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Brain diffusion‐weighted imaging in Friedreich's ataxia

Identifieur interne : 002B39 ( Main/Corpus ); précédent : 002B38; suivant : 002B40

Brain diffusion‐weighted imaging in Friedreich's ataxia

Auteurs : Giovanni Rizzo ; Caterina Tonon ; Maria Lucia Valentino ; David Manners ; Filippo Fortuna ; Cinzia Gellera ; Antonella Pini ; Alessandro Ghezzo ; Agostino Baruzzi ; Claudia Testa ; Emil Malucelli ; Bruno Barbiroli ; Valerio Carelli ; Raffaele Lodi

Source :

RBID : ISTEX:74A749AB62758B4B7AE369D7165AFEBB9A1B7E12

English descriptors

Abstract

Background:: Friedreich ataxia (FRDA) is the commonest form of autosomal recessive ataxia. This study aimed to define the extent of the brain damage in FRDA patients and to identify in vivo markers of neurodegeneration, using diffusion‐weighted imaging (DWI). Methods:: We studied 27 FRDA patients and 21 healthy volunteers using a 1.5 T scanner. Axial DW images were obtained and mean diffusivity (MD) maps were generated. Region of interests (ROIs) included medulla, pons, inferior, middle and superior cerebellar peduncles (ICP, SCP, MCP), dentate nucleus, cerebellar white matter, thalamus, caudate, putamen, pallidus, pyramidal tracts at level of posterior limb of internal capsule (PLIC), optic radiations (OR), and corpus callosum. Histograms of MD were generated for all pixels in the whole cerebral hemispheres and infratentorial compartment. Disease severity was assessed by the International Cooperative Ataxia Rating Scale (ICARS). Results:: FRDA patients had significantly higher MD values than controls in medulla (P < 0.001), ICP (P < 0.001), MCP (P < 0.01), SCP (P < 0.001), OR (P < 0.001), and at the level of the infratentorial structures such as brainstem (P < 0.01), cerebellar hemispheres (P < 0.01), and especially in the cerebellar vermis (P < 0.001). MD values were strongly correlated with disease duration and ICARS score. Discussion:: Our results showed that DWI is a suitable non‐invasive technique to quantify the extent of neurodegeneration in FRDA, that appears more extended than previously reported, showing a microstructural involvement of structures such as OR and MCP. © 2011 Movement Disorder Society

