ICP Produced by Electric Stimulation of the Brainstem, Hypothalamus and Cerebral Cortex in Cats
M. Maeda, K. Tanaka, S. Nishimura, and S. Matsuura .................. 156 Determinants of Intracranial Pressure Rebound After Brain Compression
K.E. Jakobsson, J. LOfgren, and N.N. Zwetnow ...................... 161 Direct Observation of Autonomic Nerve Activity in Experimental Acute Brain Swelling
H. Sakamoto, K. Tanaka, T. Nakamura, S. Nishimura, and S. Matsuura ...... 166
Session V: Methods of Measurement
Chairmen: M. Brock and J. Van Eijndhoven
A Comparison Between Three Methods ofICP Recording J.B. North and P.L. Reilly .................................... 177
Clinical Evaluation of the Gaeltec ICTlb Pressure Transducer Placed Subdurally P. Barlow, A.D. Mendelow, J.O. Rowan, A.E. Lawrence, and M. Barlow ..... 181
Multiple Simultaneous Recordings of ICP in Patients with Acute Mass Lesions L.F. Marshall, J. Zovickian, R. Ostrup, and J.M. Seelig ................. 184
Intracerebral Versus Intraventricular Pressure Recording G. Sundbiirg, K. Messeter, C.-H. Nordstrom, and S. Soderstrom ........... 187
XI
The Pressure Depth Curve in Anterior Fontanelle Pressure Monitoring W.C.G. Plandsoen, D.A. de Jong, A.I.R. Maas, H. Stroink, and J.H.M. van Eijndhoven ...................................... 193
Intracranial Balloon Catheter for ICP and Pressure/Volume Monitoring P.A. Villanueva ........................................... 199
Difficulties in Interpretation of Extradural Pressure (EDP). Measurement in Acutely Raised Intracranial Pressure (ICP)
M. Powell and A. Crockard ................................... 203 The Rotterdam Teletransducer: Telemetric Epidural Pressure Monitoring - Results of Comparative EDP-VFP Measurements
A.I.R. Maas and D.A. de Jong ................................. 207 The Effect of Position on Ventricular Pressure in Shunted and Unshunted Individuals. A Telemetric Study
P.H. Chapman, R. Griebel, E. Cosman, and M. Arnold ................. 213 A. Device for Prolonged Continuous Epidural ICP Measurement
N. Greib, F.R. Block, and K.E. Richard ........................... 218 Clinical Evaluation of the Cosman ICP Telesensor in Children
R.A. Minns and J.F. Shaw .................................... 222 Estimation of Cerebral Perfusion Pressure from Arterial Blood Pressure and Transcranial Doppler Recordings
R. Aaslid, T. Lundar, K.-F. Lindegaard, and H. Nornes ................. 226 Combined Intracranial Pressure and Multilevel Continuous Local Cerebral Blood Flow Monitoring: Local Perfusion Fluctuations
K.H. Manwaring, M.L. Manwaring, T. Harrington, L.P. Carter, and R.F. Spetzler 230
Non Invasive Evaluations ofIntracranial Pressure, Cerebral Blood Flow, Vascular Compliance and Oxygen Consumption Using Laser Infrared Spectroanalysis and the Skull Impedance Plethysmographic Method
N. Hayashi, T. Tsubokawa, T. Takeuchi, H. Kushi, S. Kumura, Y. Makiyama, and A. Matsumura ......................................... 235
Routine Computerized Neuromonitoring M.R. Gaab, M. Ottens, F. Busche, G. Moller, and H.A. Trost ............. 240
Session VI: Pulse Wave Form Analysis
Chairmen: J.O. Rowan and C.J. Avezaat
Frequency Response in Clinical Pressure Measuring Systems R.A. Johnston, M. Matheson, and A. Anderson ...................... 251
Pulse Wave Analysis During Progressive Intracranial Hypertension H.D. Portnoy, T. Sekino, and C. Branch ........................... 256
Development of a Clinical Monitoring System by Means of ICP Waveform Analysis
R.S. Bray, A.M. Sherwood, J.A. Halter, C. Robertson, and R.G. Grossman .... 260
XII
Influence of Intracranial Components on the Intracranial Pressure Pulse Wave (ICP-PW). (Comparison of ICP-PW in Communicating and Non-Communicating Hydrocephalus)
T. Matsumoto, Y. Kasuga, K. Kamiya, and H. Nagai. .................. 265 System Analysis of Pressure Transmission in the Intracranial Cavity
Y. Kasuga, H. Nagai, Y. Hasegawa, M. Nitta, and T. Matsumoto ........... 271 Influences of the Arterial and Venous Pressure Wave on the CSF Pulse Wave
A. Gega, Y. lida, and S. Utsumi ..................................... 276 An Analysis of the Epidural Pulse Waveform in Neurosurgical Patients
O. Hirai, H. Handa, and M. Ishikawa ............................. 281 Some Observations on the Relationship Between Cerebral Pulse Amplitude and ICP in Patients with Intracranial Hypertension
G. Tomei, S.M. Gaini, P. Rampini, R. Villani, R. Massei, and L. Beretta ...... 286 Oscillations of ICP Related to Cardiovascular Parameters
K.M. Einhaupl, C. Garner, U. Dirnagl, G. Schmieder, P. Schmiedek, G. Kufner, and J. Rieder ............................................ 290
The Correlation Between A- and B-Waves and Arterial CO2 Tension S.E. B¢>rgesen and J.O. Espersen ................................ 298
Cerebrospinal Fluid Dynamics in Patients with Plateau Waves M. Hayashi, H. Kobayashi, Y. Handa, H. Kawano, and H. Ishii ............ 305
Session VII: Consequences of Raised ICP: Structural, Functional, Vascular
Chairman: M. Gaab
Topographic Analysis of Mechanopathophysiological Alteration in Brain Tissue Produced Intracranial Hypertension
T. Tsubokawa, N. Hayashi, and S. Kimura ......................... 313 Local Shift of the Brain and Its Relation to the Tentorial Edge
N. Misu, H. Kuchiwaki, N. Hirai, H. Ishiguri, S. Takada, and N. Kageyama .... 318
Functional - Electrophysiology
The Effect of an Acute Rise in ICP on the Primary Somatosensory Pathway A. Ladds, M. Nitta, T. Tsutsui, and L. Symon ....................... 325
Auditory Brain Stem Responses in Uncal Herniation S. Nagao, H. Kuyama, Y. Houma, F. Momma, T. Nishiura, M. Suga, T. Murota, T. Tanimoto, M. Kawauchi, and A. Nishimoto ............... 331
The Effects of an Expanding Supratentorial Mass on Auditory Brain Stem Responses in Baboons
T. Tsutsui, M. Nitta, A. Ladds, and L. Symon ....................... 335
XIII
Studies of Brain Stem Evoked Potentials in Relation to Brain Shifting During Raised Intracranial Pressue Induced by a Frontal Balloon and a Temporal Balloon
H. Kuchiwaki, S. Takada, N. Misu, H. Ishiguri, J. Itoh, M. Nagasaka, N. Hirai, M. Ohta, and N. Kageyama ................................... 339
Electroencephalographic Changes During Pressure Waves of ICP Following Experimental Subarachnoid Hemorrhage
S. Yamamoto, E. Uno, H. Fujii, S. Higashi, M. Hashimoto, K. Futami, Y. Kogure, and C. Obinata ................................... 345
Auditory Brain Stem Evoked Response in Increased Intracranial Pressure Produced by Infusion Method in Cats
K. Iwata, A. Yamazaki, and H. Yuasa ............................ 351 Electrophysiological Findings During Increased Intracranial Pressure: A Clinical Study
K. Takeuchi, M. Hara, T. Shiogai, C. Kadowaki, and M. Nakamura ......... 355 Changes in Electrophysiological and Metabolic Indices of Brain Activity Associated with Elevated Intracranial Pressure and Transtentorial Herniation
D. d'Avella, P.G. Newlon, N. Pandolfo, M. Giebel, D.P. Becker, and R.L. Hayes .............................................. 360
Relationships of Regional Cerebral Blood Flow. Evoked Potential Responses, and SystemiC Hemodynamics During Intracranial Hypertension
R.C. Koehler, J.E. Backofen, R.w. McPherson, M.C. Rogers, and RJ. Traystman ........................................... 365
Relationship Between Cerebral Blood Flow and Somatosensory Evoked Potential in Increased Intracranial Pressure in Cats
J. Izumi, T. Kawase, S. Okui, Y.lizaka, and S. Toya .................. 369 The Effects of Secondary Insults on Cerebral Blood Flow (CBF) Intracranial Pressure (ICP) and Somatosensory Evoked Potentials (SEP) in Head Injured Cats
W. Lewelt, P. Newlon, L. Jenkins, J.D. Miller, R. Keenan, and D.P. Becker .... 373 Mechanisms of the Cushing Response
H. Schrader, N.N. Zwetnow, J. LOfgren, C. Hall, and L. MQrkrid .......... 378 Pulmonary Responses to Acutely Elevated Intracranial Pressure in Dogs
R.M. Millis, D.H. Wood, and c.o. Trauth .......................... 385 Autoregulation of Cerebral Blood Flow with Intracranial Hypertension: Effect of Hypoxia
C. Borel, R.C. Koehler, J.E. Backofen, M.D. Jones, Jr., and R.J. Traystman ... 389 Continuous Measurement of Local Cerebral Blood Volume by Reflectance Photometry
