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      Fatal subarachnoid hemorrhage following ischemia in vertebrobasilar dolichoectasia

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          Abstract

          Vertebrobasilar dolichoectasia (VBD) is a chronic disorder with various cerebrovascular and compressive manifestations, involving subarachnoid hemorrhage (SAH). Occurrence of SAH shortly after worsening of clinical VBD symptoms has occasionally been reported. The goal of the study was to examine this association, in particular its pathophysiology, clinical precursor signs, time course, and outcome.

          To this end, in a retrospective multicenter study, we analyzed 20 patients with VBD and SAH in regard to preceding clinical symptoms, presence of vertebrobasilar thrombosis and ischemia, outcome and neuropathological correlates.

          Median age of the 7 female and 13 male patients was 70 years (interquartile range [IQR] 18.3 years). Fourteen patients (70%) presented with new or acutely worsening posterior fossa signs at a median of 3 days prior to SAH (IQR 2, range 0.5–14). A thrombus within the VBD was detected in 12 patients (60%). Thrombus formation was associated with clinical deterioration (χ 2 = 4.38, P = 0.04) and ponto-cerebellar ischemia (χ 2 = 8.09, P = 0.005). During follow-up after SAH, 13 patients (65%) died, after a median survival time of 24 hours (IQR 66.2, range 2–264 hours), with a significant association between proven ponto-cerebellar ischemia and case fatality (χ 2 = 6.24, P = 0.01).

          The data establish an association between clinical deterioration in patients with VBD, vertebrobasilar ischemia, and subsequent SAH. Antithrombotic treatment after deterioration appears controversial and SAH outcome is frequently fatal. Our data also indicate a short window of 3 days that may allow for evaluating interventional treatment, preferably within randomized trials.

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          Most cited references29

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          Natural history of vertebrobasilar dolichoectasia.

          The long-term prognosis of patients with vertebrobasilar dolichoectasia (VBD) is unknown. The purpose of this study was to explore the natural history of VBD, evaluate its progression, and examine factors that may influence the clinical course of this condition. We conducted a prospective clinical and imaging follow-up study of 156 consecutive patients with VDB followed for an average of 11.7 years. Predictors of events were evaluated by multivariate analysis. Survival analysis was used to evaluate rates of incidence. During follow-up, 93 patients (60%) experienced at least one event: 75 patients had stroke (59 ischemic and 21 hemorrhagic), 31 patients had new compressive symptoms, and 2 patients had hydrocephalus. Events were significantly associated with the severity of VBD, i.e., diameter, height of bifurcation, and lateral displacement of the basilar artery. During follow-up VBD progressed in 43% of patients. Progression of VBD was associated with a higher morbidity and mortality. The cumulative proportion of survivors free of adverse health event was 54.1 at 5 years, 39.5 at 10 years, and 23.5 at 15 years. During follow-up, 62 patients died and stroke was the most common cause of death. The long-term prognosis of patients with vertebrobasilar dolichoectasia (VBD) depended mainly on the severity of the condition at diagnosis and on its evolutionary characteristics. Progression of VBD exposed patients to high risk of adverse events, especially stroke.
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            Vertebrobasilar dilatative arteriopathy (dolichoectasia).

            Dolichoectasia (dilatative arteriopathy) describes marked elongation, widening, and tortuosity of arteries. The intracranial vertebral and basilar arteries are preferentially involved. Dolichoectatic arteries usually have an abnormally large external diameter and a thin arterial wall, with degeneration of the internal elastic lamina, multiple gaps in the internal elastica, thinning of the media secondary to reticular fiber deficiency, and smooth muscle atrophy. The most important clinical presentations of dilatative arteriopathy include acute brain ischemia; a progressive course related to compression of cranial nerves, the brain stem, or the third ventricle; and catastrophic outcome caused by vascular rupture. Flow in dilated arteries can become bidirectional, resulting in reduced antegrade flow and thrombus formation. Elongation and angulation of arteries can stretch and distort the orifices of arterial branches, leading to decreased blood flow, especially in penetrating branches.
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              Proposed classification of nonatherosclerotic cerebral fusiform and dissecting aneurysms.

