Abstract

Sirs: Modern concepts of the pathophysiology of cerebral ischemic syndromes have been strongly influenced by modern brain imaging. The high contrast of the acute ischemic lesion on diffusion-weighted MRI (DWI) against the dark background facilitates the detection of acute lesions even when they are of minute size. For large stroke lesions, it has been repeatedly shown that acute lesions on DWI, the area of severe hypoperfusion on perfusion-weighted MRI (PWI), and the vessel status on MR angiographic images, all provide important information with regard to the underlying pathophysiology. Consequently the socalled mismatch concept between the acute DWI and PWI lesion is nowadays frequently used in clinical trials, and within institutional protocols, to estimate the potential benefit from thrombolytic treatment. Although the diagnostic information obtained in large strokes is important, the value of demonstrating acute, small DWI lesions is also very considerable. In particular, conventional T2weighted MRI and (even more so) CT may not be able to differentiate the acute from chronic lesions (or to detect a small lesion at all on CT). Because of this lack of sensitivity, a negative conventional MRI or CT often generates diagnostic uncertainty. It is not surprising that very small DWI lesions may not directly cause clinical manifestations. However, the information conveyed by the presence and morphological appearance of acute lesions may be clinically useful. The mechanism of acute stroke is often of relevance for the assignment of the stroke etiology and for an early estimation of the individual prognosis. Such new information has already led to a reassessment of the concepts of transient ischemic attacks and subcortical stroke syndromes [1, 2]. From the multiplicity of lesions and their anatomical pattern and distribution, several papers have already demonstrated that the aetiology can be inferred, e.g. hemodynamic stroke patterns versus stroke patterns in endocarditis with a proximal embolic source or cerebral vasospasm [3, 4]. In this issue of the Journal of Neurology, Cho and co-authors report their experience with the analysis of multiple cerebral infarcts in acute stroke patients. The authors investigated 67 patients with multiple acute lesions, who underwent DWI within 48 hours after symptom onset. DW images and ADC maps were used for lesion classification. Furthermore, blood markers were also analysed. In 29% of the patients there were indications of possible cardioembolism. Large artery atherosclerosis, or small vessel occlusion in multiple territories, or both in combination, were identified in 34.3%. It is a very interesting but also demanding task to investigate the origin of multiple lesions in more detail. This is particularly so when an embolic source is suspected as the cause of stroke in patients with multiple lesions. In future studies, serial MRI may ascertain the timing of events: whether repeat embolic events have occurred and are responsible for the multiplicity of the lesions or whether a single event and break up of a large embolus is responsible. In this context, transcranial ultrasound can be helpful to confirm the presence of embolic material within the blood flow to the hemispheres. It is a common procedure to use the TOAST criteria for stroke classification. However, for such a detailed analysis with very specific questions this classification may not be ideal. The demonstration of thrombus or a patent foramen ovale on trans-oesophageal echocardiography appears to provide more direct evidence. A most interesting finding in this study was that the CRP was increased in many of the patients with multiple infarcts. This should provide motivation for further investigation of this group of patients, including follow-up MRI and in depth analysis of the potential causes of a CRP elevation, in order to generate new insights into the mechanisms of stroke.

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