Patterns of ischemic posterior circulation strokes: A clinical, anatomical, and radiological review

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Patterns of ischemic posterior circulation strokes: A clinical, anatomical, and radiological review

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Alexander Salerno, Davide Strambo, Stefania Nannoni, ...

First Published September 28, 2021 Review Article 

https://doi.org/10.1177/17474930211046758

Article information

Abstract

Background

Posterior circulation and anterior circulation strokes share many clinical, pathogenetic and radiological features, although some clinical signs are highly specific to posterior circulation strokes. Arterial stenosis and occlusions occur in significant numbers in both acute posterior circulation and anterior circulation strokes, making them good candidates for endovascular treatment. Among posterior circulation strokes, basilar artery occlusions stand out because of the diagnostic and acute treatment challenges.

Methods

We reviewed the literature on clinical stroke syndromes and neuroimaging findings and systematically describe for each anatomical site of stroke the detailed clinical and radiological information (anatomical representation, diffusion weighted imaging and angiographic sequences). The principles of neuroimaging of posterior circulation strokes and the prognosis for each stroke localization are also discussed.

Review summary

Stroke syndromes in the territories of the vertebral, basilar, cerebellar, and posterior cerebral arteries are presented. Features typical of posterior circulation strokes are highlighted, including patterns of basilar artery occlusions. Clinical severity and prognosis of posterior circulation strokes are highly variable, and given that they are more difficult to detect on CT-based neuroimaging, magnetic resonance imaging is the technique of choice in suspected posterior circulation strokes. Rapid identification of arterial occlusion patterns may provide prognostic information and support acute revascularization decisions.

Conclusions

Posterior circulation stroke syndromes tightly reflect lesion localization and arterial occlusion patterns. Although many clinical and pathogenetic features are similar to anterior circulation strokes, notable differences exist in terms of clinical presentation, stroke mechanism, prognosis, and response to acute recanalization.

Keywords

Ischemic stroke, Vertebrobasilar insufficiency, Basilar artery, Magnetic Resonance Imaging, Prognosis

Stroke mechanisms and general clinical features

Posterior circulation (PC) and anterior circulation (AC) strokes share many clinical and pathophysiological features, but there are notable differences mainly related to their respective cerebrovascular anatomy and brainstem functions. Whereas age and cerebrovascular risk factors seem similar, male sex appears more frequent in PC strokes.¹

Some clinical signs are highly specific to PC strokes because of the unique brainstem functions and vascularization (Figure 1). The basilar artery, in fact, gives origin to a peculiar network of perforating and circumferential arteries, which systematically repeats itself at each anatomical level of the brainstem (Figure 2). Oculomotor deficits such as unilateral palsy of eye movements, internuclear ophthalmoplegia, and skew deviation are pathognomonic for brainstem locations of stroke.¹ This is also true for vertical nystagmus, up- or down-gaze palsy and conjugate gaze paresis to one side. Crossed syndromes and bilateral long tract signs are highly specific because of the bilateral supply of the basilar artery to the posterior fossa structures, and the frequent crossing of fiber tracts in the brainstem. Central vestibular symptoms and signs such as nausea, vertigo, conjugate nystagmus in any direction, gait and hemi-ataxia are also characteristic of brainstem and cerebellar strokes.^2,3 Lesions of the lower brainstem and cerebellum commonly cause true vertigo and conjugate horizontal/rotatory nystagmus, whereas strokes of the upper brainstem and cerebellum cause unsteadiness and gait ataxia. Infrequent but moderately specific signs are decreased level of consciousness and amnestic syndromes, which are often missed in the acute phase or mistaken for confusional state.

Figure 1. Anatomy and vascularization of the vertebrobasilar system.

Figure 2. (a) Schematization of pontine syndromes. (b) Pattern of perforating branches in the pons.

Hemispheric symptoms or signs such as aphasia, hemineglect, or conjugate eye deviation are rare in PC strokes, but may still occur due to the involvement of the thalamus; in this case, an important unilateral posterior cerebral artery (PCA) stroke can even clinically mimic an AC stroke.³ Exceptionally, cerebellar stroke can also lead to cognitive dysfunction, related to bidirectional connections with the cortex (“diaschisis”).⁴

Contrary to general belief, dysarthria^1,3 and homonymous visual field deficits¹ do not seem to be more frequent in PC than in AC strokes. However, PCA strokes more often cause isolated field deficits than middle cerebral artery (MCA) strokes.

The presence of multilevel lesions is peculiar to PC strokes. Symptoms may in fact be explained by the presence of two or more concomitant lesions. This feature is typical of PC strokes and is explained by the fact that the vertebrobasilar system stretches along multiple structures of the posterior fossa.

All mechanisms accounting for ischemic AC strokes also occur in the PC, and there are no consistent differences in their frequencies.^1,5 In the largest comparative study, lacunar strokes seemed more frequent in the PC,¹ which could be due to the high density of long tracts and cranial nerve structures in the brainstem. Therefore, small PC strokes may be more expressive than in the AC, which is less densely packed with neuronal and axonal structures.

For the same reason, acute neuroimaging (including MRI) may not show a clinical brainstem stroke (i.e. false-negative imaging). A negative MRI in face of a vascular brainstem syndrome should not preclude a stroke diagnosis. This is particularly true for patients with acute symptom onset, absence of alternative explanations, and cerebrovascular risk factors.

Finally, most studies show a lower initial stroke severity in PC strokes. This may be due to the more frequent lacunar strokes or an underrepresentation of clinical PC deficits (ataxia, gait, oculomotor signs, amnesia) in the NIHSS scale.⁶

The aim of this review is to present systematically the clinical–radiological correlations in PC strokes through the description of typical symptoms, anatomical drawings, and MRI-based examples.