scholarly journals Advances in cerebral amyloid angiopathy imaging

2019 ◽  
Vol 12 ◽  
pp. 175628641984411 ◽  
Author(s):  
Szu-Ju Chen ◽  
Hsin-Hsi Tsai ◽  
Li-Kai Tsai ◽  
Sung-Chun Tang ◽  
Bo-Chin Lee ◽  
...  
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Small Vessel Disease ◽  
Imaging Techniques ◽  
White Matter Hyperintensity ◽  
Superficial Siderosis ◽  
Clinical Aspects ◽  
Amyloid Angiopathy ◽  
Perivascular Spaces ◽  
Imaging Studies ◽  
Cerebral Amyloid

Cerebral amyloid angiopathy (CAA) is a cerebral small vessel disease caused by β -amyloid (Aβ) deposition at the leptomeningeal vessel walls. It is a common cause of spontaneous intracerebral hemorrhage and a frequent comorbidity in Alzheimer’s disease. The high recurrent hemorrhage rate in CAA makes it very important to recognize this disease to avoid potential harmful medication. Imaging studies play an important role in diagnosis and research of CAA. Conventional computed tomography and magnetic resonance imaging (MRI) methods reveal anatomical alterations, and remains as the most reliable tool in identifying CAA according to modified Boston criteria. The vascular injuries of CAA result in both hemorrhagic and ischemic manifestations and related structural changes on MRI, including cerebral microbleeds, cortical superficial siderosis, white matter hyperintensity, MRI-visible perivascular spaces, and cortical microinfarcts. As imaging techniques advance, not only does the resolution of conventional imaging improve, but novel skills in functional and molecular imaging studies also enable in vivo analysis of vessel physiological changes and underlying pathology. These modern tools help in early detection of CAA and may potentially serve as sensitive outcome markers in future clinical trials. In this article, we reviewed past studies of CAA focusing on utilization of various conventional and novel imaging techniques in both research and clinical aspects.

Hypertensive Arteriopathy and Cerebral Amyloid Angiopathy in Patients with Cognitive Decline and Mixed Cerebral Microbleeds

2020 ◽  
Vol 78 (4) ◽  
pp. 1765-1774
Author(s):  
Yuichiro Ii ◽  
Hidehiro Ishikawa ◽  
Hirofumi Matsuyama ◽  
Akihiro Shindo ◽  
Keita Matsuura ◽  
...  
Keyword(s):  
White Matter ◽  
Cerebral Amyloid Angiopathy ◽  
Small Vessel Disease ◽  
Cerebral Microbleeds ◽  
White Matter Hyperintensity ◽  
Superficial Siderosis ◽  
Amyloid Angiopathy ◽  
Age Related ◽  
Cerebral Amyloid ◽  
Occipital Lobes

Background: Hypertensive arteriopathy (HA) and cerebral amyloid angiopathy (CAA) may contribute to the development of mixed cerebral microbleeds (CMBs). Recently, the total small vessel disease (SVD) scores for HA and CAA were proposed, which are determined by a combination of MRI markers to reflect overall severity of these microangiopathies. Objective: We investigated whether or not total HA-SVD and CAA-SVD scores could be used to predict overlap of HA and CAA in patients with mixed CMBs. Methods: Fifty-three subjects with mixed CMBs were retrospectively analyzed. MRI markers (CMBs, lacunes, perivascular space, white matter hyperintensity [WMH] and cortical superficial siderosis [cSS]) were assessed. The HA-SVD score and CAA-SVD score were obtained for each subject. Anterior or posterior WMH was also assessed using the age-related white matter changes scale. Results: The two scores were positively correlated (ρ= 0.449, p < 0.001). The prevalence of lobar dominant CMB distribution (p < 0.001) and lacunes in the centrum semiovale (p < 0.001) and the severity of WMH in the parieto-occipital lobes (p = 0.004) were significantly higher in the high CAA-SVD score group. cSS was found in four patients with high CAA-SVD score who showed lobar-dominant CMB distribution and severe posterior WMH. Conclusion: Mixed CMBs are mainly due to HA. Assessing both two scores may predict the overlap of HA and CAA in individuals with mixed CMBs. Patients with a high CAA-SVD score may have some degree of advanced CAA, especially when lobar predominant CMBs, severe posterior WMH, lobar lacunes, or cSS are observed.

scholarly journals Dementia incidence and predictors in cerebral amyloid angiopathy patients without intracerebral hemorrhage

2017 ◽  
Vol 38 (2) ◽  
pp. 241-249 ◽  
Author(s):  
Li Xiong ◽  
Gregoire Boulouis ◽  
Andreas Charidimou ◽  
Duangnapa Roongpiboonsopit ◽  
Michael J Jessel ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Cerebral Amyloid Angiopathy ◽  
Small Vessel Disease ◽  
Superficial Siderosis ◽  
Amyloid Angiopathy ◽  
Perivascular Spaces ◽  
Older Individuals ◽  
Cumulative Score ◽  
Dementia Incidence ◽  
Cerebral Amyloid

