Metabolic patterns in brain 18F-fluorodeoxyglucose PET relate to aetiology in paediatric dystonia
Abstract There is a lack of imaging markers revealing the functional characteristics of different brain regions in paediatric dystonia. In this observational study, we assessed the utility of [18F]2-fluoro-2-deoxy-D-glucose (FDG)-PET in understanding dystonia pathophysiology by revealing specific re...
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| Veröffentlicht in: | Brain (London, England : 1878) England : 1878), 2023-06, Vol.146 (6), p.2512-2523 |
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| creator | Tsagkaris, Stavros Yau, Eric K C McClelland, Verity Papandreou, Apostolos Siddiqui, Ata Lumsden, Daniel E Kaminska, Margaret Guedj, Eric Hammers, Alexander Lin, Jean-Pierre |
| description | Abstract
There is a lack of imaging markers revealing the functional characteristics of different brain regions in paediatric dystonia. In this observational study, we assessed the utility of [18F]2-fluoro-2-deoxy-D-glucose (FDG)-PET in understanding dystonia pathophysiology by revealing specific resting awake brain glucose metabolism patterns in different childhood dystonia subgroups. PET scans from 267 children with dystonia being evaluated for possible deep brain stimulation surgery between September 2007 and February 2018 at Evelina London Children’s Hospital (ELCH), UK, were examined. Scans without gross anatomical abnormality (e.g. large cysts, significant ventriculomegaly; n = 240) were analysed with Statistical Parametric Mapping (SPM12). Glucose metabolism patterns were examined in the 144/240 (60%) cases with the 10 commonest childhood-onset dystonias, focusing on nine anatomical regions. A group of 39 adult controls was used for comparisons. The genetic dystonias were associated with the following genes: TOR1A, THAP1, SGCE, KMT2B, HPRT1 (Lesch Nyhan disease), PANK2 and GCDH (Glutaric Aciduria type 1). The acquired cerebral palsy (CP) cases were divided into those related to prematurity (CP-Preterm), neonatal jaundice/kernicterus (CP-Kernicterus) and hypoxic-ischaemic encephalopathy (CP-Term). Each dystonia subgroup had distinct patterns of altered FDG-PET uptake. Focal glucose hypometabolism of the pallidi, putamina or both, was the commonest finding, except in PANK2, where basal ganglia metabolism appeared normal. HPRT1 uniquely showed glucose hypometabolism across all nine cerebral regions. Temporal lobe glucose hypometabolism was found in KMT2B, HPRT1 and CP-Kernicterus. Frontal lobe hypometabolism was found in SGCE, HPRT1 and PANK2. Thalamic and brainstem hypometabolism were seen only in HPRT1, CP-Preterm and CP-term dystonia cases. The combination of frontal and parietal lobe hypermetabolism was uniquely found in CP-term cases. PANK2 cases showed a distinct combination of parietal hypermetabolism with cerebellar hypometabolism but intact putaminal-pallidal glucose metabolism. HPRT1, PANK2, CP-kernicterus and CP-preterm cases had cerebellar and insula glucose hypometabolism as well as parietal glucose hypermetabolism. The study findings offer insights into the pathophysiology of dystonia and support the network theory for dystonia pathogenesis. ‘Signature’ patterns for each dystonia subgroup could be a useful biomarker to guide differential |
| doi_str_mv | 10.1093/brain/awac439 |
| format | Article |
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There is a lack of imaging markers revealing the functional characteristics of different brain regions in paediatric dystonia. In this observational study, we assessed the utility of [18F]2-fluoro-2-deoxy-D-glucose (FDG)-PET in understanding dystonia pathophysiology by revealing specific resting awake brain glucose metabolism patterns in different childhood dystonia subgroups. PET scans from 267 children with dystonia being evaluated for possible deep brain stimulation surgery between September 2007 and February 2018 at Evelina London Children’s Hospital (ELCH), UK, were examined. Scans without gross anatomical abnormality (e.g. large cysts, significant ventriculomegaly; n = 240) were analysed with Statistical Parametric Mapping (SPM12). Glucose metabolism patterns were examined in the 144/240 (60%) cases with the 10 commonest childhood-onset dystonias, focusing on nine anatomical regions. A group of 39 adult controls was used for comparisons. The genetic dystonias were associated with the following genes: TOR1A, THAP1, SGCE, KMT2B, HPRT1 (Lesch Nyhan disease), PANK2 and GCDH (Glutaric Aciduria type 1). The acquired cerebral palsy (CP) cases were divided into those related to prematurity (CP-Preterm), neonatal jaundice/kernicterus (CP-Kernicterus) and hypoxic-ischaemic encephalopathy (CP-Term). Each dystonia subgroup had distinct patterns of altered FDG-PET uptake. Focal glucose hypometabolism of the pallidi, putamina or both, was the commonest finding, except in PANK2, where basal ganglia metabolism appeared normal. HPRT1 uniquely showed glucose hypometabolism across all nine cerebral regions. Temporal lobe glucose hypometabolism was found in KMT2B, HPRT1 and CP-Kernicterus. Frontal lobe hypometabolism was found in SGCE, HPRT1 and PANK2. Thalamic and brainstem hypometabolism were seen only in HPRT1, CP-Preterm and CP-term dystonia cases. The combination of frontal and parietal lobe hypermetabolism was uniquely found in CP-term cases. PANK2 cases showed a distinct combination of parietal hypermetabolism with cerebellar hypometabolism but intact putaminal-pallidal glucose metabolism. HPRT1, PANK2, CP-kernicterus and CP-preterm cases had cerebellar and insula glucose hypometabolism as well as parietal glucose hypermetabolism. The study findings offer insights into the pathophysiology of dystonia and support the network theory for dystonia pathogenesis. ‘Signature’ patterns for each dystonia subgroup could be a useful biomarker to guide differential diagnosis and inform personalized management strategies.
Tsagkaris et al. report that subgroups of patients with paediatric dystonia with different aetiologies show distinct patterns of 18F-FDG-PET metabolism that can be linked to the clinical signs in each group. These signature patterns could be useful imaging biomarkers to guide differential diagnosis and personalised management.</description><identifier>ISSN: 0006-8950</identifier><identifier>EISSN: 1460-2156</identifier><identifier>DOI: 10.1093/brain/awac439</identifier><identifier>PMID: 36445406</identifier><language>eng</language><publisher>US: Oxford University Press</publisher><subject>Adult ; Apoptosis Regulatory Proteins - metabolism ; Brain - metabolism ; Cerebral Palsy ; Child ; DNA-Binding Proteins - metabolism ; Dystonia - metabolism ; Dystonic Disorders - metabolism ; Fluorodeoxyglucose F18 - metabolism ; Glucose - metabolism ; Human health and pathology ; Humans ; Infant, Newborn ; Kernicterus - complications ; Kernicterus - metabolism ; Life Sciences ; Molecular Chaperones - metabolism ; Original ; Positron-Emission Tomography - methods</subject><ispartof>Brain (London, England : 1878), 2023-06, Vol.146 (6), p.2512-2523</ispartof><rights>The Author(s) 2022. Published by Oxford University Press on behalf of the Guarantors of Brain. 2022</rights><rights>The Author(s) 2022. Published by Oxford University Press on behalf of the Guarantors of Brain.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c385t-b42f9c99fcfc85a5146112fbe584b3cb2e1a1eec2e2bbecce7ab6b0bc24d1e813</citedby><cites>FETCH-LOGICAL-c385t-b42f9c99fcfc85a5146112fbe584b3cb2e1a1eec2e2bbecce7ab6b0bc24d1e813</cites><orcidid>0000-0002-3537-9714 ; 0000-0002-9637-567X ; 0000-0001-9314-2259</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,1583,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36445406$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-03970350$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Tsagkaris, Stavros</creatorcontrib><creatorcontrib>Yau, Eric K C</creatorcontrib><creatorcontrib>McClelland, Verity</creatorcontrib><creatorcontrib>Papandreou, Apostolos</creatorcontrib><creatorcontrib>Siddiqui, Ata</creatorcontrib><creatorcontrib>Lumsden, Daniel E</creatorcontrib><creatorcontrib>Kaminska, Margaret</creatorcontrib><creatorcontrib>Guedj, Eric</creatorcontrib><creatorcontrib>Hammers, Alexander</creatorcontrib><creatorcontrib>Lin, Jean-Pierre</creatorcontrib><title>Metabolic patterns in brain 18F-fluorodeoxyglucose PET relate to aetiology in paediatric dystonia</title><title>Brain (London, England : 1878)</title><addtitle>Brain</addtitle><description>Abstract