Url:
DOI: 10.1002/mds.23518

Links to Exploration step

ISTEX:74A749AB62758B4B7AE369D7165AFEBB9A1B7E12

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<div type="abstract" xml:lang="en">Background:: Friedreich ataxia (FRDA) is the commonest form of autosomal recessive ataxia. This study aimed to define the extent of the brain damage in FRDA patients and to identify in vivo markers of neurodegeneration, using diffusion‐weighted imaging (DWI). Methods:: We studied 27 FRDA patients and 21 healthy volunteers using a 1.5 T scanner. Axial DW images were obtained and mean diffusivity (MD) maps were generated. Region of interests (ROIs) included medulla, pons, inferior, middle and superior cerebellar peduncles (ICP, SCP, MCP), dentate nucleus, cerebellar white matter, thalamus, caudate, putamen, pallidus, pyramidal tracts at level of posterior limb of internal capsule (PLIC), optic radiations (OR), and corpus callosum. Histograms of MD were generated for all pixels in the whole cerebral hemispheres and infratentorial compartment. Disease severity was assessed by the International Cooperative Ataxia Rating Scale (ICARS). Results:: FRDA patients had significantly higher MD values than controls in medulla (P < 0.001), ICP (P < 0.001), MCP (P < 0.01), SCP (P < 0.001), OR (P < 0.001), and at the level of the infratentorial structures such as brainstem (P < 0.01), cerebellar hemispheres (P < 0.01), and especially in the cerebellar vermis (P < 0.001). MD values were strongly correlated with disease duration and ICARS score. Discussion:: Our results showed that DWI is a suitable non‐invasive technique to quantify the extent of neurodegeneration in FRDA, that appears more extended than previously reported, showing a microstructural involvement of structures such as OR and MCP. © 2011 Movement Disorder Society</div>
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<p>Background:: Friedreich ataxia (FRDA) is the commonest form of autosomal recessive ataxia. This study aimed to define the extent of the brain damage in FRDA patients and to identify in vivo markers of neurodegeneration, using diffusion‐weighted imaging (DWI). Methods:: We studied 27 FRDA patients and 21 healthy volunteers using a 1.5 T scanner. Axial DW images were obtained and mean diffusivity (MD) maps were generated. Region of interests (ROIs) included medulla, pons, inferior, middle and superior cerebellar peduncles (ICP, SCP, MCP), dentate nucleus, cerebellar white matter, thalamus, caudate, putamen, pallidus, pyramidal tracts at level of posterior limb of internal capsule (PLIC), optic radiations (OR), and corpus callosum. Histograms of MD were generated for all pixels in the whole cerebral hemispheres and infratentorial compartment. Disease severity was assessed by the International Cooperative Ataxia Rating Scale (ICARS). Results:: FRDA patients had significantly higher MD values than controls in medulla (P < 0.001), ICP (P < 0.001), MCP (P < 0.01), SCP (P < 0.001), OR (P < 0.001), and at the level of the infratentorial structures such as brainstem (P < 0.01), cerebellar hemispheres (P < 0.01), and especially in the cerebellar vermis (P < 0.001). MD values were strongly correlated with disease duration and ICARS score. Discussion:: Our results showed that DWI is a suitable non‐invasive technique to quantify the extent of neurodegeneration in FRDA, that appears more extended than previously reported, showing a microstructural involvement of structures such as OR and MCP. © 2011 Movement Disorder Society</p>
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<p>Friedreich ataxia (FRDA) is the commonest form of autosomal recessive ataxia. This study aimed to define the extent of the brain damage in FRDA patients and to identify in vivo markers of neurodegeneration, using diffusion‐weighted imaging (DWI).</p>
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<p>We studied 27 FRDA patients and 21 healthy volunteers using a 1.5 T scanner. Axial DW images were obtained and mean diffusivity (MD) maps were generated. Region of interests (ROIs) included medulla, pons, inferior, middle and superior cerebellar peduncles (ICP, SCP, MCP), dentate nucleus, cerebellar white matter, thalamus, caudate, putamen, pallidus, pyramidal tracts at level of posterior limb of internal capsule (PLIC), optic radiations (OR), and corpus callosum. Histograms of MD were generated for all pixels in the whole cerebral hemispheres and infratentorial compartment. Disease severity was assessed by the International Cooperative Ataxia Rating Scale (ICARS).</p>
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<p>FRDA patients had significantly higher MD values than controls in medulla (
<i>P</i>
< 0.001), ICP (
<i>P</i>
< 0.001), MCP (
<i>P</i>
< 0.01), SCP (
<i>P</i>
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<i>P</i>