Cerebral amyloid angiopathy (CAA) is a common cause of cognitive impairment in older individuals. This study aimed to investigate predictors of dementia in CAA patients without intracerebral hemorrhage (ICH). A total of 158 non-demented patients from the Stroke Service or the Memory Clinic who met the modified Boston Criteria for probable CAA were included. At baseline, neuroimaging markers, including lobar microbleeds (cerebral microbleeds (CMBs)), white matter hyperintensities (WMH), cortical superficial siderosis (cSS), magnetic resonance imaging (MRI)-visible centrum semiovale perivascular spaces (CSO-PVS), lacunes, and medial temporal atrophy (MTA) were assessed. The overall burden of small vessel disease (SVD) for CAA was calculated by a cumulative score based on CMB number, WMH severity, cSS presence and extent and CSO-PVS severity. The estimated cumulative dementia incidence at 1 year was 14% (95% confidence interval (CI): 5%–23%), and 5 years 73% (95% CI: 55%, 84%). Age (hazard ratio (HR) 1.05 per year, 95% CI: 1.01–1.08, p = 0.007), presence of MCI status (HR 3.40, 95% CI: 1.97–6.92, p < 0.001), MTA (HR 1.71 per point, 95% CI: 1.26–2.32, p = 0.001), and SVD score (HR 1.23 per point, 95% CI: 1.20–1.48, p = 0.030) at baseline were independent predictors for dementia conversion in these patients. Cognitive deterioration of CAA patients appears attributable to cumulative changes, from both vasculopathic and neurodegenerative lesions.

scholarly journals Cerebral amyloid angiopathy severity is linked to dilation of juxtacortical perivascular spaces

2015 ◽  
Vol 36 (3) ◽  
pp. 576-580 ◽  
Author(s):  
Susanne J van Veluw ◽  
Geert Jan Biessels ◽  
Willem H Bouvy ◽  
Wim GM Spliet ◽  
Jaco JM Zwanenburg ◽  
...  
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Small Vessel Disease ◽  
Amyloid Β ◽  
Amyloid Angiopathy ◽  
Perivascular Spaces ◽  
Resonance Imaging ◽  
Centrum Semiovale ◽  
Tissue Sections ◽  
Cortical Areas ◽  
Cerebral Amyloid

Perivascular spaces are an emerging marker of small vessel disease. Perivascular spaces in the centrum semiovale have been associated with cerebral amyloid angiopathy. However, a direct topographical relationship between dilated perivascular spaces and cerebral amyloid angiopathy severity has not been established. We examined this association using post-mortem magnetic resonance imaging in five cases with evidence of cerebral amyloid angiopathy pathology. Juxtacortical perivascular spaces dilation was evaluated on T2 images and related to cerebral amyloid angiopathy severity in overlying cortical areas on 34 tissue sections stained for Amyloid β. Degree of perivascular spaces dilation was significantly associated with cerebral amyloid angiopathy severity (odds ratio = 3.3, 95% confidence interval 1.3–7.9, p = 0.011). Thus, dilated juxtacortical perivascular spaces are a promising neuroimaging marker of cerebral amyloid angiopathy severity.

scholarly journals Distribution of lacunes in cerebral amyloid angiopathy and hypertensive small vessel disease

Neurology ◽  
2017 ◽  
Vol 88 (23) ◽  
pp. 2162-2168 ◽  
Author(s):  
Marco Pasi ◽  
Gregoire Boulouis ◽  
Panagiotis Fotiadis ◽  
Eitan Auriel ◽  
Andreas Charidimou ◽  
...  
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Small Vessel Disease ◽  
Small Vessel ◽  
White Matter Hyperintensity ◽  
Amyloid Angiopathy ◽  
Vessel Disease ◽  
Close Relationship ◽  
Cerebral Amyloid ◽  
Highly Correlated ◽  
The Relationship

