Artikel
Finding the reason for atypical intracerebral haemorrhage: clinical and radiological differences between patients with probable cerebral amyloid angiopathy and mixed location haemorrhage
Ursachenfindung bei atypischer intracerebraler Blutung – klinische und radiologische Unterscheidung zwischen cerebraler Amyloidangiopathie und gemischt-lokalisierten atypischen Hirnblutungen
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Autoren
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Charlotte Flüh
- University Hospital of Schleswig-Holstein, Campus Kiel, Department of Neurosurgery, Kiel, Deutschland
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Ulf Jensen-Kondering
- University Hospital of Schleswig-Holstein, Campus Kiel, Department of Radiology and Neuroradiology, Kiel, Deutschland
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Caroline Weiler
- University Hospital of Schleswig-Holstein, Campus Kiel, Department of Neurology, Kiel, Deutschland
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Gregor Kuhlenbäumer
- University Hospital of Schleswig-Holstein, Campus Kiel, Department of Neurology, Kiel, Deutschland
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Daniela Berg
- University Hospital of Schleswig-Holstein, Campus Kiel, Department of Neurology, Kiel, Deutschland
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Olav Jansen
- University Hospital of Schleswig-Holstein, Campus Kiel, Department of Radiology and Neuroradiology, Kiel, Deutschland
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Nils Margraf
- University Hospital of Schleswig-Holstein, Campus Kiel, Department of Neurology, Kiel, Deutschland
| Veröffentlicht: | 4. Juni 2021 |
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Gliederung
Text
Objective: 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. Patients regularly present to neurosurgical and neurological departments with atypical hemorrhages, but clinical differentiation between both entities is often difficult. The distinction between the two entities (CAA and mixed CMB) is clinically relevant because the risk of relevant 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, who presented to the neurovascular service between 2014 and 2019, were retrospectively identified from our database. Comprehensive comparison regarding clinical and radiological parameters was performed between the two cohorts.
Results: 96 patients were included into the study. 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.
Conclusion: CAA and mixed CMB demonstrate radiological differences in the absence of macrohaemorrhages. Susceptibility-based sequences can be used to depict considerably more microbleeds and cortical siderosis compared to GRE T2* sequences. However, more clinically available biomarkers are needed to elucidate the contribution of CAA and hypertensive angiopathy in mixed CMB patients.