M. Ishikawa, H. Handa, S. Yoshida, O. Hirai, and K. Imadaka ............ 393 Cerebrovascular Response to Elevated Intracranial Pressure
L.M. Auer and N. Ishiyama ................................... 399 Intracranial Volume Load Tolerance
N.N. Zwetnow, J. LOfgren, and H. Schrader ........................ 404
XIV
Measurement of Conductance to Cerebrospinal Fluid Outflow by the Steady-State Perfusion Method in Patients with Normal or Increased Intracranial Pressure
F. Gjerris, S.E. B¢rgesen, K. Schmidt, P.S. S¢rensen, and J. Gyring ......... 411 Cerebrospinal Fluid Flow After Pressure Infusion Cisternography in Patients with Communicating Hydrocephalus
K. Sugiura, M. Baba, T. Chishiki, E. Kamatsuka, T. Tachizawa, and N. Hayama 417 CSF Circulation in Hydrocephalus. A Study of CSF Flow in a Shunt System
C. Kadowaki, M. Hara, M. Numoto, and K. Takeuchi .................. 423 Hydrocephalic Edema: Accessory CSF Absorption of Passive Response to Ventricular Enlargement
K. Shapiro, F. Takei, A. Fried, and I. Kohn ........................ 428 Behavior of the Cisterna Magna ICP in Traumatic Coma Patients
A. Hirayama and S. Yamasaki ................................. 433 Rhythmic Brain Movement and Density Variations Shown by Rapid Sequential CT Scanning in the Human Subject
K. Lewer Allen and E.A. Bunt ................................. 437 Biomechanics and a Theoretical Model of Hydrocephalus: Application of the Finite Element Method
T. Nagashima, N. Tamaki, S. Matsumoto, and Y. Seguchi ............... 441 Benign Intracranial Hypertension and Normal Pressure Hydrocephalus: Theoretical Considerations
L. Junck ............................................... 447 Intracranial Pressure (ICP) and Positron Emission Tomographic (PET) Studies in Acute and Chronic Hydrocephalus
M. Powell, DJ. Brooks, H.A. Brockard, R.P. Beaney, K.L. Leenders, D.G.T. Thomas, T. Jones, and J. Marshall. ......................... 451
Local Cerebral Glucose Utilization in Congenital Hydrocephalic Rats by Means of the e4 C)-Deoxyglucose Method
A. Shimizu, H. Takiguchi, H. Ueno, H. Chigasaki, and S. Ishii ............ 457 Regional Cerebral Protein Synthesis in Experimental Hydrocephalus
K. Takahashi, W. Bodsch, T. Shibata, and K.-A. Hossmann .............. 463 Visual Evoked Potentials in Patients with Hydrocephalus or Intracranial Hypertension
P. Soelberg-S¢rensen, F. Gjerris, P. Selmar, and W. Trojaborg ............. 468 The Role of HydrocephalUS in Producing Clinical Deterioration After Cerebral Aneurysm Rupture
I. Papo, M. Bodosi, F.r. Merei, A. Luongo, and G. Caruselli. ............. 472 Intracranial Pressure and Cerebral Blood Flow in Patients with Communicating Hydrocephalus Following Intracranial Aneurysm Rupture
M. Hayashi, Y. Handa, H. Kobayashi, H. Kawano, H. Ishii, and T. Tsuji ...... 476 CSF Drainage and Intracranial Pressure After Subarachnoid Hermorrhage
R. Borgmann and J. Kr~kenes . . . . . . . . . . . . . . . . . . . . . . . . ......... 481
XV
"Empty Sella" and Benign Intracranial Hypertension: Endocrine and CSF Dynamic Study
C. Anile and G. Maira ....................................... 486 Stimulation of Cyclic Adenosine 3, 5-Monophosphate Formation in Rabbit Choroid Plexus by Beta-Receptor Agonists and Vasoactive Intestinal Polypeptide
M. lindvall, A. Gustafson, P. Hedner, and Ch. Owman .................. 491 Ontogeny of Sympathetic Nerves and Transport Functions in the Rabbit Choroid Plexus
Ch. Owman, M. lindvall, and B. Winbladh . . . . . . . . . . . .............. 496 Effect of Cerebroventricular Infusion of Vasopressin on Intracranial Pressure, Blood Pressure and Plasma Vasopressin
P. Soelberg-S¢>rensen and J.A. Gyring ............................ 502 Intracranial Pressure in Experimental Streptococcus Pneumoniae Meningitis in Rabbits
K.J. Goitein, M. Shapiro, and M. Ramaz .......................... 507
Session IX: Haemorrhage, Ischemia and Other Focal Lesions
Chairmen: A. Baethmann and H.A. Crockard
Experimental Intracerebral Haemorrhage: Intracranial Pressure Changes and Cerebral Blood Flow
A.D. Mendelow, R. Bullock, F.P. Nath, A. Jenkins, T. Kingman, and G.M. Teasdale ............................................ 515
The Influence of Systemic Hypertension on Intracranial Pressure and Edema Formation in Experimental Intracerebral Hemorrhage
T. Wallenfang, J. Bayer, G. Fries, and K. Schiirmann .................. 521 Investigation of Cerebral Perfusion Pressure and Edema Formation in a Hypertonic Saline Model of Cerebral Edema
Q.J. Durward, R.F. Del Maestro, A.L. Amacher, and J.K. Farrar. .......... 526 Immunohistochemical Investigation in Experimental Intracerebral Hemorrhage (ICH) and Its Correlation with Findings in Clinical Studies
T. Wallenfang, G. Fries, J. Bayer, and K. Schiirmann .................. 532 Vasogenic Brain Edema and Intracranial Pressure in Experimental Carbon Dioxide Laser Brain Lesions
H.E. James, S. Schneider, E. Tiznado, and S. Moore ................... 538 Photoactivation of Hematoporphyrin Derivative in Cat Brain: A Model of Ischemic Necrosis
M. Chopp, M.R. Glasberg, S. Teodecki, and K.M.A. Welch ............... 543 Response of ICP, CBF and ECoG to Cerebral Administration of Kinins
A. Unterberg, U. Hack, and A. Baethmann ......................... 548 The Role of Cellular Calcium Entry in Spontaneous and Traumatic Subarachnoid Hemorrhage
O.R. Hubschmann, D.C. Nathanson, and AJ. Krieger .................. 552
XVI
Changes of Capillary Permeability in Experimental Brain Tumor A. Tamura, T. Nakagomi, M. Matsutani, T. Nagashima, H. Tanaka, H. Orii, and K. Sano ................................................ 557
Segmental Vascular Resistance and CO2 Reactivity After Global Cerebral Ischemia R. Schmidt-Kastner and K.-A. Hossmann .......................... 561
Brain Tissue Pressure in Focal Cerebral Ischemia with and without Reperfusion F. Iannotti, G.P. Schielke, V. Albanese, P. Picozzi, M. Rotondo, and J.T. Hoff ............................................... 566
Session X: Therapy I: Osmotic and Other Agents
Chairmen: S. Ishii and J.W.F. Beks
Effects of Mannitol on Tissue Pressure in Focal Cerebral Ischemia G.P. Schielke, J.T. Hoff, S. Hatashita, and D.S. Kim ................... 573
How does Mannitol Reduce Edema Water in Focal Cerebral Ischemia? T. Hanamura, T. Asano, T. Shigeno, T. Mirna, E. Watanabe, and K. Takakura .. 577
The Effect of Mannitol on the Water Content of White Matter after Head Injury inMan
F. Nath and S. Galbraith ..................................... 581 The Effect of Intravenous Mannitol on Cat Pial Arteries and Veins During Normal and Elevated Intracranial Pressure
L.M. Auer and K. Haselsberger ................................. 585 Intracranial Pressure Changes Following a Bolus Infusion of Mannitol at Various Levels of PaC02 in Normal Dogs and Dogs with Experimentally Induced Intracranial Hypertension
M. Abou-Madi, D. Trop, N. Abou-Madi, and P. Ravussin ................ 590 The Effect of Furosemide on Intracranial Pressure and Cerebrospinal Fluid Formation
M. Pollay, P.A. Roberts, B. Hisey, B. Pendleton, D. Koontz, R. Smith, and F .A. Stevens .......................................... 597
Analysis of the Intracranial Response to Mannitol and Furosemide C.P. McGraw and C.O'Connor ................................. 601
The Combined Use of Mannitol and Furosemide in Treatment of Elevated Intracranial Pressure: Timing, Dosage and Delivery
P.A. Roberts, M. Pollay, F.A. Stevens, C.F. Engles, and C.B. Fullenwider. .... 605 Effect of Steroids on the Resolution Process of Edema
K. Tanaka, K. Ohata, J. Katsuyama, S. Nishimura, and A. Marmarou ........ 611 A Study of Potassium Canrenoate on Raised Intracranial Pressure and on the Metabolism of Electrolytes and Hormones
Y. Node, S. Nakazawa, K. Yajima, Y. Tsuji, and T. Hasegawa ............. 620 Reduction in Cerebrospinal Fluid Transport Mediated by Lead Acetate In Vitro in the Superior Sagittal Sinus of the Dog
J.D. Mann, J.D. Charlton, S.L. Cookson, N.E. Pederson, and R.N. Johnson ... 624
XVII
Reduction of Intracranial Pressure with Anticoagulation in Patients with Venous Sinus Thrombosis