Objective:To evaluate whether the burden of deep and lobar lacunes differs between patients with intracerebral hemorrhage (ICH) with definite/probable cerebral amyloid angiopathy (CAA) per the Boston criteria and hypertensive small vessel disease (HTN-SVD; ICH in basal ganglia, thalami, brainstem).Methods:We defined lobar and deep lacunes similar to the topographic distribution used for ICH and cerebral microbleeds (CMBs). We then compared their distribution between patients with CAA-ICH and those with strictly deep CMB and ICH (HTN-ICH). The independent associations of lacune location with the diagnosis of CAA-ICH and HTN-ICH were evaluated with multivariable models. The relationship between lobar lacunes and white matter hyperintensity (WMH) volume was evaluated by means of partial correlation analyses adjusted for age and a validated visual scale.Results:In our final cohort of 316 patients with ICH, lacunes were frequent (24.7%), with similar rates in 191 patients with CAA and 125 with HTN-ICH (23% vs 27.2%, p = 0.4). Lobar lacunes were more commonly present in CAA (20.4% vs 5.7%, p < 0.001), while deep lacunes were more frequent in HTN-ICH (15.2% vs 2.1%, p < 0.001). After correction for demographics and clinical and neuroimaging markers of SVD, lobar lacunes were associated with CAA (p = 0.003) and deep lacunes with HTN-ICH (p < 0.001). Lobar lacunes in 80% of the cases were at least in contact with WMH, and after adjustment for age, they were highly correlated to WMH volume (r = 0.42, p < 0.001).Conclusions:Lobar lacunes are associated with CAA, whereas deep lacunes are more frequent in HTN-SVD. Lobar lacunes seem to have a close relationship with WMH, suggesting a possible common origin.

Abstract P442: The Association of Amyloid and Tau Burden With Centrum Semiovale Perivascular Spaces in Cerebral Amyloid Angiopathy

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Elif Gokcal ◽  
Alex A Becker ◽  
Mitchell J Horn ◽  
Alvin S Das ◽  
Kristin Schwab ◽  
...  
Keyword(s):  
Regression Model ◽  
Cerebral Amyloid Angiopathy ◽  
Structural Mri ◽  
Ordinal Regression ◽  
White Matter Hyperintensity ◽  
Amyloid Angiopathy ◽  
Perivascular Spaces ◽  
Centrum Semiovale ◽  
Ordinal Regression Model ◽  
Cerebral Amyloid

Background: The mechanisms linking cerebral amyloid angiopathy (CAA) to enlarged perivascular spaces in centrum semiovale (CSO-EPVS) and whether other Alzheimer’s Disease (AD) pathologies might affect CSO-EPVS are unclear. We hypothesized that amyloid but not tau load would independently correlate with CSO-EPVS in CAA. Methods: Fifty prospectively enrolled nondemented probable CAA patients underwent high-resolution structural MRI, Pittsburgh compound B (PiB, for amyloid), and 18 F-flortaucipir (FTP, for tau) PET imaging. Microbleeds (all lobar, LMB) were counted and white matter hyperintensity volume (WMH) was quantified. CSO-EPVS were counted on T 2 -MRI sequence and graded using a previously validated scale (range 0-4). A multivariate ordinal regression model was used to assess the independent associations between CSO-EPVS and mean cortical amyloid as well as tau deposition, after adjusting for relevant covariates. Results: Patients had a mean age of 69.3±7.2. Age, sex, presence of hypertension, intracerebral hemorrhage (ICH), LMB counts, and WMH were not associated with CSO-EPVS grades (p>0.2 for all comparisons). Higher PiB uptake significantly correlated with increased CSO-EPVS (rho=0.45, p=0.001). Higher FTP showed a trend for correlation with CSO-EPVS (rho=0.26, p=0.069). In an ordinal regression model with CSO-EPVS grade as the dependent variable and both amyloid and tau levels included as predictors along with covariates presented above, the association of CSO-EPVS remained significant with higher PiB uptake (β=3.97, 95%CI 1.1-6.8, p=0.007) but not with FTP uptake (p=0.167). Conclusion: Results of this study suggest that CSO-EPVS is independently associated with amyloid but not with tau deposition in CAA. CSO-EPVS was not associated with age or classical vascular risk factors or presence of ICH. Our results support the view that vascular amyloid but not other AD pathologies such as tau might contribute to EPVS in patients with CAA.

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.

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

Stroke ◽  
2014 ◽  
Vol 45 (10) ◽  
pp. 2930-2935 ◽  
Author(s):  
Andreas Charidimou ◽  
Rolf H. Jäger ◽  
Andre Peeters ◽  
Yves Vandermeeren ◽  
Patrice Laloux ◽  
...  
Keyword(s):  
White Matter ◽  
Cerebral Amyloid Angiopathy ◽  
Superficial Siderosis ◽  
Amyloid Angiopathy ◽  
Perivascular Spaces ◽  
Cerebral Amyloid ◽  
Cortical Superficial Siderosis

scholarly journals Stopping “transient ischemic attacks” by antiplatelet withdrawal

2021 ◽  
Vol 3 (1) ◽  
Author(s):  
Lina Palaiodimou ◽  
Aikaterini Theodorou ◽  
Stefanos Lachanis ◽  
George P. Paraskevas ◽  
Matilda Papathanasiou ◽  
...  
Keyword(s):  
Differential Diagnosis ◽  
Cerebral Amyloid Angiopathy ◽  
Brain Mri ◽  
Superficial Siderosis ◽  
Amyloid Angiopathy ◽  
Perivascular Spaces ◽  
The Past ◽  
Cerebral Amyloid ◽  
Ischemic Attack ◽  
Cortical Superficial Siderosis

