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Global and regional cerebral blood flow

Noninvasive quantitation in patients with subarachnoid hemorrhage

Maria Granowska, Keith E. Britton, F. Afshar, Charles W. Wright, Richard R. J. Smyth, Ting Y. Lee and Cyril C. Nimmon

T he rupture of an intracranial aneurysm is usually associated with alteration or loss of consciousness with or without focal neurological signs. 14 These sequelae are attributed at least in part to alteration in cerebral blood flow (CBF) globally or regionally. 9 Arterial spasm is usually implicated. 18, 21 Subsequent cerebral angiography, an essential but invasive technique required to identify the site and surgical anatomy of the problem, may also be associated with arterial spasm, since the injected high-contrast medium may act as an oxygen

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Martin E. Weinand, L. Philip Carter, Waleed F. El-Saadany, Panayiotis J. Sioutos, David M. Labiner and Kalarickal J. Oommen

electrocorticography; and video electrocorticographic (ECoG) monitoring with depth, subdural, or epidural electrodes. Recently, there has been a trend in epilepsy centers that perform invasive monitoring to do so less often. 16 Because invasive monitoring is decreasing in surgical candidates, 1, 2, 4–6, 12–14, 16, 23, 26–28, 31, 36–39, 43, 44 there is need to improve our understanding of other pathophysiology that might be amenable to noninvasive detection. Localization of the epileptic focus using cerebral blood flow (CBF) methods is supported by the observation that SPECT

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Ian H. Johnston and A. M. Harper

H yperosmolar solutions such as mannitol and urea are widely used in neurosurgical practice, both in the control of raised intracranial pressure and for the reduction of brain bulk at operation to facilitate access. Previous studies of the effects of such solutions on cerebral blood flow have given conflicting results. 1, 5 Changes in cerebral blood flow due to infusion of hyperosmolar solutions could be of considerable clinical importance in states of raised intracranial pressure, as emphasized by the recent suggestion that they may increase an already high

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K. C. Petruk, G. R. West, M. R. Marriott, J. W. McIntyre, T. R. Overtone and Bryce K. A. Weir

T he pathophysiologic mechanisms involved in the production of decreased cerebral perfusion following subarachnoid hemorrhage (SAH) in man remain obscure. Cerebral arterial spasm has been implicated as the principal cause of morbidity and mortality after aneurysmal rupture. 1, 3, 6, 18, 33 While marked vasospasm appears to diminish cerebral blood flow, the relationship is not fully resolved. Recent clinical and experimental studies 5, 15, 35–38, 40 have failed to show a direct correlation between vasospasm, cerebral ischemia, and neurological sequelae

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J. Douglas Miller, Albert E. Stanek and Thomas W. Langfitt

D uring expansion of an intracranial mass lesion, several processes occur simultaneously. Brain adjacent to the expanding lesion is distorted, brain shift and herniation occur at a distance from the lesion, 36 and the general level of intracranial pressure (ICP) increases as compensatory mechanisms become exhausted. 17 In addition, the compressed brain may swell. 12 The final effect of such a lesion on regional and total cerebral blood flow (CBF) may therefore be complex and difficult to interpret. In a previous study 24, 25 we used a simple experimental

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Jack M. Fein and Guy Molinari

occlusion and has been reported in 115 selected cases. 1 While the clinical and radiographie indications for this procedure are currently under investigation, the assumption that such grafting techniques will augment cerebral blood flow has not been established. The canine experimental model has been useful in developing the technique of superficial temporal-to-cortical artery anastomosis because of the size of the middle cerebral vessels. Angiographic evaluation postoperatively has been of particular value in documenting patency which, however, is not necessarily

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Francis W. Gamache Jr., Ronald E. Myers and Esteban Monell

A lthough episodes of spontaneous or controlled hypotension are familiar to all clinicians, little is known about the changes that occur in the overall cerebral blood flow (CBF) or in the blood flow to specific brain regions either during or after such episodes. The local cerebral blood flow (L-CBF) refers to that which is distributed to individual neuroanatomic structures as compared to regional blood flow which is most commonly measured by determining the washout curves of gamma emitters detected by probes placed on the surface of poorly delimited, three

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Howard Yonas, Holly A. Smith, Susan R. Durham, Susan L. Pentheny and David W. Johnson

T he role played by compromised cerebral hemodynamics in the likelihood of subsequent infarction has not been clearly defined. 1, 3, 5, 22, 24 Until recently, it has not been possible to properly identify significant numbers of individuals who may be at increased hemodynamic risk for infarction. This is due in part to our inability to identify and accurately measure relevant physiological parameters. 21 With the availability of positron emission tomography (PET), which provides an integrated assessment of cerebral blood flow (CBF), blood volume, oxygen

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Central cholinergic control of cerebral blood flow in the baboon

Effect of cholinesterase inhibition with neostigmine on autoregulation and CO2 responsiveness

Minoru Aoyagi, John Stirling Meyer, Vinod D. Deshmukh, Erwin O. Ott, Yukio Tagashira, Yasuo Kawamura, Masayuki Matsuda, Amrit N. Achari and Anthony N. C. Chee

evidence for any cholinergic control of cerebral circulation. For example, it is generally accepted that cerebral blood flow (CBF) is influenced by procedures such as electrical stimulation of the parasympathetic nerves (the seventh and tenth cranial nerves), 6, 7, 14, 21, 55 and ablation or stimulation of brain-stem centers, 26, 37, 42, 44, 57, 60, 62 as well as administration of neurotransmitters and their antagonists. 9, 11, 25, 35, 38, 41, 54, 59 Some possible functional significance of this neurogenic control of the cerebral circulation has been adduced from

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Jun Harada, Akira Takaku, Shunro Endo, Naoya Kuwayama and Osamu Fukuda

C hildren sometimes exhibit a surprising ability to recover from neurological impairments caused by cerebrovascular events. On the other hand, once irreversible damage has occurred, they suffer severe sequelae such as delays in mental and motor development. Clarification of the critical levels for ischemia in the developing brain is indispensable in an effort to better understand cerebrovascular disorders in children. Many reports, both clinical and experimental, have been published on the critical level of cerebral blood flow (CBF) during cerebral ischemia