Abstract P429: Hospital Level Diagnostic Disparities of Cerebral Amyloid Angiopathy in the United States Nationwide Hospitalizations

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Urvish K Patel ◽  
Nandakumar Nagaraja
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
The United States ◽  
Cross Sectional Study ◽  
Teaching Hospitals ◽  
Amyloid Angiopathy ◽  
Urban Teaching ◽  
Hospital Level ◽  
Cross Sectional ◽  
Northeast Region ◽  
Cerebral Amyloid

Background/Objective: There is limited knowledge of the nationwide prevalence of cerebral amyloid angiopathy (CAA) diagnosis and disparity amongst US hospitalization. The aim of this study is to assess the prevalence of CAA diagnosis and identify hospital-level disparity in the CAA diagnosis amongst US hospitalizations. Methods: A cross-sectional study was performed using the National Inpatient Sample [2016-2017] for adult hospitalizations. We extracted a cohort of patients with a diagnosis of CAA using ICD 10 code. Age was categorized as <50 years, 50-59, 60-69, 70-79, and ≥80 years. Weighted analysis using chi-square and multivariable survey logistic regression was performed to identify the prevalence of CAA and evaluate the diagnostic disparity of CAA amongst USA hospitalization. Results: Out of total 60,609,519 US hospitalizations, 16040 (0.027%) had a diagnosis of CAA. Patients with CAA were of higher age 71-80 years (39.9% vs 16.4%), ≥81 years (36.4% vs 14.9%), men (48.1% vs 42.1%), white (71.5% vs 67.5%), and more likely admitted to urban-teaching hospitals (83.9% vs 66.0%), Northeast region hospitals (26.5% vs 18.8%), and hospitals with large bed-size (65.7% vs 51.2%) compared to patients without CAA (p<0.0001). On regression analysis, urban non-teaching (aOR 2.1; 95%CI 1.6-2.9; ref=rural), urban-teaching hospitals [5.4 (4.1-7.2); ref=rural], median size hospital [1.3 (1.1-1.5); ref=small], and large bed size hospitals [2.3 (2-2.7); ref=small] had higher odds of diagnosis of CAA. Compared to the Northeast region, Midwest [0.8 (0.7-0.97)] and South [0.7 (0.6-0.8)] region hospitals had lower odds of a diagnosis of CAA. Conclusion: CAA was present in 0.03% of hospitalized patients in 2016-17. It was more commonly diagnosed in urban teaching, urban non-teaching, large and medium bed size hospitals compared to rural and small bed size hospitals. Lack of awareness of CAA diagnosis in rural and small hospitals could be a potential factor for these disparities.

scholarly journals Cerebral amyloid angiopathy: a cross-sectional study in a single center in Northeastern Brazil

2020 ◽  
Vol 78 (5) ◽  
pp. 277-281
Author(s):  
Marx Lima de BARROS-ARAÚJO ◽  
Irapuá Ferreira RICARTE ◽  
Edward MONTALVERNE FILHO ◽  
Guilherme Marconi Guimarães Martins HOLANDA ◽  
Ícaro Araújo de SOUSA ◽  
...  
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Outpatient Service ◽  
Brain Magnetic Resonance Imaging ◽  
Tertiary Hospital ◽  
Cross Sectional Study ◽  
Northeastern Brazil ◽  
Amyloid Angiopathy ◽  
Cross Sectional ◽  
Age Related ◽  
Cerebral Amyloid

ABSTRACT Background: Cerebral amyloid angiopathy (CAA) is a cerebrovascular disorder caused by progressive deposition of β-amyloid peptides in the walls of small and medium-sized cortical and leptomeningeal vessels. Until today, the prevalence of CAA is unknown in our region. Objective: This study aims to analyze the prevalence of this entity in a specific elderly population in a tertiary hospital in Northeastern Brazil. Methods: A cross-sectional, retrospective study with the enrollment of patients aged 65 or older followed in the neurological outpatient service of the Universidade Federal do Piauí, Brazil, who underwent brain magnetic resonance imaging (MRI) from July 2016 to June 2018. Results: One hundred and seventy-four patients were enrolled, of whom 100 were women (57.4%) and 74, men (42.6%), aged from 65 to 91 years old (median age 73.27). Nine patients were excluded from the study due to unavailability of MRI sequences needed for an appropriate analysis. Out of the 165 remaining patients, 12 (7.2%) had established the diagnosis of CAA, according to the modified Boston criteria. Conclusion: The prevalence of CAA in our study was like those of medical literature, with a progressive age-related increase.

