A restricted subarachnoid hemorrhage in the cortical sulcus in cerebral amyloid angiopathy: could it be a warning sign?

Katoh, Masahito; Yamada, Masami; Asaoka, Katsuyuki; Aoki, Takeshi; Imamura, Hiroyuki; Kashiwazaki, Daina; Takano, Kazuya; Aida, Toshimitsu

doi:10.1016/j.surneu.2006.11.028

Cited by 43 publications

(39 citation statements)

References 4 publications

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“…25 Increasing data support the hypothesis that cSS might precede lobar ICH in patients with CAA. 15,[26][27][28] In a recent retrospective study, 51 patients with cSS and no apparent cause other than CAA were identified through a single-center systematic database search and followed up for a median of 35.3 months. 15 Over this period, 24 patients (47.1%) experienced any new "intracranial hemorrhage" (ICH or acute convexity subarachnoid hemorrhage): 18 patients (35.3%) had an ICH, of which 13 were at the site of preexisting siderosis.…”

Section: Resultsmentioning

confidence: 99%

Cortical superficial siderosis and intracerebral hemorrhage risk in cerebral amyloid angiopathy

et al. 2013

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Objective: To investigate whether cortical superficial siderosis (cSS) on MRI, especially if disseminated (involving more than 3 sulci), increases the risk of future symptomatic lobar intracerebral hemorrhage (ICH) in cerebral amyloid angiopathy (CAA).Methods: European multicenter cohort study of 118 patients with CAA (104 with baseline symptomatic lobar ICH) diagnosed according to the Boston criteria. We obtained baseline clinical, MRI, and follow-up data on symptomatic lobar ICH. Using Kaplan-Meier and Cox regression analyses, we investigated cSS and ICH risk, adjusting for known confounders.Results: During a median follow-up time of 24 months (interquartile range 9-44 months), 23 of 118 patients (19.5%, 95% confidence interval [CI]: 12.8%-27.8%) experienced symptomatic lobar ICH. Any cSS and disseminated cSS were predictors of time until first or recurrent ICH (logrank test: p 5 0.0045 and p 5 0.0009, respectively). ICH risk at 4 years was 25% (95% CI: 7.6%-28.3%) for patients without siderosis; 28.9% (95% CI: 7.7%-76.7%) for patients with focal siderosis; and 74% (95% CI: 44.1%-95.7%) for patients with disseminated cSS (log-rank test: p 5 0.0031). In Cox regression models, any cSS and disseminated cSS were both independently associated with increased lobar ICH risk, after adjusting for $2 microbleeds and age (hazard ratio: 2.53; 95% CI: 1.05-6.15; p 5 0.040 and hazard ratio: 3.16; 95% CI: 1.35-7.43; p 5 0.008, respectively). These results remained consistent in sensitivity analyses including only patients with symptomatic lobar ICH at baseline. Conclusions:Our findings indicate that cSS, particularly if disseminated, is associated with an increased risk of symptomatic lobar ICH in CAA. cSS may help stratify future bleeding risk in CAA, with implications for prognosis and treatment. Neurology ® 2013;81:1666-1673 GLOSSARY CAA 5 cerebral amyloid angiopathy; CI 5 confidence interval; CMB 5 cerebral microbleed; cSS 5 cortical superficial siderosis; FLAIR 5 fluid-attenuated inversion recovery; GRE 5 gradient-recalled echo; HR 5 hazard ratio; ICH 5 intracerebral hemorrhage.Sporadic cerebral amyloid angiopathy (CAA) is a highly prevalent, age-related small-vessel disease 1 caused by amyloid-b deposition in cortical and leptomeningeal vessel walls. 2 CAA is a major cause of lobar intracerebral hemorrhage (ICH), particularly in elderly patients.2-5 Spontaneous ICH is one of the most catastrophic forms of stroke, with a high risk of recurrence [6][7][8] ; CAA-related lobar ICH may carry a greater risk than deep ICH presumed to be due to hypertensive arteriopathy, 8,9 but this is currently difficult to predict. Predisposing factors for lobar ICH and lobar ICH recurrence in CAA include APOE e4 and e2 alleles, 10 hemorrhagic neuroimaging markers of CAA such as lobar cerebral microbleeds (CMBs), 11 and anticoagulant or antiplatelet use. 12 Little is known about cortical superficial siderosis (cSS), a recently identified neuroimaging marker of CAA, 13 and the risk of subsequent

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Section: Resultsmentioning

confidence: 99%

Cortical superficial siderosis and intracerebral hemorrhage risk in cerebral amyloid angiopathy

et al. 2013

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“…Focal subarachnoid hemorrhage has been reported as a presenting feature of amyloid angiopathy, 10 and superficial siderosis on MRI has been observed as an early imaging finding in amyloid angiopathy patients with Alzheimer disease. 11 There is also evidence on autopsy that subarachnoid hemorrhage, particularly in cerebral sulci, may be a primary source of hemorrhage in amyloid angiopathy.…”