K. Einhaupl, C. Garner, P. Schmiedek, R. Haberl, U. Dirnagl, H.W. Pfister, and P. Franz ................................................ 629
Session XI: Head Injury and Other Clinical Uses of ICP Monitoring
Chairmen: D.P. Becker and H. Nagai
Role of Intracranial Pressure Monitoring in the Management of Occult Traumatic Intradural Hematoma
Y.M. Kohi, G.M. Teasdale, L.S. Murray, S.L. Galbraith, and P. Driscol. ...... 635 The Application of ICP Monitoring in Deciding Surgical Management
M. Hara, C. Kadowaki, M. Nakamura, H. Watanabe, T. Shiogai, M. Ogashiwa, M. Numoto, and K. Takeuchi. ................................. 639
Cerebral Blood Flow Changes in Hypertensive Intracerebral Hematoma Y. Yamada, T. Shima, S. Matsumura, Y. Okada, T. Hatayama, and S. Okita ... 643
Pressure-Volume Dynamics in Head-Injured Patients: A Preliminary Study A.L Maset, A. Marmarou, J.D. Ward, and H.F. Young .................. 647
Changes of Glasgow Coma Score and ICP During the Development of Acute Epidural Hematoma
H. Sakai, H. Takagi, H. Ohtaka, T. Tanabe, T. Ohwada, and K. Yada ........ 652 Pupillary Abnormalities, Elevated Intracranial Pressure and Mass Lesion Location
L.F. Marshall, J.M. Cotten, S. Bowers-Marshall, and J.M. Seelig ........... 656 The Relationship Between Intracranial Pressure, Cerebral Perfusion Pressure and Outcome in Head Injured Patients: The Critical Level of Cere bral Perfusion Pressure
H. Tsutsumi, K. Ide, T. Mizutani, H. Takahashi, H. Tanabe, H. Kuroki, H. Toyooka, K. Mii, and K. Takakura ............................ 661
Impact of Cerebral Perfusion Pressure on Survival Following Head Trauma C.P. McGraw, C.B. Shields, J.W. Gamel, and R.A. Greenberg ............. 667
Clinical Analysis of Intracranial Hypertension in Severe Head Injury M. Yano, Y. Ikeda, S. Kobayashi, and T. Otsuka ..................... 671
Increased ICP and Systemic Hypotension During the First 72 Hours Following Severe Head Injury
J.M. Seelig, M.R. Klauber, B.M. Toole, and S. Bowers-Marshall. ........... 675 Local Basal Ganglia and Brain Stem Blood Flow in the Head Injured Patient Using Stable Xenon Enhanced CT Scanning
T.R. Harrington, K. Manwaring, and J. Hodak ....................... 680 Correlation of Acute ICP and CBF with CT Scan and Neuropsychological Recovery in Severe Head Injury
B.P. Uzzell, W.D. Obrist, C.A. Dolinskas, and J.L. Jaggi ................ 687 The Influence ofIntracranial Pressure and Clinico-Neurological Findings on Outcome in Patients with Diencephalic Tumors
K. Richard, R. Knipprath, E. Godehardt, H. Herrmann, and R. Firsching ..... 691
XVIII
Clinical Experience of 780 Cases of Postoperative ICP Monitoring H. Takagi, Y. Miyasaka, S. Morii, T. Ohwada, and K. Yada .............. 695
Nursing and ICP: Studies of Two Clinical Problems: Study 1: Effects of Passive Turning and Lateral Neck Flexion
P.H. Mitchell, D. Amos, and C. Astley ............................ 701 Study 2: Effects of Touching and Talking in Children
P.H. Mitchell, F.B. Johnson, B. Habermann-little, D. Van Inwegen-Scott, and D. Tyler ............................................. 702
The Problems of Averaging ICP Records by Eye D. Price and P. Driscoll ...................................... 705
Intracranial Pressure in the Early Stage after SAH M. Mokry and L.M. Auer .................................... 713
Session XII: Therapy II: Anesthesia, Pharmacology and Cerebral Metabolic Depressants
Chairmen: S.L. Galbraith and S. Cotev
ICP and CBF Reactivity to Isoflurane and Nitrous Oxide During Normocarbia, Hypocarbia and Intracranial Hypertension
M. Albin, L. Bunegin, and J. Gelineau ............................ 719 Effect of Isoflurane on Intracranial Pressure in Patients with Intracranial Mass Lesions
M. Belopavlovic and A. Buchthal ............................... 725 Isoflurane and Intracranial Pressure
B. Mazzarella, P. Mastronardi, T. Cafiero, G. Gargiulo, A. Frangiosa, C. Tomassino, L. Stella, and A. De Chiara ......................... 732
Effects of Etomidate, Sodium Pentothal and Lidocaine on Cerebral Elastance F.J. Gilsanz, R. Garcia de Sola, J.1. Lora-Tomayo, P. Mateos, and C. Hernandez ............................................ 736
Elimination of Ventilator-Related ICP Fluctuations by Special Techniques of Artificial Ventilation
R. Schedl, M. Baum, H. Benzer, P. Fasol, G. Ittner, N. Mutz, and H. Spangler ............................................. 740
Intracranial Pressure and Other Variables During Simultaneous Ventilation Compression Cardiopulmonary Resuscitation
N. Bircher and P. Safar ...................................... 747 Control of Intracranial Pressure in Traumatic Brain Injury. Our Experience with Gammahydroxybutyric Acid or Thiopental and Fentanyl
P. Dabadie, P. Maurette, J.F. Brule, C. Kays, J. Destandeau, J.P. Castel, and P. Erny ................................................ 750
The Effects of Gammahydroxybutyrate and Sodium Thiopentone on Intracranial Pressure in Severe Head Injury
J.R.S. Leggate, N.M. Dearden, and J.D. Miller ...................... 754
XIX
Cerebral Vasoconstriction with Fluosol DA as a Means of Acutely Reducing ICP J.P. Muizelaar, E.P. Wei, H.A. Kontos, and D.P. Becker ................. 758
The Effect of Dimethylsulfoxide (DMSO) on Intracranial Pressure and Outcome After Severe Head Injury
L.H. Pitts, M.P. Lovely, and H.M. Bartkowski ....................... 762 Failure of Prophylactic Barbiturate Coma in the Prevention of Death Due to Uncontrollable Intracranial Hypertension in Patients with Severe Head Injury
J.D. Ward, J.D. Miller, S. Choi, A. Marmarau, H.A. Lutz, P. Newlon, R. Keenan, and D.P. Becker .......................................... 766
The Outcome with Barbiturate Therapy in Severe Head Injuries M. Yano, Y. Ikeda, S. Kobayashi, Y. Yamamoto, and T. Otsuka ........... 769
Treatment for Severe Head Injury. A Comparative Study of Nizofenone and Barbiturate
A. Tamura, T. Kurihara, H. Nakayama, H. Nihei, O. Gotoh, and K. Sano ..... 774
Summaries
Progress in the Analysis of Intracranial Pressure Dynamics A. Marmarou ............................................ 781
Raised ICP in Head Injury, Its Significance, Causes, and Therapy T.W. Langfitt ............................................ 789
Subject Index .............................................. 795
Aaslid, R. 226 1
Abou-Madi, M. 590 Abou-Madi, N. 590 Adams, J.H. 35 Albanese, V. 566 Albin, M.S. 719 Amacher, A.L. 526 Amos, D. 701 Andersen, N.E.O. III Anderson, A. 251 Anile,C. 486 Arnold, M. 213 Asano, T. 577 Astley, C. 701 Auer, L.M. 399, 585, 713 Avezaat, C.J. 48, 99 Baba, M. 417 Backofen, J.E. 365,389 Baethmann, A. 548 Barlow, M. 181 Barlow,P. 181 Bartkowski, H.M. 30,
762 Baum,M. 740 Bayer, J. 521,532 Beaney, R.P. 451 Beck, J. 62,68 Becker, D.P. 9,25,108,
360,373,758,766 Belopavlovic, M. 725 Benzer, H. 740
Beretta, L. 286 Bircher, N. 747 Blake, G. 20 Block, F .R. 218 Bodosi, M. 472 Bodsch, W. 463 Borel, C. 389 B¢rgesen, S.E. 289,411 Borgmann, R. 481 Bowers-Marshal, S. 656,
675 Branch, C. 256 Bray, R.S. 260 Brondsted, H.E. 111 Brooks, D.1. 451 Brule, J.F. 750 Buchthal, A. 735 Bullock, R. 20, 515 Bunegin, L. 719 Bunt, E.A. 437 Busche, F. 240 Cafiero, T. Carter, L.P. 230 Caruselli, G. 472 Castel, J.P. 750 Chapman, P.H. 213 Chariton, J.D. 624 Chigasaiki, H. 457 Chishiki, T. 417 Choi, S. 766 Chopp, M. 543
Clifton, G.L. 9, 25 Cookson, S.L. 624 Cosman, E. 213 Cotten, J.M. 656 Crockard, H.A. 203,451 Dabadie, P. 750 d'Avella, D. 360 De Chiara, A, 732 De Jong, D.A. 193, 207 De Salles, A.A.F. 25 Dearden, N.M. 754 Del Maestro, R.F. 526 Destandeau, J. 750 Dirnagl, U. 290,629 Dolinskas, C.A. 687 Doyle, D. 35 Driscol, P. 635, 705 Du Trevou, M. 20 Duhaine, A. Durward, Q.y. 526 Einhiiupl, K.M. 290, 629 Ekstedt, J. 54,132 Engles, C.F. 605 Erny, P. 750 Espersen, J.O. 298 Farrar, J.K. 526 Fasol, P. 740 Favier, J. 20 Firsching, R. 691 Franz, P. 629 Friden, H. 54, 132
i The address of each first mentioned author is indicated below the according contribution heading. Page, in which contribution commences
XXI
