Unruptured intracranial aneurysm as a cause of cerebral ischemia.
ABSTRACT Unruptured intracranial artery aneurysms (IAs) can be revealed by cerebral ischemia. Little is known on the clinical course and outcome of patients with this condition. We report our findings in a consecutive series of 15 such patients.
We retrospectively analyzed patients with ischemic stroke (IS) or transient ischemic attack (TIA), unruptured IA on the symptomatic cerebral artery, and no other potential cause of cerebral ischemia consecutively treated in a tertiary stroke unit.
Fifteen patients (ten women, and five men) were identified. Their mean age was 49.7 years (range, 37-80 years). Ten patients presented with IS, and five with TIA. The median diameter of IA was 7.5mm (range, 2.5-23 mm). Aneurysm thrombosis was found on imaging in 9/10 patient with IS, and 1/5 patients with TIA (p=0.017). Thirteen patients were given an antiplatelet agent. Mean follow-up until last visit or treatment of aneurysm was 393 days (median 182 days; range, 6-1825 days). There was no ischemic recurrence. Partial or complete recanalization of aneurysm thrombosis occurred in 7/10 patients. Two patients, both with initial aneurysmal thrombosis and on antiplatelet therapy, experienced aneurysm rupture.
Unruptured IA is a rare cause of IS/TIA. IS is associated with aneurysm thrombosis. Our findings suggest that aneurysm thrombosis is a dynamic process which is associated with a low rate of ischemic recurrence on antiplatelet therapy but may be followed by subarachnoid hemorrhage.
Article: Cerebral aneurysm as an exacerbating factor in stroke pathology and a therapeutic target for neuroprotection.[show abstract] [hide abstract]
ABSTRACT: Stroke remains a major cause of death in the US and around the world. Despite major scientific advances in our understanding of stroke pathology, the only FDA-approved drug for ischemic stroke is tissue plasminogen activator (tPA). Moreover, the therapeutic window for tPA is confined to the acute phase of stroke, thereby greatly limiting its benefits to less than 3% of ischemic stroke patients. Many treatment strategies for stroke have targeted the subacute or chronic phase in an effort to abrogate the secondary cell death that ensues after the initial stroke insult. Here, we advance the hypothesis that blood vessel disruption, or aneurysm, in the brain is an exacerbating factor for stroke, especially in the evolution of the penumbra or peri-infarct area. A better understanding of aneurysm, specifically its dynamic onset and juxtaposition to the ischemic brain tissue should facilitate the development of novel strategies for attenuating the secondary cell death associated with stroke. To this end, we discuss the laboratory and clinical evidence implicating aneurysm formation in stroke and also provide insights on how stem cell therapy may prove efficacious in combating aneurysm and stroke.Current pharmaceutical design 05/2012; 18(25):3663-9. · 4.41 Impact Factor