There is a lack of imaging markers revealing the functional characteristics of different brain regions in paediatric dystonia. In this observational study, we assessed the utility of [18F]2-fluoro-2-deoxy-D-glucose (FDG)-PET in understanding dystonia pathophysiology by revealing specific resting awake brain glucose metabolism patterns in different childhood dystonia subgroups. PET scans from 267 children with dystonia being evaluated for possible deep brain stimulation surgery between September 2007 and February 2018 at Evelina London Children’s Hospital (ELCH), UK, were examined. Scans without gross anatomical abnormality (e.g. large cysts, significant ventriculomegaly; n = 240) were analysed with Statistical Parametric Mapping (SPM12). Glucose metabolism patterns were examined in the 144/240 (60%) cases with the 10 commonest childhood-onset dystonias, focusing on nine anatomical regions. A group of 39 adult controls was used for comparisons. The genetic dystonias were associated with the following genes: TOR1A, THAP1, SGCE, KMT2B, HPRT1 (Lesch Nyhan disease), PANK2 and GCDH (Glutaric Aciduria type 1). The acquired cerebral palsy (CP) cases were divided into those related to prematurity (CP-Preterm), neonatal jaundice/kernicterus (CP-Kernicterus) and hypoxic-ischaemic encephalopathy (CP-Term). Each dystonia subgroup had distinct patterns of altered FDG-PET uptake. Focal glucose hypometabolism of the pallidi, putamina or both, was the commonest finding, except in PANK2, where basal ganglia metabolism appeared normal. HPRT1 uniquely showed glucose hypometabolism across all nine cerebral regions. Temporal lobe glucose hypometabolism was found in KMT2B, HPRT1 and CP-Kernicterus. Frontal lobe hypometabolism was found in SGCE, HPRT1 and PANK2. Thalamic and brainstem hypometabolism were seen only in HPRT1, CP-Preterm and CP-term dystonia cases. The combination of frontal and parietal lobe hypermetabolism was uniquely found in CP-term cases. PANK2 cases showed a distinct combination of parietal hypermetabolism with cerebellar hypometabolism but intact putaminal-pallidal glucose metabolism. HPRT1, PANK2, CP-kernicterus and CP-preterm cases had cerebellar and insula glucose hypometabolism as well as parietal glucose hypermetabolism. The study findings offer insights into the pathophysiology of dystonia and support the network theory for dystonia pathogenesis. ‘Signature’ patterns for each dystonia subgroup could be a useful biomarker to guide differential diagnosis and inform personalized management strategies.
Tsagkaris et al. report that subgroups of patients with paediatric dystonia with different aetiologies show distinct patterns of 18F-FDG-PET metabolism that can be linked to the clinical signs in each group. These signature patterns could be useful imaging biomarkers to guide differential diagnosis and personalised management.