Blood–brain barrier breakdown as a novel mechanism underlying cerebral hyperperfusion syndrome

Ivens, Sebastian; Szendro, Gabriel; Greenberg, George; Friedman, Alon; Shelef, Ilan

doi:10.1007/s00415-009-5384-z

Cited by 50 publications

(44 citation statements)

References 26 publications

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“…Because ICH is thought to be a result of cerebral hyperperfusion syndrome, a condition arising from baroreceptor dysregulation of cerebral blood flow and free radical-mediated endothelial damage in the preoperative chronically hypoperfused state, it is possible that CAS procedures are more likely to result in postoperative hyperperfusion. 2,3,14,15 Recently, Park et al 16 reported hyperperfusion after carotid stenting of individuals at high risk was directly related to the location of the atheromatous lesion; stent deployment within the carotid bulb body was associated with a 6-fold higher rate of hyperperfusion relative to stent deployment within apical lesions. Similar reports are absent in the endarterectomy literature.…”

Section: Discussionmentioning

confidence: 99%

Intracranial Hemorrhage Is Much More Common After Carotid Stenting Than After Endarterectomy

McDonald

Cloft

Kallmes

2011

Stroke

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Background and Purpose-Intracranial hemorrhage (ICH) is a rare and devastating complication of carotid revascularization. We sought to determine the prevalence of, type of, and risk factors associated with ICH among recipients of carotid endarterectomy (CEA) and carotid angioplasty and stenting (CAS) within the National Inpatient Sample (NIS). Methods-Postoperative cases of ICH after CEA (International Classification of Disease 9 th edition [ICD-9]: 38.12) or CAS (ICD-9: 00.63) were retrieved from the 2001 to 2008 NIS. Clinical presentation (asymptomatic versus symptomatic), discharge status, in-hospital mortality, demographics, and hospital characteristics were extracted from NIS data. Charlson indices of comorbidity were determined based on ICD-9 and clinical classification software codes. Multivariate regression was used to determine the impact of revascularization procedure type and symptom status on adverse outcomes, including ICH, in-hospital mortality, and unfavorable discharge status. Results-Among 57 663 486 NIS hospital admissions, 215 012 CEA and 13 884 CAS procedures were performed.Symptomatic presentations represented the minority of CEA (Nϭ10 049; 5%) and CAS cases (Nϭ1251; 10%). ICH occurred significantly more frequently after CAS than CEA in both symptomatic (4.4% versus 0.8%; PϽ0.0001) and asymptomatic presentations (0.5% versus 0.06%; PϽ0.0001). Multivariate regression suggested that symptomatic presentations (versus asymptomatic) and CAS procedures (versus CEA) were both independently predictive of 6-fold to 7-fold increases in the frequency of postoperative ICH. ICH was independently predictive in a 30-fold increased risk of mortality before discharge. Conclusions-CAS procedures are associated with elevated adverse outcomes, including ICH, in-hospital death, and unfavorable discharges, especially among symptomatic presentations. (Stroke. 2011;42:2782-2787.)

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Section: Discussionmentioning

confidence: 99%

Intracranial Hemorrhage Is Much More Common After Carotid Stenting Than After Endarterectomy

McDonald

Cloft

Kallmes

2011

Stroke

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“…[5][6][7] Risk factors for hyperperfusion have been proposed, including high-grade stenosis, poor collateral circulation, high blood pressure, age, and bloodbrain barrier breakdown. [7][8][9][10][11] Nevertheless, the underlying pathophysiology of HPS has not been well evaluated due to its low incidence (0.7%-3%). 7,9,12 The generally accepted explanation emphasizes a failure of autoregulation after sudden augmentation of cerebral blood inflow following carotid stent placement.…”

mentioning

confidence: 99%

Stenotic Transverse Sinus Predisposes to Poststenting Hyperperfusion Syndrome as Evidenced by Quantitative Analysis of Peritherapeutic Cerebral Circulation Time

Lin

Chang

Tsai

et al. 2014

American Journal of Neuroradiology

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BACKGROUND AND PURPOSE:Hyperperfusion syndrome is a devastating complication of carotid stent placement. The shortening of cerebral circulation time after stent placement is seen as a good indicator of the development of hyperperfusion syndrome. The purpose of our study was to evaluate whether patients with ipsilateral transverse sinus stenosis are prone to having shortened cerebral circulation time after stent placement, subsequently leading to the possible development of hyperperfusion syndrome.

