scholarly journals Diagnostic Utility of Amyloid PET in Cerebral Amyloid Angiopathy-Related Symptomatic Intracerebral Hemorrhage

2014 ◽  
Vol 34 (5) ◽  
pp. 753-758 ◽  
Author(s):  
Jean-Claude Baron ◽  
Karim Farid ◽  
Eamon Dolan ◽  
Guillaume Turc ◽  
Siva T Marrapu ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Cerebral Amyloid Angiopathy ◽  
Visual Analysis ◽  
Diagnostic Value ◽  
Amyloid Angiopathy ◽  
Amyloid Pet ◽  
Healthy Elderly ◽  
Symptomatic Intracerebral Hemorrhage ◽  
Significant Difference ◽  
Cerebral Amyloid

By detecting β-amyloid ( Aβ) in the wall of cortical arterioles, amyloid positron emission tomography (PET) imaging might help diagnose cerebral amyloid angiopathy (CAA) in patients with lobar intracerebral hemorrhage (I-ICH). No previous study has directly assessed the diagnostic value of 11-Pittsburgh compound B (PiB) PET in probable CAA-related I-ICH against healthy controls (HCs). 11C-PiB-PET and magnetic resonance imaging (MRI) including T2* were obtained in 11 nondemented patients fulfilling the Boston criteria for probable CAA-related symptomatic I-ICH (sl-ICH) and 20 HCs without cognitive complaints or impairment. After optimal spatial normalization, cerebral spinal fluid (CSF)-corrected PiB distribution volume ratios (DVRs) were obtained. There was no significant difference in whole cortex or regional DVRs between CAA patients and age-matched HCs. The whole cortex DVR was above the 95% confidence limit in 4/9 HCs and 10/11 CAA patients (sensitivity = 91%, specificity = 55%). Region/frontal or occipital ratios did not have better discriminative value. Similar but less accurate results were found using visual analysis. In patients with sl-ICH, 11C-PiB-PET has low specificity for CAA due to the frequent occurrence of high 11C-PiB uptake in the healthy elderly reflecting incipient Alzheimer's disease (AD), which might also be present in suspected CAA. However, a negative PiB scan rules out CAA with excellent sensitivity, which has clinical implications for prognostication and selection of candidates for drug trials.

Amyloid-PET in cerebral amyloid angiopathy

Neurology ◽  
2017 ◽  
Vol 89 (14) ◽  
pp. 1437-1438 ◽  
Author(s):  
Nicolas Raposo ◽  
Joshua A. Sonnen
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Amyloid Angiopathy ◽  
Amyloid Pet ◽  
Cerebral Amyloid

Clinical and neuropathologic analysis of intracerebral hemorrhage in patients with cerebral amyloid angiopathy

2019 ◽  
Vol 176 ◽  
pp. 110-115
Author(s):  
Taro Yanagawa ◽  
Masaki Takao ◽  
Masami Yasuda ◽  
Tomoya Kamide ◽  
Hiroki Sato ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Cerebral Amyloid Angiopathy ◽  
Amyloid Angiopathy ◽  
Cerebral Amyloid

Abstract 36: The Boston Criteria V2.0 for Cerebral Amyloid Angiopathy: Updated Criteria and Multicenter MRI-Neuropathology Validation

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Andreas Charidimou ◽  
Gregoire Boulouis ◽  
Matthew Frosch ◽  
Jean-Claude Baron ◽  
Marco Pasi ◽  
...  
Keyword(s):  
White Matter ◽  
Intracerebral Hemorrhage ◽  
Diagnostic Accuracy ◽  
Cerebral Amyloid Angiopathy ◽  
Brain Mri ◽  
Amyloid Angiopathy ◽  
Perivascular Spaces ◽  
Validation Sample ◽  
Temporal Validation ◽  
Cerebral Amyloid

