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Visible infarction on CT after stroke—what does it tell?
  1. R Kay,
  2. A C F Hui
  1. Department of Medicine and Therapeutics, Prince of Wales Hospital, Shatin, Hong Kong
  1. Correspondence to:
 Professor R Kay; 

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There are many predictors of functional outcome after stroke, among which consciousness level on admission, concentration of blood glucose, and radiological extent of the infarct or haematoma spring into mind. Not all infarcts are visible on CT, especially in the first few hours. In the paper by Wardlaw et al on 452–458,1 among 12 550 patients who were enrolled in the International Stroke Study (1991–96) only 50% had visible infarction, even up to 48 hours after stroke.

Compared with patients without visible infarction, those who had were 25% more likely to have a poor outcome (defined as death or dependency) at six months. There was, however, neither an association between visible infarction and subsequent haemorrhagic transformation of the infarct (which occurred in less than 1% of all patients), nor any interaction between visible infarction and treatment allocation (aspirin or heparin) with the six month outcome.

As functional outcome reflects the amount of brain infarcted, it can be expected that early visualisation of this process will lead to a poorer outcome. On the other hand, haemorrhagic transformation of the infarct is a multifactorial process dependent not only on the size of the infarct, but also on the blood pressure, blood coagulability, and a host of other factors such as whether and when reperfusion has occurred. Thus, early visualisation of infarction may not independently predict haemorrhagic transformation.

Ever since the late 1990s, when thrombolytic treatment gained approval from the US Food and Drug Administration for the treatment of cerebral infarction within 3 hours of onset, there has been intense interest in visualising infarction as early as possible. A variety of “early infarct signs” on CT, such as loss of cortical grey-white matter differentiation and loss of the insular ribbon, have been proposed,2 but these signs are generally subtle and lacking in interrater agreement. Posterior fossa strokes are also not included in such schemes. Newer techniques (diffusion weighted imaging and perfusion imaging) using MR are much more sensitive but are not as widely available as CT. Even in centres where MR is available, there are many logistic reasons why CT remains the imaging modality of first choice.3

What, then, is the value of CT when infarction is not seen? Most importantly, it is more reliable than MR in ruling out cerebral haemorrhage. It may even predict a better prognosis, although much depends on other factors. If the CT is performed within 3 hours of stroke, it helps to identify patients suitable for thrombolytic therapy,4 provided that it is read by a specialist. Perhaps the biggest drawback of a “negative CT” is that it cannot confirm that any infarction has taken place. This makes giving potentially harmful therapies rather awkward, and does little to reassure the patient’s family.


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