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Clinical characteristics and outcome in expansive compared with steno-occlusive mural hematoma in spontaneous
Lukas Mayer-Suess1, Benjamin Dejakum1,2, Gudrun Ratzinger3
1Department of Neurology, Medical University of Innsbruck, Innsbruck, Austria.
Insights
Spontaneous cervical artery dissection (sCeAD) has two forms: steno-occlusive and expansive. While both can cause stroke, the expansive type shows delayed diagnosis and higher rates of aneurysm formation, though long-term outcomes are similar.
Area of Science:
- Neurology
- Vascular Imaging
- Stroke Research
Background:
- Spontaneous cervical artery dissection (sCeAD) is a leading cause of ischemic stroke in young adults.
- sCeAD presents with distinct vessel wall imaging phenotypes: steno-occlusive or expansive mural hematomas.
- The pathophysiological differences between these sCeAD phenotypes remain unclear.
Purpose of the Study:
- To compare clinical characteristics and long-term recurrence rates between expansive and steno-occlusive mural hematomas in acute sCeAD.
- To investigate potential differences in the underlying pathophysiology based on acute morphological presentation.
Main Methods:
- Retrospective analysis of MRI scans from the ReSect-study cohort of sCeAD patients.
- Patients were categorized into steno-occlusive (stenosis without expansion) or expansive (expansion without stenosis) hematoma groups.
- Exclusion of patients with mixed pathologies to ensure distinct group analysis.
Main Results:
- Of 221 patients, 84.6% had steno-occlusive and 15.4% had expansive hematomas.
- Expansive dissections had significantly longer diagnosis times (17.8 vs 7.8 days) and higher rates of preceding upper respiratory infection (26.5% vs 12.3%).
- While functional outcomes and recurrence rates were similar, expansive hematomas were associated with more residual aneurysms (41.2% vs 11.5%).
Conclusions:
- Clinical outcomes and recurrence rates do not necessitate differential treatment or follow-up based on acute sCeAD morphology.
- Current findings suggest no clear difference in acute aetiopathogenesis between steno-occlusive and expansive mural hematomas.
- Further mechanistic studies are required to understand potential pathomechanistic distinctions between sCeAD phenotypes.
Background:
Spontaneous cervical artery dissection (sCeAD) is one of the prime causes of ischemic stroke in young adults. Based on vessel wall imaging, steno-occlusive or expansive wall hematomas can be distinguished. It is unclear whether these two distinct morphological phenotypes reflect different pathophysiological processes.
Aim:
We aim to evaluate differences in clinical characteristics and long-term recurrence between patients with expansive and steno-occlusive mural wall hematoma in the acute phase.
Methods:
Participants of the ReSect-study, one of the largest single-center cohort studies with long-term follow-up of sCeAD patients, with sufficient magnetic resonance imaging (MRI) were included. All available MRI scans were retrospectively evaluated for patients dichotomized to two groups: (1) mural hematoma causing steno-occlusive pathologies without expansion of total vessel diameter (steno-occlusive hematoma), and (2) mural hematoma causing vessel diameter expansion without lumen stenosis (expansive hematoma). Patients with mixed steno-occlusive and expansive vessel pathologies were excluded from the analysis.
Results:
In total, 221 individuals were available for analysis. The pathognomonic vessel wall hematoma was steno-occlusive in 187 (84.6%) and expansive in 34 (15.4%). No difference was seen in patient demographics, clinical status at admission, laboratory parameters, family history, or the frequency of clinical stigmata for connective tissue disorders. Both patients with expansive and steno-occlusive mural hematoma had a high likelihood of suffering cerebral ischemia (64.7 vs 79.7). Still, time from symptom onset to diagnosis was significantly longer in those with expansive dissection (17.8 vs 7.8 days, p = 0.02). Those with expansive dissections were more likely to have upper respiratory infection within 4 weeks prior to dissection (26.5% vs 12.3%, p = 0.03). Upon follow-up, functional outcome was identical and groups did not differ in rate of sCeAD recurrence, but those with expansive mural hematoma at baseline more frequently had residual aneurysmal formation (41.2% vs 11.5%, p < 0.01).
Conclusions:
As cerebral ischemia was frequent in both, our clinical results do not advise for differential treatment or follow-up based on the acute morphological phenotype. There was no clear evidence of a different aetiopathogenesis between patients with steno-occlusive or expansive mural hematoma in the acute phase. More mechanistic approaches are needed to elucidate potential differences in pathomechanism between both entities.
Data Access:
Anonymized data not published within this article will be made available by request from any qualified investigator.
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