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Article: Abnormal diffusion tensor in nonsymptomatic familial amyotrophic lateral sclerosis with a causative superoxide dismutase 1 mutation

TitleAbnormal diffusion tensor in nonsymptomatic familial amyotrophic lateral sclerosis with a causative superoxide dismutase 1 mutation
Authors
KeywordsALS
DTI
Familial
Nonsymptomatic
SOD1 mutation
Issue Date2008
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/1053-1807/
Citation
Journal Of Magnetic Resonance Imaging, 2008, v. 27 n. 1, p. 8-13 How to Cite?
Abstract
Purpose: To determine whether diffusion abnormalities can be observed in nonsymptomatic family members with a known causative Cu/Zn superoxide dismutase mutation (asymptomatic familial amyotrophic lateral sclerosis; AFALS +SOD1) in a family with autosomal dominant familial amyotrophic lateral sclerosis (ALS) using diffusion tensor imaging (DTI). Materials and Methods: A total of eight AFALS +SOD1 subjects (aged 17-43 years) were age-matched with 13 healthy controls (aged 19-45 years) without SOD1 mutations. DTI was carried out on a 1.5T scanner. The diffusion index maps derived were then normalized spatially for voxel-based analysis, region of interest (ROI)-based analysis was also carried out. Results: Our voxel-based and ROI-based analysis showed that AFALS +SOD1 subjects have decreased fractional anisotropy (FA) (0.5401 vs. 0.5168, P < 0.05) and increased tensor trace (TT) (2.5854 × 10 -3 mm 2/second vs. 2.6226 × 10 -3 mm 2/second, P < 0.04) at the posterior limb of the internal capsule compared to the control subjects. Increased radial diffusivity (E (2,3)/2) was detected on both sides (right = 0.5710 × 10 -3 mm 2/second vs. 0.5943 × 10 -3 mm 2/second, P < 0.05; left = 0.5666 × 10 -3 mm 2/second vs. 0.5872 × 10 -3 mm 2/second, P < 0.05). No significant change in axial diffusivity (E 1) was detected. Conclusion: Abnormal diffusivity was found at the posterior limb of the internal capsule in AFALS +SOD1 subjects, hitherto unreported. Our results suggest that DTI may detect diffusion abnormalities in AFALS +SOD1 subjects before symptoms develop. © 2007 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/68021
ISSN
2013 Impact Factor: 2.788
ISI Accession Number ID
References

 

