Cerebellovascular Disease: MR imaging

Abstract

Cerebellovascular disease refers to a group of cerebellar conditions related to its blood supply. In part I, we assessed cerebellar infarcts in relation to vascular territories. First, we critically appraised the existing classification system of small cerebellar infarcts, and propose to classify small cerebellar infarcts according to anatomical location instead of presumed border zones in between perfusion territories. This is expected to improve clinicoradiological correlation and may allow for a more reliable and reproducible classification. Still, the holy grail in stroke medicine remains to link infarcts with the responsible diseased artery by direct imaging of involved perfusion territories. This brings us to our next objective, which was to develop an innovative imaging technique to visualise cerebellar arterial perfusion territories in vivo. In order to visualise the cerebellar PICA-perfusion territories, we studied 14 healthy subjects with super-selective ASL MRI. By labelling both vertebral arteries, we were able to distinguish the territories supplied by one vertebral artery (PICA) from those supplied by both vertebral arteries (AICA and SCA) and from the contralateral vertebral artery (contralateral PICA). We demonstrated the high variability in the extent of the PICA, but also showed that the medial posterior inferior cerebellar surfaces were invariably perfused by the PICA. Our next goal was to investigate the occurrence and topographical patterns of incidental cerebellar infarcts in a cohort of 636 patients with arterial disease from the SMART-Medea study. Unlike cerebellar infarcts studied in the symptomatic stage, small cerebellar infarcts proved to outnumber large cerebellar infarcts by a factor of almost 20. We also found that the overwhelming majority of cerebellar infarcts comprised small infarct cavities within the cerebellar cortex. These cavities will be the subject of part II of this thesis, which begins with a radiological-pathological validation study. In 40 whole cerebella scanned with 7T ex vivo MRI, we found that 20 out of 22 cerebellar cavities were located in the cortex, and these were therefore named cerebellar cortical infarct cavities. All cavities retrieved on histopathological examination were compatible with an ischaemic origin. Additionally, we translated our findings towards lower field-strengths (1.5T) in vivo. This allowed us to study the epidaemiology of cerebellar cortical infarct cavities in the 636 patients from the SMART-Medea study, and found a significant relationship with markers of atherosclerosis, imaging markers of atherothromboembolic cerebrovascular disease, and worse physical but not mental functioning. In our final study, we observed cerebellar cortical infarct cavities ≤ 1.5 cm in 16 of 46 patients with a recent vertebrobasilar TIA or stroke and a symptomatic vertebral artery stenosis ≥50% from the Vertebral Artery Stenting Trial. Since only one of these 16 patients was known with a prior history of vertebrobasilar TIA or stroke, cerebellar cortical infarct cavities should be added to the spectrum of common incidental brain infarcts detectible on routine MRI. Identification of cerebellar cortical infarct cavities on MRI not only increases the visible burden of brain infarcts, but also adds insights to the temporal and spatial distribution of brain infarcts.