Fried,A. 74,118,428 Fries, G. 521,532 Fujii, H. 345 Fullenwider, C.B. 605 Futami, K. 345 Gaab, M.R. 240 Gabra-Sanders, T. 43 Gaini, S.M. 286 G~braHh,S. 3,581,635 Gamel, J.w. 667 Garcia de Sola, R. 736 Gargiulo, G. Garner, C. 290,629 Gasparian, S.S. 89 Gega, A. 276 Gelineau, J. 719 Gennarelli, T. 15 Giebel, M. 360 Gilsanz, FJ. 736 Gjerris, F. 111 , 411, 468 Glasberg, M.R. 543 Godehardt, E. 691 Goitein, KJ. 507 Gotoh, O. 774 Graham, D.1. 35 Greenberg, R.A. 667 Greib, N. 218 Griebel, R. 213 Grossman, R.G. 260 Gustafson, A. 491 Gyring,J.111,411,502 Haberl, R. 629 Habermann-Little, B. 702 Hack, U. 548 Hall, C. 378 Halter, J .A. 260 Hanamura, T. 577 Handa,H. 146,281,393 Handa, Y. 305,476 Hara, M. 355,423, 639 Harrington, T.R. 230,
680 Hasegawa, T. 620 Hasegawa, Y. 271 Haselsberger, K. 585 Hashimoto, M. 345
XXII
Hashimoto, T. 30 Hatashita, S. 573 Hatayama, T. 643 Hayama, N. 417 Hayashi, M. 305,476 Hayashi, N. 235,313 Hayes, R.L. 360 Hedner,P. 491 Hernandez, C. 736 Herrmann, H. 691 Higashi, S. 345 Hirai,N. 318,339 Hirai, O. 146,281,393 Hirayama, A. 433 Hisey, B. 597 Hodak, J. 680 Hoff, J.T. 566,573 Hossman, K.A. 463,561 Houma, Y. 331 Hubschmann, O.R. 552 Iannotti, F. 566 Ide, K. 661 Iida, Y. 276 Iizaka, Y. 369 Ikeda, Y. 671,769 Imadaka, K. 393 Ishiguri, H. 318, 339 Ishii,H. 305,476 Ishii, S. 151,457 Ishikawa, M. 146,281,
393 Ishiyama, N. 399 Itoh, J. 339 Ittner, G. 740 Iwata, K. 351 Izumi, J. 369 Jaggi, J.L. 687 Jakobsson, K.E. 161 James, H.E. 538 Jenkins, A. 515 Jenkins, L. 373 Johnson, F.B. 702 Johnson, R.N. 624 Johnston, R.A. 251 Jones, T. 451 Jones, Jr., M.D. 389
Junek, L. 447 Kadowaki, C. 355,423 Kageyama, N. 318,339 Kamatsuka, E. 417 Kamiya, K. 265 Kasuga, Y. 265,271 Katsuyama, J. 611 Kawano,H. 305,476 Kawase, T. 369 Kawauchi, M. 331 Kays, C. 750 Keenan, R. 373, 766 Kim, D.S. 573 Kimura, S. 235,313 Kingman, T. 515 Kinoshita, Y. 128 Klauber, M.R. 675 Knipprath, R. 691 Kobayashi, H. 305,476 Kobayashi, S. 671,769 Koehler, R.C. 365,389 Kogure, Y. 345 Kohi, Y.M. 635 Kohn, I. 74,428 Kontos, H.A. 25,758 Koontz, D. 597 Kosteljanetz, M. 123 Kr£kenes, J. 481 Krieger, AJ. 552 Kuboyama, K. 128 Kuchiwaki, H. 318,339 Kufner, G. 290 Kurihara, T. 774 Kuroki, H. 661 Kushi, H. 235 Kuyama, H. 331 Ladds, A. 325, 335 Langfitt, T.W. 789 Lawrence, A.E. 35,181 Leenders, K.L. 451 Leggate, J.R.S. 754 Lewelt, W. 373 Lewer Allen, K. 437 Lindegaard, K.F. 226 Lindvall, M. 491, 496 Little, B.H. 701
LOfgren, J. 161,378,404 Lora-Tamayo, J.1. 736 Love, J.A. 132 Lovely, M.P. 762 Lundar, T. 226 Luongo, A. 472 Lutz, H.A. 9,25,766 Maas, A.I.R. 193, 207 Maeda, M. 151,156 Maira, G. 486 Makiyama, Y. 235 Mann, J.D. 624 Manwaring, K.H. 230,
680 Manwaring, M.L. 230 Marmarou, A. 9,25,108,
611,647,781 Marshall, J. 451 Marshall, L.F. 184,656 Marshall, S.B. Maset, A.L. 9,25,647 Massei, R. 286 Mastronardi, P. Mateos, P. 736 Matheson, M.S. 251 Matsumoto, S. 441 Matsumoto, T. 265, 271 Matsumura, A. 235 Matsumura, S. 643 Matsutani, M. 557 Matsuura, S. 156,166 Maurette, P. 750 Mazzarella, B. McGraw, C.P. 601,667 McLellan, D.R. 35 McPherson, R.W. 365 Mendelow, A.D. 3, 181,
515 Merei, F.T. 472 Messeter, K. 187 Mii, K. 661 Miller, J.D. 43,105,373,
754, 766 Millis, R.M. 385 Mirna, T. 577 Minns, R.A. 222
Misu, N. 318,339 Mitchell, P.H. 701 Miyasaka, Y. 695 Miyazaki, M. 151 Mizutani, T. 661 Mokry, M. 713 Moller, G. 240 Momma, F. 331 Moore, S. 538 Morii, S. 695 Morkrid, L. 378 Moulton, R.J. 9,25 Muizelaar, J.P. 25, 758 Murota, T. 331 Murray, L.S. 635 Mutz, N. 740 Nagai, H. 365,271 Nagao, S. 331 Nagasaka, M. 339 Nagashima, T. 441,557 Nakagomi, T. 557 Nakamura, M. 355,639 Nakamura, T. 108,166 Nakayama, H. 774 Nakazawa, S. 620 Nath, F.P. 515,581 Nathanson, D.C. 552 Newlon, P.G. 360,373,
766 Nihei, H. 774 Nishimoto, A. 331 Nishimura, S. 156,166,
611 Nishiura, T. 331 Nitta, M. 271,325,335 Node, Y. 620 Nordstrom, C.H. 187 Nomes, H. North, J.B. 177 Numoto, M. 423,639 Nyary, I. 142 Obinata, C. 345 Obrist, W.D. 687 O'Connor, C. 601 Ogashiwa, M. Ohata, K. 611
Ohta, M. 339 Ohtaka, H. 652 Ohwada, T. 652,695 Okada, Y. 643 Okita, S. 643 Okui, S. 369 Orii, H. 557 Ostrup, R. 184 Otsuka, T. 671, 769 Ottens, M. 240 Owman, Ch. 491, 496 Pandolfo, S.N. 360 Papo,1. 472 Pastuszko, M. 15 Pederson, N.E. 624 Pendleton, B. 597 Pfister, H.W. 629 Picozzi, P. 566 Pitts, L.H. 30, 762 Plandsoen, W.C.G. 193 Pogiiani, L. 30 Pollay, M. 597, 605 Poortvliet, D.C.J. 79 Portnoy, H.D. 256 Powell, M. 203,451 Price, D. 705 Rabow, L. 25 Rakier, A.J. 89 Ramaz, M. 507 Rampini, P. 286 Ravussin, P. 590 Razumovsky, A.E. 89 Reilly, P.L. 177 Richard, K.E. 218,691 Rieder, J. 290 Roberts, P.A. 597,605 Robertson, C. 260 Rogers, M.C. 365 Rosner, M.J. 137 Rotondo, M. 566 Rowan, J.O. 181 Safar, P. 747 Sakai, H. 652 Sakamoto, H. 108, 166 Sakamoto, T. 15 Sakamoto, W. 108
XXIII
Salton, R.A. 62, 68 Sano,K. 557,774 Schedl, R. 740 Schettini, A. 62, 68 Schielke, G.P. 566, 573 Schmidt, K. 411 Schmidt-Kastner, R. 561 Schmiedek, P. 290,629 Schmieder, G. 290 Schneider, S. 538 Schrader, H. 378,404 Schiirmann, K. 521,532 Seelig, J.M. 184,656,
675 Seguchi, Y. 441 Sekino, T. 256 Selmar, P. 468 Shakhno~ch,A.R. 89 Shapiro, H.M. Shapiro, K. 74,118,428 Shapiro, M. 507 Shaw, J.F. 222 Sherwood, A.M. 260 Shibata, T. 463 Shields, C.B. 667 Shigeno, T. 577 Shima, T. 643 Shimada, N. 128 Shimizu, A. 457 Shiogai, T. 355,639 Sliwka, S. 48, 84 Smith, R. 597 Soderstrom, S. 187 SQrensen, P.S. 411,
468,502 Spangler, H. 740 Spetzler, R.F. 230 Stella, L. 732 Stevens, F .A. 597, 605 Stroink, H. 193 Suga, M. 331 Sugiura, K. 417
XIV
Sundbarg, G. 187 Symon, L. 325,335 Tachizawa, T. 417 Taguchi, J. 128 Takada,S. 318,339 Takagi, H. 652,695 Takahashi, H. 661 Takahashi, K. 151,463 Takakura, K. 577,661 Takei, F. 74,428 Takeuchi, K. 355,423,
639 Takeuchi, T. 235 Takiguchi, H. 457 Talcizawa, H. 43,105 Tamaki, N. 441 Tamu~, A. 557,774 Tana,be, H. 661 Tanabe, T. 652 Tanaka, K. 156,166,
557,611 Taneda, M. 128 Tanimoto, T. 331 Tans, J.TJ. 79 Teasdale, G.M. 3,515,
635 Teodecki, S. 543 Thibault, L. 15 Thomas, D.G.T. 451 Tiznado, E. 538 Tomasino, C. 732 Tomei, G. 15,286 Toole, B.M. 675 Toya,S. 369 Toyooka, H. 661 Traystman, R.J. 365,389 Trojaborg, W. 468 Trop, D. 590 Trouth, C.O. 385 Trost, H.A. 240 Tsubokawa, T. 235,313
Tsuji, T. 476,620 Tsutsui, T. 325,335 Tsutsumi, H. 661 Tyler, D. 702 Ueno, H. 457 Uno,E. 345 Unterberg, A. 548 Utsumi, S. 276 Uzzell, B.P. 687 Vajda, J. 142 Van Eijndhoven, J.H.M.
48,99,193 Villani, R. 286 Villanueva, P.A. 199 Van Inwegen-Scott, D.
701 Wallenfang, T. 521,532 Walsh, E.K. 62, 68 Ward, J.D. 9,25,647,
766 Watanabe, E. 577 Watanabe, H. 639 Wei, E.P. 758 Welch, K.M.A. 543 Winbladh, B. 496 Wiser, R. 15 Wood, D.H. 385 Yada, K. 652,695 Yajima, K. 620 Yamada, Y. 643 Yamamoto, S. 345 Yamamoto, Y. 769 Yamasaki, S. 433 Yamazaki, A. 351 Yang, M. 25 Yano, M. 671,769 Yoshida, S. 393 Young, H.F. 647 Yuasa, H. 351 Zo~ckian, J. 184 Zwetnow, N.N. 161,378,
404
Chairmen: T. W. Langfitt and G. M. Teasdale
Causes and Consequences of Raised Intracranial Pressure in Head Injuries. G.M. Teasdale, A.D. Mendelow, and S. Galbraith
Dynamics of Intracranial Pressure Rise in Severely Head Injured Patients. A. Marmarou, A.L. Maset, J.D. Ward, R.J. Moulton, H.A. Lutz, G.L. Clifton, and D.P. Becker
ICP After Experimental Diffuse Head Injuries. T. Gennarelli, M. Pastuszko, T. Sakamoto, G. Tomei, A. Duhaine, R. Wiser, and L. Thibault
The Value of CT Scan Density Measurements After Human Head Injury: A Comparative Study Using Microgravimetric Measurement of Brain Specific Gravity. R Bullock, G. Blake, M. du Trevou, and J. Favier
Causal Factors in the Development of Brain Lactic Acidosis: Relationship Between Intracranial Pressure, CSF Lactate and CSF-CKBB After Severe Head Injury. L. Rabow, A.A.F. DeSalles, M. Yang, A.L. Maset, H. Kontos, H.A. Lutz, J.D. Ward, . RY. Moulton, G.L. Clifton, P. Muizelaar, A. Marmarou, and D.P. Becker
Changes in Brain Phosphorus Metabolism in Rats Following Fluid Percussion Injury. T. Hashimoto, L.H. Pitts, L. Pogiiani, and H.M. Bartkowski
Brain Damage in Non-Missile Head Injury Secondary to High Intracranial Pressure. D. Graham, A.E. Lawrence, J.H. Adams, D. Doyle, and D.R McLellan
Causes and Consequences of Raised Intracranial Pressure in Head Injuries
G.M. Teasdale, A.D. Mendelow, and S. Galbraith
Institute of Neurological Sciences, Southern General Hospital, Glasgow G51 4 TF (U.K.)
