Intracranial Cerebral Artery Dissection of Anterior Circulation as a Cause of Convexity Subarachnoid Hemorrhage

Abstract

Background: Convexity subarachnoid hemorrhage (cSAH), defined as intrasulcal bleeding restricted to hemispheric convexities, has several etiologies: reversible cerebral vasoconstriction syndrome, cerebral amyloid angiopathy, and internal carotid artery (ICA) stenosis or occlusion. However, it remains unknown whether cerebral artery dissection causes cSAH. Methods: We retrospectively investigated patients admitted to our hospital between 2005 and 2013 with ischemic stroke or transient ischemic attack caused by cerebral artery dissection. Cerebral artery dissection was diagnosed by cervical or cerebral magnetic resonance imaging (MRI) or computed tomography (CT) showing a wall hematoma. CT angiography, ultrasonography, or intra-arterial digital-subtraction angiography detected cerebral artery dissection if a double lumen, string sign, intimal flap, or dissecting aneurysm was observed at a nonbifurcation site. We used CT or MRI to detect cSAH, which was defined as blood collection restricted to one or few cerebral sulci without extending to the basal cisterns, ventricles, or Sylvian and interhemispheric fissures. Demographic, neuroimaging, treatment, and prognostic data were collected. Results: In total, 82 patients were diagnosed with ischemic stroke caused by cerebral artery dissection. The following arteries were affected: the ICA (9 patients), anterior cerebral artery (ACA; 12 patients), middle cerebral artery (MCA; 12 patients), vertebral artery (37 patients), basilar artery (5 patients), posterior cerebral artery (2 patients), and posterior inferior cerebellar artery (4 patients). In addition, 1 patient presented with simultaneous dissection in both the vertebral and internal carotid arteries, and 6 patients (7%) presented with cSAH (3 men and 3 women, age 39-67 years). The MCA was dissected in four cases and the ACA in two cases, with cSAH frequencies of 33 (4 of 12) and 17% (2 of 12), respectively, in those vessels. Artery dissection in the vertebrobasilar artery system was not responsible for cSAH (0 of 48). In all the MCA dissection cases, cSAH occurred in the arterial border zone between the ACA and MCA territories. Although 2 patients showed early reperfusion with temporary cSAH enlargement, cSAH was self-limiting. Antithrombotic treatment did not complicate the clinical course when used in 4 patients during acute or subacute phases. All patients achieved a 3-month poststroke modified Rankin Scale of 0-2. Conclusion: Our data suggest that cSAH caused by intracranial cerebral artery dissection is not rare. Further investigations are needed to elucidate the precise mechanism underlying cSAH in cerebral artery dissection.

Acute ischemic stroke with contralateral convexal subarachnoid hemorrhage: two cases report

“…Moreover, cSAH has been described to occur invariably on the side with acute ischemic stroke, and it is notably unusual for cSAH to occur on the opposite side of the infarct territory. To date, there have been few reports about infarction with contralateral cSAH caused by RCVS, ICA dissection, embolic stroke of undetermined source, and CAA [8–10, 15]. This paper presented two cases of acute ischemic stroke with contralateral cSAH due to ICA atherosclerotic occlusion and cardioembolic stroke, respectively.…”

The insidious appearance of the dissecting aneurysm: Imaging findings and related pathophysiology. A report of two cases

“…After review of the literature we found that the majority of cases of dissecting aneurysm of the intracranial ICA were located in the supraclinoid segment. 13,18,21–24 However, our two cases illustrate the use of CTA in the early detection of the outpouch in the reformatted MPR images as the possible site of the initial transmural rupture of the dissecting aneurysm.…”

Subarachnoid haemorrhage due to intracranial vertebral artery dissection presenting with atypical cauda equina syndrome features: case report

“…In our case, a convexal/subconvexal focus of blood affecting the parietal lobule was seen, which could explain why the patient developed headache, facial nerve palsy, and confusion. In various case series of cSAH, reported features have included focal and transient motor and/or sensory symptoms (42–73%), including facial nerve palsy and pronator drift [15, 16]; headache (18–65%); and confusion (9.8%) [17–20]. Although cSAH by definition spares the basal cistern and Sylvian fissures (which our case does not), descriptions of cSAH have been made even when these regions are not spared [21–23].…”