ArticleActa neurochirurgica2024
Clinical and radiologic distinctions between familial cavernous malformation syndrome and cerebral amyloid angiopathy.
Article in Acta neurochirurgica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
purposeFamilial cerebral cavernous malformation syndrome (FCCM) is characterized by multiple hemorrhagic lesions and is sometimes mistaken for cerebral amyloid angiopathy (CAA).
methodsWe compared clinical and radiologic characteristics in patients with definite (N = 32) and presumed FCCM (n = 76) to patients with definite (N = 29) and probable CAA (N = 21).
resultsPatients with CAA were older (78.6 years CAA vs. 43.4 FCCM; p < 0.0001), had cognitive complaints (66.0% CAA vs. 8.3% FCCM; p < 0.0001), and less likely to have a family history (4.0% CAA vs. 50.9% FCCM; p < 0.0001). FCCM patients were more likely to have at least 1 Zabramski type 2 lesion (0 CAA vs. 79.6% FCCM; p < 0.0001). Presence of any subcortical white matter hemorrhagic lesion (23.0% CAA vs. 99.1% FCCM; p < 0.0001), a lesion in either the basal ganglia, internal capsule or cerebellum (28.0% CAA vs 79.6% FCCM; p < 0.0001) and a subcortical white matter to cortical ribbon distribution of hemorrhagic lesions ≥ 1.0 was predictive of FCCM (6.0% CAA vs 83.9% FCCM; p < 0.0001). CAA patients more commonly had white matter disease, sulcal subarachnoid hemorrhage, and severely enlarged perivascular spaces in the centrum. However, none of the latter features were unique to CAA. FCCM patients meeting Boston 2.0 criteria for CAA (n = 14) had additional factors that helped distinguish them from CAA.
conclusionsPatients with FCCM can be reliably distinguished from CAA by accurately applying the Boston 2.0 criteria, assessing hemorrhagic lesion distribution and types, and assessing for clinical features unique to FCCM. FCCM criteria are proposed. The frequent finding of leukoaraiosis and enlarged perivascular spaces in the centrum semiovale in FCCM patients deserves further investigation.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.