Cortical subarachnoid haemorrhage in the elderly: a recurrent event probably related to cerebral amyloid angiopathy

Raposo, Nicolas; Viguier, Alain; Cuvinciuc, Victor; Calvière, Lionel; Cognard, Christophe; Bonneville, Fabrice; Larrue, Vincent

doi:10.1111/j.1468-1331.2010.03214.x

Cited by 89 publications

(70 citation statements)

References 20 publications

(30 reference statements)

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“…Accumulating evidence suggests that cortical superficial siderosis (cSS) [5][6][7][8] and MRI-visible centrum semiovale (ie, cerebral hemisphere white matter) perivascular spaces (CSO-PVS) are new imaging markers of CAA, which may reflect distinct but related aspects of pathophysiology. However, the precise relationship between CSO-PVS and other imaging manifestations of CAA, including cSS and lobar CMBs, has not been explored.…”

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confidence: 99%

White Matter Perivascular Spaces Are Related to Cortical Superficial Siderosis in Cerebral Amyloid Angiopathy

Charidimou

Jäger

Peeters

et al. 2014

Stroke

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Consecutive CAA patients (according to the original Boston criteria 9 ; ie, not including cSS as a criterion) from an ongoing multicenter Background and Purpose-We set out to investigate whether MRI-visible centrum semiovale perivascular spaces (CSO-PVS), a potential biomarker of impaired interstitial fluid drainage in sporadic cerebral amyloid angiopathy, is associated with cortical superficial siderosis (cSS), reflecting recurrent hemorrhage from severe leptomeningeal and superficial cortical vascular amyloid. Methods-Retrospective multicenter cohort study of possible/probable cerebral amyloid angiopathy according to the Boston criteria. PVS were rated in basal ganglia and CSO (CSO-PVS) on axial T2-weighted sequences, using a validated 4-point visual rating scale and were classified as high (score >2) or low degree (score ≤2) for prespecified analyses. Independent risk factors for high CSO-PVS degree were investigated in logistic regression. Results-The

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confidence: 99%

White Matter Perivascular Spaces Are Related to Cortical Superficial Siderosis in Cerebral Amyloid Angiopathy

Charidimou

Jäger

Peeters

et al. 2014

Stroke

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“…1,4 Recent studies have identified cortical superficial siderosis (cSS) as another manifestation of CAA. [5][6][7][8] In CAA, cSS has a characteristic predilection for the cerebral convexities, reflecting linear blood residues in the superficial layers of the cerebral cortex or in the subarachnoid space. [8][9][10] cSS may have clinical relevance as an important cause of transient focal neurologic episodes (sometimes called "amyloid spells"), 11,12 and a potential "warning sign" for future symptomatic ICH.…”

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confidence: 99%

Prevalence and mechanisms of cortical superficial siderosis in cerebral amyloid angiopathy

et al. 2013

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Objective: We investigated the prevalence and clinical-radiologic associations of cortical superficial siderosis (cSS) in patients with probable cerebral amyloid angiopathy (CAA) compared to those with intracerebral hemorrhage (ICH) not attributed to CAA. Methods:We conducted a retrospective multicenter cohort study of 120 patients with probable CAA and 2 comparison groups: 67 patients with either single lobar ICH or mixed (deep and lobar) hemorrhages; and 22 patients with strictly deep hemorrhages. We rated cSS, ICH, white matter changes, and cerebral microbleeds.

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“…Patients first presenting with TFNEs also had a higher total SVD summary score (mean 6 SD; 3.5 6 1.3 vs 2.9 6 1.2; p , 0.001) and this remained significant in an ordinal logistic regression, adjusting for age vascular risk factors (adjusted OR [2][3][4] in patients with cognitive symptoms and 3 [3][4] in those with TFNEs, both p , 0.001). 28 This was almost entirely driven by a higher number of CMBs (1 in ICH patients vs 5 [3][4][5][6][7][8][9][10][11][12][13] in patients with cognitive symptoms and 7 in those with TFNEs, p 5 0.001 and p , 0.001; see tables e-1 and e-2 and figure e-1 at Neurology.org for details). DISCUSSION We demonstrated that patients with probable CAA without symptomatic ICH first presenting with TFNEs bore a higher burden of quantifiable SVD-related damage compared to patients with probable CAA first evaluated for cognitive symptoms.…”

