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Effects of nifedipine on intracranial pressure in neurosurgical patients with arterial hypertension

Akio Tateishi, Takanobu Sano, Hiroshi Takeshita, Toshihisa Suzuki, and Hisao Tokuno

nifedipine administered to treat arterial hypertension in patients with decreased intracranial compliance. This study documents the effects of nifedipine, given through a nasogastric tube, on ICP and cerebral perfusion pressure (CPP) in neurosurgical patients with arterial hypertension occurring in the setting of acute cerebral disorders. Clinical Material and Methods This study was approved by the local Institutional Human Studies Committee, and informed consent was obtained from all patients or their closest relatives. The characteristics of eight patients and

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Responses to experimental subarachnoid hemorrhage in the spontaneously breathing primate

Charles Rothberg, Bryce Weir, Thomas Overton, and Michael Grace

-slope-index method. The values were not corrected for arterial CO 2 levels. The rCBF determinations were performed at regular intervals both before and after the intracranial insult. Mean arterial blood pressure (MaBP) was measured continuously through a femoral artery catheter. Intracranial pressure (ICP) was monitored in the right midparietal area using an intracranial, extradural hydrostatic pressure device. 1 Cerebral perfusion pressure (CPP) was calculated as CPP (mm Hg) = MaBP (mm Hg) − ICP (mm Hg). 6 Cerebrovascular resistance (CVR) was calculated 7 as We have

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Novel index for predicting mortality during the first 24 hours after traumatic brain injury

Hakseung Kim, Hack-Jin Lee, Young-Tak Kim, Yunsik Son, Peter Smielewski, Marek Czosnyka, and Dong-Joo Kim

L owered cerebral blood flow (CBF) is an immediate consequence of traumatic brain injury (TBI). 35 The subsequent secondary ischemic insult in the brain is a well-known phenomenon; hence, maintaining an adequate level of CBF is considered to be one of the primary objectives during the management of TBI. 6 Normally, the cerebral circulation maintains a relatively constant CBF, despite the fluctuations in cerebral perfusion pressure (CPP), through an intrinsic, homeostatic mechanism known as cerebral autoregulation. 25 However, this mechanism often fails in

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Monitoring of autoregulation using laser Doppler flowmetry in patients with head injury

Joseph M. K. Lam, John N. K. Hsiang, and Wai S. Poon

T he essence of head injury management is the provision of optimum conditions for recovery from damage already sustained and the avoidance of development of secondary brain injury. Cerebral ischemia is an important cause of secondary brain insult that can affect outcome in the head-injured patient. 23 Maintenance of adequate cerebral perfusion pressure (CPP) is important in preventing cerebral ischemia and even improves the function of ischemic brain tissue. 24, 26 The normal human cerebral circulation has the ability to maintain a stable cerebral blood flow

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Experimental cerebral oligemia and ischemia produced by intracranial hypertension

Part 1: Pathophysiology, electroencephalography, cerebral blood flow, blood-brain barrier, and neurological function

Lawrence F. Marshall, Felix Durity, Robert Lounsbury, David I. Graham, Frank Welsh, and Thomas W. Langfitt

control animals. In Group 2, with 15 animals, oligemia was produced by abruptly elevating the ICP to within 20 torr of the systolic SAP and maintaining this level of perfusion for 15 minutes ( Fig. 1 ). The infusion was abruptly terminated at 15 minutes and the ICP allowed to fall spontaneously. Complete ischemia was produced in the 15 animals in Group 3 by rapidly elevating the ICP to 20 torr above systolic SAP for 15 minutes, followed by restitution of normal cerebral perfusion pressure (CPP) as in Group 2. Fig. 1. Representative tracing obtained during 15

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Early changes of intracranial pressure, perfusion pressure, and blood flow after acute head injury

Part 1: An experimental study of the underlying pathophysiology

Ernst G. Pfenninger, Andreas Reith, Dieter Breitig, Ad Grünert, and Friedrich W. Ahnefeld

therefore only be extrapolated from experimental findings in animals. In such animal studies, the ICP measured immediately after trauma varied from unchanged to moderate change, up to very marked ICP elevations. 14, 16, 24 Besides ICP, the cerebral perfusion pressure (CPP) is a very important parameter determining the integrity of cerebral neurons. We could not find any information in the literature about early changes in CPP after acute head injury in experimental animals. Cerebral circulation depends not only on the level of ICP, which of course counteracts CPP, but

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Effects of head elevation on intracranial hemodynamics in patients with ventriculoperitoneal shunts

Sotaro Higashi, Kazuya Futami, Hiroshi Matsuda, Junkoh Yamashita, Masaaki Hashimoto, Mitsuhiro Hasegawa, Kazuhiko Tokuda, Mahmood Hassan, and Kinichi Hisada

negative ventricular fluid pressure (VFP) that is caused by the hydrodynamic characteristics of valves when patients are in the upright position. Many authors have shown that, when the head is elevated, patients who have shunts with DP valves develop significantly negative VFP, whereas normal subjects have VFP near atmospheric pressure. 3, 10, 16, 19 Although the effects of head elevation on VFP have been investigated in subjects having a variety of shunt types, the effect of postural changes on cerebral blood flow (CBF) as well as on cerebral perfusion pressure (CPP

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Cerebral and cardiovascular responses to changes in head elevation in patients with intracranial hypertension

Quentin J. Durward, A. Lorne Amacher, Rolando F. Del Maestro, and William J. Sibbald

60° of head elevation. The rapid rise in ICP precipitated within 5 seconds of the change in head position was partially controlled by cerebrospinal fluid (CSF) venting. The patient was lowered back to 30°, and the ICP fell, but further CSF venting was required. Systemic Hemodynamics The mean SAP (recorded at the level of the foramen of Monro) fell with the progressive increase in head elevation (r = 0.98; p < 0.001) ( Fig. 4 left ), whereas the cerebral perfusion pressure (CPP) was not significantly affected by 15° or 30° of head elevation ( Fig. 4

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ICP, CPP, and PRx in traumatic brain injury and aneurysmal subarachnoid hemorrhage: association of insult intensity and duration with clinical outcome

Teodor Svedung Wettervik, Anders Hånell, Timothy Howells, Elisabeth Ronne Engström, Anders Lewén, and Per Enblad

T raumatic brain injury (TBI) and aneurysmal subarachnoid hemorrhage (aSAH) are two types of acute brain injury with high rates of mortality and neurological sequelae. 1 , 2 Both severe TBI and aSAH patients are at high risk of developing secondary brain injury. Neurointensive care (NIC) in these patients aims to prevent, monitor, detect, and treat secondary insults to avoid secondary brain injury. 3 The traditional main NIC variables are intracranial pressure (ICP) and cerebral perfusion pressure (CPP), and recently pressure reactivity index (PRx) is

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Origin and evolution of plateau waves

Experimental observations and a theoretical model

Michael J. Rosner and Donald P. Becker

. , 38 confirmed this mild reduction in CBF in four of five patients; their fifth patient had blood flow measurements only slightly higher than baseline. However, plateau waves have always been described in association with marked reductions in cerebral perfusion pressure (CPP); this is in contrast to small reductions reported in CBF. This suggests that plateau waves occur in association with marked reductions in cerebral vascular resistance (CVR) consistent with generally intact autoregulation. One would expect CBV to increase under these circumstances, 11, 29, 34