Abstract Introduction Transient ischemic attack (TIA) is considered to be an important risk factor for the development of ischemic stroke and requires complete etiopathogenic evaluation and prompt initiation of secondary prevention treatment. In addition, an accurate differential diagnosis should be performed in order to exclude other disorders mimicking TIA. Methods In this case report, we describe the clinical and neuroimaging evaluation and the differential diagnosis of a patient with suspected crescendo TIAs. Results A 79-year-old man presented with recurrent episodes of right-sided numbness over the past 7 months, despite different single and dual antiplatelet therapies that were sequentially prescribed for suspected TIAs. Brain MRI revealed cortical superficial siderosis, symmetrical periventricular leukoencephalopathy and enlarged perivascular spaces. Cerebral amyloid angiopathy was considered in the differential diagnosis of the patient. Antiplatelet withdrawal was recommended and led to complete remission of the patient’s transient focal neurological episodes (TFNE) that were initially misdiagnosed as TIAs. Discussion Cortical superficial siderosis has been implicated as a key neuroimaging feature of cerebral amyloid angiopathy, a diagnosis which can be supported by the additional radiological findings of symmetrical white matter hyperintensities and enlarged perivascular spaces. Antiplatelet treatment in patients with cortical superficial siderosis may increase the frequency and severity of TFNE, while it increases exponentially the risk of intracerebral hemorrhage. The present case highlights that recognition of cortical superficial siderosis is crucial in the management of patients presenting with transient focal neurological symptoms that can be misdiagnosed as recurrent TIAs.

Abstract TP432: Predictors for Dementia Conversion in Cerebral Amyloid Angiopathy From a Stroke Unit

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Li Xiong ◽  
Raffaella Valenti ◽  
Andreas Charidimou ◽  
Gregoire Boulouis ◽  
Duangnapa Roongpiboonsopit ◽  
...  
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Stroke Unit ◽  
Cox Regression ◽  
Superficial Siderosis ◽  
P Value ◽  
Amyloid Angiopathy ◽  
Perivascular Spaces ◽  
Cox Regression Analysis ◽  
Cerebral Amyloid

Objective: Cerebral amyloid angiopathy (CAA) is increasing recognized as a cause of cognitive impairment and dementia in older individuals. This study aimed to investigate predictors of dementia, including imaging markers, in CAA patients from a stroke unit. Methods: A total of 71 non-demented patients from a stroke unit were included according to modified Boston Criteria for probable CAA with available cognitive follow up. These CAA patients included both patients with and patients without previous intracerebral hemorrhage (ICH). At baseline, neuroimaging markers, including lobar microbleeds (CMBs), white matter hyperintensities (WMH), cortical superficial siderosis (cSS) and MRI-visible centrum semiovale perivascular spaces (CSO-PVS) were assessed. The small vessel disease (SVD) score for CAA was calculated by the scores of CMBs, WMH, cSS and CSO-PVS. The association between these neuroimaging markers and dementia conversion was analyzed. Results: The median follow up time is 1.91 years (quartiles 1.14-4.23 years). Fourteen (19.72%) CAA patients developed dementia during follow up period. Thirty-seven CAA patients (52.11%) had previous symptomatic ICH. Age, lobar CMBs≥20 and SVD score were selected from the univariate Cox-regression analysis with p value less than 0.1 (Table1). In a backward stepwise multivariabte analysis including age, previous ICH history and either SVD score or number of CMBs, age and SVD score independently predicted dementia conversion (Table 1). The individual neuroimaging markers for SVD related brain damage (CSO-PVS, cSS, lobar MBs and WMH) did not predict dementia conversion for probable CAA patients. Conclusion: Our results demonstrate that cognitive deterioration of CAA patients appears attributed to cumulative CAA related vasculopathic changes.

scholarly journals Small vessel disease burden in cerebral amyloid angiopathy without symptomatic hemorrhage

Neurology ◽  
2017 ◽  
Vol 88 (9) ◽  
pp. 878-884 ◽  
Author(s):  
Gregoire Boulouis ◽  
Andreas Charidimou ◽  
Michael J. Jessel ◽  
Li Xiong ◽  
Duangnapa Roongpiboonsopit ◽  
...  
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Small Vessel Disease ◽  
Summary Score ◽  
Small Vessel ◽  
Amyloid Angiopathy ◽  
Perivascular Spaces ◽  
Cognitive Symptoms ◽  
Vessel Disease ◽  
Age Related ◽  
Cerebral Amyloid

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 = 205) or an outpatient memory clinic (n = 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 = 97) demonstrated a higher prevalence of cSS (p < 0.0001), higher WMH volumes (p = 0.03), and a trend toward higher CMB counts (p = 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 = 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.

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