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Are multiple acute small subcortical infarctions caused by embolic mechanisms?
  1. B Norrving
  1. Department of Clinical Neuroscience, Lund University Hospital, Sweden
  1. Correspondence to:
 Dr B Norrving
 Department of Neurology, Lund University Hospital, Lund S-22185, Sweden;

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Multiple lacunar infarct mechanisms

In this issue the paper by Chowdhury et al (see page 1416)1 is an important addition to the list of recent publications that challenge traditional concepts on the mechanisms of acute ischaemic stroke. According to conventional teaching, an acute ischaemic stroke is characterised by infarction confined to a single localised (focal) region of the brain. However, new neuroimaging techniques—in particular diffusion weighted magnetic resonance imaging (dw-MRI)—have modified this view.

In a recent study,2 scattered lesions in one vascular territory or multiple lesions in multiple vascular territories were actually more common than single lesions. Although dw-MRI is very sensitive in the ultra-early detection of cerebral ischaemia, it should be recognised that the dw-MRI lesions are not equivalent with infarction. Dw-MRI abnormalities may be reversible if the level of ischaemia is mild, or if early reperfusion occurs—for example, by means of thrombolytic therapy. Nevertheless, dw-MRI findings may give clues to underlying pathophysiology.

Scattered or multiple acute ischaemic lesion patterns have been associated with embolism from cardiac or large artery sources,2 which, in particular, should also be logically plausible if cortical territories are involved. However, in the present series of 10 patients with multiple infarcts mainly confined to subcortical regions,1 an embolic source was found in only one case. Could an embolic source have been over-looked? The possibility cannot be excluded because the patients were not investigated with trans-oesophageal ultrasound (which might have disclosed atherosclerotic aortic arch disease, for example); however, it appears unlikely.

The dw-MRI findings suggested that the subcortical lesions had occurred within several weeks rather than at exactly the same time. Also in this field, concepts have changed: the acute phase of ischaemic stroke is much more dynamic than previously thought. A recent dw-MRI study3 disclosed early recurrent lesions on neuroimaging in one third of all patients within the first week, while clinical recurrence was evident in only 2%. Accepting that embolism is the unlikely cause in the present series, what other mechanisms may cause a clustering of multifocal cerebral ischaemia? At present, the answer is unknown but systemic factors like blood pressure regulation, haemorheological factors, infection, endothelial dysfunction, and possibly even stress might contribute. The present study underscores current gaps in the knowledge of precipitating causes of acute cerebral ischaemia—an under-investigated topic.

The present study also highlights recent insights that “silent” or “covert” cerebral infarcts are severalfold more common than ischaemic stroke, i.e. infarcts that present with the acute onset of focal neurological deficits. According to a recent analysis, less than 7% of all cerebrovascular lesions are associated with overt clinical symptoms, i.e. fulfilling the definition of stroke.4 Covent cerebrovascular lesions are important determinants for cognitive dysfunction, dementia, recurrent stroke, and death.

Recent technological advances have provided us with the tools for research into these issues. Progress in diagnosis and prevention of overt and covert cerebrovascular disease will require an open mind, ready to challenge traditional concepts of cerebrovascular disease.

Multiple lacunar infarct mechanisms


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