</description><subject>Adult</subject><subject>Apoptosis Regulatory Proteins - metabolism</subject><subject>Brain - metabolism</subject><subject>Cerebral Palsy</subject><subject>Child</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Dystonia - metabolism</subject><subject>Dystonic Disorders - metabolism</subject><subject>Fluorodeoxyglucose F18 - metabolism</subject><subject>Glucose - metabolism</subject><subject>Human health and pathology</subject><subject>Humans</subject><subject>Infant, Newborn</subject><subject>Kernicterus - complications</subject><subject>Kernicterus - metabolism</subject><subject>Life Sciences</subject><subject>Molecular Chaperones - metabolism</subject><subject>Original</subject><subject>Positron-Emission Tomography - methods</subject><issn>0006-8950</issn><issn>1460-2156</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>TOX</sourceid><sourceid>EIF</sourceid><recordid>eNqFkc1v1DAQxS1ERZfCkSvKEQ6h_t7khKqqpUiL2kN7tsbOZGvkjYPtFPa_J9tdyseF00gzb35PM4-QN4x-YLQVpzaBH07hOzgp2mdkwaSmNWdKPycLSqmum1bRY_Iy56-UMim4fkGOhZZSSaoXBL5gARuDd9UIpWAacuWH6pFaseay7sMUU-ww_tiuw-Rixurm4rZKGKBgVWIFWHwMcb3d7Y2AnYeSZly3zSUOHl6Rox5CxteHekLuLi9uz6_q1fWnz-dnq9qJRpXaSt63rm1717tGgZrvYIz3FlUjrXCWIwOG6Dhya9E5XILVllrHZcewYeKEfNxzx8lusHM4lATBjMlvIG1NBG_-ngz-3qzjg2GUC861nAnv94T7f_auzlZm16OiXVKh6MPO7d3BLcVvE-ZiNj47DAEGjFM2fCm5Vo2gepbWe6lLMeeE_RObUbPL0Dx-2xwynPVv_zzkSf0rtN_ecRr_w_oJv-iqJQ</recordid><startdate>20230601</startdate><enddate>20230601</enddate><creator>Tsagkaris, Stavros</creator><creator>Yau, Eric K C</creator><creator>McClelland, Verity</creator><creator>Papandreou, Apostolos</creator><creator>Siddiqui, Ata</creator><creator>Lumsden, Daniel E</creator><creator>Kaminska, Margaret</creator><creator>Guedj, Eric</creator><creator>Hammers, Alexander</creator><creator>Lin, Jean-Pierre</creator><general>Oxford University Press</general><scope>TOX</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>1XC</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-3537-9714</orcidid><orcidid>https://orcid.org/0000-0002-9637-567X</orcidid><orcidid>https://orcid.org/0000-0001-9314-2259</orcidid></search><sort><creationdate>20230601</creationdate><title>Metabolic patterns in brain 18F-fluorodeoxyglucose PET relate to aetiology in paediatric dystonia</title><author>Tsagkaris, Stavros ; Yau, Eric K C ; McClelland, Verity ; Papandreou, Apostolos ; Siddiqui, Ata ; Lumsden, Daniel E ; Kaminska, Margaret ; Guedj, Eric ; Hammers, Alexander ; Lin, Jean-Pierre</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c385t-b42f9c99fcfc85a5146112fbe584b3cb2e1a1eec2e2bbecce7ab6b0bc24d1e813</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Adult</topic><topic>Apoptosis Regulatory Proteins - metabolism</topic><topic>Brain - metabolism</topic><topic>Cerebral Palsy</topic><topic>Child</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Dystonia - metabolism</topic><topic>Dystonic Disorders - metabolism</topic><topic>Fluorodeoxyglucose F18 - metabolism</topic><topic>Glucose - metabolism</topic><topic>Human health and pathology</topic><topic>Humans</topic><topic>Infant, Newborn</topic><topic>Kernicterus - complications</topic><topic>Kernicterus - metabolism</topic><topic>Life Sciences</topic><topic>Molecular Chaperones - metabolism</topic><topic>Original</topic><topic>Positron-Emission Tomography - methods</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tsagkaris, Stavros</creatorcontrib><creatorcontrib>Yau, Eric K C</creatorcontrib><creatorcontrib>McClelland, Verity</creatorcontrib><creatorcontrib>Papandreou, Apostolos</creatorcontrib><creatorcontrib>Siddiqui, Ata</creatorcontrib><creatorcontrib>Lumsden, Daniel E</creatorcontrib><creatorcontrib>Kaminska, Margaret</creatorcontrib><creatorcontrib>Guedj, Eric</creatorcontrib><creatorcontrib>Hammers, Alexander</creatorcontrib><creatorcontrib>Lin, Jean-Pierre</creatorcontrib><collection>Oxford University Press Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Brain (London, England : 1878)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tsagkaris, Stavros</au><au>Yau, Eric K C</au><au>McClelland, Verity</au><au>Papandreou, Apostolos</au><au>Siddiqui, Ata</au><au>Lumsden, Daniel E</au><au>Kaminska, Margaret</au><au>Guedj, Eric</au><au>Hammers, Alexander</au><au>Lin, Jean-Pierre</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Metabolic patterns in brain 18F-fluorodeoxyglucose PET relate to aetiology in paediatric dystonia</atitle><jtitle>Brain (London, England : 1878)</jtitle><addtitle>Brain</addtitle><date>2023-06-01</date><risdate>2023</risdate><volume>146</volume><issue>6</issue><spage>2512</spage><epage>2523</epage><pages>2512-2523</pages><issn>0006-8950</issn><eissn>1460-2156</eissn><abstract>Abstract