Introduction
There is still disagreement about the value of monitoring and treating Intracranial Pres­ sure (ICP) in severely head injured patients (Stuart et al. 1983). This reflects continuing uncertainties about what mechanisms are responsible for increased ICP, if these differ in different injuries, and also doubts about the relationship between ICP and brain damage. We review a range of investigations we have performed on severely injured adults in order to study changes in the volumes of the intracranial constituents that may indicate raised ICP after head injury. The results provide a basis for understanding the causes and con­ sequences of traumatic intracranial hypertension.
Patients and Methods
The patients were managed in an intensive care unit; they did not receive steroids, man­ nitol was used sparingly and patients were ventilated only for respiratory indications. The type of injury was determined from CT scan findings.
Water content cerebral white matter was determined by a gravimetric technique (Galbraith et al. 1984) in biopsies taken at operation. Cerebral blood volume (CBV) was measured from CT scans taken before and after the intravenous injection of iodide contrast (Mendel ow et al. 1983). Ventricular volume was measured by a CT scan tech­ nique and used as an index of changes in Cerebrospinal Fluid (CSF) volume (Murphy et al. 1983). In some patients Cerebral Blood Flow (CBF) was measured by the Xenon 133 intravenous injection technique; (Mendelow et al. 1985).
Results
Brain Water Content
Both diffusely and focally injured groups had low specific gravities, suggesting the presence of oedema. (Galbraith et al. 1984). Calculated water content was 78.3 ± 7% in seven dif­ fuse injuries and 80.8 ± 6.8 in ten focal injuries. The most striking correlation was an association between a high water content in the white matter around an intracranial
Intracranial Pressure VI Eds.: J. D. Miller, G.M. Teasdale, J. O. Rowan, S. L. Galbraith, and A. D. Mendelow © Springer-Verlag Berlin Heidelberg 1986
3
•
65 70 80 90 100
H 20/g Tissue ( S.G. Method)
Fig. 1. Relationship between ICP and brain water in white matter surrounding a traumatic intra­ cranial haematoma (Data from Galbraith et al. 1984)
haematoma and the level of ICP postoperatively (Fig. 1). By contrast, in patients with diffuse injury water content and ICP were not correlated.
Cerebral Blood Volume
The values of CBV ranged between 2% and 8% in 23 focally injured and 19 diffusely injured patients (Mendelow et al. 1983). In neither case was a high blood volume asso­ ciated with elevated ICP, nor did CBV correlate with arterial PaC02 or CBF.
CSF Volume
The mean ventricular volume was 29.4 ± 5.2 ml in 16 patients studied after evacuation of an intracranial haematoma and there was a significant correlation between a decreasing volume and increased ICP (Murphy et al. 1983). Furthermore, in 4 out of 5 of these patients who were studied serially, an increase in the ventricular size was accompanied
4
by a reduction in ICP. The volume of each of the lateral ventricles was measured in 31 patients with an extradural haematoma studied pre-operatively. The results showed that not only was the ventricle contralateral to the haematoma usually larger in relation to the ipsilateral ventricle, the total volume of the two ventricles could be increased above normal. This occurred when there was a mid-line shift of more than 1 cm and when the CT scan showed obliteration of the third ventricle and basal cisterns (Findlay et al. 1983), a finding that indicates that an obstruction to CSF outflow could contribute to the increase of ICP.
Although 22 patients with a diffuse injury had small ventricles (mean 6.1 ± 1.1 ml) they were younger and there was not a relationship between ventricle size and ICP. Indeed these diffusely injured patients also showed a striking association between obliteration of the third ventricle and basal cisterns on the CT scan and an increased intracranial pressure (Teasdale et al. 1984) Fig. 2.
Fig. 2. Relationship between modal ICP and the CT Scan Appearances of CSF spaces. (From Teasdale E et al. 1984, by permission Ed J Neurol. Nsurg & Psychiat)
Cerebral Blood Flow and ICP
lCP (mm Hgl
•
33 patients with a focal injury tended to have a low CBF, particularly when the ICP was high (Mendelow et al. 1985). By contrast, in 22 patients with a diffuse injury CBF was higher and did not decline with a raised ICP (Table 1).
5
Table 1. Mean values of cerebral blood flow CBF (iSEM) ml/l00g/min related to type of injury and modal ICP (Data from Mendelow et al. 1985)
Types of Injury Low ICP High ICP <20mmHg >20mmHg
Focal 43.2 ±4 36.1 ± 3.5 (n = 17) (n = 16)
Diffuse 50.5 ±4.8 49.4 ± 8.7 (n = 16) (n = 6)
Conclusions
1. Causes of Raised ICP in Different Injuries
We suggest that in patients with a diffuse injury, increased ICP can not be explained by changes in a single intracranial constituent. Instead, varying combinations of increased brain water content, increased CBV, and obstruction to CSF outflow are responsible. An obstruction in CSF flow also occurs in patients with an intracranial space occupying lesion and may contribute to raised ICP before operation. On the other hand, when pressure remains high after operation, it then appears to reflect the severity of swelling in the brain around the lesion. This is mainly due to oedema and as this dissipates, pres­ sure declines.
2. Consequences of Raised ICP in Different Injuries
Raised ICP does not itself directly cause brain damage, instead it does so only by second­ arily producing ischaemia, either focal or diffuse. In patients with a haematoma, ischae­ mia due to increased ICP and shift clearly cause deterioration and secondary brain damage (Galbraith and Teasdale 1981). By contrast, there is no evidence that increased ICP reduces CBF in diffuse injury (Obrist et al. 1984). Although ischaemia may occur when ICP is> 40 mmHg and Cerebral perfusion Pressure (CPP) is low, high ICP is rare in adult patients with diffuse injury and usually is a terminal event.
It is clear that fatal diffuse primary brain damage can be sustained without a rise in intracranial pressure. Of 82 patients identified at post mortem to have sustained diffuse axonal injury, 32 had no signs of raised ICP and when these were present there was usually an associated haematoma or severe contusion (Table 2). We therefore suggest that the well established correlation between increased ICP and worse outcome of dif­ fuse injury can be explained by the level of intracranial pressure being an indication of the established damage, rather than a primary cause of progressive damage.
6
Table 2. Occurrence of sign of increased ICP and associated features in 82 patients with post mortem evidence of diffuse axonal injury. (Data from series of Graham et al. 1985)
Intracranial haematoma
32 patients
2 (6%)
23 (72%)
PM Signs of t ICP
50 patients
14 (28%)
49 (98%)
If, as we suggest, raised ICP often reflects traumatic brain damage rather than producing it, is there any value in monitoring ICP? We think that there is and that the benefit varies with the kind of injury (Table 3):
Table 3. Causes and Consequences of Traumatic Intracranial Hypertension
Type of Cause of t ICP Cerebral Significance of t ICP injury Mass tH20 tCBV CSF Blood
obst Flow
Focal Normal Ischaemia and Pre-op ++ + ? + or secondary Post-op - ++ ? ? low brain damage
Diffuse ± ± ± ± Normal ? Measure of or Established high damage
Measurements of ICP have a clear role in patients with a mass lesion whether or not the patient is in coma. They are especially useful with an occult haematoma, in whom the need for operation is in doubt. ICP is also a reliable index of the degree and progress of post operative swelling. In patients with a diffuse injury, measurements of ICP are less useful and in these patients intensive treatment of ICP has uncertain benefits which may be outweighed by the potential hazards. When a patient in coma has a normal CT scan, ICP monitoring is rarely necessary, unless there are at least two adverse features such as abnormal motor response, a history of hypotension or age over 40 years. (Narayan et al. 1982).
7
References
Findlay G, Kohi Y, Matheson M, Murray L, Teasdale G (1983). Volumetric analysis of the contra­ lateral dilated ventricle. J Neurol Neurosurg & Psychiat 46: 368
Galbraith S, Teasdale G (1981) Predicting the need for operation in the patient with an occult trau­ matic intracranial haematoma. J Neurosurg 55:75-81
Galbraith S, Cardoso E, Patterson J, Marmarou A (1984). The water content of white matter after head injury in man. In: Go KG and Baethmann AF. Recent Progress in the Study and Therapy of Brain Oedema. Plenum Publishing Corporation pp 323-330
Graham DI, Lawrence AE, Hume Adams J, Doyle D, McLellan D (1986). Brain Damage Secondary to a High Intracranial Pressure in Head Injury. In: ICP VI. Eds. Miller JD, Teasdale G, Rowan JR, Galbraith S, Mendelow AD. Springer-Verlag, Berlin Heidelberg
Mendelow AD, Teasdale G, Teasdale E, Matheson M, Russell T (1983). Cerebral Blood Volume and Intracranial Pressure in Head Injured Patients. In: ICP V. Ed. Ishii S, Nagai H, Brock M. Springer­ Verlag. Berlin Heidelberg p495-500
Mendelow AD, Teasdale GM, Russell T, Flood J, Patterson J, Murray GD (1985). Cerebral Blood Flow and Perfusion Pressure in Human Head Injury. J Neurosurgery (In Press)
Murphy A, Teasdale E, Matheson M, Galbraith S, Teasdale G (1983). Relationships between CT indices of brain swelling and Intracranial Pressure after head injury. In: ICP V. Ed. Ishii S, Nagai H, Brock M. Springer-Verlag. Berlin Heidelberg p562-566
Narayan RK, Kishore PRS, Becker DP et al. (1982) Intracranial Pressure: to Monitor or not to Monitor? A review of our experience with severe head injury. J Neurosurg 56:650-659
Obrist WD, Langfitt TW, Jaggi JC, Cruz J, Gennarelli TA (1984). Cerebral Blood Flow and meta­ bolism in comatose patients with acute head injury: Relationship to intracranial pressure. J Neurosurg 61:241-253
Stuart GG, Merry GS, Smith JA, Yelland JDN (1983). Severe head injury managed without intra­ cranial pressure monitoring. J Neurosurg 59:601-605
Teasdale E, Cardoso E, Galbraith S, Teasdale G (1984). CT Scan in Severe Diffuse Head Injury: Physiological and Clinical Correaltions. J Neurol Neurosurg & Psychiat 47:600-603
8
Dynamics of Intracranial Pressure Rise in Severely Head Injured Patients*
A. Marmarou, A.L. Maset, J.D. Ward, R.J. Moulton, H.A. Lutz, G.L. Clifton, and D.P. Becker
Division of Neurosurgery, Box 508, MeV Station, Richmond, VA 23298 (USA)
Our work and studies by other investigators have shown that the single most frequent cause of death in aggressively managed head injured patients is uncontrollable intra­ cranial hypertension (Becker 1977, Marshall 1979). Studies in Richmond indicate that high ICP was initially present in two-thirds of those patients without intracranial space­ occupying lesions who were comatose upon admission. Half of the patients who developed intracranial hypertension, or in whom elevated ICP persisted, died despite therapy. Raised ICP continues as the most frequent cause of death in head injury yet the sequence of events which leads to raised ICP is poorly understood. Our studies of ICP dynamics impli­ cate at least three parameters which contribute to the level of pressure; the rate of fluid formation (If), the outflow resistance offered to the egress of fluid (Ro), and a component (Pv) identifying the vascular contribution to ICP. The objective of this study was to measure the changes in these parameters in head-injured patients and determine the relative contribution of CSF and vascular components to the ICP.
