Enlarged perivascular spaces are brain vascular changes in which the space between blood vessels and the pia mater enlarges locally. Despite recent efforts, their etiology and significance are not well understood yet by the research community, which is limited by technical challenges in the quantitative evaluation of enlarged perivascular spaces. Enlarged perivascular spaces are believed to result from either hypertension, obstruction, inflammation, atrophy, or recently, even glymphatic clearance. The emergence of new results on the significance of associations between enlarged perivascular spaces and multiple neurovascular disorders - such as stroke or vascular dementia - strongly encourages the community to overcome the technical limitations and understand the enlargement of perivascular spaces in depth.
Research into enlarged perivascular spaces has been limited by technical challenges in their quantification. These challenges stem from the fact that perivascular spaces can be numerous - leading to time-consuming manual counting - and most importantly, that the cut-off between normal and enlarged perivascular space is loosely defined. Despite standardization initiatives, there is still substantial variability in the quantification of perivascular spaces from one study to another. Most of the research into perivascular spaces is realized using categorical scores which only coarsely summarize the enlarged perivascular space burden. In addition, the detailed analysis of potential quantification mistakes with other local cerebrovascular abnormal changes is often omitted. Recently, automatic quantification methods have emerged, but they are either imperfect, incomplete or used in a few studies. In this research series, we would like to aggregate articles that promote a more precise quantification of enlarged perivascular spaces and demonstrate results on their etiology and clinical relevance for cerebral disorders.
We welcome submissions on original research articles or reviews targeting fine-grained quantification of perivascular spaces with applications to their etiology and clinical relevance. More precisely, we are interested in articles that treat the following theme (but not limited to):
• Localization of perivascular in the brain beyond the centrum semiovale, basal ganglia, brainstem, and hippocampus: sub-regions and other brain regions
• Asymmetry of perivascular space distribution
• Enlarged perivascular spaces - symptom mapping
• Extraction of shape and volumetric features
• Enlarged perivascular spaces mimics: differential diagnosis between enlarged perivascular spaces and similar local brain changes
• Multi-modal MRI analysis of enlarged perivascular spaces
Novel methods that demonstrate to achieve such quantification are very welcome, and methods that can combine it with association studies on determinants and pathologies will be favored.
Beyond those cited above, examples of relevant determinants, pathologies, and medication could include:
• Brain damage
• Brain functional networks
• Steroid response and stress responses
• Loss of white matter or changes in myelination
• Anti-seizure medications
• Chemotherapeutics
Enlarged perivascular spaces are brain vascular changes in which the space between blood vessels and the pia mater enlarges locally. Despite recent efforts, their etiology and significance are not well understood yet by the research community, which is limited by technical challenges in the quantitative evaluation of enlarged perivascular spaces. Enlarged perivascular spaces are believed to result from either hypertension, obstruction, inflammation, atrophy, or recently, even glymphatic clearance. The emergence of new results on the significance of associations between enlarged perivascular spaces and multiple neurovascular disorders - such as stroke or vascular dementia - strongly encourages the community to overcome the technical limitations and understand the enlargement of perivascular spaces in depth.
Research into enlarged perivascular spaces has been limited by technical challenges in their quantification. These challenges stem from the fact that perivascular spaces can be numerous - leading to time-consuming manual counting - and most importantly, that the cut-off between normal and enlarged perivascular space is loosely defined. Despite standardization initiatives, there is still substantial variability in the quantification of perivascular spaces from one study to another. Most of the research into perivascular spaces is realized using categorical scores which only coarsely summarize the enlarged perivascular space burden. In addition, the detailed analysis of potential quantification mistakes with other local cerebrovascular abnormal changes is often omitted. Recently, automatic quantification methods have emerged, but they are either imperfect, incomplete or used in a few studies. In this research series, we would like to aggregate articles that promote a more precise quantification of enlarged perivascular spaces and demonstrate results on their etiology and clinical relevance for cerebral disorders.
We welcome submissions on original research articles or reviews targeting fine-grained quantification of perivascular spaces with applications to their etiology and clinical relevance. More precisely, we are interested in articles that treat the following theme (but not limited to):
• Localization of perivascular in the brain beyond the centrum semiovale, basal ganglia, brainstem, and hippocampus: sub-regions and other brain regions
• Asymmetry of perivascular space distribution
• Enlarged perivascular spaces - symptom mapping
• Extraction of shape and volumetric features
• Enlarged perivascular spaces mimics: differential diagnosis between enlarged perivascular spaces and similar local brain changes
• Multi-modal MRI analysis of enlarged perivascular spaces
Novel methods that demonstrate to achieve such quantification are very welcome, and methods that can combine it with association studies on determinants and pathologies will be favored.
Beyond those cited above, examples of relevant determinants, pathologies, and medication could include:
• Brain damage
• Brain functional networks
• Steroid response and stress responses
• Loss of white matter or changes in myelination
• Anti-seizure medications
• Chemotherapeutics