Pial vasodilation and moderate hyperaemia following carotid endarterectomy: new MRI diagnostic signs in hyperperfusion/reperfusion syndrome?

Thurley, Peter; Altaf, N.; Dineen, Robert A.; MacSweeney, Shane; Auer, Dorothee P.

doi:10.1007/s00234-009-0527-6

Cited by 4 publications

(6 citation statements)

References 3 publications

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“…However, larger samples are needed to verify if the definition based on the MV is more syndrome specific. The mean increases in CBFV on the ipsilateral and contralateral sides are consistent with other studies [38,48,49]. …”

Section: Discussionsupporting

confidence: 82%

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Hyperperfusion Syndrome after Carotid Endarterectomy and Carotid Stenting

Buczek

Karliñski²,

Kobayashi³

et al. 2013

Cerebrovasc Dis

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Background: Hyperperfusion syndrome (HS) is a relatively rare but possibly serious complication of carotid revascularization procedures. Impaired cerebral autoregulation and postrevascularization changes in cerebral blood flow are the main mechanisms involved in the development of HS. Most up-to-date studies addressing this issue are retrospective and tend to concentrate on carotid endarterectomy (CEA), neglecting carotid stenting (CAS). Our aim was to compare the frequency of clinical signs of HS and hyperperfusion detected by transcranial Doppler (TCD) in patients undergoing CAS or CEA due to carotid stenosis. Methods: In this prospective observational study, we evaluated 61 patients scheduled for routine CAS or CEA. Each patient was examined by a neurologist before and after the revascularization procedure to assess the clinical status. Severe headache, ocular or facial pain, confusion, visual disturbances, epileptic seizures or any focal deficits not caused by cerebral ischemia were considered clinical signs of HS. Peak systolic velocity (PSV), end-diastolic velocity, mean velocity (MV), and pulsatility index were measured by TCD once before and twice after the intervention (within 6 h after and 2-5 days after the procedure). Hyperperfusion was defined as a >100% increase in the middle cerebral artery (MCA) blood velocity, evaluated separately for PSV and MV after the procedure compared with the baseline value. Cerebrovascular reactivity (CVR) was evaluated with a TCD acetazolamide test before the intervention. Results: CAS (n = 33) and CEA (n = 28) patients were included in the study. There was no difference between the groups in the frequency of clinical signs of HS (21.2 vs. 21.4%) and ratio of TCD hyperperfusion (12.1 vs. 14.3%). In the CAS group, ipsilateral MCA velocity significantly increased directly after the intervention and 2-5 days later, while it increased in the CEA group only 2-5 days after the intervention. The sensitivity and specificity of hyperperfusion, defined by MV, for HS signs were 38.5 and 93.8%, respectively, whereas those defined by PSV were 30.8 and 89.6%, respectively. The sensitivity and specificity of impaired CVR (<25%) for HS signs were 63.6 and 73.5%, respectively. Conclusions: There is no difference in the frequency of HS clinical signs and hyperperfusion detected by TCD between patients after CAE and CAS. Clinical signs suggested HS does not always correspond with TCD hyperperfusion. However, both the CVR test and TCD measurements of MCA velocity can help identify patients at high risk for HS.

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Section: Discussionsupporting

confidence: 82%

“…Conversely, changes in perfusion or CBFV >100% after the procedure may remain clinically silent [19,22,34,35]. Some researchers suggest that the term HS should be replaced with reperfusion syndrome [34,36,37,38]. Therefore, we intentionally refrained from defining HS.…”

Section: Discussionmentioning

confidence: 99%

Hyperperfusion Syndrome after Carotid Endarterectomy and Carotid Stenting

Buczek

Karliñski²,

Kobayashi³

et al. 2013

Cerebrovasc Dis

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“…Thurley et al (2009) described a similar unilateral leptomeningeal enhancement in a patient exhibiting headache, vomiting, seizure and hypertension after endarterectomy.…”

Section: Reperfusion Syndromementioning

confidence: 82%

“…We believe that the finding described by Grunwald et al (2009) and Thurley et al (2009) may be related to a clinical syndrome of hyperperfusion that is not complicated by intracranial hemorrhage. Our patients with leptomeningeal enhancement after CAS ( Figure 3) did not exhibit the classical symptoms of cerebral hyperperfusion, such as transitory focal deficit, unilateral migraine and seizures.…”

Section: Reperfusion Syndromementioning

confidence: 89%

Decreased Cerebral Perfusion in Carotid Artery Stenosis, Carotid Angioplasty and Its Effects on Cerebral Circulation

Tavares¹,

Caldas²

2012

Advances in the Treatment of Ischemic Stroke

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“…While CT, positron emission tomography, MR perfusion and TCD have all been used to assess leptomeningeal collateral blood flow in a variety of different disorders, the most effective single method to visualize leptomeningeal collateral blood flow in humans remains through angiographic assessment (Mori et al, 2009;Derdeyn et al, 1999;Thurley et al, 2009;Wu et al, 2008). However, a combination of multiple imaging modalities is ideal to gain a greater understanding of blood flow in the ischemic cortex (Bang et al, 2008;Wu et al, 2008;Kim et al, 2009).…”

Section: Clinical Importance Of Leptomeningeal Collateralsmentioning

confidence: 99%