There is a lack of imaging markers revealing the functional characteristics of different brain regions in paediatric dystonia. In this observational study, we assessed the utility of [18F]2-fluoro-2-deoxy-D-glucose (FDG)-PET in understanding dystonia pathophysiology by revealing specific resting awake brain glucose metabolism patterns in different childhood dystonia subgroups. PET scans from 267 children with dystonia being evaluated for possible deep brain stimulation surgery between September 2007 and February 2018 at Evelina London Children’s Hospital (ELCH), UK, were examined. Scans without gross anatomical abnormality (e.g. large cysts, significant ventriculomegaly; n = 240) were analysed with Statistical Parametric Mapping (SPM12). Glucose metabolism patterns were examined in the 144/240 (60%) cases with the 10 commonest childhood-onset dystonias, focusing on nine anatomical regions. A group of 39 adult controls was used for comparisons. The genetic dystonias were associated with the following genes: TOR1A, THAP1, SGCE, KMT2B, HPRT1 (Lesch Nyhan disease), PANK2 and GCDH (Glutaric Aciduria type 1). The acquired cerebral palsy (CP) cases were divided into those related to prematurity (CP-Preterm), neonatal jaundice/kernicterus (CP-Kernicterus) and hypoxic-ischaemic encephalopathy (CP-Term). Each dystonia subgroup had distinct patterns of altered FDG-PET uptake. Focal glucose hypometabolism of the pallidi, putamina or both, was the commonest finding, except in PANK2, where basal ganglia metabolism appeared normal. HPRT1 uniquely showed glucose hypometabolism across all nine cerebral regions. Temporal lobe glucose hypometabolism was found in KMT2B, HPRT1 and CP-Kernicterus. Frontal lobe hypometabolism was found in SGCE, HPRT1 and PANK2. Thalamic and brainstem hypometabolism were seen only in HPRT1, CP-Preterm and CP-term dystonia cases. The combination of frontal and parietal lobe hypermetabolism was uniquely found in CP-term cases. PANK2 cases showed a distinct combination of parietal hypermetabolism with cerebellar hypometabolism but intact putaminal-pallidal glucose metabolism. HPRT1, PANK2, CP-kernicterus and CP-preterm cases had cerebellar and insula glucose hypometabolism as well as parietal glucose hypermetabolism. The study findings offer insights into the pathophysiology of dystonia and support the network theory for dystonia pathogenesis. ‘Signature’ patterns for each dystonia subgroup could be a useful biomarker to guide differential diagnosis and inform personalized management strategies.
Tsagkaris et al. report that subgroups of patients with paediatric dystonia with different aetiologies show distinct patterns of 18F-FDG-PET metabolism that can be linked to the clinical signs in each group. These signature patterns could be useful imaging biomarkers to guide differential diagnosis and personalised management.</abstract><cop>US</cop><pub>Oxford University Press</pub><pmid>36445406</pmid><doi>10.1093/brain/awac439</doi><tpages>12</tpages><orcidid>https://orcid.org/0000-0002-3537-9714</orcidid><orcidid>https://orcid.org/0000-0002-9637-567X</orcidid><orcidid>https://orcid.org/0000-0001-9314-2259</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Apoptosis Regulatory Proteins - metabolism Brain - metabolism Cerebral Palsy Child DNA-Binding Proteins - metabolism Dystonia - metabolism Dystonic Disorders - metabolism Fluorodeoxyglucose F18 - metabolism Glucose - metabolism Human health and pathology Humans Infant, Newborn Kernicterus - complications Kernicterus - metabolism Life Sciences Molecular Chaperones - metabolism Original Positron-Emission Tomography - methods |
| title | Metabolic patterns in brain 18F-fluorodeoxyglucose PET relate to aetiology in paediatric dystonia |
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