Cerebral Amyloid Angiopathy and Transient Focal Neurological Episodes

Charidimou, Andreas; Werring, David J.

doi:10.1159/000353989

Cited by 8 publications

(11 citation statements)

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“…76 Instead, the presentation may be with transient focal neurological symptoms (TFNS) or 'amyloid spells'. 82 TFNS, especially manifesting with spreading paraesthesias, are more likely to occur when the cSAH is localised to the central sulcus, which is in close proximity to the primary motor and sensory cortices. visual symptoms) and negative (e.g.…”

Section: Radiotherapymentioning

confidence: 99%

“…visual symptoms) and negative (e.g. 82,85 It is imperative to make a distinction between TFNS and sensory transient ischaemic attacks, which may be instead included in the referral note, but will tend to only have negative symptoms without migration. 82 TFNS, especially manifesting with spreading paraesthesias, are more likely to occur when the cSAH is localised to the central sulcus, which is in close proximity to the primary motor and sensory cortices.…”

Section: Radiotherapymentioning

confidence: 99%

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Cerebral amyloid angiopathy: Review of clinico‐radiological features and mimics

et al. 2018

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Cerebral amyloid angiopathy (CAA) is an important cause of lobar intracerebral haemorrhage (ICH) in the elderly, but has other clinico-radiological manifestations. In the last two decades, certain magnetic resonance imaging (MRI) sequences, namely gradient-recalled echo imaging and the newer and more sensitive susceptibility-weighted imaging, have been utilised to detect susceptibility-sensitive lesions such as cerebral microbleeds and cortical superficial siderosis. These can be utilised sensitively and specifically by the Modified Boston Criteria to make a diagnosis of CAA without the need for 'gold-standard' histopathology from biopsy. However, recently, other promising MRI biomarkers of CAA have been described which may further increase precision of radiological diagnosis, namely chronic white matter ischaemia, cerebral microinfarcts and lobar lacunes, cortical atrophy, and increased dilated perivascular spaces in the centrum semiovale. However, the radiological manifestations of CAA, as well as their clinical correlates, may have other aetiologies and mimics. It is important for the radiologist to be aware of these clinico-radiological features and mimics to accurately diagnose CAA. This is increasingly important in a patient demographic that has a high prevalence for use of antiplatelet and antithrombotic medications for other comorbidities which inherently carries an increased risk of ICH in patients with CAA.

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Section: Radiotherapymentioning

confidence: 99%

Section: Radiotherapymentioning

confidence: 99%

Cerebral amyloid angiopathy: Review of clinico‐radiological features and mimics

et al. 2018

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“…Patients first presenting with TFNEs also had a higher total SVD summary score (mean 6 SD; 3.5 6 1.3 vs 2.9 6 1.2; p , 0.001) and this remained significant in an ordinal logistic regression, adjusting for age vascular risk factors (adjusted OR [2][3][4] in patients with cognitive symptoms and 3 [3][4] in those with TFNEs, both p , 0.001). 28 This was almost entirely driven by a higher number of CMBs (1 in ICH patients vs 5 [3][4][5][6][7][8][9][10][11][12][13] in patients with cognitive symptoms and 7 in those with TFNEs, p 5 0.001 and p , 0.001; see tables e-1 and e-2 and figure e-1 at Neurology.org for details). DISCUSSION We demonstrated that patients with probable CAA without symptomatic ICH first presenting with TFNEs bore a higher burden of quantifiable SVD-related damage compared to patients with probable CAA first evaluated for cognitive symptoms.…”

Section: Resultsmentioning

confidence: 99%

“…The 2 main outpatient settings through which patients with CAA without ICH come to medical attention are stroke services (where patients are commonly seen for transient focal neurologic episodes [TFNEs]) 9,10 and memory clinics (where patients are evaluated for cognitive symptoms or subjective cognitive complaints). 11 It has been shown that patients with CAA first seen for acute neurologic symptoms often develop recurrent symptoms and are at high risk of developing subsequent ICH, [12][13][14] while an association with higher risk of bleeding has not been described in memory clinic patients, who demonstrate cognitive decline over time.…”

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confidence: 99%

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Small vessel disease burden in cerebral amyloid angiopathy without symptomatic hemorrhage

et al. 2017

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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 5 205) or an outpatient memory clinic (n 5 442) 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 5 97) demonstrated a higher prevalence of cSS (p , 0.0001), higher WMH volumes (p 5 0.03), and a trend toward higher CMB counts (p 5 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 5 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. Neurology ® 2017;88:878-884 GLOSSARY BG 5 basal ganglia; CAA 5 cerebral amyloid angiopathy; CI 5 confidence interval; CMB 5 cerebral microbleed; CSO 5 centrum semiovale; cSS 5 cortical superficial siderosis; FLAIR 5 fluid-attenuated inversion recovery; ICH 5 intracerebral hemorrhage; IQR 5 interquartile range; OR 5 odds ratio; PVS 5 perivascular spaces; SVD 5 small vessel disease; TE 5 echo time; TFNE 5 transient focal neurologic episode; WMH 5 white matter hyperintensity.Sporadic cerebral amyloid angiopathy (CAA) is characterized by progressive deposition of b-amyloid in the walls of cortical and leptomeningeal small arteries, resulting in vessel dysfunction and brain parenchymal injury. CAA is common in older individuals and, when severe, can lead to devastating consequences including intracerebral hemorrhage (ICH) and dementia. 1,2While definite diagnosis relies on pathology, clinical and neuroimaging criteria (the Boston criteria) can reliably identify CAA in older patients with lobar hemorrhage.3,4 More recently, an updated version of these criteria has demonstrated that the presence of $2 lobar cerebral microbleeds (CMBs) in patients without large hemorrhage is specific for moderate to severe CAA pathology presence in older individuals seen in a h...

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