Author Affiliations
  1. The University of Hong Kong
  2. University of Birmingham
DC FieldValueLanguage
dc.contributor.authorNg, MCen_HK
dc.contributor.authorHo, JTen_HK
dc.contributor.authorHo, SLen_HK
dc.contributor.authorLee, Ren_HK
dc.contributor.authorLi, Gen_HK
dc.contributor.authorCheng, TSen_HK
dc.contributor.authorSong, YQen_HK
dc.contributor.authorHo, PWLen_HK
dc.contributor.authorFong, GCYen_HK
dc.contributor.authorMak, Wen_HK
dc.contributor.authorChan, KHen_HK
dc.contributor.authorLi, LSWen_HK
dc.contributor.authorLuk, KDKen_HK
dc.contributor.authorHu, Yen_HK
dc.contributor.authorRamsden, DBen_HK
dc.contributor.authorLeong, LLYen_HK
dc.date.accessioned2010-09-06T06:00:35Z-
dc.date.available2010-09-06T06:00:35Z-
dc.date.issued2008en_HK
dc.identifier.citationJournal Of Magnetic Resonance Imaging, 2008, v. 27 n. 1, p. 8-13en_HK
dc.identifier.issn1053-1807en_HK
dc.identifier.urihttp://hdl.handle.net/10722/68021-
dc.description.abstractPurpose: To determine whether diffusion abnormalities can be observed in nonsymptomatic family members with a known causative Cu/Zn superoxide dismutase mutation (asymptomatic familial amyotrophic lateral sclerosis; AFALS +SOD1) in a family with autosomal dominant familial amyotrophic lateral sclerosis (ALS) using diffusion tensor imaging (DTI). Materials and Methods: A total of eight AFALS +SOD1 subjects (aged 17-43 years) were age-matched with 13 healthy controls (aged 19-45 years) without SOD1 mutations. DTI was carried out on a 1.5T scanner. The diffusion index maps derived were then normalized spatially for voxel-based analysis, region of interest (ROI)-based analysis was also carried out. Results: Our voxel-based and ROI-based analysis showed that AFALS +SOD1 subjects have decreased fractional anisotropy (FA) (0.5401 vs. 0.5168, P < 0.05) and increased tensor trace (TT) (2.5854 × 10 -3 mm 2/second vs. 2.6226 × 10 -3 mm 2/second, P < 0.04) at the posterior limb of the internal capsule compared to the control subjects. Increased radial diffusivity (E (2,3)/2) was detected on both sides (right = 0.5710 × 10 -3 mm 2/second vs. 0.5943 × 10 -3 mm 2/second, P < 0.05; left = 0.5666 × 10 -3 mm 2/second vs. 0.5872 × 10 -3 mm 2/second, P < 0.05). No significant change in axial diffusivity (E 1) was detected. Conclusion: Abnormal diffusivity was found at the posterior limb of the internal capsule in AFALS +SOD1 subjects, hitherto unreported. Our results suggest that DTI may detect diffusion abnormalities in AFALS +SOD1 subjects before symptoms develop. © 2007 Wiley-Liss, Inc.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/1053-1807/en_HK
dc.relation.ispartofJournal of Magnetic Resonance Imagingen_HK
dc.rightsJournal of Magnetic Resonance Imaging. Copyright © John Wiley & Sons, Inc.en_HK
dc.subjectALSen_HK
dc.subjectDTIen_HK
dc.subjectFamilialen_HK
dc.subjectNonsymptomaticen_HK
dc.subjectSOD1 mutationen_HK
dc.subject.meshAdolescenten_HK
dc.subject.meshAdulten_HK
dc.subject.meshAmyotrophic Lateral Sclerosis - enzymology - genetics - pathologyen_HK
dc.subject.meshAnisotropyen_HK
dc.subject.meshDiffusion Magnetic Resonance Imaging - methodsen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImage Processing, Computer-Assisteden_HK
dc.subject.meshMaleen_HK
dc.subject.meshMutationen_HK
dc.subject.meshStatistics, Nonparametricen_HK
dc.subject.meshSuperoxide Dismutase - geneticsen_HK
dc.titleAbnormal diffusion tensor in nonsymptomatic familial amyotrophic lateral sclerosis with a causative superoxide dismutase 1 mutationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1053-1807&volume=27&issue=1&spage=8&epage=13&date=2008&atitle=Abnormal+diffusion+tensor+in+nonsymptomatic+familial+amyotrophic+lateral+sclerosis+with+a+causative+superoxide+dismutase+1+mutation.en_HK
dc.identifier.emailHo, SL:slho@hku.hken_HK
dc.identifier.emailSong, YQ:songy@hkucc.hku.hken_HK
dc.identifier.emailHo, PWL:hwl2002@hku.hken_HK
dc.identifier.emailLuk, KDK:hcm21000@hku.hken_HK
dc.identifier.emailHu, Y:yhud@hku.hken_HK
dc.identifier.authorityHo, SL=rp00240en_HK
dc.identifier.authoritySong, YQ=rp00488en_HK
dc.identifier.authorityHo, PWL=rp00259en_HK
dc.identifier.authorityLuk, KDK=rp00333en_HK
dc.identifier.authorityHu, Y=rp00432en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/jmri.21217en_HK
dc.identifier.pmid18022844en_HK
dc.identifier.scopuseid_2-s2.0-37849027014en_HK
dc.identifier.hkuros143686en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-37849027014&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume27en_HK
dc.identifier.issue1en_HK
dc.identifier.spage8en_HK
dc.identifier.epage13en_HK
dc.identifier.isiWOS:000252104100002-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridNg, MC=7202076279en_HK
dc.identifier.scopusauthoridHo, JT=55166751200en_HK
dc.identifier.scopusauthoridHo, SL=25959633500en_HK
dc.identifier.scopusauthoridLee, R=7408202795en_HK
dc.identifier.scopusauthoridLi, G=35767974200en_HK
dc.identifier.scopusauthoridCheng, TS=7404082613en_HK
dc.identifier.scopusauthoridSong, YQ=7404921212en_HK
dc.identifier.scopusauthoridHo, PWL=25027612100en_HK
dc.identifier.scopusauthoridFong, GCY=7004978754en_HK
dc.identifier.scopusauthoridMak, W=22948344000en_HK
dc.identifier.scopusauthoridChan, KH=7406034963en_HK
dc.identifier.scopusauthoridLi, LSW=7501450364en_HK
dc.identifier.scopusauthoridLuk, KDK=7201921573en_HK
dc.identifier.scopusauthoridHu, Y=7407116091en_HK
dc.identifier.scopusauthoridRamsden, DB=7102612805en_HK
dc.identifier.scopusauthoridLeong, LLY=7004323766en_HK

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