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Paradoxical embolisation and cerebral white matter lesions in dementia

¹ University of Manchester, Division of Psychiatry, Education and Research Centre, Wythenshawe Hospital, Wythenshawe, Manchester M23 9LT, UK, ² Radboud University Nijmegen Medical Centre, Department of Psychiatry (961), PO Box 9101, 6500 HB, Nijmegen, the Netherlands, ³ Vascular Studies Unit, Academic Surgery Unit, University of Manchester, South Manchester University Hospital, Wythenshawe, Manchester M23 9LT, ⁴ Imaging Science & Biomedical Engineering, University of Manchester, Manchester M13 9PT, UK

Correspondence: Prof Alan Jackson, Division of Imaging Science, The Medical School, University of Manchester, Oxford Rd, Manchester M13 9PT, UK. E-mail: alan.jackson{at}manchester.ac.uk

The study aimed to examine the relationship between spontaneous cerebral emboli (SCE), patent foramen ovale (PFO) and white matter hyperintensities (WMH) on cerebral MRI in patients with Alzheimer's disease (AD) and vascular dementia (VaD). SCE were identified by transcranial Doppler of the middle cerebral artery for 1 h. A "significant" v-aCS (venous-to-arterial circulation shunt indicative of PFO; 15 embolic signals within 12 cardiac cycles) was detected by intravenous injection of "air in saline" ultrasound contrast. Deep white matter hyperintensities (DWMH) and periventricular hyperintensities (PVH) were assessed using Schelten's scale. After correction for cardiovascular risk factors, both DWMH and PVH were significantly associated with the presence of a PFO in AD (β = 0.31, p = 0.02 for DWMH, odds ratio 8.7, p = 0.011 for PVH) but not in VaD. No consistent relationship was found between SCE and WMH in AD. In VaD, the severity of DWMH was negatively correlated with SCE (β = –0.55; p = 0.001). In conclusion, the presence of a significant venous-to-arterial shunt is associated with more severe DWMH in AD, and may play a part in the aetiology of the disorder. In addition, there is a significant negative correlation between SCE and DWMH in VaD, which supports the hypothesis that VaD may be the result of ischaemic injury, predominantly reflecting embolic aetiology.

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