Cortical ischemic lesion burden measured by DIR is related to carotid artery disease severity.

نویسندگان

  • Doriana Landi
  • Paola Maggio
  • Domenico Lupoi
  • Paola Palazzo
  • Claudia Altamura
  • Emma Falato
  • Riccardo Altavilla
  • Stefano Vollaro
  • Angela Daniela Coniglio
  • Francesco Tibuzzi
  • Francesco Passarelli
  • Mauro Silvestrini
  • Patrizio Pasqualetti
  • Fabrizio Vernieri
چکیده

BACKGROUND Over time, exposure to cerebrovascular risk factors and carotid artery disease may cause multiple asymptomatic brain cortical and subcortical microinfarcts, which are commonly found at brain autopsy. So far, lack of convenient neuroimaging tools limited the investigation of grey matter ischemic damage in vivo. We applied the Double Inversion Recovery (DIR) sequence to explore the impact of carotid artery disease on intracortical ischemic lesion load in vivo, taking into account the impact of demographic characteristics and vascular risk factors. METHODS DIR was acquired in 62 patients with common cerebrovascular risk factors stratified in three groups according to carotid artery disease severity. Intracortical lesions scored on DIR (DIRlns) were classified by vascular territory, lobe and hemisphere. White matter hyperintensities (WMHs) volume was also quantified on Fluid Attenuated Inversion Recovery sequence (FLAIR). RESULTS Among demographic characteristics and cerebrovascular risk variables explored, General Linear Model indicated that age and carotid artery disease were significantly associated to DIRlns. After correcting for age, DIRlns load was found to be significantly dependent on carotid artery stenosis severity (F(2, 58) = 5.56, p = 0.006). A linear positive correlation between DIRlns and WMHs was found after correcting for age (p = 0.003). CONCLUSIONS Carotid disease severity is associated with DIRlns accrual. Microembolism and impaired cerebral hemodynamics may act as physiopathological mechanisms underlying cortical ischemic damage. The role of other factors, such as small vessel disease and the possible interaction with carotid disease, remains to be further explored.

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عنوان ژورنال:
  • Cerebrovascular diseases

دوره 39 1  شماره 

صفحات  -

تاریخ انتشار 2015