Ischaemic Cavities in the Cerebellum: An Ex Vivo 7-Tesla MRI Study with Pathological Correlation. De Cocker L, van Veluw S, Biessels G et al. Cerebellar Cortical Infarct Cavities and Vertebral Artery Disease. De Cocker L, Compter A, Kappelle L, Luijten P, Hendrikse J, Van der Worp H. Cerebellar Cortical Infarct Cavities: Correlation With Risk Factors and MRI Markers of Cerebrovascular Disease. De Cocker LJ, Kloppenborg RP, van der Graaf Y, Luijten PR, Hendrikse J, Geerlings MI. Cerebellar infarct patterns: The SMART-Medea study. De Cocker LJ, Geerlings MI, Hartkamp NS, Grool AM, Mali WP, Van der Graaf Y, Kloppenborg RP, Hendrikse J. This is generally due to concomitant brainstem infarction, or compressive hydrocephalus, rather than cerebellar infarction in itself. Unusual complications include:Ĭlinical differential considerations include The mortality related to cerebellar infarcts is higher than that of other vascular territories. Only cortical cerebellar infarcts smaller than 0.5 cm in the DWI positive initial stage tend to become imperceptible on routine MRI scans, due to shrinkage and infarct retraction after healing 12. They are easily observed on MRI (and CT) due to high intrinsic contrast between CSF within the cavity and the adjacent parenchyma. Small cerebellar infarcts are often only detected as an incidental (cerebellar cortical) infarct cavity, which are most often smaller than 1 cm and typically involve the cerebellar cortex 10,11. Finally, large and small cerebellar infarcts tend to heal with cavitation, leaving a CSF-filled cavity surrounded by a rim of gliosis 10. In this stage, infarcts may also be seen as areas of parenchymal contrast enhancement, which appears around 1 week and may be visible up to 2 to 4 months after infarction. Also around 10 days, (subacute) infarcts may become hard to identify due to a phenomenon known as “fogging” 9. Brain swelling peaks at about 3 days, after which infarcts diminish in size and diffusion (pseudo-)normalizes after around 10 days (1-4 weeks) 9. In the acute stage, cerebellar infarcts are first seen as hyperintense areas on DWI because of cytotoxic edema with restricted diffusion, after which they soon become hyperintense on FLAIR and T2WI as well 9. Typical features of infarction such as early loss of grey-white differentiation, hypoattenuation and edema, progressing to chronic encephalomalacia may be identified in the relevant vascular territories. These infarcts often involve the apex of cerebellar fissures, which has been referred to as the 'apex-of-fissure' or ' depth-of-fissure' sign 10,14,15. While larger cerebellar infarcts in general involve the cerebellar cortex with a varying amount of adjacent white matter ('arbor vitae'), most small cerebellar infarcts involve the cerebellar cortex in isolation, thus with sparing of white matter 9,10,13. Radiographic featuresĬerebellar infarcts tend to involve the cerebellar cortex 9,10. In the symptomatic stage, they may remain unrecognized because they only present with minor or non-specific clinical findings, because MRI is not performed, or because they may be overlooked on MRI, especially if performed beyond the acute stage of restricted diffusion 9. Small cerebellar infarcts frequently only present as an incidental finding on imaging studies after healing 11,12. Examination findings include incoordination, ataxia, and horizontal nystagmus. Patients may also present with altered conscious state or coma. Many of the symptoms of cerebellar infarction are non-specific, such as nausea, vomiting, dizziness, unsteadiness, and headache, and the clinical diagnosis relies on a focussed neurological examination and a reasonable index of suspicion. However, their true incidence may be much higher, since most cerebellar infarcts are small and may remain unrecognized 10-12. Cerebellar infarcts account for ~2% (range 1.5-2.3%) of all cerebral infarctions 1,2.
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