<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Rua C</submitter><funding>University of Oxford Medical Sciences Division COVID-19 Research Response Fund</funding><funding>Cambridge Centre for Parkinson-Plus</funding><funding>NIHR Oxford Biomedical Research Centre</funding><funding>Medical Research Council</funding><funding>NIHR Cambridge Biomedical Research Centre</funding><funding>National Institute for Health Research (NIHR)</funding><funding>NIHR Oxford Health Biomedical Research Centre</funding><funding>Wellcome Trust</funding><funding>BHF Centre of Research Excellence, Oxford</funding><funding>Academy of Medical Sciences/The Health Foundation Clinician Scientist Fellowship</funding><pagination>4121-4130</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7616766</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>147(12)</volume><pubmed_abstract>Post-mortem studies have shown that patients dying from severe acute respiratory syndrome coronavirus (SARS-CoV-2) infection frequently have pathological changes in their CNS, particularly in the brainstem. Many of these changes are proposed to result from para-infectious and/or post-infection immune responses. Clinical symptoms such as fatigue, breathlessness, and chest pain are frequently reported in post-hospitalized coronavirus disease 2019 (COVID-19) patients. We propose that these symptoms are in part due to damage to key neuromodulatory brainstem nuclei. While brainstem involvement has been demonstrated in the acute phase of the illness, the evidence of long-term brainstem change on MRI is inconclusive. We therefore used ultra-high field (7 T) quantitative susceptibility mapping (QS</pubmed_abstract><journal>Brain : a journal of neurology</journal><pubmed_title>Quantitative susceptibility mapping at 7 T in COVID-19: brainstem effects and outcome associations.</pubmed_title><pmcid>PMC7616766</pmcid><funding_grant_id>103838</funding_grant_id><funding_grant_id>203139/Z/16/Z</funding_grant_id><funding_grant_id>NIHR203312</funding_grant_id><funding_grant_id>BRC-1215-20008</funding_grant_id><funding_grant_id>225924/Z/22/Z</funding_grant_id><funding_grant_id>098436/Z/12/B</funding_grant_id><funding_grant_id>220258</funding_grant_id><funding_grant_id>0009118</funding_grant_id><funding_grant_id>MC_UU_00030/14</funding_grant_id><funding_grant_id>NIHR203316</funding_grant_id><funding_grant_id>BRC-1215-20014</funding_grant_id><pubmed_authors>Outtrim JG</pubmed_authors><pubmed_authors>Menon DK</pubmed_authors><pubmed_authors>Lupson VC</pubmed_authors><pubmed_authors>Ersche KD</pubmed_authors><pubmed_authors>Stamatakis EA</pubmed_authors><pubmed_authors>Pattinson K</pubmed_authors><pubmed_authors>Manktelow A</pubmed_authors><pubmed_authors>Newcombe VFJ</pubmed_authors><pubmed_authors>Chatfield DA</pubmed_authors><pubmed_authors>Clare S</pubmed_authors><pubmed_authors>Rowe JB</pubmed_authors><pubmed_authors>Sawcer SJ</pubmed_authors><pubmed_authors>Neubauer S</pubmed_authors><pubmed_authors>Bullmore ET</pubmed_authors><pubmed_authors>McDonald R</pubmed_authors><pubmed_authors>Qiu L</pubmed_authors><pubmed_authors>Williams GB</pubmed_authors><pubmed_authors>Rodgers CT</pubmed_authors><pubmed_authors>Clarke WT</pubmed_authors><pubmed_authors>Cassar M</pubmed_authors><pubmed_authors>Rua C</pubmed_authors><pubmed_authors>Ezra M</pubmed_authors><pubmed_authors>Raman B</pubmed_authors></additional><is_claimable>false</is_claimable><name>Quantitative susceptibility mapping at 7 T in COVID-19: brainstem effects and outcome associations.</name><description>Post-mortem studies have shown that patients dying from severe acute respiratory syndrome coronavirus (SARS-CoV-2) infection frequently have pathological changes in their CNS, particularly in the brainstem. Many of these changes are proposed to result from para-infectious and/or post-infection immune responses. Clinical symptoms such as fatigue, breathlessness, and chest pain are frequently reported in post-hospitalized coronavirus disease 2019 (COVID-19) patients. We propose that these symptoms are in part due to damage to key neuromodulatory brainstem nuclei. While brainstem involvement has been demonstrated in the acute phase of the illness, the evidence of long-term brainstem change on MRI is inconclusive. We therefore used ultra-high field (7 T) quantitative susceptibility mapping (QS</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Dec</publication><modification>2025-04-04T02:26:43.925Z</modification><creation>2025-04-04T02:26:43.925Z</creation></dates><accession>S-EPMC7616766</accession><cross_references><pubmed>39375207</pubmed><doi>10.1093/brain/awae215</doi></cross_references></HashMap>