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Hyperperfusion

Cerebrovascular Carotid spasm Compromise of ECA ostium Hyperfusion syndrome Contrast encephalopathy Transient symptomatic cerebral ischemia Global Focal Carotid dissection Carotid perforation Hyperperfusion syndrome Acute stent thrombosis Major ischemic stroke Cerebral hemorrhage... [Pg.563]

Coutts SB, Hill MD, Hu WY Hyperperfusion syndrome toward a stricter definition. Neurosurgery 2003 53 1053— 1058 discussion 1058-1060. [Pg.566]

Abou-Chebl A, YadavJS, Reginelli JR Bajzer C, Bhatt D, Krieger DW. Intracranial hemorrhage and hyperperfusion syndrome... [Pg.567]

Hypermetabolism - hyperperfusion based on 1 1 relationship between VO2, VCO2, QO2... [Pg.166]

KaribeH.,ZarowG. J., GrahamS. H., and WeinsteinP.R. (1994) Mild intraischemic hypothermia reduces postischemic hyperperfusion, delayed postischemic hypoperfusion, blood-brain barrier disruption, brain edema, and neuronal damage volume after temporary focal cerebral ischemia in rats. J. Cereb. Blood Flow Metab. 14, 620-627. [Pg.60]

Spontaneous recanalization, at least of middle cerebral artery occlusion, occurs in up to two-thirds of patients within a week of stroke onset, many in the first 48 hours (Fieschi et al. 1989 Kaps et al. 1992 Zanette et al. 1995 Arnold et al. 2005). In general, the CT identified and functional outcomes are both better with recanalization and reperfusion, and even with early hyperperfusion, than if the middle cerebral artery remains occluded (Wardlaw et al. 1993 Marchal et al. 1996b Barber et al. 1998b). [Pg.51]

Marchal G, Beaudouin V, Rioux P et al. (1996a). Prolonged persistence of substantial volumes of potentially viable brain tissue after stroke. A correlative PET-CT study with voxel-based data analysis. Stroke 27 599-606 Marchal G, Furlan M, Beaudouin V et al. (1996b). Early spontaneous hyperperfusion after stroke. A marker of favourable tissue outcome Brain 119 409-419 Meyer JS, Ohara K, Muramatsu K (1993). [Pg.54]

Headache ipsilateral to the operation may herald cerebral hyperperfusion (van Mook et al. 2005 Adhiyaman and Alexander 2007), but it may also be due to something akin to cluster headache and caused by subtle damage to the sympathetic plexus around the carotid artery... [Pg.296]

Naylor AR, Evans J, Thompson MM et al. (2003). Seizures after carotid endarterectomy hyperperfusion, dysautoregulation or hypertensive encephalopathy European Journal of Vascular Endovascular Surgery 26 39-44... [Pg.301]

A lack of close correlation between COHb levels and the severity of CO toxicity is well recognized (Mannaioni et al, 2006) this clearly suggests the involvement of other factors. These other factors most probably include xanthine oxidase-derived reactive oxygen species, which are produced due to hyperperfusion following the initial hypoxia. This inference is supported by several animal studies (Sokal and KraUcowska, 1985 Thom, 1992 Zhang and Piantadosi, 1992). [Pg.280]

Salnja, S., White, RJ. Hereditary hemorrhagic telangiectasia of the hver hyperperfusion with relative ischemia. Poverty amidst plenty. Radiology 2004 230 25-27... [Pg.841]

The microcirculatory changes associated with shock are complex and difficult to study. Although some mediators such as endothelin-1 cause vasoconstriction, other mediators, such as adenosine and nitric oxide, yield vasodilation. These changes result in hypoperfusion or hyperperfusion depending on the area. As these microcirculatory changes fail to maintain adequate organ perfusion, more widespread sympathetic nervous system activation and vasoconstriction ensue. [Pg.480]

Moore D.E., Herscovitch P., Schiffmann R., Selective arterial distribution of cerebral hyperperfusion in Eabry disease. Journal of Neuroimaging 11 (2001) 303-307. [Pg.585]

Moore D.E., Scott L.T., Gladwin M.T., Altarescu G., Kaneski C., Suzuki K., Pease-Fye M., Eerri R., Brady R.O., Herscovitch P., Schiffmann R., Regional cerebral hyperperfusion and nitric oxide pathway dysregulation in Fabry disease reversal by enzyme replacement therapy. Circulation 104(2001) 1506-1512. [Pg.585]

Posterior reversible encephalopathy syndrome Hyperperfusion syndrome post carotid endarterectomy Conventional MR imaging findings... [Pg.165]

Rarely, other disease entities such as HTV or other viral encephalopathies, tumor, and acute donyelinafion can present with acute neurologic deficits and patterns of edema on conventional images suggestive of stroke. Similar to PRES and hyperperfusion syndrome following carotid endarterectomy, DW images shows elevated diffusion. [Pg.167]

Fig. 7.20 Hyperperfusion syndrome following carotid endarterectomy (CEA). Seventy-nine-year-old female 1 week after CEA with status epUepticus. T2-weighted image demonstrates gray and white matter hypeiintensity in the left frontal lobe, suggestive of acute infarction. There is no decreased diffusion on... Fig. 7.20 Hyperperfusion syndrome following carotid endarterectomy (CEA). Seventy-nine-year-old female 1 week after CEA with status epUepticus. T2-weighted image demonstrates gray and white matter hypeiintensity in the left frontal lobe, suggestive of acute infarction. There is no decreased diffusion on...
Xan, G.S. and C.C. Phatouros, Cerebral hyperperfusion syndrome post-carotid artery stenting. J Med Imaging Radiat Oncol, 2009. 53(1) p. 81-6. [Pg.173]

In many acnte stroke patients, spontaneons resoln-tion of the arterial lesion(s) before the time of presentation resnlts in spontaneous reperfusion of some or all of the previously ischemic tissue. Various studies have found that spontaneous reperfusion occurs in 16% of patients scanned within 8 h of stroke onset [10], and 33% of patients scanned within 48 h of onset [11], hi this reperfused tissue, vasodilation that persists even after the reduction in perfusion pressure has resolved often results in postischemic hyperperfusion, which is... [Pg.182]


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See also in sourсe #XX -- [ Pg.47 , Pg.65 , Pg.136 , Pg.137 , Pg.288 ]




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Carotid endarterectomy hyperperfusion

Hyperperfusion syndrome

Postischemic hyperperfusion

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