scholarly journals Subarachnoid and Subdural Hemorrhages in Lobar Intracerebral Hemorrhage Associated With Cerebral Amyloid Angiopathy

Stroke ◽  
2019 ◽  
Vol 50 (6) ◽  
pp. 1567-1569 ◽  
Author(s):  
Alain Viguier ◽  
Nicolas Raposo ◽  
Sofia Patsoura ◽  
Lionel Calviere ◽  
Jean François Albucher ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Cerebral Amyloid Angiopathy ◽  
Amyloid Angiopathy ◽  
Subdural Hemorrhages ◽  
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.

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 Cognitive Impairment Before Intracerebral Hemorrhage Is Associated With Cerebral Amyloid Angiopathy

Stroke ◽  
2018 ◽  
Vol 49 (1) ◽  
pp. 40-45 ◽  
Author(s):  
Gargi Banerjee ◽  
Duncan Wilson ◽  
Gareth Ambler ◽  
Karen Osei-Bonsu Appiah ◽  
Clare Shakeshaft ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Intracerebral Hemorrhage ◽  
Cerebral Amyloid Angiopathy ◽  
Amyloid Angiopathy ◽  
Cerebral Amyloid

Clinical features of non-hypertensive lobar intracerebral hemorrhage related to cerebral amyloid angiopathy

2010 ◽  
Vol 17 (6) ◽  
pp. 823-829 ◽  
Author(s):  
M. Hirohata ◽  
M. Yoshita ◽  
C. Ishida ◽  
S. I. Ikeda ◽  
A. Tamaoka ◽  
...  
Keyword(s):  
Intracerebral Hemorrhage ◽  
Clinical Features ◽  
Cerebral Amyloid Angiopathy ◽  
Amyloid Angiopathy ◽  
Cerebral Amyloid
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