scholarly journals Acute diffusion-weighted imaging lesions in cerebral amyloid angiopathy-related convexal subarachnoid hemorrhage

2017 ◽  
Vol 38 (2) ◽  
pp. 225-229 ◽  
Author(s):  
Markus Beitzke ◽  
Christian Enzinger ◽  
Alexander Pichler ◽  
Gerit Wünsch ◽  
Franz Fazekas
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Amyloid Angiopathy ◽  
Diffusion Weighted Imaging ◽  
Superficial Siderosis ◽  
Amyloid Angiopathy ◽  
Cross Sectional ◽  
Diffusion Weighted ◽  
Patient Groups ◽  
Cerebral Amyloid ◽  
Convexal Subarachnoid Hemorrhage

Small acute diffusion-weighted imaging (DWI) lesions can accompany intracerebral hemorrhage due to cerebral amyloid angiopathy (CAA). We therefore examined the occurrence of such lesions in the context of CAA-related convexal subarachnoid hemorrhage (cSAH) both in a cross-sectional and longitudinal manner. DWI lesions were noted in 14/29 (48%) patients at their index cSAH and 12/21 patients (57%) showed acute small DWI lesions at follow-up MRI. Forty-four of 71 (62%) DWI lesions were spatially related to areas of cortical superficial siderosis. Clarification of the implications of our finding needs the investigation of larger patient groups.

scholarly journals Cerebral Amyloid Angiopathy-Related Atraumatic Convexal Subarachnoid Hemorrhage: An ARIA before the Tsunami

2015 ◽  
Vol 35 (5) ◽  
pp. 710-717 ◽  
Author(s):  
Eva Martínez-Lizana ◽  
María Carmona-Iragui ◽  
Daniel Alcolea ◽  
Manuel Gómez-Choco ◽  
Eduard Vilaplana ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Amyloid Angiopathy ◽  
Functional Disability ◽  
Superficial Siderosis ◽  
Csf Biomarkers ◽  
Amyloid Angiopathy ◽  
Cerebral Amyloid ◽  
Convexal Subarachnoid Hemorrhage

Atraumatic convexal subarachnoid hemorrhage (cSAH) in elderly patients is a rare entity that has been associated with cerebral amyloid angiopathy (CAA) and intracerebral hematomas (ICH). To characterize this entity and to study these associations, 22 patients over 60 with cSAH were included in a multicenter ambispective cohort study. Clinical data, magnetic resonance imaging (MRI) studies, APOE genotyping, and cerebrospinal fluid (CSF) biomarkers were evaluated. Results were compared with data from healthy controls (HC), non-cSAH CAA patients (CAAo), and Alzheimer disease patients. Convexal subarachnoid hemorrhage presented with transient sensory or motor symptoms. At follow-up (median 30.7 months), 5 patients had died, 6 survivors showed functional disability (modified Rankins Scale (mRS) > 2), and 12 cognitive impairment. Four patients had prior ICH and six had an ICH during follow-up. CSF-Aβ40 and Aβ42 levels were lower in cSAH and CAAo compared with HC. Convexal subarachnoid hemorrhage presented an APOE-ε2 overrepresentation and CAAo had an APOE-ε4 overrepresentation. On MRI, all patients fulfilled CAA-modified Boston criteria and 9 showed cortical ischemia in the surrounding cortex or the vicinity of superficial siderosis. The neuropathologic study, available in one patient, showed severe CAA and advanced Alzheimer-type pathology. Convexal subarachnoid hemorrhage in the elderly is associated with cognitive impairment and lobar ICH occurrence. Our findings support the existence of an underlying CAA pathology.

scholarly journals β-Amyloid in CSF

Neurology ◽  
2016 ◽  
Vol 88 (2) ◽  
pp. 169-176 ◽  
Author(s):  
Ellis S. van Etten ◽  
Marcel M. Verbeek ◽  
Jeroen van der Grond ◽  
Ronald Zielman ◽  
Sanneke van Rooden ◽  
...  
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Clinical Symptoms ◽  
White Matter Hyperintensity ◽  
Superficial Siderosis ◽  
Csf Biomarkers ◽  
Amyloid Angiopathy ◽  
Cross Sectional ◽  
Mutation Carriers ◽  
Β Amyloid ◽  
Cerebral Amyloid

