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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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Guy Rosenthal, Rene O. Sanchez-Mejia, Nicolas Phan, J. Claude Hemphill III, Christine Martin and Geoffrey T. Manley

critically ill patients leave the intensive care unit for imaging and entail the risk of secondary insults associated with patient transport. Loss of cerebral autoregulation often occurs after severe TBI. 2 , 21 The loss of autoregulation in the cerebral vasculature can lead either to hypoperfusion resulting in cerebral ischemia or to hyperemia that contributes to increased ICP. 26 Both these phenomena can contribute to secondary injury after severe TBI. Recent evidence suggests that patients with impaired autoregulation may have better outcomes when CPP is maintained

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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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Domenico G. Iacopino, Alfredo Conti, Calogero Battaglia, Clotilde Siliotti, Tullio Lucanto, Letterio B. Santamaria and Francesco Tomasello

N itrous oxide is administered routinely in anesthesia for neurosurgical procedures. For a long time this agent was considered to have little effect on cerebral circulation and autoregulation; 4, 13, 36 however, there have been a number of reports describing adverse effects on cerebrovascular hemodynamics in both humans and animals. Increased intracranial pressure, CBF, and CMRO 2 and reduced cerebral autoregulation have been extensively reported, 4, 6, 7, 11, 15, 17, 21, 24, 31, 38, 42 but the magnitudes of these changes are still under debate. In the

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

exhibit exquisite control over CBF since CBF “automatically” returns to normal when T A /Ro balances a change in P TM 28 ( Fig. 9 ). Any increase in P TM causes stretch of the vessel wall, signaling for an increase in vasomotor tone ( Fig. 12 ), while any decrease in P TM causes vessel collapse, the signal for a decrease in tone (the Bayliss reflex 1 ). Thus, the limits of vasomotor tone define the pressure-flow characteristics of cerebral autoregulation. 10, 12 Control of flow is actually accomplished by changes in vasomotor tone over all the arteries as well as

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Richard J. Nelson, Sheila Perry, Tony K. Hames and John D. Pickard

reactivity has already been employed in studies of extracranial vascular disease. 56, 65 To use TCD in the place of existing methods of measuring cerebrovascular reactivity assumes that the caliber and flow velocity profiles of the basal cerebral arteries are not significantly altered by changes in PaCO 2 and that changes in mean flow velocity accurately reflect changes in regional CBF. The development of delayed cerebral ischemia after subarachnoid hemorrhage (SAH) is strongly related to the loss of normal cerebral autoregulation 19, 42, 44, 54 and reactivity 62 and

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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

The purpose of this study was to determine whether patients with minor head injury experience impairments in cerebral autoregulation. Twenty-nine patients with minor head injuries defined by Glasgow Coma Scale (GCS) scores of 13 to 15 underwent testing of dynamic cerebral autoregulation within 48 hours of their injury using continuous transcranial Doppler velocity recordings and blood pressure recordings. Twenty-nine age-matched normal volunteers underwent autoregulation testing in the same manner to establish comparison values. The function of the autoregulatory response was assessed by the cerebral blood flow velocity response to induced rapid brief changes in arterial blood pressure and measured as the autoregulation index (ARI).

Eight (28%) of the 29 patients with minor head injury demonstrated poorly functioning or absent cerebral autoregulation versus none of the controls, and this difference was highly significant (p = 0.008). A significant correlation between lower blood pressure and worse autoregulation was found by regression analysis in head-injured patients (r = 0.6, p < 0.001); however, lower blood pressure did not account for the autoregulatory impairment in all patients. Within this group of head-injured patients there was no correlation between ARI and initial GCS or 1-month Glasgow Outcome Scale scores. This study indicates that a significant number of patients with minor head injury may have impaired cerebral autoregulation and may be at increased risk for secondary ischemic neuronal damage.

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Afroditi Despina Lalou, Marek Czosnyka, Joseph Donnelly, John D. Pickard, FMedSci, Eva Nabbanja, Nicole C. Keong, Matthew Garnett and Zofia H. Czosnyka

studies (i.e., Mathew et al., 24 , 25 Schmidt et al., 35 , 36 and Tanaka et al. 40 ) have correlated normal CBF before shunting with a positive outcome. Those studies, however, only relied on measurements of CBF alone, and there are many more that contradicted this finding or were inconclusive on whether higher or lower CBF was associated with a better postsurgical outcome. 1–5 Other studies have indicated that the ability of the brain to maintain a constant CBF in response to changes in cerebral perfusion pressure (CPP)—termed cerebral autoregulation—may be of

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Yuji Handa, Minoru Hayashi, Hiroaki Takeuchi, Tetsuya Kubota, Hidenori Kobayashi and Hirokazu Kawano

to what degree it should be continued during the time course of cerebral vasospasm. No studies have dealt expressly with these problems, and it is difficult to investigate them systematically in clinical cases for ethical reasons. Our previous experimental study in primates demonstrated that cerebral autoregulation is greatly impaired when the severity of vasospasm is at its maximum. 26 In order to solve the above problems in hemodynamic therapy, it is important to study how the time course of the impairment of autoregulation correlates with the time course of

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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