BACKGROUND: Small cerebellar cavities (≤15 mm) are often observed coincidentally in ageing subjects and have also been associated with migraine. Although generally assumed to be of ischaemic origin, descriptive imaging studies are sparse and imaging findings have not been correlated with histopathology. We aimed to investigate whether small ischaemic cavities in the cerebellum show characteristic infarct patterns that might be helpful for diagnostic imaging. METHODS: We examined 40 whole postmortem cerebella with 7-tesla MRI ex vivo for the presence of small ischaemic cavities. The scan protocol included a T2-, T2*- and fluid-attenuated inversion recovery-weighted sequence for all specimens. We investigated to which degree small ischaemic cavities affect the cortical, juxtacortical and/or deep subcortical regions of the cerebellum. In a subset of the cavities identified, we correlated the imaging data with histopathological findings. This was performed by cutting the particular cerebellar specimen into 5-mm-thick slices. Serial sections were performed if cavities remained unidentified macroscopically. RESULTS: Twenty-two cavities were seen on ex vivo MRI in 8 out of 40 examined cerebella. Twenty out of 22 cerebellar cavities were located in the cortex, and only 2 in the deep white matter, with no cavities located in the juxtacortical white matter. None of the 20 cerebellar cortical cavities showed extension into the juxtacortical white matter on MRI, although in 1 cortical cavity some surrounding gliosis was seen to extend into the juxtacortical white matter. Nine out of 22 cavities were sampled for pathological correlation, including 7 cerebellar cortical cavities and both cavities or lacunes in the deep white matter. Three out of 7 cortical and both the deep cavities were histopathologically verified as cavities of ischaemic origin, while the remaining cortical cavities could not be retrieved upon histopathologic examination. Some microscopic gliosis was seen to extend into the juxtacortical white matter of all confirmed cortical cavities. CONCLUSION: Knowledge of typical infarct patterns may facilitate the detection and characterisation of cerebellar ischaemic cavities in vivo. Cerebellar cortical cavities appeared to be much more common than deep cavities and presented on imaging as a full-thickness defect in the cerebellar cortex without extension in the adjacent white matter.
BACKGROUND: Small cerebellar cavities (≤15 mm) are often observed coincidentally in ageing subjects and have also been associated with migraine. Although generally assumed to be of ischaemic origin, descriptive imaging studies are sparse and imaging findings have not been correlated with histopathology. We aimed to investigate whether small ischaemic cavities in the cerebellum show characteristic infarct patterns that might be helpful for diagnostic imaging. METHODS: We examined 40 whole postmortem cerebella with 7-tesla MRI ex vivo for the presence of small ischaemic cavities. The scan protocol included a T2-, T2*- and fluid-attenuated inversion recovery-weighted sequence for all specimens. We investigated to which degree small ischaemic cavities affect the cortical, juxtacortical and/or deep subcortical regions of the cerebellum. In a subset of the cavities identified, we correlated the imaging data with histopathological findings. This was performed by cutting the particular cerebellar specimen into 5-mm-thick slices. Serial sections were performed if cavities remained unidentified macroscopically. RESULTS: Twenty-two cavities were seen on ex vivo MRI in 8 out of 40 examined cerebella. Twenty out of 22 cerebellar cavities were located in the cortex, and only 2 in the deep white matter, with no cavities located in the juxtacortical white matter. None of the 20 cerebellar cortical cavities showed extension into the juxtacortical white matter on MRI, although in 1 cortical cavity some surrounding gliosis was seen to extend into the juxtacortical white matter. Nine out of 22 cavities were sampled for pathological correlation, including 7 cerebellar cortical cavities and both cavities or lacunes in the deep white matter. Three out of 7 cortical and both the deep cavities were histopathologically verified as cavities of ischaemic origin, while the remaining cortical cavities could not be retrieved upon histopathologic examination. Some microscopic gliosis was seen to extend into the juxtacortical white matter of all confirmed cortical cavities. CONCLUSION: Knowledge of typical infarct patterns may facilitate the detection and characterisation of cerebellar ischaemic cavities in vivo. Cerebellar cortical cavities appeared to be much more common than deep cavities and presented on imaging as a full-thickness defect in the cerebellar cortex without extension in the adjacent white matter.
Authors: Laurens J L De Cocker; A Compter; L J Kappelle; P R Luijten; J Hendrikse; H B Van der Worp Journal: Neuroradiology Date: 2016-05-28 Impact factor: 2.804
Authors: Hille Koppen; Inge H Palm-Meinders; Werner H Mess; Ruud W Keunen; Gisela M Terwindt; Lenore J Launer; Mark A van Buchem; Mark C Kruit; Michel D Ferrari Journal: Neurology Date: 2016-03-11 Impact factor: 9.910
Authors: Laurens J L De Cocker; Mirjam I Geerlings; Nolan S Hartkamp; Anne M Grool; Willem P Mali; Yolanda Van der Graaf; Raoul P Kloppenborg; Jeroen Hendrikse Journal: Neuroimage Clin Date: 2015-02-09 Impact factor: 4.881
Authors: Laurens Jl De Cocker; Arjen Lindenholz; Jaco Jm Zwanenburg; Anja G van der Kolk; Maarten Zwartbol; Peter R Luijten; Jeroen Hendrikse Journal: Neuroimage Date: 2016-11-18 Impact factor: 6.556
Authors: Melissa A Batson; Natalia Petridou; Dennis W J Klomp; Maarten A Frens; Sebastiaan F W Neggers Journal: PLoS One Date: 2015-08-10 Impact factor: 3.240