Posterior circulation stroke: still a Cinderella disease

BMJ 2013; 346 doi: http://dx.doi.org/10.1136/bmj.f3552 (Published 14 June 2013) Cite this as: BMJ 2013;346:f3552
  1. Hedley C A Emsley, consultant neurologist
  1. 1Department of Neurology, Royal Preston Hospital, Preston PR2 9HT, UK
  1. hedley.emsley{at}lthtr.nhs.uk

Improved clinical recognition, specific diagnostic imaging, and studies of treatment are urgently needed to optimise care

Although enormous strides have been made recently in hyperacute stroke care in the United Kingdom, one stroke presentation continues to pose particular challenges. Clinicians who treat patients with a transient ischaemic attack (TIA) or ischaemic stroke that affects the posterior circulation face difficulties in making the diagnosis, accessing imaging, and treating the condition effectively. Healthcare professionals in emergency settings urgently need to acquaint themselves with the signs of the acute neurological deficits associated with posterior circulation stroke.

Posterior circulation stroke accounts for about a fifth of the estimated 150 000 strokes that occur in the UK each year.1 Simple screening methods have been devised to identify patients with an acute stroke or TIA and ensure early intervention. The “face arm speech test” (FAST) score in particular has been developed to assess whether a patient is likely to have had an acute stroke and may be a candidate for intravenous thrombolysis. This score was primarily evaluated in a cohort of unselected patients with acute stroke, most of whom had anterior circulation (carotid territory) stroke.

Clinical features of stroke affecting the posterior circulation (usually in the territory of the vertebrobasilar system) differ substantially from those of anterior circulation stroke. Common posterior circulation symptoms include visual disturbance, vertigo, and ataxia (box). The face arm speech test score does not include these features and is positive in only 61% of patients with posterior circulation stroke.2

Common clinical features of posterior circulation stroke

  • Unilateral, bilateral, or crossed sensory loss or weakness

  • Visual disturbance (such as diplopia and homonymous hemianopia)

  • Unsteadiness or ataxia

  • Dysarthria

  • Dysphagia

  • Vertigo

  • Nausea and vomiting

  • Drowsiness

  • Various other features, including other cranial nerve deficits

Patients with anterior circulation stroke usually have clinical features that conform to a readily identifiable pattern. After successful initiatives to raise awareness, these patients are often swiftly connected with appropriate hyperacute stroke pathways on hospital arrival (or even after pre-hospital alert by a paramedic), although a need for further development and training in the community to improve pre-hospital recognition of stroke has recently been highlighted.3

However, it is difficult to recognise posterior circulation TIA and stroke, and considerable delays occur often. A recent cross sectional study of patients with acute stroke who were treated with intravenous thrombolysis found that the intervals to referral and treatment were significantly longer for posterior circulation strokes than for anterior circulation strokes.4 A recent analysis of all potential ischaemic events during the 90 days preceding ischaemic stroke within a prospective population based incidence study highlighted an important problem: transient isolated brainstem symptoms that do not satisfy traditional definitions of TIA commonly precede definite vertebrobasilar stroke.5

The risk of early recurrent stroke is high in patients with vertebrobasilar stenosis.6 However, there is rarely a second chance at diagnosis when the diagnosis of posterior circulation TIA or stroke is delayed or missed, and the result may be death or substantial disability, including devastating outcomes such as locked-in syndrome. It is therefore crucial that posterior circulation stroke is detected and diagnosed earlier.

Computed tomography of the brain has far lower sensitivity than magnetic resonance imaging in the diagnosis of posterior circulation ischaemia, especially when diffusion weighted magnetic resonance imaging is used.7 Brain magnetic resonance imaging can be invaluable in confirming the location of a lesion, but it can be difficult to perform in unwell patients with acute stroke. It also has longer scan acquisition times than computed tomography, which can introduce delay in treatment.8 Moreover, the appropriate selection of magnetic resonance imaging as the imaging modality of choice relies on the initial clinical suspicion of posterior circulation stroke, which is challenging, as already discussed.

Because computed tomography remains the first line brain imaging modality for acute stroke in the UK, it may be preferable to harness its full potential. In some cases, computed tomography angiography can rapidly identify the cause of a posterior circulation stroke lesion, including the location and severity of vascular lesions such as atheromatous disease or arterial dissection. This technique may have greater sensitivity for vertebral artery dissection than magnetic resonance angiography or ultrasound, but further studies on imaging techniques and radiographic criteria in this condition are needed.9

Treatment of posterior circulation cerebral ischaemia is also not straightforward. Initial medical management strategies for posterior circulation TIA are the same as for anterior circulation TIA. Patients with posterior circulation ischaemic stroke are potentially eligible for intravenous thrombolysis, but there are important areas of uncertainty. The role of endovascular therapy for posterior circulation acute ischaemic stroke is not clear. There are no clear selection criteria for acute neurosurgical intervention. It is also unclear exactly how patients with vertebral artery dissection or vertebral artery stenosis should be selected for secondary prevention interventions.

Of 656 participants in the recent Interventional Management of Stroke (IMS) trial III,10 which compared intravenous thrombolysis with intra-arterial treatment against intravenous thrombolysis alone, the brainstem or cerebellum was the presumptive location of stroke in only 2% of patients. Patients with basilar artery occlusion will not be included in the UK interventional stroke trial—Pragmatic Ischaemic Stroke Thrombectomy Evaluation (PISTE).11

Furthermore, patient selection, referral, and transfer for neurosurgical interventions such as external ventricular drainage for hydrocephalus due to mass effect from posterior circulation infarction can vary greatly.12 In patients with confirmed vertebral artery dissection, it is unclear whether antiplatelet treatment or anticoagulation is the best treatment approach. This question is currently being investigated by the Cervical Artery Dissection in Stroke Study (CADISS).13 For vertebral artery stenosis, it is not known whether vertebral artery stenting is superior to medical treatment, a question that the Vertebral Artery Ischaemia Stenting Trial (VIST) aims to answer.14 A second trial is also investigating stenting for symptomatic vertebral artery stenosis.15 Given the high risk of early recurrence of stroke in vertebrobasilar stenosis, urgent investigation and treatment are crucial, similar to carotid endarterectomy for symptomatic carotid stenosis.

Diagnosis and treatment trials have focused mainly on anterior circulation stroke. There is a clear need for studies that assess the optimal imaging protocols for posterior circulation stroke and treatment trials conducted solely in patients with posterior circulation stroke.


Cite this as: BMJ 2013;346:f3552


  • Competing interests: I have read and understood the BMJ Group policy on declaration of interests and declare the following interests: I am the local principal investigator (at Lancashire Teaching Hospitals NHS Foundation Trust) for the Vertebral Artery Ischaemia Stenting Trial (VIST) and the current chairman of the British Association of Stroke Physicians Training and Education Committee. I am also a member of the Stroke Association research awards committee and the National Institute for Health and Care Excellence (NICE) evidence resources reference panel.

  • Provenance and peer review: Not Commissioned; externally peer reviewed.