LETTER TO THE EDITOR

LETTER TO THE EDITOR

M. Ng and P. Singh University of Cambridge, Cambridge, UK Correspondence: M. Ng, University of Cambridge School of Clinical Medicine, Hills Road, Cambridge, CB2 0SP, UK (tel.: +44 7816 789382; fax: +44 1223 336709; e-mail: [email protected]).

Keywords: dementia, lacunar infarction, small vessel disease, vascular pathology doi:10.1111/ene.12610 Received: 21 September 2014 Accepted: 8 October 2014 Dear Editor, We read with interest the study by Kitagawa et al. [1] which found that lacunar infarction, especially if multiple, is significantly associated with incident dementia. They used lacunar infarction as a surrogate marker of small vessel disease (SVD), defining it as a supratentorial hypointensity of a specified size. Lacunar infarcts are thought to result primarily from SVD occluding a small perforating artery supplying deep structures of the brain [2]. The group’s findings support

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the previously proposed theory that SVD causes cognitive decline and plays an important role in the pathogenesis of dementia [3]. Small vessel pathology can result in ischaemia or haemorrhage. Other markers of SVD on brain magnetic resonance imaging (MRI) besides lacunar infarction include white matter hyperintensities, cerebral microbleeds and visible perivascular spaces, easily imaged parenchymal lesions which reflect underlying vessel changes [2]. The mechanisms that result in these parenchymal lesions are heterogeneous and poorly understood and use of lacunar infarction as a marker of SVD may be an oversimplification. Importantly, small subcortical infarcts may not be the result of SVD but of embolic causes. Adachi et al. found that large vessel disease can result in small lacunarlike infarcts. They propose that the other markers of white matter hyperintensities and visible perivascular spaces should be used to distinguish these from pure lacunar infarcts resulting from SVD [4]. Staals et al. suggest that a ‘total SVD burden score’ might be better suited to reflect the total brain damage caused by SVD. It takes into account all of the individual markers on brain MRI, which are all considered consequences of SVD, irrespective of potentially different pathogeneses. The score is higher in patients presenting with acute lacunar infarction

compared with acute cortical stroke and it is associated with vascular risk factors [3]. The score has not yet been validated for dementia or cognitive decline but it is potentially a more representative marker of total brain SVD and may help to further elucidate the role of SVD in dementia, particularly if the pathogenetic mechanisms underlying the different individual features are better characterized. Disclosure of conflicts of interest The authors declare no financial or other conflicts of interest. References

1. Kitagawa K, Miwa K, Yagita Y, Okazaki S, Sakaguchi M, Mochizuki H. Association between carotid stenosis or lacunar infarction and incident dementia in patients with vascular risk factors. Eur J Neurol 2015; 22: 187–192. 2. Pantoni L. Cerebral small vessel disease: from pathogenesis and clinical characteristics to therapeutic challenges. Lancet Neurol 2010; 9: 689–701. 3. Staals J, Makin SDJ, Doubal FN, Dennis MS, Wardlaw JM. Stroke subtype, vascular risk factors, and total MRI brain small-vessel disease burden. Neurology 2014; 83: 1228–1234. 4. Adachi T, Kobayashi S, Yamaguchi S, Okada K. MRI findings of small subcortical ‘lacunar-like’ infarction resulting from large vessel disease. J Neurol 2000; 247: 280–285.

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EUROPEAN JOURNAL OF NEUROLOGY

Use of lacunar infarction as a marker of small vessel disease

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Use of lacunar infarction as a marker of small vessel disease.

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