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“…Seizures caused by the osmotic BBB disruption procedure in oncological patients (Neumann-Haefelin et al 2002;Marchi et al 2007) and seizures observed in cerebral hyperperfusion syndrome (Ivens et al 2010) are typical examples to this condition.…”

Section: Dementiamentioning

confidence: 99%

Physiology and Pathophysiology of Cerebral Microcirculation

Dalkara

2014

PanVascular Medicine

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The brain uses more energy than any other organ in the body and relies on uninterrupted supply of glucose and oxygen via blood flow. Blood flow in human gray matter is in the range of 40-70 mL/100 mL/min and is regulated to match the metabolic demand of the brain region supplied. Majority of the nutrient and waste exchange takes place at microcirculation. Penetrating arteries supplying the brain branch into arterioles and terminate in an extensive network of capillaries. The total length of capillaries in 1 mm 3 of human cortex is about 50 cm. Unlike other organs where temporary closing or recruitment of capillaries matches the varying tissue O 2 demand, in the brain, this is likely regulated by heterogeneity of red blood cell transit times across capillaries. Increases in neuronal activity also cause an enhanced blood flow to the active brain area. This neurovascular coupling is regulated by multiple mechanisms: adenosine and lactate produced as end products of the enhanced metabolism couple neural activity with flow by inducing vasodilation. As a specific mechanism to the brain, glutamate-induced Ca 2+ increases in astrocytes, and interneurons play an important role to translate neuronal activity (assessed by monitoring glutamate released to the extracellular space) to vasoactive signals such as arachidonic acid metabolites and nitric oxide (NO). K + released onto smooth muscle cells through Ca 2+ -activated K + channels on astrocyte endfeet plasmalemma can also induce dilation during neuronal activity. Majority of the regulation takes place around arterioles. Relative contributions of the above pathways to blood flow increase vary in different brain regions. Another unique feature of cerebral circulation is the blood-brain barrier (BBB) that limits and regulates entry of blood constituents (including ions) to the CNS parenchyma. A close interaction between the endothelia and pericytes as well as astrocytes is required for development and functioning of the neurovascular unit and BBB. The ratio of pericytes to endothelial cells is much higher in the cerebral microcirculation compared to other tissues. Pericytes may play a role in distribution of microvascular blood flow depending on the very focal demand as a final step of flow regulation after the arterioles. This flow regulation with fine spatial resolution may be essential for tissues with high functional specialization such as the brain and retina. Retinal microvessels appear particularly dependent on pericytes. Pericyte loss in the retinal microvessels is a hallmark of diabetic retinopathy. The microvascular injury induced by ischemia/reperfusion plays a critical role in determining tissue survival after recanalization in focal cerebral ischemia by disrupting the blood-brain barrier integrity and inducing microcirculatory clogging (no-reflow). Radicals produced during ischemia/reperfusion afflict microvessels more heavily compared to larger vessels. Effective suppression of oxidative/nitrative stress during pharmacological or interventional reopeni...

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Blood–brain barrier breakdown as a novel mechanism underlying cerebral hyperperfusion syndrome

Cited by 50 publications

References 26 publications

Intracranial Hemorrhage Is Much More Common After Carotid Stenting Than After Endarterectomy

Intracranial Hemorrhage Is Much More Common After Carotid Stenting Than After Endarterectomy

Stenotic Transverse Sinus Predisposes to Poststenting Hyperperfusion Syndrome as Evidenced by Quantitative Analysis of Peritherapeutic Cerebral Circulation Time

Physiology and Pathophysiology of Cerebral Microcirculation

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