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Neurosurgical Forum: Letters to the Editor To The Editor Harold A. Wilkinson , M.D., Ph.D. Massachusetts General Hospital Boston, Massachusetts 195 196 Abstract Object The aim of this study was to compare the effects of two different treatment protocols on physiological characteristics and outcome in patients with brain trauma. One protocol was primarily oriented toward reducing intracranial pressure (ICP), and the other primarily on maintaining cerebral perfusion pressure (CPP). Methods A series of

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Michael J. Rosner and Irene B. Coley

E levation of the head of the bed has been standard neurosurgical practice for management of intracranial pressure (ICP). 1, 2, 4 Yet, such elevation has been shown to be capable of elevating ICP and even inducing pressure waves. 1, 3 More recently, we have provided laboratory and clinical evidence linking pressure waves to cerebral perfusion pressure (CPP) decrements. 9–11 These latter observations have led us in the present study to examine CPP as a function of head elevation. In our recent descriptions of the “vasodilatory cascade,” we have pointed out

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Pressure-volume index as a function of cerebral perfusion pressure

Part 2: The effects of low cerebral perfusion pressure and autoregulation

W. John Gray and Michael J. Rosner

P revious studies of the relationship of cerebral perfusion pressure (CPP) changes to “brain stiffness, ” whether measured by compliance, elastance, volume pressure response, or pressure-volume index (PVI), have suggested that at normal levels of intracranial pressure (ICP), “brain stiffness” does not change significantly when CPP is changed within the 50- to 160-mm Hg range. 1, 10, 18 Recent work by us in cats has shown that deep barbiturate anesthesia nearly obliterates the relationship between PVI and CPP, but under light anesthesia cats showed a

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Pressure-volume index as a function of cerebral perfusion pressure

Part 1: The effects of cerebral perfusion pressure changes and anesthesia

W. John Gray and Michael J. Rosner

relatively constant despite changes in cerebral perfusion pressure (CPP) over the 60- to 170-mm Hg range. 8, 9, 14, 18, 20, 32, 41 Autoregulation of CBF is accomplished by changes in the cerebrovascular resistance (CVR) achieved by alterations in the caliber of the vessels. 10, 11, 20, 26, 32 A consequence of constant flow and changing vessel size is a change in the cerebral blood volume (CBV); 36 however, CBF is influenced by other factors, including PaCO 2 , 15, 35, 43 blood viscosity, 16, 19, 30 and many anesthetic agents. 12 The PVI for a normal neuraxis has

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Michael J. Rosner, Sheila D. Rosner, and Alice H. Johnson

I n the process of better understanding Lundberg's Plateau and B wave phenomena, a general model evolved that could be used to predict the appearance and behavior of many intracranial pressure (ICP) events and that provided a theoretical basis for the management of ICP problems in general. 58, 61 We have termed this model the “complex vasodilatory/vasoconstriction cascade” 29, 57, 60 ( Figs. 1 – 3 ). By stabilizing cerebral perfusion pressure (CPP) at higher levels, we found that ICP could be better controlled without cerebral ischemia. Fig. 1. The

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Neurosurgical Forum: Letters to the Editor To The Editor Julio Cruz , M.D., Ph.D. Medical College of Pennsylvania and Hahnemann University Philadelphia, Pennsylvania 365 367 This letter is in regard to a recently published paper (Rosner MJ, Rosner SD, Johnson AH: Cerebral perfusion pressure: management protocol and clinical results. J Neurosurg 83: 949–962, December, 1995). The paper is an expansion of previously published work. 6 Figures 1 through 3 are very similar to Figs. 1, 2, and 4 of the authors

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Georgios V. Varsos, Angelos G. Kolias, Peter Smielewski, Ken M. Brady, Vassilis G. Varsos, Peter J. Hutchinson, John D. Pickard, and Marek Czosnyka

T he circulation of cerebral blood flow (CBF) is driven by cerebral perfusion pressure (CPP), which is defined as the vascular pressure gradient across the cerebral bed and can be calculated as the difference between arterial blood pressure (ABP) and pressure in cortical or bridging veins. 15 , 24 Due to difficulties in measuring the pressure of bridging veins, invasive intracranial pressure (ICP) measurements are used instead as an approximation, defining CPP as ABP − ICP. 1 , 26 , 34 , 39 Cerebral perfusion pressure in clinical practice is considered

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Ingunn R. Rise and Ole J. Kirkeby

number of studies that have been published on the subject, there is considerable controversy regarding the role of this agent in cerebrovascular regulation. The combination of high intracranial pressure and hypotension is common in many patients in neurosurgical wards, and maintenance of autoregulation is crucial for these patients. Cerebral vasomotor responses to changes in cerebral perfusion pressure (CPP) serve protective functions. Loss of vasomotor reactivity leads to a poor outcome in patients who receive neurosurgical intensive care 20, 32 because the

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Albert Català-Temprano, Gemma Claret Teruel, Francisco José Cambra Lasaosa, Martí Pons Ódena, Antoni Noguera Julián, and Antonio Palomeque Rico

traumatic brain injury . J Neurotrauma 17 : 451 – 553 , 2000 3 Chesnut RM : Avoidance of hypotension: conditio sine qua non of successful head injury management . J Trauma 42 : 5 Suppl S4 – S9 , 1997 4 Daley M , Pourcyrous M , Timmons S , Leffler CH : Assessment of cerebrovascular autoregulation: changes of highest modal frequency of cerebrovascular pressure transmission with cerebral perfusion pressure . Stroke 35 : 1952 – 1956 , 2004 5 Downard C , Hulka F , Mullins RJ , Piatt J , Chesnut R , Quint P , : Relationship of

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Zeev Feldman, Malcolm J. Kanter, Claudia S. Robertson, Charles F. Contant, Christopher Hayes, Michael A. Sheinberg, Cynthia A. Villareal, Raj K. Narayan, and Robert G. Grossman

E levated intracranial pressure (ICP) or inadequate cerebral perfusion pressure (CPP) and cerebral blood flow (CBF) are common causes of secondary brain damage in head-injured patients. In patients with raised ICP, it is a common practice to position the patient in bed with the head elevated above the level of the heart. Kenning, et al. , 4 reported that elevating the head to 45° or 90° significantly reduced ICP. However, some studies suggest that head elevation may also lower the CPP. Durward, et al. , 2 studied the effect of head elevation at 0