              The aim of this study is to classify nonatherosclerotic aneurysms unrelated to the branching zones (including fusiform aneurysms and dissecting aneurysms). Damage to the internal elastic lamina (IEL) is often an associated factor in the pathogenesis of aneurysm formation. In this study, 85 nonatherosclerotic aneurysms arising from an arterial trunk unrelated to the branching zones were classified into four different types, based on the lesional patterns of the IEL and the state of the intima. Type 1 corresponded to classic dissecting aneurysms, the pathogenesis of which was characterized by acute widespread disruption of the IEL without intimal thickening. Patients with Type 1 aneurysms had an ominous clinical course, and many presented with sudden subarachnoid hemorrhage with frequent rebleeding. Type 2 aneurysms were segmental ectasias, which had an extended and/or fragmented IEL with intimal thickening. Weakness of the arterial wall caused by the damaged IEL was assumed to be compensated by the intimal thickening. The luminal surface of the thickened intima was smooth without thrombus formation. The patients with Type 2 aneurysms had a placid clinical course. Type 3 aneurysms were dolichoectatic dissecting aneurysms, pathologically characterized by fragmentation of the IEL, multiple dissections of thickened intima, and organized thrombus in the lumen. Most of them were symptomatic and progressively enlarged over time. Type 4 aneurysms were saccular aneurysms unrelated to the branching zones. They arose in areas with minimally disrupted IEL without intimal thickening, and there was a risk of rupture. There was a strong relationship between the pathological features of the aneurysms and their clinical courses. This classification may provide a rationale for modes of treatment.
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                Author and article information

                Journal
                Medicine (Baltimore)
                Medicine (Baltimore)
                MEDI
                Medicine
                Wolters Kluwer Health
                0025-7974
                1536-5964
                July 2016
                08 July 2016
                : 95
                : 27
                : e4020
                Affiliations
                [a ]Stroke Center, Service de Neurologie, Département des Neurosciences Cliniques, Centre Hospitalier Universitaire Vaudois (CHUV) and University of Lausanne, Lausanne, Switzerland
                [b ]Department of Interventional Neurology and Stroke, Institute of Neurosciences, Saket City Hospital, New Delhi, India
                [c ]Service de Neurologie, Département des Neurosciences Cliniques, Hôpitaux Universitaires de Genève (HUG), Geneva, Switzerland
                [d ]Service de Neurologie, Fondation Hopale, Berck-sur-Mer, France
                [e ]Service de Pathologie Clinique, Hôpitaux Universitaires de Genève (HUG), Geneva, Switzerland
                [f ]The Comprehensive Stroke Center, Tufts University Medical Center, Boston, MA
                [g ]Servizio di Neurologia, Ospedale Regionale di Lugano, Lugano
                [h ]Neurologische Klinik, Kantonsspital Aarau, Aarau, Switzerland
                [i ]Stroke Unit and Division of Internal and Cardiovascular Medicine, Ospedale Santa Maria della Misericordia, Perugia, Italy
                [j ]Department of Neurology and Neurosurgery, Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht, The Netherlands.
                Author notes
                []Correspondence: P. Michel, Stroke Center, Service de Neurologie, Département des Neurosciences Cliniques, Centre Hospitalier Universitaire Vaudois, Rue du Bugnon, Lausanne, Switzerland (e-mail: patrik.michel@ 123456chuv.ch ).
                Article
                04020
                10.1097/MD.0000000000004020
                5058812
                27399083
                5c5e67fa-0434-4857-ae89-d969b9c2dbef
                Copyright © 2016 the Author(s). Published by Wolters Kluwer Health, Inc. All rights reserved.

                This is an open access article distributed under the Creative Commons Attribution License 4.0, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. http://creativecommons.org/licenses/by/4.0

                History
                : 9 February 2016
                : 7 April 2016
                : 2 June 2016
                Categories
                5300
                Research Article
                Observational Study
                Custom metadata
                TRUE

                dolichoectasia,ischemia,stroke,subarachnoid hemorrhage,vertebrobasilar

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