Ultrafast magnetic resonance imaging protocols in stroke

Although the approval of recombinant tissue plasminogen activator (rtPA) for the treatment of acute ischaemic stroke has been based on the primary imaging technique of conventional cerebral computerised tomography (CT),¹ newer and more refined magnetic resonance (MR) techniques are unrelentlessly extending into this particular field of emergency medicine, stimulated by the important hope that these new techniques could help to prolong the therapeutic time window beyond the 3 hour limit in selected patients. Several recent papers have clearly demonstrated that the mismatch concept,² though leading to diagnostic pitfalls in a small number of cases as well, seems to be helpful in selecting patients for “late” fibrinolysis. It has been shown that the rapidity with which the inevitable core infarction augments into the tissue at risk ( =  penumbra) does not only depend on external parameters like perfusion pressure, blood glucose level, body temperature, or oxygen saturation (to mention only a few), but is strongly influenced by individual, predefined anatomical features of the cerebral vasculature like the configuration of the circle of Willis and the collateralising potential of the leptomeningeal anastomoses at the cortical level.³

The indication for systemic fibrinolysis in acute stroke is not dependent on the angiological proof of an intracranial arterial occlusion. The conflict between the desire to base fibrinolysis on pathophysiologically relevant knowledge, and the urge of the therapeutic time window with an exponentially decreasing benefit from lysis over time led to a decision in favour of the time requirements. It could be argued, however, that patients without a visible arterial occlusion would not need fibrinolysis at all, and should not be exposed to its intrinsic risks.

With this in mind the idea to subject nearly every acute stroke patient to an ultrafast MR imaging protocol including T1, T2, fluid attenuated inversion recovery (FLAIR), and diffusion weighted imaging (DWI) sequences in addition to three dimensional time-of-flight MR to visualise the major cerebral arteries appears very attractive even though this technology and the corresponding expertise is not available yet over 24 hours in most places. Until now, the most convincing argument against this refined diagnostic work-up of the acute stroke patient was the limitation of time. This is no longer valid, however, and postprocessing efforts lasted only 7 minutes, during which time the patient was returned to the ward. With this ultra fast MRI technique, even the handling of restless and uncooperative patients did not seem to be a problem anymore—another important argument often posed against MR imaging in the very acute phase of stroke.

A technique like the one described by U-King-Im et al (this issue, pp 1002–5), supplemented by an additional haemosiderin-sensitive gradient echo sequence for the detection of previous haemorrhages might initiate profound changes in the protocols for the management of acute stroke patients irrespective whether ischaemic or haemorrhagic in origin. Realistic hopes are that: (1) ideal candidates for fibrinolysis could be pinpointed; (2) the time window for fibrinolysis could be prolonged on an individual basis; (3) the risk of intracerebral haemorrhage could be reduced by excluding patients without a visible arterial lesion; and (4) patients with multiple haemosiderin remnants indicating previous brain haemorrhages could be excluded as well, because of their excessive bleeding risk. In patients with peracute brain haemorrhage, recombinant activated Factor VII could be applied to stop the growth of the haematoma.⁴ If this works, only two major obstacles still seem to be present: the patients’ cardiac pacemakers and defibrillators, and the costs.