Study Population
This report describes the information gathered thus far in a study population of 42 severely head injured patients, Glasgow coma score 8 or less, admitted to the intensive care unit within 6 to 18 hours from the time of injury. Ofthis patient group, in which the primary diagnoses are listed in Table 1, access to the CSF compartment via ventri­ cular catheter for volume manipulation and ICP measurement was possible in 34 patients. Pressure volume testing was restricted to this cohort.
Table 1. Primary diagnosis - Patient study group (N = 34)
Closed Head Injury Epidural Intracerebral Hematoma Subdural Hematoma Intraventricular Hemorrhage
l3 5 8 6 2
*This project was funded by the National Institutes of Health, NS-12587
Intracranial Pressure VI Eds.: 1. D. Miller, G. M. Teasdale, 1. O. Rowan, 9 s. L. Galbraith, and A. D. Mendelow © Springer-Verlag Berlin Heidelberg 1986
Methods
All patients were undergoing continuous monitoring of ICP and pressure dynamics stud­ ies as part of a standard clinical protocol. The pressure transducer (Gould model P23) for measurement of ICP was referenced to the level of the external auditory canal and with the patient bed elevated 20 degrees above the horizontal plane. In general, the tech­ niques used in determining CSF formation, outflow resistance and vascular pressure by volume manipulation are those reported previously (Marmarou et al. 1976, Marmarou et al. 1978). Briefly described, following stabilization in the ICP, a small bolus of CSF (0.5- 1.5 rnl) was removed and the pressure volume index (PVI) which describes the intra­ cranial compliance was estimated from the equation PVIw = dV/log (Po/Pm). The ele­ ments of this equation are the pressure volume index computed from withdrawal (PVIw), the volume of the bolus (dV), initial pressure prior to removal (Po), and the minimum pressure reached immediately following withdrawal (Pm). Next, the volume (Vmax) necessary to limit the pressure rise to bolus injection (Pmax) (usually 25 mmHg) was computed using the equation Vmax = (PVIw) (log Plimit/Po). Subsequent injections of volume were kept below this limit. Following this calculation, two to three bolus injec­ tions were performed and the initial pressure (Po), peak pressure (Pp), and volume addi­ tion (dV) were obtained from the pressure response to calculate the pressure volume index from injection (PVIi) using the equation PVIi = dV/(log Pp/Po). The resistance to outflow (Ro) was calculated from the same pressure response to bolus addition using the equation
Ro = t2Po/(PVIi)Log [(P2/Pp) (Pp-Po) /P2-Po)]
where pressure P2 refers to a pressure point on the return trajectory at time t2 (usually selected at 2 minutes). The withdrawal maneuver, in addition to providing a measure of the PVI, also permitted the calculation of CSF formation. A small amount of fluid (2-4 cc) was removed and the initial (Po), minimum (Pm), and a pressure point Pion the return trajectory at time tl was inserted in the equation
Iform = (PVI/tl) (log Pi/Pm)
for estimation of fluid formation. The remaining Pv parameter in the steady state equation was estimated by with­
drawing fluid at the estimated formation rate using a motorized syringe pump. This maneuver shunts the newly formed fluid and essentially cancels the gradient of ICP necessary to absorb fluid. Thus, the new equilibrium pressure reached was considered the vascular contribution to ICP.
Results
Comparison ofPVI determination by bolus injection of withdrawal
As described in the methods section, the first maneuver was a small bolus withdrawal to estimate the pressure volume index. The withdrawal index (PVIw) was compared
10
to subsequent indices obtained by bolus injection (PVIb). This is an important considera­ tion since at high ICP levels it was not always possible to add volume. A total of 68 com­ parisons were made (Table 2) and were analyzed as a function of steady state ICP level. It can be seen from Table 2 that the withdrawal PVIw compares favorably with indices obtained from bolus injection. This close agreement held throughout the range of pressure above and below 15 mmHg.
Table 2. Comparison of PVI by bolus injection and withdrawal methods (N = 23; M ± SD)
ICP PVI (ml) PVI (ml) N P mmHg withdrawal injection studies
<15 18.9 (7.7) 18.4 (6.9) 28 NS.90:>P>'80
>15 17.1 (5.5) 17.0 (5.2) 40 NS 1 :>P>.90
Rate of fluid formation
In patients with steady state ICP levels less than 15 mHg, the rate of fluid formation averaged 0.337(SD 0.10) ml/min (Table 3). This is equivalent to 485 ml/day and is very close to the accepted normal value of 500 ml/day. As ICP levels increased, the mean value of CSF formation decreased moderately to 0.296 (SD 0.06) ml/min. This repre­ sents a 12% reduction compared to the low pressure group. However, these values are still within normal range. It is important to note the wide variation of fluid formation in the ICP range of 15 to 25 mmHg. In two patients, the rate of fluid formation exceed­ ed 0.7 ml/min, and we believe this represents edema clearance through the CSF system. This was confirmed in both patients by withdrawing fluid at the estimated formation rate for several hours, and by recording fluid volume at a reduced sustained level of pressure.
Table 3. CSF formation in head injured patients
ICP Studies Patients Study CSF formation (ml/min) SD mmHg N N mean range
<15 14 13 0.337 0.13-0.49 0.10
15-25 37 19 0.300 0.13-0.74 0.127
>25 9 6 0.296 0.25-0.40 0.060
Resistance to CSF absorption
Table 4 compares the resistance to CSF absorption measured by bolus technique in patient groups with steady state ICP levels above and below 15 mmHg. The mean value
11
Table 4. CSF outt1ow resistance in head injured patients
ICP Studies Patients CSF outt1ow resistance SIG mmHg N N mean range SD
<15 11 11 16.0 4.7-30.2 8.76
>15 11 11 11.75 2.9-28.3 6.3 .20>p>.10
of resistance below 15 mmHg equalled 16.0 mmHg/ml/min, a five fold increase above normal values for bolus resistance. The average resistance values in the high pressure group were also above normal but not statistically different from the low pressure mean.
CSF component of ICP
Accepting the notion that the CSF component of ICP is given by the product of CSF formation and resistance, as described by the steady state equation, we can now deter­ mine the percentage of ICP rise caused by fluid absorption. The mean steady state ICP of this patient group equalled 18.87 mmHg, representing an ICP rise of 8.87 mmHg above the estimated normal opening pressure of 10 mmHg. The formation resistance product (If*Ro) for bolus techniques was calculated as (0.35*3.0) or 1.05 mmHg. Thus, at an opening pressure of 10 mmHg, the CSF component accounts for 10.5% of steady state pressure. A pressure of 8.95 was considered as normal Pv. The percentage rise of ICP due to CSF component was calculated by the equation:
%ICPcsf = [ (If* Ro) exp - (If* Ro) norm l/ICP rise x 100%
and
%ICPvasc = [ (Pvexp - Pvnorm) IICP rise 1 * 100%
Inserting the measured values obtained in Table 5 we find that the component of rep rise of this patient group due to CSF absorption accounts for 31 % of the ICP elevation. The remainder, or the estimated rise due to a vascular component equals 68.5%.
Table 5. Contribution of CSF and vascular factors to raised ICP in head injured patients with measures of If and Ro
Patients ICP ICP rise If Ro %L'iIcp (csf) %L'iIcp (vase) N mmHg mmHg ml/min ml/min/Hg estimated
11 18.87 8.87 0.326 11.75 31.34 68.66
SD (3.56) 3.31 (0.14) (6.33) 17.3
12
Estimation of CSF and Vascular component of ICP in patients with measures of formation, resistance, and Py from withdrawal tests
Independent measures of If and Ro using bolus manipulation, and Pv from withdrawal tests were obtained in 9 patients (Table 6). The mean ICP level of this patient group averaged 19.97 mmHg. The rise above accepted normal opening pressure of 10 mmHg equaled 9.97 mmHg. Inserting the values for If, Ro and measured Pv, the percentage rise due to the CSF system equaled 22.9% while the measured contribution of the vas· cular compartment equaled 73.42%. Adding the CSF and Vascular components, we have accounted for 96% of the ICP rise.
Table 6. Contribution of CSF and vascular factors to raised ICP in head injured patients with Independent measure of If, Ro, and Py (N = 9)
ICP tdcp If Ro Py %ICPcsf %ICPpy
Mean 19.97 9.97 0.268 12.18 16.27 22.90 73.42
SE 2.5 2.36 0.022 3.16 2.17 6.94 7.26
Summary
We must consider that these data were obtained during the course of treatment and represent in the majority of cases, the combined effect of Mannitol, hyperventilation, drainage, and barbiturates. Despite aggressive therapy, ICP remained elevated and 20% of the patients studied went on to develop intractable ICP and eventual neurologic death. The results of these studies suggest that although absorption is moderately impaired, the increased resistance does not account for an appreciable elevation of ICP in this patient group. Fluid formation was within normal1imits thus not adding further challenge to the absorptive mechanism and increasing ICP. It must also be noted that these techniques used to assess fluid formation measure the sum of newly formed CSF and ventricular clearance of edema fluid. In two patients, the rate of fluid forma­ tion exceeded 0.75 rnI/min and was sustained for several hours suggesting fluid clearance by the CSF compartment. However, the fact that net fluid formation approaches 500 rnI/day and is reasonably constant over the first 5 days post injury, indicates that ventri­ cular clearance of edema is minimal during this period in the majority of patients.