Section: Discussionmentioning

confidence: 99%

Crescendo Transient Aura Attacks

Izenberg

Aviv

Demaerschalk

et al. 2009

Stroke

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Background and Purpose-Diagnosis of transient ischemic attack can be difficult because many mimics exist. We report the clinical and neuroimaging features of a distinct hemorrhagic transient ischemic attack mimic. Methods-Case series. Results-We describe 4 elderly patients presenting with a cluster of stereotyped somatosensory migraine auras, initially referred for "crescendo transient ischemic attacks". Neuroimaging in each patient revealed an unexpected finding of spontaneous focal subarachnoid hemorrhage conforming to a cortical sulcus in the contralateral hemisphere. We postulate that the episodic aura symptoms corresponded to recurrent cortical spreading depression triggered by the presence of subarachnoid blood, and speculate that such episodes could be a presenting feature of cerebral amyloid angiopathy in the absence of typical cerebral microbleeds or history of cognitive impairment. Conclusions-Focal subarachnoid hemorrhage can present clinically with transient repetitive migraine auras. Awareness of this entity is important because misdiagnosis as cerebral ischemic events could lead to incorrect treatment. We recommend that elderly patients presenting with a cluster of new unexplained migraine auras should be investigated ideally with MRI to detect focal subarachnoid hemorrhage.

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“…11 Pathologic studies of patients with CAA show that many amyloid-laden arteries are present in the leptomeninges. 19,20 Human autopsy studies have revealed that involvement of the leptomeningeal arteries occurs in early stages of CAA followed by extension of CAA to arterioles in the allocortex and the midbrain.…”

Section: Recurrent Hemorrhage (Intracerebral Hemorrhage)mentioning

confidence: 99%

“…Diverse etiologies have been posited for its occurrence, including cortical vein occlusions, posterior reversible leukoencephalopathy syndrome (PRES), reversible cerebral vasoconstriction syndrome (RCVS), coagulopathy, cocaine use, lupus vasculitis, cavernoma, brain abscesses, and cerebral amyloid angiopathy (CAA). [1][2][3][4][5][6][7][8][9][10][11][12][13] Existing information about this condition is largely derived from case reports and small case series, which carry inherent referral and diagnostic biases. We undertook this study to systematically evaluate and review the potential causes and patterns of clinical and radiologic presentation of localized cSAH from the inpatient population at our institution.…”

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confidence: 99%

Atraumatic convexal subarachnoid hemorrhage

Kumar¹,

Goddeau²,

Selim³

et al. 2010

Neurology

252

146

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Objective: To identify patterns of clinical presentation, imaging findings, and etiologies in a cohort of hospitalized patients with localized nontraumatic convexal subarachnoid hemorrhage.Methods: Twenty-nine consecutive patients with atraumatic convexal subarachnoid hemorrhage were identified using International Classification of Diseases-9 code from 460 patients with subarachnoid hemorrhage evaluated at our institution over a course of 5 years. Retrospective review of patient medical records, neuroimaging studies, and follow-up data was performed.Results: There were 16 women and 13 men between the ages of 29 and 87 years. Two common patterns of presentations were observed. The most frequent presenting symptom in patients Յ60 years (n ϭ 16) was a severe headache (n ϭ 12; 75%) of abrupt onset (n ϭ 9; 56%) with arterial narrowing on conventional angiograms in 4 patients; 10 (p ϭ 0.003) were presumptively diagnosed with a primary vasoconstriction syndrome. Patients Ͼ60 years (n ϭ 13) usually had temporary sensory or motor symptoms (n ϭ 7; 54%); brain MRI scans in these patients showed evidence of leukoaraiosis and/or hemispheric microbleeds and superficial siderosis (n ϭ 9; 69%), compatible with amyloid angiopathy (n ϭ 10; p Ͻ 0.0001). In a small group of patients, the presentation was more varied and included lethargy, fever, and confusion. Four patients older than 60 years had recurrent intracerebral hemorrhages in the follow-up period with 2 fatalities. Conclusion:Convexal subarachnoid hemorrhage is an important subtype of nonaneurysmal subarachnoid bleeding with diverse etiologies, though a reversible vasoconstriction syndrome appears to be a common cause in patients 60 years or younger whereas amyloid angiopathy is frequent in patients over 60. These observations require confirmation in future studies. Atraumatic localized convexal subarachnoid hemorrhage (cSAH) is an unusual presentation of subarachnoid bleeding, in which the bleeding is localized to the convexities of the brain without involvement of the adjacent parenchyma or extension into the interhemispheric fissures, basal cisterns, or ventricles. Since most saccular aneurysms arise from the circle of Willis, aneurysmal rupture is an unlikely source of cSAH. Diverse etiologies have been posited for its occurrence, including cortical vein occlusions, posterior reversible leukoencephalopathy syndrome (PRES), reversible cerebral vasoconstriction syndrome (RCVS), coagulopathy, cocaine use, lupus vasculitis, cavernoma, brain abscesses, and cerebral amyloid angiopathy (CAA). 1-13Existing information about this condition is largely derived from case reports and small case series, which carry inherent referral and diagnostic biases. We undertook this study to systematically evaluate and review the potential causes and patterns of clinical and radiologic presentation of localized cSAH from the inpatient population at our institution.

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A restricted subarachnoid hemorrhage in the cortical sulcus in cerebral amyloid angiopathy: could it be a warning sign?

Cited by 43 publications

References 4 publications

Cortical superficial siderosis and intracerebral hemorrhage risk in cerebral amyloid angiopathy

Cortical superficial siderosis and intracerebral hemorrhage risk in cerebral amyloid angiopathy

Crescendo Transient Aura Attacks

Atraumatic convexal subarachnoid hemorrhage

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