Introduction: The Boston criteria are used worldwide for in vivo diagnosis of cerebral amyloid angiopathy (CAA). Given substantial advances in CAA research, we aimed to update the Boston criteria and externally validate their diagnostic accuracy across the spectrum of CAA-related presentations and across international sites. Methods: As part of an International CAA Association multicenter study, we identified patients age 50 or older with potential CAA-related clinical presentations (spontaneous intracerebral hemorrhage, cognitive impairment, or transient focal neurological episodes), available brain MRI, and histopathologic assessment for the diagnosis of CAA. We derived Boston criteria v2.0 by selecting MRI features to optimize diagnostic specificity and sensitivity in a pre-specified derivation sample (Boston cases 1994 to 2012, n=159), then externally validated in pre-specified temporal (Boston cases 2012-2018, n=59) and geographical (non-Boston cases 2004-2018; n=123) validation samples and compared their diagnostic accuracy to the currently used modified Boston criteria. Results: Based on exploratory analyses in the derivation sample, we derived provisional criteria for probable CAA requiring presence of at least 2 strictly lobar hemorrhagic lesions (intracerebral hemorrhage, cerebral microbleed, or cortical superficial siderosis focus) or at least 1 strictly lobar hemorrhagic lesion and 1 white matter characteristic (severe degree of visible perivascular spaces in centrum semiovale or white matter hyperintensities multispot pattern). Sensitivity/specificity of the criteria were 74.8/84.6% in the derivation sample, 92.5/89.5% in the temporal validation sample, 80.2/81.5% in the geographic validation sample, and 74.5/95.0% in cases across all samples with autopsy as the diagnostic gold standard. The v2.0 criteria for probable CAA had superior accuracy to the currently modified Boston criteria (p<0.005) in the autopsied cases. Conclusion: The Boston criteria v.2.0 incorporate emerging MRI markers of CAA to enhance sensitivity without compromising their high specificity. Validation of the criteria across independent patient settings firmly supports their adoption into clinical practice and research.

Abstract WP397: Longitudinal Sex Differences in Cerebral Amyloid Angiopathy

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Michael Maniskas ◽  
Jacob Hudobenko ◽  
Akhiko Urayama ◽  
Louise McCullough ◽  
Bharti Manwani
Keyword(s):  
Mouse Model ◽  
Cerebral Amyloid Angiopathy ◽  
Cognitive Deficits ◽  
Elderly Women ◽  
Amyloid Plaque ◽  
Amyloid Angiopathy ◽  
Female Mice ◽  
Plaque Deposition ◽  
Significant Difference ◽  
Cerebral Amyloid

Background: Cerebral amyloid angiopathy (CAA) is the most common cause of lobar intracerebral hemorrhage in the aging population. It is mostly a consequence of amyloid beta40 (Aβ40) deposition within the cerebral blood vessels. A recent study has shown that this amyloid plaque deposition is more prevalent in the brain of elderly women compared to men. The increase in amyloid plaque deposition is linked to increased cerebral microbleeds (CMBs) and reduced cognition. The major objective of this study to discern if a sexual dichotomy existed in CMBs and cognition using mouse model of CAA. Methods: We used the Tg-SwDI mouse (“CAA mouse”, harboring Swedish, Dutch, and Iowa mutations of human amyloid precursor protein) model that develops Aβ deposits and cognitive deficits at 3-4 months. Cognitive deficits were analyzed using Fear Conditioning (FC) in pre-symptomatic (3 month) and (12 month) old male and female mice. Briefly, mice were acclimated to the FC chamber for a 2 minute training trial to record baseline. After 1 hour rest, mice were placed back in the chamber for 2 minutes, where they received a 2 millisecond shock (1,000 u/amp). Day 2, activity was recorded for 3 minutes and this measure was compared to baseline to determine Mean Inactive State (MIS-seconds). Mice were euthanized following FC, and brains scanned ex vivo using a MRI T2 Star sequence to assess for CMBs. Results: FC showed a significant difference in MIS (p<0.05) between male (3 and 12 months old) and female (3 months only) mice, n=6/group, suggesting that aged females had significantly lower MIS (Figure 1). MRI showed that aged female mice had more CMBs compared to aged male mice (females, 15.3±7 vs. males 0.25 ±0.2, n= 3/group, p=0.05. Conclusion: In a mouse model of CAA, our results demonstrate that aged females have increased CMBs as compared to males, which may be contributing to decreased cognition as seen on FC. Ongoing studies are designed to further understand the etiology of this sex difference.

Subacute Cognitive Decline in an 86-Year-Old Woman With Prior Lobar Intracerebral Hemorrhage

2021 ◽  
pp. 192-194
Author(s):  
Stephen W. English ◽  
James P. Klaas
Keyword(s):  
Intracerebral Hemorrhage ◽  
Cognitive Decline ◽  
Temporal Lobe ◽  
Cerebral Amyloid Angiopathy ◽  
Mass Effect ◽  
Amyloid Angiopathy ◽  
Left Temporal Lobe ◽  
Epileptiform Discharges ◽  
Cerebral Amyloid ◽  
T2 Hyperintensity