We conclude that, with exception of those patients with subarachnoid hemorrhage where Ro is high (Marmarou et al. 1976, Kosteljanetz 1984) CSF absorption parameters playa minor role in the sequence of events leading to raised ICP in head injury which lends support to the concept that the rise of ICP is effected by edema, and swollen tissue is mediated by a vascular mechanism.
13
References
Becker, D.P., Miller, J.D., Ward, J.D., Greenberg, R.P., Young, H.F., Sakalas, R. (1977) The outcome from severe head injury with early diagnosis and intensive management. J. Neurosurg. 47:491- 502
Kosteljanetz, M. (1984) CSF dynamics in patients with subarachnoid and/or intraventricular hemor­ rhage. J. Neurosurg. 60:940-946
Marmarou, A., Shapiro, K., Shulman, K. (1976) Isolating factors leading to sustained elevations of the ICP. In: Intracranial Pressure III, J.W.F. Beks, D.A. Bosch, M. Brock (eds.), Springer-Verlag, Berlin, pp. 33-36
Marmarou, A., Shulman, K., Rosende, R. (1978) A nonlinear analysis of the cerebrospinal fluid system and intracranial pressure dynamics. J. Neurosurg. 48: 332-334
Marshall, L.F., Smith, R.W., Shapiro, H.M. (1979) The outcome with aggressive treatment in severe head injuries. I. The significance of intracranial pressure monitoring. J. Neurosurg. 50:20-25
14
ICP After Experimental Diffuse Head Injuries
T. Gennarelli, M. Pastusko, T. Sakamoto, G. Tomei, A. Duhaine, R. Wiser, and L. Thibault
Division of Neurosurgery, University of Pennsylvania, 3400 Spruce Street, Philadelphia, PA 19104 (USA)
We have previously shown that ICP rises transiently, but to high values, after reversible cerebral concussion induced by sagittal plane angular acceleration in the monkey (1) and that for equally severe concussions produced by coronal plane angular acceleration, the ICP rises much less dramatically (2). We now present data on more severe diffuse injuries produced by coronal plane acceleration and on concussion produced by horizontal plane acceleration.
Methods
Physiological monitors were attached to 86 anesthetized adult 5-9 kg monkeys or baboons using 80% nitrous oxide and either 1) phencyclidine (one or more doses of 1 mg/kg) or 2) ketamine (5-8 mg/kg) and Veterinary Innovar (lcc/16 kg); droperidol plus fentanyl anesthesia. ICP was measured through a hollow, right angle subarachnoid bolt inserted into the right frontal bone connected by fluid-filled teflon tubing to a mano­ metrically calibrated pressure transducer. ICP was recorded before, and for at least two hours after injury, except for the actual time of the injury when, because of transducer saturation, it was temporarily disconnected (for 30 seconds before and 10 seconds after injury). All animals spontaneously ventilated through an endotracheal tube and had normal resting blood gases.
Injuries were produced by the Penn I or Penn II acceleration devices preVIOUSlY described (3). Briefly, a single non-impact, controlled, angular acceleration was delivered to the head so that it moved only in a single plane. Three injury planes were investigated. Thirty-one animals incurred sagittal plane motions with the head moving posterior to anterior. These, as well as 7 of 44 animals that were given a left to right coronal plane acceleration, have been subjects of previous reports (1,2). Horizontal plane acceleration was given to 11 subjects, so that the head moved torsionally from right to left about its vertical axis. The angular displacement was 60 degrees in all cases, but the magnitude of acceleration was varied from 0.5 to 2 x 105 radians/sec2. Post injury neurological observations were made and the subjects were sacrificed for pathologic or biochemical analyses at various times.
Coma was defined as the absence of eye opening and behavioral contact with the environment when the effects of deep anesthesia were no longer present (4). The ani­ mals were divided into several categories of injury for this report, based on the duration
Intracranial Pressure VI Eds.: J. D. Miller, G. M. Teasdale, J. o. Rowan, S. L. Galbraith, and A. D. Mendelow © Springer.Veriag Berlin Heidelberg 1986
15
of post traumatic coma. In increasing severity, these injuries are mild concussion (coma <3 min); cerebral concussion (CC) (coma 3-15 min); mild diffuse axonal injury (mild DAI), coma 15-120 min; diffuse axonal injury (coma >2 hr) without or with promi­ nant respiratory disturbances of the cluster breathing type (5).
Results
Cerebral Concussion (see Fig. 1) Cerebral concussion was produced in all three injury directions. Of 31 sagittal injuries,
there were 6 mild concussions and 25 concussions. Coronal motion caused concussion in 15 of 44 experiments and all 11 horizontal plane experiments had concussion injury. The maximum ICP/Control ICP in mild concussion was 3.64 and for concussion in the coronal, horizontal and sagittal planes were 1.25,2.91 and 6.55. Thus sagittal injury, even mild concussion, produced larger rises in ICP than the other two motions. Figure 1 also shows that in sagittal concussion the ICP returned toward normal much more slowly.
ICP AFTER CONCUSSION ICP/ICP CONTROL
7 ~----------------------------------------------,
Fig. 1 c M-CC-S TIME AFTER INJURY (minute .. ) + CC-C <) Cc-s b. CC-H
Abbreviations in figures: M-CC = Mild cerebral concussion (coma < 3 min), CC-C, S, H = Cerebral concussion from Coronal, Sagittal, or Horizontal plane acceleration; coma 4-15 minutes, M-DAI-C = Mild Diffuse Axonal injury from coronal plane acceleration (coma 15-120 minutes), DAI-C = Diffuse axonal injury from coronal motions (coma> 2 hours), R-DAI-C = Diffuse axonal injury with cluster respirations
16
Prolonged traumatic coma (see Fig. 2) Prolonged traumatic coma or DAI occurred only after coronal acceleration. Figure 2
demonstrates that as the duration and severity of DAI increased from mild DAI (n = 10), through DAI without cluster breathing (n = 13), to DAI with cluster breathing (n = 6), the magnitude and duration of elevated ICP increased. Subjects with cluster breathing had the worst neurological signs and outcome and were separated from those without respiratory disturbance because they clearly had more severe injury. The maximum ICP (% of control) for each group was 393, 800, and 993 respectively and the duration of the ICP elevation was 10, 35 and 120 minutes after injury.
ICP AFTER PROLONGED COMA 10
ICP/ICP CONTROL
Fig. 2 M-OAI-C TIME AFTER INJURY (minutes)
C + OAI-C 0 R-MJ-C
Figure 3 compares the maximum ICP of the seven injuries. They are shown in increasing severity from left to right except that the three cerebral concussions are of equal severity. Thus the rise of ICP in cerebral concussion is very different depending on the direction of head motion that caused the concussion; sagittal concussions, even mild ones, had higher elevations of ICP than those produced by horizontal or coronal acceleration. Though ICP was even higher in the DAI injuries, the ICP associated with sagittal concus­ sion exceeded that in mild DAI, despite the latter being an injury associated with much longer coma and more severe pathologic abnormalities.
17
ICP/CONTROL
9
8
7
Fig. 3 INCREASING SEVERllY OF INJURY
Discussion
We conclude that the ICP rise after acceleration injury is not entirely dependent on the magnitude of the coma produced, because animals with mild DAI had lower ICP values than did sagittally injured animals with shorter, concussive comas. Similarly, we feel that immediate ICP elevations are not related to the amount of primary brain damage present since coronally injured animals with mild DAI had more axonal damage than did sagittal animals. Rather, we feel that the immediate ICP elevation is an independent phenomenon related to the direction of head movement. ICP immediately after injury is more sensitive to sagittal than to horizontal or coronal motions. This would seem to be unlikely if vasoparalysis of cortical vessels was a direct result of acceleration. In all three directions, cortical vessels are subjected to the same forces since the vessels are randomly distributed throughout the brain. Instead we favor the hypothesiS that the ICP rises because of loss of pressure autoregulation induced by activation of lower brain stem centers, a location apparently more stressed by sagittal motion than by other directions.
In addition, the effect that respiratory disturbance may play in acute ICP elevations must be considered. Though transient irregularities of rate and volume occur frequently in all types of cerebral concussion and DAI, none is as prominent as the cluster respira­ tions that characterize the most severe injuries. This pattern is associated with under­ ventilation and hypercapnia. These may augment the peak and prolong the duration of the ICP rise that is due to trauma induced vasoparalysis. The localization of cluster breathing to the tegmental region of the lower pons and upper medulla (5) also supports the hypothesis that rises in ICP immediately after injury result from acceleration induced tissue strains in the lower brains tern.
18
Summary
Previously we showed that the rises in ICP were accompanied by rises in mean arterial blood pressure (MAP) (1). We posed the dilemma of whether the increased ICP was a consequence of impaired pressure autoregulation due to the rise in MAP or, rather, that the MAP rose in compensation for a primary rise in ICP. Subsequently, we showed that, for equal levels of injury, the direction of head motion was important and that sagittal motions produced greater ICP elevation than did coronal plane motion (2). This sugges­ ted a differential effect on brainstem centers responsible for blood pressure control.
We now present evidence that 1) for equal levels of injury, namely cerebral concussion, coronal plane head motions produce less ICP change than sagittal motions, with hori­ zontal motions in between and 2) that ICP elevations increase with increasing injury severity through the spectrum of diffuse brain injury from concussion to DAI. These data continue to support the hypothesis that raised ICP immediately after head injury has its origin in the lower brainstem.
References
1. Gennarelli, TA, Czernicki, Z, Segawa, H, et aI., (1980) ICP in Experimental Head Injury, in Intra­ cranial Pressure IV, Shulman, K, Marmarou, A, Miller, JD, et. al. (eds), Springer-Verlag, Berlin, pp.28-32
2. Gennarelli, TA, Marcincin, RP, Thibault, LE and Thompson, CJ, (1983), Effect of Direction of Head Movement on ICP in Experimental Head Injury, in Intracranial Pressure V, Ishii, S., Nagai, H, and Brock, M (eds), Springer-Verlag, Berlin, pp. 483-486
3. Gennarelli, TA, (1983), Head Injury in Man and Experimental Animals: Clinical Aspects, Acta Neurochir, Suppl. 32, 1-13
4. Gennarelli, TA, Thibault, LE, Adams, JH, et al., (1982), Diffuse Axonal Injury and Traumatic Coma in the Primate, Ann. Neurol, 12:564-574
5. Plum, F and Posner, JB, (1980), in The Diagnosis of Stupor and Coma, Davis, Philadelphia, p. 34
19
The Value of CT Scan Density Measurements After Human Head Injury: A Comparative Study Using Microgravimetric Measurement of Brain Specific Gravity
R. Bullock, G. Blake, M. du Trevou, and J. Favier
Department of Neurosurgery, University of Natal and Wentworth Hospital, P/Bag Jacobs, 4026, Durban (South Africa)
Introduction
Following human head injury, complex pathophysiological processes interact, and controversy exists regarding the role of brain oedema and brain engorgement, both of which may occur, superimposed upon diffuse axonal injury and hypoxic brain damage. Both engorgement and oedema may be a cause of raised intracranial pressure. (Adams et al. 1982).