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 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 Plasma Amyloid-Beta Levels in a Pre-Symptomatic Dutch-Type Hereditary Cerebral Amyloid Angiopathy Pedigree: A Cross-Sectional and Longitudinal Investigation

2021 ◽  
Vol 22 (6) ◽  
pp. 2931
Author(s):  
Pratishtha Chatterjee ◽  
Michelle Tegg ◽  
Steve Pedrini ◽  
Anne M. Fagan ◽  
Chengjie Xiong ◽  
...  
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Amyloid Beta ◽  
Single Molecule ◽  
Amyloid Angiopathy ◽  
Longitudinal Analyses ◽  
Cross Sectional ◽  
Cerebral Amyloid ◽  
Using Data ◽  
Larger Sample

Plasma amyloid-beta (Aβ) has long been investigated as a blood biomarker candidate for Cerebral Amyloid Angiopathy (CAA), however previous findings have been inconsistent which could be attributed to the use of less sensitive assays. This study investigates plasma Aβ alterations between pre-symptomatic Dutch-type hereditary CAA (D-CAA) mutation-carriers (MC) and non-carriers (NC) using two Aβ measurement platforms. Seventeen pre-symptomatic members of a D-CAA pedigree were assembled and followed up 3–4 years later (NC = 8; MC = 9). Plasma Aβ1-40 and Aβ1-42 were cross-sectionally and longitudinally analysed at baseline (T1) and follow-up (T2) and were found to be lower in MCs compared to NCs, cross-sectionally after adjusting for covariates, at both T1(Aβ1-40: p = 0.001; Aβ1-42: p = 0.0004) and T2 (Aβ1-40: p = 0.001; Aβ1-42: p = 0.016) employing the Single Molecule Array (Simoa) platform, however no significant differences were observed using the xMAP platform. Further, pairwise longitudinal analyses of plasma Aβ1-40 revealed decreased levels in MCs using data from the Simoa platform (p = 0.041) and pairwise longitudinal analyses of plasma Aβ1-42 revealed decreased levels in MCs using data from the xMAP platform (p = 0.041). Findings from the Simoa platform suggest that plasma Aβ may add value to a panel of biomarkers for the diagnosis of pre-symptomatic CAA, however, further validation studies in larger sample sets are required.

scholarly journals Cross-sectional and longitudinal differences in peak skeletonized white matter mean diffusivity in cerebral amyloid angiopathy

2020 ◽  
Vol 27 ◽  
pp. 102280
Author(s):  
Cheryl R. McCreary ◽  
Andrew E. Beaudin ◽  
Arsenije Subotic ◽  
Angela M. Zwiers ◽  
Ana Alvarez ◽  
...  
Keyword(s):  
White Matter ◽  
Cerebral Amyloid Angiopathy ◽  
Mean Diffusivity ◽  
Amyloid Angiopathy ◽  
Cross Sectional ◽  
Cerebral Amyloid

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.

Does a Graduate Course in Fluency Disorders Make a Difference?

2010 ◽  
Vol 20 (1) ◽  
pp. 10-14 ◽  
Author(s):  
Evelyn R. Klein ◽  
Barbara J. Amster
Keyword(s):  
Undergraduate Students ◽  
Graduate Programs ◽  
The United States ◽  
Cross Sectional Study ◽  
Sectional Study ◽  
Graduate Course ◽  
Cross Sectional ◽  
Fluency Disorders ◽  
Introductory Course ◽  
Communicative Disorders

Abstract A study by Yaruss and Quesal (2002), based on responses from 134 of 239 ASHA accredited graduate programs, indicated that approximately 25% of graduate programs in the United States allow students to earn their degree without having coursework in fluency disorders and 66% of programs allow students to graduate without clinical experience treating people who stutter (PWS). It is not surprising that many clinicians report discomfort in treating PWS. This cross-sectional study compares differences in beliefs about the cause of stuttering between freshman undergraduate students enrolled in an introductory course in communicative disorders and graduate students enrolled and in the final weeks of a graduate course in fluency disorders.