An 86-year-old woman with a history of hypertension, hyperlipidemia, coronary artery disease, and hypothyroidism sought care for subacute, progressive cognitive decline. Five months earlier, she was hospitalized for a small, left temporal, lobar, intracerebral hemorrhage with associated receptive aphasia. Over the next several months, she had a precipitous cognitive decline. She was prescribed memantine by her primary physician because of concern for dementia. One month before seeking care, she was found unconscious in her bathroom, which was believed to be an unwitnessed seizure. Brain magnetic resonance imaging 1 month before the current evaluation showed a prior, small, left temporal hemorrhage and diffuse lobar microhemorrhages on gradient echo imaging, focal leptomeningeal gadolinium enhancement in the left temporal lobe, and multifocal T2 hyperintensity with mass effect, maximal in the left temporal lobe. Electroencephalography showed multifocal, independent epileptiform discharges. She underwent open biopsy of the left temporal lobe, which indicated focal granulomatous inflammation causing vascular destruction, with β‎-amyloid plaques within the cortical and leptomeningeal vessels. The findings were consistent with a diagnosis of amyloid-β‎-related angiitis in the setting of severe cerebral amyloid angiopathy. Because of concern for subclinical seizures and epileptiform discharges on electroencephalography, the patient was started on levetiracetam without substantial change in her mental status. After the biopsy findings demonstrated inflammatory changes consistent with amyloid-β‎-related angiitis, she was started on intravenous methylprednisolone, followed by transition to prednisone. After 6 months of treatment, she had significant clinical and radiographic improvement. Follow-up magnetic resonance imaging at that time showed interval improvement in the T2 hyperintensity and mass effect in the left temporal lobe. She was again independent with her activities of daily living, and memantine was discontinued. Cerebral amyloid angiopathy encompasses a heterogeneous group of diseases characterized by amyloid-β‎ peptide deposition. The most common clinical manifestation of cerebral amyloid angiopathy is lobar intracerebral hemorrhage, which can be multifocal and recurrent but can also result in cerebral ischemia and ischemic leukoencephalopathy.

scholarly journals Risk of Intracerebral Hemorrhage and Mortality After Convexity Subarachnoid Hemorrhage in Cerebral Amyloid Angiopathy

Stroke ◽  
2019 ◽  
Vol 50 (9) ◽  
pp. 2562-2564 ◽  
Author(s):  
Lionel Calviere ◽  
Alain Viguier ◽  
Sofia Patsoura ◽  
Vanessa Rousseau ◽  
Jean-François Albucher ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Intracerebral Hemorrhage ◽  
Cerebral Amyloid Angiopathy ◽  
Amyloid Angiopathy ◽  
Cerebral Amyloid

scholarly journals Clinical and radiological differences between patients with probable cerebral amyloid angiopathy and mixed cerebral microbleeds

2020 ◽  
Vol 267 (12) ◽  
pp. 3602-3608 ◽  
Author(s):  
Ulf R. Jensen-Kondering ◽  
Caroline Weiler ◽  
Patrick Langguth ◽  
Naomi Larsen ◽  
Charlotte Flüh ◽  
...  
Keyword(s):  
Cerebral Amyloid Angiopathy ◽  
Cerebral Microbleeds ◽  
Superficial Siderosis ◽  
Periventricular White Matter ◽  
Amyloid Angiopathy ◽  
Imaging Features ◽  
Significant Difference ◽  
Comprehensive Comparison ◽  
Cerebral Amyloid ◽  
Cortical Superficial Siderosis

Abstract Background The key imaging features of cerebral amyloid angiopathy (CAA) are lobar, cortical, or cortico-subcortical microbleeds, macrohaemorrhages and cortical superficial siderosis (cSS). In contrast, hypertensive angiopathy is characterized by (micro) haemorrhages in the basal ganglia, thalami, periventricular white matter or the brain stem. Another distinct form of haemorrhagic microangiopathy is mixed cerebral microbleeds (mixed CMB) with features of both CAA and hypertensive angiopathy. The distinction between the two entities (CAA and mixed CMB) is clinically relevant because the risk of haemorrhage and stroke should be well balanced if oral anticoagulation is indicated in CAA patients. We aimed to comprehensively compare these two entities. Methods Patients with probable CAA according to the modified Boston criteria and mixed CMB without macrohaemorrhage were retrospectively identified from our database. Comprehensive comparison regarding clinical and radiological parameters was performed between the two cohorts. Results Patients with CAA were older (78 ± 8 vs. 74 ± 9 years, p = 0.036) and had a higher prevalence of cSS (19% vs. 4%, p = 0.027) but a lower prevalence of lacunes (73% vs. 50%, p = 0.018) and deep lacunes (23% vs. 51%, p = 0.0003) compared to patients with mixed CMB. Logistic regression revealed an association between the presence of deep lacunes and mixed CMB. The other collected parameters did not reveal a significant difference between the two groups. Conclusions CAA and mixed CMB demonstrate radiological differences in the absence of macrohaemorrhages. However, more clinically available biomarkers are needed to elucidate the contribution of CAA and hypertensive angiopathy in mixed CMB patients.

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