Objective:To investigate CSF biomarkers in presymptomatic and symptomatic mutation carriers with hereditary cerebral hemorrhage with amyloidosis–Dutch type (HCHWA-D), a model for sporadic cerebral amyloid angiopathy, and to determine the earliest deposited form of β-amyloid (Aβ).Methods:HCHWA-D mutation carriers and controls were enrolled in the cross-sectional EDAN (Early Diagnosis of Amyloid Angiopathy Network) study. The HCHWA-D group was divided into symptomatic carriers with a previous intracerebral hemorrhage and presymptomatic carriers. CSF concentrations of Aβ40, Aβ42, total tau, and phosphorylated tau181 proteins were compared to those of controls of a similar age. Correlations between CSF biomarkers, MRI markers, and age were investigated with multivariate linear regression analyses.Results:We included 10 symptomatic patients with HCHWA-D (mean age 55 ± 6 years), 5 presymptomatic HCHWA-D carriers (mean age 36 ± 13 years), 31 controls <50 years old (mean age 31 ± 7 years), and 50 controls ≥50 years old (mean age 61 ± 8 years). After correction for age, CSF Aβ40 and Aβ42 were significantly decreased in symptomatic carriers vs controls (median Aβ40 1,386 vs 3,867 ng/L, p < 0.001; median Aβ42 289 vs 839 ng/L, p < 0.001) and in presymptomatic carriers vs controls (median Aβ40 3,501 vs 4,684 ng/L, p = 0.011; median Aβ42 581 vs 1,058 ng/L, p < 0.001). Among mutation carriers, decreasing CSF Aβ40 was associated with higher lobar microbleed count (p = 0.010), increasing white matter hyperintensity volume (p = 0.008), and presence of cortical superficial siderosis (p = 0.02).Conclusions:Decreased levels of CSF Aβ40 and Aβ42 occur before HCHWA-D mutation carriers develop clinical symptoms, implicating vascular deposition of both Aβ species as early steps in cerebral amyloid angiopathy pathogenesis. CSF Aβ40 and Aβ42 may serve as preclinical biomarkers of cerebral amyloid angiopathy pathology.

scholarly journals The Characteristics of Superficial Siderosis and Convexity Subarachnoid Hemorrhage and Clinical Relevance in Suspected Cerebral Amyloid Angiopathy

2015 ◽  
Vol 39 (5-6) ◽  
pp. 278-286 ◽  
Author(s):  
Jun Ni ◽  
Eitan Auriel ◽  
Jenelle Jindal ◽  
Alison Ayres ◽  
Kristin M. Schwab ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Intracerebral Hemorrhage ◽  
Cerebral Amyloid Angiopathy ◽  
Epileptiform Activity ◽  
Brain Mri ◽  
Superficial Siderosis ◽  
Amyloid Angiopathy ◽  
Cerebral Bleeding ◽  
Cerebral Amyloid

