We searched PubMed (from 1990 to August, 2011) with the terms “basilar artery occlusion” and “basilar artery thrombosis”. We also identified relevant published work by searching the reference lists of articles retrieved by our search and from our own files. Reports published in English, Finnish, French, German, Italian, and Swedish were reviewed. The final reference list was generated on the basis of originality and relevance to the broad scope of this Review.
ReviewBasilar artery occlusion
Introduction
The vertebral and basilar arteries supply blood to many large and small vessels in the posterior circulation. Occlusions of the posterior circulation arteries cause about a fifth of all strokes. When the basilar artery is occluded, clinical presentation ranges from mild transient symptoms to devastating strokes. Basilar artery occlusion (BAO) is rare. It accounts for about 1% of all strokes and is reported in about 8% of patients with symptomatic vertebrobasilar territory ischaemia.1, 2 At our institutions (since 2004), about ten individuals per year with BAO from Bern, and between ten and 15 from Helsinki, have been treated with thrombolysis. From these numbers, we estimate the incidence of BAO to be about one patient per 100 000 a year, or a maximum of a few individuals per 100 000. Patients are usually elderly, but younger people or even children can have BAO.3, 4
Abercrombie was probably the first clinician to publish a clinical and pathological description of BAO in 1828,5 and Hayem is quoted frequently for his detailed clinicopathological report from 1868.6 Table 1 summarises landmarks in BAO research that have been important for current understanding and advances in management.5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20 Technical developments during the past few decades have improved the diagnosis and management of BAO greatly. Non-invasive imaging has contributed to a better understanding of clinical-anatomical correlations and serves as a basis for rapid diagnosis and treatment. Furthermore, many recanalisation techniques have been developed that help to reperfuse brain tissue jeopardised by ischaemia and to improve patients' outcomes.
Nevertheless, the disorder is still devastating for many patients and their families, and further research is needed to secure improvements in the diagnosis and treatment of BAO. In this Review, we discuss pathophysiology and causes of BAO and its clinical presentation and diagnosis, and we summarise clinical outcomes and current management of the disorder. We hope that a better understanding of BAO will increase the number of patients who get early and optimum treatment and that the future will bring new treatment options.
Section snippets
Anatomy
The basilar artery is joined to the brainstem via penetrating median, paramedian, and short and long circumferential branches,21 which are connected by anastomotic channels in 42–67% of people.22 The section of the basilar artery from the vertebral artery junction to the anterior inferior cerebellar artery is generally referred to as the proximal segment, the middle part from the anterior inferior cerebellar artery to the superior cerebellar artery is called the middle segment, and the area
Pathophysiology and causes
The most frequent causes of BAO are atherosclerotic occlusions resulting from local thrombosis due to severe stenosis and embolic occlusions from cardiac and large artery sources. In autopsy series, atherosclerosis was reported as the most common cause of BAO and was usually extensive and not restricted to the basilar artery.7, 25 In studies in which imaging was used for diagnosis of BAO, atherosclerosis was noted in 26–36% of patients, emboli in 30–35%, other causes (including dissection of
Anatomical-clinical correlations
Clinical symptoms and signs depend on the location of occlusion in the basilar artery and on the anatomical regions affected by the resulting ischaemia (table 2). Labauge and colleagues8 surveyed 17 of their own patients and 265 from elsewhere. Of 257 patients with adequate angiograms, 58% were monosegmental, 23% were plurisegmental, and 18% had complete BAO. The extent of the infarct that results from BAO depends mainly on the collaterals (figure 2). In patients with slowly occluding
Prodromal symptoms
Up to two-thirds of patients with BAO have prodromal transient ischaemic attacks, minor strokes, or other symptoms, which are more frequent with atherosclerotic than embolic occlusions.7, 8, 26 In the BASICS registry,18 19% of patients had prodromal transient ischaemic attacks and 19% had prodromal minor strokes. Vertigo and headaches are the most common prodromal symptoms. Other prodromal symptoms and signs include a decrease in consciousness, yawning, double vision, visual-field deficits,
Differential diagnosis
Several disorders can mimic BAO (table 3). When recognised early, the outcome of BAO can be improved with thrombolysis. Therefore, rapid diagnosis is essential. Whenever a patient with decreased consciousness shows brainstem signs such as cranial nerve palsy combined with contralateral or bilateral long-tract signs, BAO should be considered. Extensor jerks and spasms and decerebrate posturing arising with BAO are sometimes mistaken for grand mal seizures and postictal state,43, 53 and acute
Neuroimaging
CT and CT angiography, MRI and magnetic resonance (MR) angiography, and transcranial doppler and colour-coded duplex sonography allow non-invasive or minimally invasive diagnosis in the acute stage of BAO.55 Moreover, CT perfusion imaging and diffusion-weighted and perfusion-weighted MRI provide information on haemodynamics in the capillaries of ischaemic tissue. A combination of these techniques is referred to as multimodal CT or multimodal MRI, and they are standard care at many comprehensive
Management
Table 4 summarises BAO outcomes after various treatments and interventions.17, 18, 19, 20, 49, 72, 73, 74, 75, 76, 77, 78, 79, 80, 81, 82 Figure 5, based on studies listed in table 4, presents data on recanalisation, survival, and functional outcomes.
Considerations for improving management
Systematic analyses have shown that most patients with BAO receive intra-arterial thrombolysis;17, 18 however, unlike the expectations of many investigators, results do not support unequivocal superiority of the intra-arterial over intravenous technique.17, 18 The effect of intravenous thrombolysis is probably not much different from that of intra-arterial thrombolysis, and in patients with mild-to-moderate deficits, intravenous thrombolysis might even be superior. However, undoubtedly,
Conclusions
During the past few decades, BAO has evolved from an almost uniformly fatal disease to a treatable disorder. Prompt recanalisation of the basilar artery can substantially enhance a patient's chances of survival and good functional recovery. However, the best recanalisation approach has not been defined in randomised trials. Current endovascular techniques recanalise 80–90% of all blocked basilar arteries. Nevertheless, many recanalisation procedures are futile, so the outlook for many patients
Search strategy and selection criteria
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