Since the advent of modern high resolution CT scanning, several authors have quali­ tatively described appearances consistent with various patterns of brain oedema (Miller et al. 1980) and diffuse brain engorgement (Bruce et al. 1981). However, few studies have, as yet, correlated CT scan appearances with objective measurement of brain oedema, cerebral blood flow or tissue histology.
Patients and Methods
Two groups of severely head injured patients were studied. Thirty-one patients with diffuse head injury underwent white matter sampling at the time of establishment of intracranial pressure monitoring via a right frontal burrhole. In none of these patients was a focal brain lesion present in the right frontal region.
In twenty-nine patients white matter samples were obtained at the time of resection of an intracerebral haematoma or focal contusion. A rongeur biopsy was made from the periphery of the lesion, after it had been removed. The majority of these patients with focal lesions subsequently underwent ICP monitoring. The mean ICP for the first 24 hours of monitoring was recorded for each patient and case notes were retrospec­ tively analysed to establish the incidence of ischaemic episodes prior to surgery. The site of white matter sampling was located on the CT scans by annotating two dimen­ sionalline diagrams at the time of surgery. A standardised 12 mm2 region of interest was then marked at this site for the appropriate CT scan cut using the cursor facility of the GE8800 scanner and the mean value of three readings of CT density was used. The CT scanner was calibrated weekly using phantoms of known density.
White matter specimens were immediately immersed in a solution of Bromobenzene and Kerosene to prevent evaporative water loss during transit. Specific gravity was measured using the microgravimetric method. (Shigeno and Brock 1982).
20 Intracranial Pressure VI Eds.: 1. D. Miller, G. M. Teasdale, 1. O. Rowan, S. L. Galbraith, and A. D. Mendelow © Springer-Verlag Berlin Heidelberg 1986
Results
Good correlation was found between white matter S.G. and CT scan density values (Fig. 1) (r = 0.650; P < 0.001). The mean white matter S.G. for the 29 patients who sustained focal injury was 1.0335 ± 0.0008. This was significantly below the normal range (P < 0.05). Mean ICP for this group was Significantly elevated (Table 1).
1050
1045
C.T. density-Houndsfield units
Fig. 1. Relationship between white matter specific gravity and CT Scan density in sixty severely head injured patients
The mean white matter S.G. for the 31 patients who sustained diffuse injuries did not differ significantly from the normal value (Table 1).
Within this group however, 17 patients had CT density values of 36 Hounsfield Units or greater (Table 2). These patients were thought to represent diffuse brain engorgement. (Vide infra) White matter S.G. for this sub-group was above the normal value, and ICP was slightly raised (Table 2).
21
Table 1. White matter specific gravity, CT scan density and ICP values in 60 severely head injured patients
White matter CT density n specific gravity (Hounsfield Units) ICP(mmHg)
Diffuse injury 31 1.0374 ± 0.0007 35.4 ± 0.7
Focal injury 29 1.0335 ± 0.0008a 30.8±0.7
Normals 1.0380 ± 0.0006b "25-35"
aSignificantly above or below normal value (P < 0.05).
bValue from Takagi et al. (1981), Bullock et al. (1985). All values given as means ± SEM.
19 ± 3
28 ±3a
<20
Table 2. White matter specific gravity, CT scan density, ICP and incidence of ischaemic episodes in 2 subgroups of patients with diffuse injury
White matter CT density ICP Ischaemia n specific gravity (Hounsfield (mmHg) (%)
Units)
Normals 1.0380 ± 0.0006a "25-35" <20
aTagaki et al. (1981), Bullock et al. (1985). All values given as means ± SEM
Five patients with diffuse injuries had CT density values of 30 H. U. or less. These patients were thought to represent "diffuse brain oedema". The mean white matter S.G. for these 5 patients was considerably lower than the normal value and mean Iep was markedly raised (Table 2).
Influence of Hypoxia/Ischaemia
Of the 60 patients studied, 14 (23%) had undergone documented episodes of hypoxia (P02 < 65 mmHg) or hypotension (MABP < 60 mmHg). Only 3 of these patients had sustained focal injuries. Five hypoxic patients manifested "diffuse brain engorgement" (Table 2) and 4 demonstrated "diffuse brain oedema". Thus, only two ischaemic head injured patients had white matter specific gravity values in the normal range. Mean ICP for the ischaemic patients was 25 ± 8 mmHg.
No relationship was found between ICP and white matter S.G. either for the group as a whole, or for the focal and diffuse injury groups when tested separately (Fig. 2).
22
1050
1045
50 60
Fig. 2. White matter specific gravity and intracranial pressure in sixty severely head injured patients
Discussion
The microgravimetric method of measurement of brain S.G. has provided a means of objectively validating CT scan observations in humans. Although Takagi et al. (1981) have documented a relationship between CT scan density and brain specific gravity, this has not yet been reported after head injury.
Of our 60 patients, 17 demonstrated white matter S.G. values above the normal range. This could be explained by an increase in tissue solids or a decrease in water con­ tent. The close correlation between high white matter S.G. and CT scan density values argues against methodological errors after sampling.
Shigeno et al. (1982) have demonstrated that change in cerebral blood volume (CBV) can account for S.G. changes in cat white matter up to 0.001. Our patients with high white
23
matter S.G. and high CT density therefore probably represent "diffuse brain engorgement". This accords with the observations of Obrist et al. (1984) who report increased cerebral blood flow (CBF) in 55% of their severely head injured patients. Episodes of hypoxia/ischaemia were strongly associated with "diffuse brain oedema" in our patients (Table 2). These patients had high ICP, and probably represent global brain perfusion failure, with consequent oedema and reduced CBF and CBV.
In patients with focal injury, we have demonstrated significantly reduced perifocal white matter S.G. and this accords with the observations of Galbraith et al. (1984). However, this reduced S.G. may be caused not only by increased brain water, but by perifocal CBV reduction, or oligaemia. Although S.G. was significantly reduced in most patients with focal injury, CT density values were within the given "normal range" of 25 to 35 Hounsfield Units (Fig. 1) for many of these patients. We feel that this given range of normal white matter CT density may be erroneously wide and could be narrowed.
CT density measurements appear to reflect changes in brain S.G. and should be further evaluated against other indicators of cerebral oedema and brain engorgement, such as NMR scanning, CBF measurement and cerebral arteriovenous oxygen differences
(AVD02)'
References
Adams, J.H. et al. (1982) Brain damage in non-missile head injury. Observations in man and sub­ human primates. In Thomas Smith W, Cavanagh J.B. (eds). Recent advances in Neuropathology. Churcill Livingstone, Edinburgh.
Bullock, R. et al. (1985) Brain specific Gravity & CT Scan density measurements after Human Head injury. J Neurosurg. (In press).
Bruce, D.A. et al. (1981) Diffuse cerebral swelling following head injuries in chidren. The syndrome of "malignant brain oedema". J Neurosurg 54: 170-178
Galbraith, S. et al. (1984) The water content of white matter after head injury in man. In Go K.G., Baethmann A (eds). Recent Progress in the Study and Therapy of Brain Oedema. Plenum Press, New York.
Miller, J.D. et al. (1980) Computed Tomography in Brain Oedema due to Trauma. In Cervos-Navarro H, Ferszt R (eds). Brain Oedema. Raven Press, New York.
Obrist, W.O. et al. (1984) Cerebral blood flow and metabolism in comatose patients with acute head injury. J Neurosurg 61:241-253.
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Causal Factors in the Development of Brain Lactic Acidosis: Relationship Between Intracranial Pressure, CSF Lactate, and CSF-CKBB After Severe Head Injury
L. Rabow, A.A.F. DeSalles, M. Yang, A. Maset, H. Kontos, H.A. Lutz, J.D. Ward, R.Y. Moulton, G.L. Clifton, P. Muizelaar, A. Marmarou, and D.P. Becker
Division of Neurological Surgery, Department of Surgery, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA (USA)
Introduction
Although there is a consensus that a high lactate level in the cerebrospinal fluid (CSF) after head injury is a grave prognostic sign, it is still debated whether the lactate is detrimental to the brain, or if CSF-Iactic acidosis is only reflecting a derangement of brain metabolism.
Lactate is the end product of glycolysis, a result of inability to metabolize pyruvate in lack of oxygen. As there is no metabolism going on in the CSF, the post-tra~matic CSF-Iactate has to emanate from brain tissue or from the blood through a breakdown of the blood-brain barrier. Since the CSF-Iactate is usually higher and remains high even after normalization of blood lactate, this latter possibility is less likely to occur. Increased CSF-Iactate may thus be due to generalized or, more likely, localized ischemia/ hypoxia, although other possibilities have to be considered, such as changes in intracel­ lular enzyme activity (lactate dehydrogenase, pyruvate dehydrogenase complex) or simply derangement of the normal metabolic pathways.
To study the relationship between CSF-Iactate production and the extent of the primary parenchymal brain injury, we have chosen to compare post-traumatic lactate levels in the CSF with those of CSF-CKBB activity in severely head-injured patients. CKBB, the anodal brain-type isoenzyme of creatine kinase, has been shown by Hedman and Rabow (1979), Nordby and Urdahl (1982), and by Bakay and Ward (1983) to rise very rapidly after a parenchymal brain damage. The rise is supposedly due to a destruc­ tion (anatomical and/or functional) of the cell membrane with a release of intracellular components into the extracellular space
Materials and Methods
A study was carried out on 29 patients, 21 males and 8 females, aged 9-62 years (median age 25 years) with severe head injury, defined as not obeying commands, not uttering any words, and remaining with eyes continuously closed, i.e., Gl