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Factors that predict basilar artery occlusion outcome
Acute basilar artery occlusion is a known cause of brain stem infarction that is often fatal. The most physiological way of treating this condition is recanalisation of the occluded artery to revascularise endangered ischemic brain. Thrombolysis by intravenous recombinant tissue plasminogen activator (rtPA) brings substantial clinical benefit in acute stroke, however, a large number of patients do not respond to this treatment. Intra-arterial thrombolysis may improve overall outcome in patients with basilar artery occlusion but predicting benefit of therapy is still difficult in the individual patient. The crucial issue in acute basilar artery occlusion is defining the predictors for successful recanalisation and improved outcome.
Arnold et al1 (pp 857) have tried to define clinical and radiological predictors of recanalisation and outcome in acute basilar artery occlusion. They found that a low National Institutes of Health Stroke Scale (NIHSS) score and vessel recanalisation (as seen on the angiogram) were associated with a favourable outcome. Complete recanalisation was seen in 8/40 (20%) cases whereas partial recanalisation was achieved in 24/40 (60%) cases, and a favorable outcome was seen in 14/40 (35%). This suggests that even partial recanalisation of basilar artery occlusion may bring about a favourable outcome. Angiographic recanalisation was seen more often in patients in whom intra-arterial thrombolysis was started within six hours of onset of symptoms and when the admission computed tomography (CT) scan showed a dense basilar artery occlusion sign, which represents a large diameter clot (embolic origin) in an artery with otherwise normal lumen. On the contrary, if the basilar artery is already stenosed due to atherosclerosis, it may not appear dense when occluded totally. This may be a possible explanation for the presence of the dense basilar artery (BA) sign being favourable for recanalisation, since, in this situation, thrombolysis will cause normalisation of the arterial lumen. In this series, the predictors of poor outcome were presence of quadriplegia and coma suggesting extensive brainstem compromise. This is similar to the observation of poor outcome in middle cerebral artery (MCA) stroke patients where the perfusion-weighted CT lesion volume was more than 100 ml.2 Other studies have shown that small diffusion-weighted imaging lesions predict a favourable outcome.3 The length of the basilar artery occlusion and the state of the collaterals are other independent variables affecting survival.
The existence of the ischaemic penumbra for several hours following acute occlusion of the arterial blood supply to the brain is the basis for acute revascularisation treatment in ischaemic stroke. Depending on the location of the occlusion in a vessel and the degree of collateral blood flow, the duration of the ischaemic penumbra varies from individual to individual. It is worthwhile to identify patients in whom the parenchyma may be salvageable after longer time periods; these patients may benefit from late recanalisation treatments. The identification and quantification of the penumbra before the initiation of definite revascularisation may be of immense benefit in identifying patients who may have a favourable outcome irrespective of the therapeutic window.
The emergence of diffusion- and perfusion-weighted magnetic resonance imaging (MRI) techniques have revolutionised the role of MRI in the evaluation of patients with acute stroke. Until recently, the diffusion–perfusion mismatch model provided a simple and feasible means to identify the ischaemic penumbra, but studies have now demonstrated that the simple diffusion–perfusion mismatch model is only a rough approximation of the ischaemic penumbra. There has been a paradigm shift towards a variety of novel concepts regarding MRI and the ischaemic penumbra. These include (i) diffusion–perfusion mismatch does not optimally define the penumbra; (ii) early diffusion lesions are in part reversible and often include both irreversibly infarcted tissue and penumbra; (iii) the visible zone of perfusion abnormality overestimates the penumbra by including regions of benign oligaemia; (iv) MRI is a very practical method for acute stroke imaging; and (v) therapeutic salvage of the ischaemic penumbra has been demonstrated in humans with the use of diffusion-perfusion MRI.4 The results of ongoing thrombolysis trials involving evaluation of stroke patients with MRI may contribute further to the prediction of outcome in cases of acute basilar artery occlusion.
The astroglial protein S100B is a marker of cerebral tissue damage. A single S100B value <0.4 μg/l obtained 48–96 hours after stroke onset indicates successful clot lysis <6 hours in MCA/M1 occlusion with a high degree of accuracy.5 A single S100B value may serve as a surrogate marker of early and sufficient recanalisation in large scale thrombolytic studies and thus help optimise doses of thrombolytic agents to reduce haemorrhagic complications.
Lastly, I think the time has come for the formulation of an outcome scale based on the evidence available from various studies on predictors of recanalisation and outcome of acute basilar artery occlusion treated with intra-arterial thrombolysis, and assessment of the scale in further studies with large numbers of patients.
Factors that predict basilar artery occlusion outcome
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