EVALUATION OF THE UNITED KINGDOM NATIONAL EXTERNAL QUALITY ASSESSMENT SERVICE 2008 (UK NEQAS 2008) GUIDELINES FOR THE DIAGNOSIS OF SUBARACHNOID HEMORRHAGE USING SPECTROPHOTOMETRIC XANTHOCHROMIA: A RETROSPECTIVE STUDY

2009 ◽  
Vol 32 (6S) ◽  
pp. 5
Author(s):  
A Gangloff ◽  
L Nadeau
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Amyloid Angiopathy ◽  
Viral Encephalitis ◽  
Objective Evaluation ◽  
Final Diagnosis ◽  
Amyloid Angiopathy ◽  
The United Kingdom ◽  
Cerebral Amyloid ◽  
The One ◽  
The Uk

Objective: Evaluation of the UK NEQAS 2008 guidelines for the interpretation of spectrophotometric xanthochromia. Method: A search of the laboratory database for all the xanthochromia test results between May 1st 2008 and May 1st 2009 was performed. Medical charts were reviewed for patients of Hôpital de l’Enfant-Jésus (HEJ) that had at least one detectable pigment (bilirubin, oxyhemoglobin, or methemoglobin). Xanthochromia results obtained with 4 different criteria (Chalmers original, Modified Chalmers, Duiser and UK NEQAS 2008) were compared. Results: We reviewed 41 medical charts (2 patients with duplicate lumbar punctures (LP) for a total of 43 LP). For these 41 patients there were 11 positive xanthochromia results, 5 of which were in concordance with a final diagnosis of subarachnoid hemorrhage (SAH). The diagnosis of the 6 other positive xanthochromia results were as follow: meningeal spread of a lymphoma, cerebral amyloid angiopathy, exertional headache, viral encephalitis with a possibility of petechiaes on the cerebral CT and second LP. Interpretation (negative/positive) of 40/43 LP was identical for the 4 methods. 2 LP were positive with Duiser and UK NEQAS 2008 but negative with Chalmers approaches (final diagnosis: SAH and cerebral amyloid angiopathy). 1 LP was positive only by the Duiser method (viral encephalitis). Conclusions: UK NEQAS 2008 guidelines identified all SAH but are sensitive to traumatic and pathologic meningeal lesions. Except for a case of viral encephalitis with a suspicion of cerebral petechiaes on CT, UK NEQAS 2008 gave xanthochromia results similar to the one in use at HEJ (Duiser). Chalmers original and Modified Chalmers methods missed one of the five SAH.

Cerebral Amyloid Angiopathy in Combination with Paroxysmal Atrial Fibrillation

2020 ◽  
Vol 25 (4) ◽  
pp. 31-37
Author(s):  
A. A. Kornilova ◽  
O. V. Lagoda ◽  
M. M. Tanashyan
Keyword(s):  
Atrial Fibrillation ◽  
Cerebral Amyloid Angiopathy ◽  
Paroxysmal Atrial Fibrillation ◽  
Past History ◽  
Laboratory Data ◽  
Clinical Manifestations ◽  
Cerebral Haemorrhage ◽  
Exclusion Criterion ◽  
Amyloid Angiopathy ◽  
Cerebral Amyloid

The present article addresses the definition of cerebral amyloid angiopathy (CAA) and its symptoms based on the analysis of the medical case; the issues of diagnosis and treatment of this pathology are discussed. The Boston criteria, which became the basis for diagnosis, study of clinical manifestations and progression of CAA and approaches to its therapy, are presented. Methods and modes of neuroimaging, including magnetic resonance imaging (MRI), which verify micro cerebral haemorrhage, are described. At the same time, the role and significance of cardiac arrhythmias in the genesis of ischemic stroke are discussed, and scales for assessing the risk of its occurrence are presented. The observation of the neurological, somatic, neuroimaging, neuropsychological status of a 62-year-old patient confirms quite rare combination of probable CAA, paroxysmal atrial fibrillation and repeated hemorrhagic functional apoplexy (FA). The relevance of the case described, is a complex clinical dilemma based on mutually exclusive recommendations for the pharmacological correction of such conditions. It is emphasized that in many multicenter clinical studies on the effectiveness of antithrombotic medication (antiaggregants, anticoagulants) in the treatment and prevention of ischaemic functional apoplexy , an important exclusion criterion is a hemorrhagic stroke in past history (including the multiple changes in haemostasis indicators). Taking into account the obtained clinical and laboratory data in the dynamics, the tactics of treating the described patient were determined. The results of studies related to the treatment of comorbid pathology that should become the subject of the development of a personalized algorithm for managing patients in each specific case, are discussed.

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