Background and Aims: Systematic studies of superficial siderosis (SS) and convexity subarachnoid hemorrhage (cSAH) in patients with suspected cerebral amyloid angiopathy (CAA) without lobar intracerebral hemorrhage (ICH) are lacking. We sought to determine the potential anatomic correlation between SS/cSAH and transient focal neurological episodes (TFNE) and whether SS/cSAH is predictor of future cerebral hemorrhagic events in these patients. Methods: We enrolled 90 consecutive patients with suspected CAA (due to the presence of strictly lobar microbleeds (CMBs) and/or SS/cSAH) but without the history of symptomatic lobar ICH who underwent brain MRI including T2*-weighted, diffusion-weighted imaging and fluid-attenuated inversion recovery sequences from an ongoing single center CAA cohort from 1998 to 2012. Evaluation of SS, cSAH and CMBs was performed. Medical records and follow-up information were obtained from prospective databases and medical charts. TFNE was defined according to published criteria and electroencephalogram reports were reviewed. Results: Forty-one patients (46%) presented with SS and/or cSAH. The prevalence of TFNE was significantly higher in those with SS/cSAH (61 vs. 10%; p < 0.001) and anatomically correlated with the location of cSAH, but not SS. The majority of TFNE in patients with SS/cSAH presented with spreading sensory symptoms. Intermittent focal slowing on electroencephalogram was present in the same area as SS/cSAH in 6 patients, but no epileptiform activity was found in any patients. Among those with available clinical follow-up (76/90 patients, 84%), ten patients with SS/cSAH (29%, median time from the scan for all patients with SS/cSAH: 21 months) had a symptomatic cerebral bleeding event on follow up (average time to events: 34 months) compared with only 1 event (2.4%, 25 months from the scan) in patients without SS/​cSAH (time to event: 25 months) (p = 0.001). The location of hemorrhages on follow-up scan was not in the same location of previously noted SS/cSAH in 9 of 10 patients. Follow-up imaging was obtained in 9 of 17 patients with cSAH and showed evidence of SS in the same location as initial cSAH in all these 9 cases. Conclusions: SS/cSAH is common in patients with suspected CAA without lobar intracerebral hemorrhage and may have a significantly higher risk of future cerebral bleeding events, regardless of the severity of the baseline CMB burden. The findings further highlight a precise anatomical correlation between TFNE and cSAH, but not SS. Distinct from transient ischemic attack or seizure, the majority of TFNE caused by SS/cSAH appear to present with spreading sensory symptoms.

Contribution of Convexal Subarachnoid Hemorrhage to Disease Progression in Cerebral Amyloid Angiopathy

Stroke ◽  
2015 ◽  
Vol 46 (6) ◽  
pp. 1533-1540 ◽  
Author(s):  
Markus Beitzke ◽  
Christian Enzinger ◽  
Gerit Wünsch ◽  
Martin Asslaber ◽  
Thomas Gattringer ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Disease Progression ◽  
Cerebral Amyloid Angiopathy ◽  
Amyloid Angiopathy ◽  
Cerebral Amyloid ◽  
Convexal Subarachnoid Hemorrhage

scholarly journals Evolution of DWI lesions in cerebral amyloid angiopathy

Neurology ◽  
2017 ◽  
Vol 89 (21) ◽  
pp. 2136-2142 ◽  
Author(s):  
Susanne J. van Veluw ◽  
Arne Lauer ◽  
Andreas Charidimou ◽  
Narimene Bounemia ◽  
Li Xiong ◽  
...  
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Small Vessel Disease ◽  
Hemorrhagic Transformation ◽  
Superficial Siderosis ◽  
Amyloid Angiopathy ◽  
Cross Sectional ◽  
Small Diffusion ◽  
Cerebral Amyloid ◽  
Cortical Superficial Siderosis

Objective:To address the pathophysiologic nature of small diffusion-weighted imaging (DWI) lesions in patients with cerebral amyloid angiopathy (CAA) who underwent serial MRI. Specifically, we tested (1) whether DWI lesions occurred preferentially in individuals with prior DWI lesions, (2) the cross-sectional association with chronic cortical cerebral microinfarcts (CMIs), and (3) the evolution of DWI lesions over time.Methods:Patients with probable CAA (n = 79) who underwent at least 2 MRI sessions were included. DWI lesions were assessed at each available time point. Lesion appearance and characteristics were assessed on available structural follow-up images. Presence and burden of other neuroimaging markers of small vessel disease (white matter hyperintensities, cerebral microbleeds, cortical superficial siderosis, and chronic cortical CMIs) were assessed as well.Results:Among 221 DWI scans (79 patients with 2 DWI scans; 40 with ≥3), 60 DWI lesions were found in 28 patients. Patients with DWI lesions at baseline were not more likely to have additional DWI lesions on follow-up compared to patients without DWI lesions at baseline. DWI lesions were associated with chronic cortical CMIs and cortical superficial siderosis, but not with other markers. For 39/60 DWI lesions, >1 MRI sequence was available at follow-up to determine lesion evolution. Twenty-four (62%) were demarcated as chronic lesions on follow-up MRI. Five appeared as cavitations, 18 as noncavitated infarcts, and 1 underwent hemorrhagic transformation.Conclusions:Based on their neuroimaging signature as well as their association with chronic cortical CMIs, DWI lesions appear to have an ischemic origin and represent one part of the CMI spectrum.

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