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Near-infrared spectroscopy use in patients with head injury

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

T he pathophysiological mechanisms excited after severe head injury are complex and poorly understood. The contribution of brain ischemia, however, is recognized; there is growing concern that ischemic insults continue to occur after the primary cerebral insult and that some of these could be avoidable. 23, 24 Major contributions to the evolution of this concept have been derived from monitoring cerebral perfusion pressure (CPP), cerebral blood flow (CBF), and cerebral oxygenation with jugular oximetry. 2, 3, 6, 7, 14, 25 Detection of cerebral events after

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Blood pressure and intracranial pressure-volume dynamics in severe head injury: relationship with cerebral blood flow

Gerrit J. Bouma, J. Paul Muizelaar, Kuniaki Bandoh, and Anthony Marmarou

cerebrovascular bed. 12 Vascular compressibility in turn can be considered a function of stiffness of the vessel wall and intravascular (transmural) pressure. Thus, factors that influence the cerebrovasculature may affect both the ICP (by changes in vascular volume) and the PVI (by alterations in stiffness of the vessel wall and intravascular pressure). The role of changes in systemic blood pressure or cerebral perfusion pressure (CPP) is of particular interest in this regard, as these greatly influence both cerebrovascular diameter (and thus volume) as well as intravascular

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Local cerebral blood flow autoregulation following “asymptomatic” cerebral venous occlusion in the rat

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

vessels in response to changes in cerebral perfusion pressure (CPP), resulting in a constant CBF. 5, 7, 14, 25, 30 Cerebral blood flow autoregulation is impaired in the presence of severe head injury, acute stroke, space-occupying lesions, acute intracranial hypertension itself, and other disorders. The brain is left unprotected against the potentially harmful effect of blood pressure changes under these pathological conditions. 2, 4, 19, 25 The current experiment was designed to examine local autoregulation (the lower limit of autoregulation [LLA]) in brains

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Continuous measurement of jugular venous oxygen saturation in response to transient elevations of blood pressure in head-injured patients

John B. Fortune, Paul J. Feustel, Carl G. M. Weigle, and A. John Popp

shows the tracing of the calculated cerebral perfusion pressure (CPP) and cerebral extraction of oxygen (CEO 2 ) defined as the difference between SaO 2 and SjvO 2 during the same 70-minute period. 8 As anticipated, increases in CPP resulted in marked decreases in CEO 2 , suggesting that the driving force for this increased CBF may be the increased CPP. Elevations in ICP for these short periods also appear to be related to increased blood flow, most likely via vascular distention. Fig. 3. Left and Center: Representative tracing of the measurements of

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Management of severe cerebral edema in the metabolic encephalopathy of Reye-Johnson syndrome

Joan L. Venes, Bennett A. Shaywitz, and Dennis D. Spencer

encephalopathy of Reye-Johnson syndrome is most likely due to severe hypoglycemia and/or cerebral ischemia secondary to poor cerebral perfusion pressure. Early diagnosis and rapid intervention to control these parameters is mandatory to ensure full neurological recovery. This report outlines the treatment modalities that have been evolved for the management of these children, and discusses four cases in which either cerebral perfusion pressure or blood glucose levels were not well maintained. The outcome was poor in all cases. Management of Reye-Johnson Syndrome

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Effects of increased intracranial pressure on cerebral blood volume, blood flow, and oxygen utilization in monkeys

Robert L. Grubb Jr., Marcus E. Raichle, Michael E. Phelps, and Robert A. Ratcheson

-test after the data were subjected to a logarithmic transformation. Experimental Design Two series of experiments were carried out as follows: Group 1 (10 Animals) Control values of CBF, CBV, and CMRO 2 were obtained at the animals' normal ICP. Cerebral perfusion pressure was decreased by infusion into the cisterna magna of artificial cerebrospinal fluid (CSF) 19 maintained at 37°C. The ICP was kept constant by means of a suspended reservoir containing the artificial CSF. The resultant ICP in the cisterna magna was continuously monitored. The ICP was raised

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Relationship between transcranial Doppler-determined pulsatility index and cerebrovascular resistance: an experimental study

Marek Czosnyka, Hugh K. Richards, Helen E. Whitehouse, and John D. Pickard

noninvasive detection of decreased cerebral perfusion pressure (CPP) or increased intracranial pressure (ICP) after severe head injury, 4, 6 cardiac arrest, 17 and in hydrocephalus. 31 Laboratory phantom models demonstrate that pulsatility can be affected both by proximal and distal vascular resistances. Whereas a rise in proximal resistance decreases, a rise in distal resistance increases blood flow pulsatility. 12, 15 Clinical ultrasound investigations of the umbilical 2, 26 and peripheral 22 circulation show that pulsatility increases when the distal vascular

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Adverse effects of pentobarbital on cerebral venous oxygenation of comatose patients with acute traumatic brain swelling: relationship to outcome

Julio Cruz

(66 cases), early postoperative CT scans revealed predominantly diffuse brain swelling as well. Thus, pentobarbital was administered exclusively at the time when refractory ICP was not associated with surgical intracranial mass lesions. Monitoring and Management In the intensive care unit all patients underwent routine monitoring of electrocardiogram tracings, body temperature, mean systemic arterial pressure (MAP), ICP, cerebral perfusion pressure (CPP), defined as the difference between MAP and mean ICP), arterial and jugular bulb oxyhemoglobin saturation

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Outcome following decompressive craniectomy for malignant swelling due to severe head injury

Bizhan Aarabi, Dale C. Hesdorffer, Edward S. Ahn, Carla Aresco, Thomas M. Scalea, and Howard M. Eisenberg

.1097/00005373-200106000-00013 30 Cruz J , Jaggi JL , Hoffstad OJ : Cerebral blood flow, vascular resistance, and oxygen metabolism in acute brain trauma: redefining the role of cerebral perfusion pressure? . Crit Care Med 23 : 1412 – 1417 , 1995 10.1097/00003246-199508000-00016 31 Dam Hieu P , Sizun J , Person H , Besson G : The place of decompressive surgery in the treatment of uncontrollable post-traumatic intracranial hypertension in children . Childs Nerv Syst 12 : 270 – 275 , 1996 32 De Luca GP , Volpin L , Fornezza U , Cervellini P , Zanusso

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The effect of mannitol on cerebral blood flow

An experimental study

Ian H. Johnston and A. M. Harper

intracranial pressure by increasing cerebral blood volume. 6 The aim of the present study has been to examine the effect of one of the more commonly used hyperosmolar solutions, 20% mannitol, on cerebral blood flow both at normal and increased intracranial pressure, and to relate the observed changes in blood flow to changes in cerebral perfusion pressure, cerebrovascular resistance, and cerebral metabolic rate. Methods Baboons weighing between 9 and 12 kg were used. Anesthesia was induced using phencyclidine hydrochloride (10 mg) and thiopentone sodium (60 mg), and