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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 306 308 One of the most undesirable features of performing clinical research is addressing potential misinformation. Even though mathematically elegant, the paper by Yoshihara, et al. (Yoshihara M, Bandoh K, Marmarou A: Cerebrovascular carbon dioxide reactivity assessed by intracranial pressure dynamics in severely head injured patients. J

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Guy L. Clifton, Halcott T. Haden, John R. Taylor, and Michael Sobel

measurement of CBF at rest and during hypercapnia as an index of cerebrovascular collateral reserve capacity in patients with carotid artery occlusion. The rationale for this dynamic test is that cerebral vessels dilate to preserve CBF distal to a flow-limiting arterial lesion. If the cerebral circulation is maximally dilated, it has a decreased capacity to dilate further in response to hypercapnia. Published data evaluating this test have established that the mean CO 2 reactivity in hemispheres ipsilateral to carotid artery occlusion is lower than the mean CO 2

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Bo Voldby, Erna M. Enevoldsen, and Finn T. Jensen

than those in Grades III and IV. 12 A few human studies have suggested a correlation between defective cerebrovascular reactivity and cerebral vasospasm 7, 11, 14 and raised intracranial pressure. 7 We have previously reported that regional cerebral blood flow (rCBF) and cerebral metabolic rate of oxygen (CMRO 2 ) are decreased following SAH, and that this decrease correlates with the degree of angiographic vasospasm. 34 In the present study, we have investigated the cerebral autoregulation and the CO 2 reactivity in patients with recent SAH, with special

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Christian Zweifel, Andrea Lavinio, Luzius A. Steiner, Danila Radolovich, Peter Smielewski, Ivan Timofeev, Magdalena Hiler, Marcella Balestreri, Peter J. Kirkpatrick, John D. Pickard, Peter Hutchinson, and Marek Czosnyka

C erebrovascular pressure reactivity reflects the capability of smooth muscle tone in the walls of cerebral arteries and arterioles to react to changes in transmural pressure (cerebral vessels constrict in response to an increase in CPP, and vice versa). Cerebrovascular pressure reactivity represents a key element of cerebral autoregulation, although the two terms should not be used interchangeably because vascular responses can occur outside the range of cerebral autoregulation. 7 , 25 With increasing ABP, intact cerebrovascular pressure reactivity will

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Masaaki Yoshihara, Kuniaki Bandoh, and Anthony Marmarou

of arterial blood gases. A report of the ACCP section on respiratory pathophysiology. Chest 83: 666–670, 1983 3. Cold GE , Jensen FT , Malmros R : The cerebrovascular CO 2 reactivity during the acute phase of brain injury. Acta Anaesth Scand 21 : 222 – 231 , 1977 Cold GE, Jensen FT, Malmros R: The cerebrovascular CO 2 reactivity during the acute phase of brain injury. Acta Anaesth Scand 21: 222–231, 1977 4. Cold GE , Jensen FT , Malmros R : The effects of PaCO 2 reduction on

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David J. Mikulis, Gregory Krolczyk, Hubert Desal, William Logan, Gabrielle deVeber, Peter Dirks, Michael Tymianski, Adrian Crawley, Alex Vesely, Andrea Kassner, David Preiss, Ron Somogyi, and Joseph A. Fisher

. Fig. 5. Case 1. Cerebrovascular reactivity maps obtained before EMDS (upper) and 5 (center) and 7 (lower) months after EMDS. Yellow/red/orange values indicate positive reactivity with yellow being the highest (see scale with CVR values as indicated). Blue and pale blue mark negative reactivity with pale blue being most negative. Black arrows indicate improved CVR in the immediate vicinity of the flap, which is marked by the presence of a surgical clip artifact ( red asterisk , artifact is also seen on adjacent images). The artifact is more prominent on

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Giovanni Muscas, Christiaan Hendrik Bas van Niftrik, Jorn Fierstra, Marco Piccirelli, Martina Sebök, Jan-Karl Burkhardt, Antonios Valavanis, Athina Pangalu, Luca Regli, and Oliver Bozinov

, 23 or cerebrovascular reactivity (CVR). 11 , 15 The application of intraoperative high-field MRI may deliver such information directly after the bypass anastomosis. By obtaining functional MRI blood oxygenation level–dependent (BOLD) volumes during repeated cycles of apnea, CVR can be measured at the brain tissue level. We previously reported the feasibility of intraoperative 3-T MRI BOLD-CVR and its preliminary application for neurovascular surgery. 6 The purpose of this study was to assess whether intraoperative BOLD-CVR can offer hemodynamic information at the

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Chia-Cheng Chang, Hiroyuki Asada, Toshiro Mimura, and Shinichi Suzuki

, : Cerebral ischemia and white matter edema in experimental hydrocephalus: a combined in vivo MRI and MRS study . Brain Res 757 : 295 – 298 , 1997 3 Chang CC , Kanno H , Yamamoto I , Kuwana N : Cerebrovascular reactivity to acetazolamide in alert patients with cerebral infarction: usefulness of first-pass radionuclide angiography using 99mTc-HMPAO in monitoring cerebral haemodynamics . Nucl Med Commun 22 : 1119 – 1122 , 2001 4 Chang CC , Kuwana N , Ito S , Ikegami T : Impairment of cerebrovascular reactivity in patients with normal

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Per Kristian Eide, Angelika Sorteberg, Gunnar Bentsen, Pål Bache Marthinsen, Audun Stubhaug, and Wilhelm Sorteberg

measurements only. “Cerebrovascular pressure reactivity” refers to the ability of the smooth muscles of the cerebral arterial vessel wall to respond to changes in the transmural pressure. This phenomenon has also been called “myogenic autoregulation,” or “Bayliss mechanism.” 6 Cerebral perfusion depends on the inflow pressure (ABP), the outflow pressure (sagittal sinus pressure), and resistance to flow within the system (that is, inflow resistance primarily of the arteries and arterioles and outflow resistance primarily of bridging veins and lateral lacunae). Myogenic

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Fangyi Zhang, Shane M. Sprague, Farrokh Farrokhi, Matthew N. Henry, Minnette G. Son, and Dennis G. Vollmer

I t is well established that CBF decreases significantly following TBI in clinical patients 19, 43 and in experimental animal models. 3, 6, 17, 19, 44 Clinically, cerebrovascular reactivity to hypercapnia has also been shown to be impaired, especially during the acute stage following severe head injury. 8, 13, 20 In animal studies, there is evidence that hypercapnic cerebral vasodilation is either attenuated or abolished depending on the degree of injury in different TBI models. 17, 20, 21, 34, 44 Recently, authors of reports have suggested that