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Marek Czosnyka, Piotr Smielewski, Stefan Piechnik, Luzius A. Steiner, and John D. Pickard

.4 ± 11.1 0.007 25 ± 15 CPP (mm Hg) 44 ± 10.5 0 68 ± 14.9 0 100 ± 15.1 * Zone F represents ABP that is too low, Zone G represents the range of adequate ABP, and Zone H represents ABP that is too high. Probability values were determined for a comparison of parameters in Zones F and G and for a comparison of parameters in Zones G and H by using the Mann—Whitney test. Continuous Monitoring of Autoregulation The most promising application of the Mx results from its ability to trace changes in cerebral autoregulation over

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Leonardo Rangel-Castilla, Jaime Gasco, Haring J. W. Nauta, DaviD O. Okonkwo, and Claudia S. Robertson

T he outcome of severe TBI has improved with advances in intensive care monitoring and treatment, most notably in Lund, Sweden, and Richmond, Virginia, in the second half of the 20th century. An understanding of the physiology, pathophysiology, monitoring, and treatment of cerebral autoregulation is key in the evolution of the critical care management of severe TBI. Cerebral pressure autoregulation is the specific intrinsic ability to maintain constant CBF over a range of blood pressures. Metabolic cerebral autoregulation is the ability of the brain to

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Elisabeth C. Jünger, David W. Newell, Gerald A. Grant, Anthony M. Avellino, Saadi Ghatan, Colleen M. Douville, Arthur M. Lam, Rune Aaslid, and H. Richard Winn

T he cerebral circulation has a capacity to maintain blood flow at a relatively constant level during changes in blood pressure. This phenomenon, known as cerebral autoregulation, is usually observed between a mean arterial blood pressure (MABP) of approximately 50 and 150 mm Hg. 14, 26 Cerebral autoregulation can be impaired or absent following severe closed head injury. 4–6, 8, 9, 21, 22, 25, 26 Impairments in autoregulation may contribute by several mechanisms to secondary neuronal injury following head injury. Lowered cerebral perfusion pressure (CPP

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Harold D. Portnoy, Michael Chopp, Craig Branch, and Michael B. Shannon

pressure. For abbreviations see Definitions. The failure of an amplitude change in the SAPW to produce a similar alteration in amplitude of the CSFPW and SSPW could be explained by autoregulation, which maintains a constant cerebral blood flow despite fluctuations in Ps. Compensatory alterations in vessel diameter cause this nonlinearity. 18, 30, 33, 34 Less readily explained are the changes in wave contour during inhalation of 100% O 2 and 100% O 2 + IVI. The XFRa spectra are not flat. This, of itself, would not be significant since attenuation of higher

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Erna M. Enevoldsen and Finn T. Jensen

preserved autoregulation seen in severely injured brain tissue is a false autoregulation which is not caused by the active vasoconstrictor response to an increase in blood pressure found in normal brain tissue. In a previous publication, 6 we showed that cerebral ischemia did not occur in head injury if the intraventricular pressure (IVP) was kept below 45 mm Hg. On the contrary, hyperemia, mostly in the form of so-called tissue-peak hyperemia, was always present in the most severely injured brain tissue during the acute phase. The hyperemia increased during

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Hiroyuki Nakase, Kiyoshi Nagata, Hiroyuki Otsuka, Toshisuke Sakaki, and Oliver Kempski

occlusion, and the vessels were occluded with platelet aggregates by means of a dye-mediated photochemical reaction. We have reported that this model is minimally invasive, clinically relevant, and reproducible. 22–24 In this model, animals with asymptomatic cortical vein occlusion could be selected by using fluorescence angiography and regional (r)CBF data. 22, 24 Autoregulation of CBF is the intrinsic ability of the brain to maintain a constant perfusion in the face of blood pressure changes; it is defined as the dilation and constriction of cerebral resistance

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Gerrit J. Bouma and J. Paul Muizelaar

I ntravascular volume expansion, alone or in combination with induced hypertension, has been proposed to be useful in the prevention and treatment of focal cerebral ischemia caused by arterial occlusive disorders or by vasospasm after subarachnoid hemorrhage. The beneficial effect of this treatment on regional cerebral blood flow (rCBF), neuroelectrical activity, and clinical symptoms has been demonstrated both in laboratory investigations 13, 28, 31, 35 and in clinical situations, 12, 23, 29 and has been related to impaired autoregulation in ischemic brain

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Mauro Ursino, Marco Giulioni, and Carlo Alberto Lodi

, pulsatility index (PI), and peak-to-peak velocity amplitude. However, the way these parameters are related and affected by changes in cerebral hemodynamics and ICP are still not sufficiently understood and are the subject of many recent experimental and clinical investigations. 7–10, 22, 24, 25, 32, 33, 36, 38 One rationale is that the relationships among ICP, systemic arterial pressure (SAP), cerebral blood volume, CBF, and autoregulation are very complicated and may lead to complex dynamic changes in the intracranial values. 14, 34, 35 Such complexity is reflected in

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W. Lewelt, L. W. Jenkins, and J. Douglas Miller

pressure (ICP), and cerebral vasospasm. The effects of reduced perfusion pressure would be greatly accentuated if there were a failure of normal cerebral autoregulation, such that cerebral blood flow (CBF) was reduced passively with the fall in perfusion pressure instead of remaining within normal limits until a critical value was reached, as occurs under normal circumstances. Because many severe head injuries are caused by automobile accidents and because multiple injuries are frequent under such circumstances, arterial hypotension is not uncommon in comatose head

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Julian Zipfel, Juliane Engel, Konstantin Hockel, Ellen Heimberg, Martin U. Schuhmann, and Felix Neunhoeffer

S evere traumatic brain injury (sTBI) in children is associated with significant morbidity and mortality. Among other causes, elevation of intracranial pressure (ICP) leads to secondary brain damage due to compromised cerebral perfusion. Cerebral autoregulation balances arterial blood pressure variation and contributes to a stable cerebral perfusion. 1–3 Most importantly, impaired cerebrovascular reactivity can persist at “normal” ICP levels and is associated with an unfavorable outcome in brain-injured adult and pediatric patients. 4 , 5 Furthermore