P1-109: LONGITUDINAL EVOLUTION OF CONNECTOPATHIES MEDIATED BY CEREBRAL MICROHEMORRHAGES IN CEREBRAL AMYLOID ANGIOPATHY VS. MILD TRAUMATIC BRAIN INJURY

2006 ◽  
Vol 14 (7S_Part_5) ◽  
pp. P313-P313
Author(s):  
Kenneth A. Rostowsky ◽  
Alexander S. Maher ◽  
Nahian F. Chowdhury ◽  
Andrei Irimia
2016 ◽  
Vol 159 (1) ◽  
pp. 19-19
Author(s):  
Yoichi Nakayama ◽  
Yohei Mineharu ◽  
Yoshiki Arakawa ◽  
Sei Nishida ◽  
Hirofumi Tsuji ◽  
...  

2016 ◽  
Vol 159 (1) ◽  
pp. 15-18 ◽  
Author(s):  
Yoichi Nakayama ◽  
Yohei Mineharu ◽  
Yoshiki Arawaka ◽  
Sei Nishida ◽  
Hirofumi Tsuji ◽  
...  

2021 ◽  
pp. 10.1212/CPJ.0000000000001055
Author(s):  
Mohamed Ridha ◽  
Yasmin Aziz ◽  
Joseph Broderick

A 67-year-old man was referred from ophthalmology for possible cerebral amyloid angiopathy (CAA) discovered during work-up of possible optic neuropathy. MRI (figure 1) demonstrated innumerable periventricular, brainstem, and cortical cerebral microhemorrhages (CMH). Scattered, non-specific white matter hyperintensities was seen on T2-weighted imaging without surrounding hypointense rim. He had no hypertension, and the distribution was uncharacteristic for CAA. Despite absent family history of stroke or seizure, testing for familial cerebral cavernous malformation (FCCM) identified a pathogenic mutation of KRIT1 (c.382G>T).


2021 ◽  
Vol 23 (2) ◽  
pp. 223-233
Author(s):  
Panagiotis Fotiadis ◽  
Marco Pasi ◽  
Andreas Charidimou ◽  
Andrew D. Warren ◽  
Kristin M. Schwab ◽  
...  

Background and Purpose Cerebral amyloid angiopathy (CAA) is a common pathology of the leptomeningeal and cortical small vessels associated with hemorrhagic and non-hemorrhagic brain injury. Given previous evidence for CAA-related loss of cortical thickness and white matter volume, we hypothesized that CAA might also cause tissue loss in the basal ganglia.Methods We compared basal ganglia volumes expressed as a percentage of total intracranial volume (pBGV) of non-demented patients with sporadic and hereditary CAA to age-matched healthy control (HC) and Alzheimer’s disease (AD) cohorts.Results Patients with sporadic CAA had lower pBGV (n=80, 1.16%±0.14%) compared to HC (n=80, 1.30%±0.13%, <i>P</i><0.0001) and AD patients (n=80, 1.23%±0.11%, <i>P</i>=0.001). Similarly, patients with hereditary CAA demonstrated lower pBGV (n=25, 1.26%±0.17%) compared to their matched HC (n=25, 1.36%±0.15%, <i>P</i>=0.036). Using a measurement of normalized basal ganglia width developed for analysis of clinical-grade magnetic resonance images, we found smaller basal ganglia width in patients with CAA-related lobar intracerebral hemorrhage (ICH; n=93, 12.35±1.47) compared to age-matched patients with hypertension-related deep ICH (n=93, 13.46±1.51, <i>P</i><0.0001) or HC (n=93, 15.45±1.22, <i>P</i><0.0001). Within the sporadic CAA research cohort, decreased basal ganglia volume was independently correlated with greater cortical gray matter atrophy (r=0.45, <i>P</i><0.0001), increased basal ganglia fractional anisotropy (r=–0.36, <i>P</i>=0.001), and worse performance on language processing (r=0.35, <i>P</i>=0.003), but not with cognitive tests of executive function or processing speed.Conclusions These findings suggest an independent effect of CAA on basal ganglia tissue loss, indicating a novel mechanism for CAA-related brain injury and neurologic dysfunction.


2019 ◽  
Vol 15 ◽  
pp. P48-P49
Author(s):  
Nelly Joseph-Mathurin ◽  
Richard J. Perrin ◽  
Nigel J. Cairns ◽  
Erin E. Franklin ◽  
Chengjie Xiong ◽  
...  

2019 ◽  
Vol 15 ◽  
pp. P1125-P1126
Author(s):  
Nelly Joseph-Mathurin ◽  
Richard J. Perrin ◽  
Nigel J. Cairns ◽  
Erin E. Franklin ◽  
Chengjie Xiong ◽  
...  

2015 ◽  
Vol 36 (1) ◽  
pp. 40-54 ◽  
Author(s):  
Yael D Reijmer ◽  
Susanne J van Veluw ◽  
Steven M Greenberg

Cerebral amyloid angiopathy (CAA) is a common form of cerebral small vessel disease and an important risk factor for intracerebral hemorrhage and cognitive impairment. While the majority of research has focused on the hemorrhagic manifestation of CAA, its ischemic manifestations appear to have substantial clinical relevance as well. Findings from imaging and pathologic studies indicate that ischemic lesions are common in CAA, including white-matter hyperintensities, microinfarcts, and microstructural tissue abnormalities as detected with diffusion tensor imaging. Furthermore, imaging markers of ischemic disease show a robust association with cognition, independent of age, hemorrhagic lesions, and traditional vascular risk factors. Widespread ischemic tissue injury may affect cognition by disrupting white-matter connectivity, thereby hampering communication between brain regions. Challenges are to identify imaging markers that are able to capture widespread microvascular lesion burden in vivo and to further unravel the etiology of ischemic tissue injury by linking structural magnetic resonance imaging (MRI) abnormalities to their underlying pathophysiology and histopathology. A better understanding of the underlying mechanisms of ischemic brain injury in CAA will be a key step toward new interventions to improve long-term cognitive outcomes for patients with CAA.


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