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Peter J. Kirkpatrick, Piotr Smielewski, Marek Czosnyka, David K. Menon and John D. Pickard

also increased in two of these events ( Fig. 4 center ). The close correlation between the signal changes of all parameters suggests that the increased ICP was a consequence of rising CBF and cerebral blood volume. Miscellaneous Of the remaining 12 events (31%), 11 were associated with a rise in ICP and fall in CPP, and one with a rise in CPP. Changes in HbO 2 , Hb, flow velocity, and LDF occurred without any significant time lag ( Fig. 4 right ) and were accompanied by SjO 2 changes in nine cases. The recordings in this group were complex, precluding

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Marek Czosnyka, Piotr Smielewski, Stefan Piechnik, Eric A. Schmidt, Pippa G. Al-Rawi, Peter J. Kirkpatrick and John D. Pickard

be a “plateau wave.” Almost all authors agree that plateau waves are provoked by rapidly increasing cerebral blood volume (CBV). 17, 23, 32 What distinguishes a plateau wave from other ICP vasogenic waves is its specific mechanism: Rosner and Becker 34 developed an elegant theoretical model of a vasodilatory cascade, which includes a time-dependent positive feedback loop between vasodilation caused by decreasing cerebral perfusion pressure (CPP) and ICP. This process, once initiated, remains active until maximum vasodilation is reached, associated with the

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Peter J. Kirkpatrick, Pietr Smielewski, Peter C. Whitfield, Marik Czosnyka, David Menon and John D. Pickard

above chromophores from optical attenuation within the brain. 5 An absolute measure of changing brain Hb saturation and blood volume is possible and has provided a means of monitoring the cerebrovascular response to certain therapeutic manipulations in critically ill infants. 6 In the larger adult head, only reflectance spectroscopy (scattered light sampled by an ipsilateral receiving probe) is possible. An estimation of light path length can be calculated, 28 but the contribution from extracranial tissues remains unresolved; therefore the use of NIRS in the adult

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Ming-Yuan Tseng, Pippa G. Al-Rawi, Marek Czosnyka, Peter J. Hutchinson, Hugh Richards, John D. Pickard and Peter J. Kirkpatrick

contents. This ICP-reducing effect persisted for more than 180 minutes (p <0.01). Likewise, a maximum increase in CPP by 21.24% (95% CI 12.52–29.96%, p <0.01) was observed at 30 minutes. This CPP-enhancing effect persisted for more than 90 minutes (p <0.05). The CVP was in a biphasic pattern; a brief increase by 29.97% (95% CI 13.23–46.81%, p <0.01) at the end of infusion, followed by a brief reduction by 17.97% (95% CI 9.06–26.88%, p <0.01) at 90 minutes. These rates indicated an initial plasma expansion, following by volume contraction. Results From TCD

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Rupert Kett-White, Peter J. Hutchinson, Pippa G. Al-Rawi, Marek Czosnyka, Arun K. Gupta, John D. Pickard and Peter J. Kirkpatrick

clipping until the end of surgery were calculated, taking into account the 6-minute dead-volume time. For baseline data, periods during CSF drainage and temporary clipping were excluded. Relationships in the combined data were explored by grouping a parameter into interval “bins” (for example, MAP into 10-mm Hg bins) and comparing the values of another variable for each group by using ANOVA (Statgraphics; Manugistics, Rockville, MD). Significance of the distribution (for example, brain tissue PO 2 at different MAP intervals) was tested using the nonparametric Kruskal

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Peter J. Hutchinson, Mark T. O'Connell, Pippa G. Al-Rawi, Lynn B. Maskell, Rupert Kett-White, Arun K. Gupta, Hugh K. Richards, David B. Hutchinson, Peter J. Kirkpatrick and John D. Pickard

heterogeneity of the brain, particularly along the course of a 30-mm-membrane catheter. In fact, in one patient the glucose concentration obtained using the 10-mm membrane was higher than that measured using the 30-mm membrane. One explanation for this may be that the whole of the 10-mm membrane was located in well-perfused tissue, whereas the distal part of the 30-mm membrane dialyzed a volume of tissue with lower glucose levels. Several types of perfusion fluids have been applied in clinical microdialysis, including saline, Ringer's solution, artificial cerebrospinal fluid

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Ming-Yuan Tseng, Peter J. Hutchinson, Hugh K. Richards, Marek Czosnyka, John D. Pickard, Wendy N. Erber, Stephen Brown and Peter J. Kirkpatrick

, Lundar T , Finset A : Cognitive outcome after aneurysmal subarachnoid hemorrhage: time course of recovery and relationship to clinical, radiological, and management parameters . Neurosurgery 60 : 649 – 657 , 2007 17 Jennett B , Bond M : Assessment of outcome after severe brain damage . Lancet 1 : 480 – 484 , 1975 18 Kassell NF , Peerless SJ , Durward QJ , Beck DW , Drake CG , Adams HP : Treatment of ischemic deficits from vasospasm with intravascular volume expansion and induced arterial hypertension . Neurosurgery 11 : 337

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Arun K. Gupta, Peter J. Hutchinson, Tim Fryer, Pippa G. Al-Rawi, Dot A. Parry, Pawan S. Minhas, Rupert Kett-White, Peter J. Kirkpatrick, Julian C. Mathews, Steve Downey, Franklin Aigbirhio, John Clark, John D. Pickard and David K. Menon

during normocapnia, which was 31.1 mm Hg. Comparison of PvO 2 and PbO 2 The values of PbO 2 were different from the derived values of PvO 2 in all cases, with the value of PvO 2 higher in all but one patient. This observation can be explained by considering the locations from which the two forms of data are measured. The PvO 2 is a measurement of O 2 tension in the end capillary, whereas PbO 2 is a measurement of tissue O 2 tension averaged over a volume of tissue that is still undetermined, but is likely to be a few cubic millimeters in size and

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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

lead to vasoconstriction and a reduction of cerebral blood volume. Under the condition of a finite pressure-volume compensatory reserve, this reduction of cerebral blood volume will produce a decrease in ICP, a condition that is usually not met in patients after a decompressive craniectomy or in those with an external ventricular drain. When cerebrovascular pressure reactivity is impaired, cerebral blood volume—and therefore ICP—will increase or decrease passively (in the same direction) in response to changes in ABP. The assessment of cerebrovascular pressure