Section: Resultsmentioning

confidence: 99%

“…11 It has been shown that patients with CAA first seen for acute neurologic symptoms often develop recurrent symptoms and are at high risk of developing subsequent ICH, [12][13][14] while an association with higher risk of bleeding has not been described in memory clinic patients, who demonstrate cognitive decline over time.…”

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confidence: 99%

Small vessel disease burden in cerebral amyloid angiopathy without symptomatic hemorrhage

et al. 2017

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Objective: Cerebral amyloid angiopathy (CAA) is a common age-related small vessel disease (SVD). Patients without intracerebral hemorrhage (ICH) typically present with transient focal neurologic episodes (TFNEs) or cognitive symptoms. We sought to determine if SVD lesion burden differed between patients with CAA first presenting with TFNEs vs cognitive symptoms.Methods: A total of 647 patients presenting either to a stroke department (n 5 205) or an outpatient memory clinic (n 5 442) were screened for eligibility. Patients meeting modified Boston criteria for probable CAA were included and markers of SVD were quantified, including cerebral microbleeds (CMBs), perivascular spaces, cortical superficial siderosis (cSS), and white matter hyperintensities (WMHs). Patients were classified according to presentation symptoms (TFNEs vs cognitive). Total CAA-SVD burden was assessed using a validated summary score. Individual neuroimaging markers and total SVD burden were compared between groups using univariable and multivariable models.Results: There were 261 patients with probable CAA included. After adjustment for confounders, patients first seen for TFNEs (n 5 97) demonstrated a higher prevalence of cSS (p , 0.0001), higher WMH volumes (p 5 0.03), and a trend toward higher CMB counts (p 5 0.09). The total SVD summary score was higher in patients seen for TFNEs (adjusted odds ratio per additional score point 1.46, 95% confidence interval 1.16-1.84, p 5 0.013). Conclusions:Patients with probable CAA without ICH first evaluated for TFNEs bear a higher burden of structural MRI SVD-related damage compared to those first seen for cognitive symptoms. This study sheds light on neuroimaging profile differences across clinical phenotypes of patients with CAA without ICH. Neurology ® 2017;88:878-884 GLOSSARY BG 5 basal ganglia; CAA 5 cerebral amyloid angiopathy; CI 5 confidence interval; CMB 5 cerebral microbleed; CSO 5 centrum semiovale; cSS 5 cortical superficial siderosis; FLAIR 5 fluid-attenuated inversion recovery; ICH 5 intracerebral hemorrhage; IQR 5 interquartile range; OR 5 odds ratio; PVS 5 perivascular spaces; SVD 5 small vessel disease; TE 5 echo time; TFNE 5 transient focal neurologic episode; WMH 5 white matter hyperintensity.Sporadic cerebral amyloid angiopathy (CAA) is characterized by progressive deposition of b-amyloid in the walls of cortical and leptomeningeal small arteries, resulting in vessel dysfunction and brain parenchymal injury. CAA is common in older individuals and, when severe, can lead to devastating consequences including intracerebral hemorrhage (ICH) and dementia. 1,2While definite diagnosis relies on pathology, clinical and neuroimaging criteria (the Boston criteria) can reliably identify CAA in older patients with lobar hemorrhage.3,4 More recently, an updated version of these criteria has demonstrated that the presence of $2 lobar cerebral microbleeds (CMBs) in patients without large hemorrhage is specific for moderate to severe CAA pathology presence in older individuals seen in a h...

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Cortical subarachnoid haemorrhage in the elderly: a recurrent event probably related to cerebral amyloid angiopathy

Cited by 89 publications

References 20 publications

White Matter Perivascular Spaces Are Related to Cortical Superficial Siderosis in Cerebral Amyloid Angiopathy

White Matter Perivascular Spaces Are Related to Cortical Superficial Siderosis in Cerebral Amyloid Angiopathy

Prevalence and mechanisms of cortical superficial siderosis in cerebral amyloid angiopathy

Small vessel disease burden in cerebral amyloid angiopathy without symptomatic hemorrhage

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