Article
Intracranial dissecting aneurysms – clinical parameters shed light on a distinct pathophysiology
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Authors
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Martin N. Stienen
- Department of Neurosurgery, University Hospital Geneva, Geneva, Switzerland
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Vitor Mendes Pereira
- Division of Neuroradiology, Department of Medical Imaging, and Division of Neurosurgery, Department of Surgery, Toronto Western Hospital, University Health Network, Toronto, Ontario
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Karl Schaller
- Department of Neurosurgery, University Hospital Geneva, Geneva, Switzerland
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Philippe Bijlenga
- Department of Neurosurgery, University Hospital Geneva, Geneva, Switzerland
| Published: | June 2, 2015 |
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Outline
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Objective: Spontaneous intracranial artery dissection (IAD) is an uncommon cause of ischemic stroke, subarachnoid hemorrhage, headache, and/or focal neurological deficit caused by mass effect. It is defined by the occurrence of a hematoma in the wall of an intracranial artery. Given the small size of intracranial arteries, the diagnosis of characteristic imaging features is challenging, which leads to under diagnosing of IAD. Pathophysiological insights as well as clinical / therapeutical implications of IAD are thus limited.
Method: Retrospective analysis of all patients with diagnosis of IAD that were entered into the prospective @neurIST study (Bijlenga P et al., Stroke 2013;44:3018-26). Characteristics of patients with IAD were compared to a) a healthy control population (n=213) and b) a control population with saccular intracranial aneurysms (n=931) from the @neurIST study.
Results: A total of 17 patients with IAD (12 ruptured / 5 unruptured) were identified. Patients with IAD had a median age of 54 years and the majority was male (58%). When compared to healthy volunteers, risk factors for IAD were smoking (OR 3.8; 95% CI 1.2-12.7), treated- (OR 4.8; 95% CI 1.6-14) or untreated hypertension (OR 5.6; 95% CI 1.6-20). When compared to a population with saccular aneurysms, treated- (OR 2.9; 95% CI 1-8.1) or untreated hypertension (OR 5.2; 95% CI 1.6-16.8) remained significant risk factors, while smoking showed a tendency (OR 2.5; 95% CI 0.8-8.2). The location of the lesion differed largely to the population with saccular aneurysms (72% vs. 16% posterior circulation, p<0.01). Conversely as found with saccular aneurysms, the risk of IAD to rupture was highest in small lesions and decreased with size.
Conclusions: IAD are rare lesions and are mostly found in male patients in the fifth decade. Since smoking, hypertension and posterior circulation are highly associated with IAD (even when compared to saccular aneurysms), the pathophysiological mechanism underlying IAD seems to be distinct and to rely even more on mechanical wall stress of the parent vessel. Our observations made in a European population is concordant with observations made in a Japanese population (Ono H et al., Stroke. 2013;44:126-131).