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<i>P</i>
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<i>P</i>
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<i>P</i>
< 0.001). MD values were strongly correlated with disease duration and ICARS score.</p>
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<p>Our results showed that DWI is a suitable non‐invasive technique to quantify the extent of neurodegeneration in
<i>FRDA</i>
, that appears more extended than previously reported, showing a microstructural involvement of structures such as OR and MCP. © 2011 Movement Disorder Society</p>
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<affiliation>MR Spectroscopy Unit, Department of Internal Medicine, Aging and Nephrology, University of Bologna, Bologna, Italy</affiliation>
<description>Correspondence: MR Spectroscopy Unit, Department of Internal Medicine, Aging and Nephrology, University of Bologna, Via Massarenti 9, 40138 Bologna, Italy</description>
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<publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher>
<place>
<placeTerm type="text">Hoboken</placeTerm>
</place>
<dateIssued encoding="w3cdtf">2011-03</dateIssued>
<dateCaptured encoding="w3cdtf">2010-06-21</dateCaptured>
<dateValid encoding="w3cdtf">2010-10-18</dateValid>
<copyrightDate encoding="w3cdtf">2011</copyrightDate>
</originInfo>
<language>
<languageTerm type="code" authority="rfc3066">en</languageTerm>
<languageTerm type="code" authority="iso639-2b">eng</languageTerm>
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<extent unit="figures">3</extent>
<extent unit="tables">4</extent>
<extent unit="references">35</extent>
<extent unit="words">7096</extent>
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<abstract lang="en">Background:: Friedreich ataxia (FRDA) is the commonest form of autosomal recessive ataxia. This study aimed to define the extent of the brain damage in FRDA patients and to identify in vivo markers of neurodegeneration, using diffusion‐weighted imaging (DWI). Methods:: We studied 27 FRDA patients and 21 healthy volunteers using a 1.5 T scanner. Axial DW images were obtained and mean diffusivity (MD) maps were generated. Region of interests (ROIs) included medulla, pons, inferior, middle and superior cerebellar peduncles (ICP, SCP, MCP), dentate nucleus, cerebellar white matter, thalamus, caudate, putamen, pallidus, pyramidal tracts at level of posterior limb of internal capsule (PLIC), optic radiations (OR), and corpus callosum. Histograms of MD were generated for all pixels in the whole cerebral hemispheres and infratentorial compartment. Disease severity was assessed by the International Cooperative Ataxia Rating Scale (ICARS). Results:: FRDA patients had significantly higher MD values than controls in medulla (P < 0.001), ICP (P < 0.001), MCP (P < 0.01), SCP (P < 0.001), OR (P < 0.001), and at the level of the infratentorial structures such as brainstem (P < 0.01), cerebellar hemispheres (P < 0.01), and especially in the cerebellar vermis (P < 0.001). MD values were strongly correlated with disease duration and ICARS score. Discussion:: Our results showed that DWI is a suitable non‐invasive technique to quantify the extent of neurodegeneration in FRDA, that appears more extended than previously reported, showing a microstructural involvement of structures such as OR and MCP. © 2011 Movement Disorder Society</abstract>
<note type="additional physical form">Author Roles and Disclosures</note>
<note type="content">*Relevant conflicts of interest/financial disclosures: Nothing to report. Full financial disclosures and author roles can be found in the online version of this article.</note>
<subject lang="en">
<genre>Keywords</genre>
<topic>Friedreich's ataxia</topic>
<topic>MRI</topic>
<topic>diffusion‐weighted imaging</topic>
</subject>
<relatedItem type="host">
<titleInfo>
<title>Movement Disorders</title>
</titleInfo>
<titleInfo type="abbreviated">
<title>Mov. Disord.</title>
</titleInfo>
<genre type="Journal">journal</genre>
<subject>
<genre>article category</genre>
<topic>Research Article</topic>
</subject>
<identifier type="ISSN">0885-3185</identifier>
<identifier type="eISSN">1531-8257</identifier>
<identifier type="DOI">10.1002/(ISSN)1531-8257</identifier>
<identifier type="PublisherID">MDS</identifier>
<part>
<date>2011</date>
<detail type="volume">
<caption>vol.</caption>
<number>26</number>
</detail>
<detail type="issue">
<caption>no.</caption>
<number>4</number>
</detail>
<extent unit="pages">
<start>705</start>
<end>712</end>
<total>8</total>
</extent>
</part>
</relatedItem>
<identifier type="istex">74A749AB62758B4B7AE369D7165AFEBB9A1B7E12</identifier>
<identifier type="DOI">10.1002/mds.23518</identifier>
<identifier type="ArticleID">MDS23518</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2011 Movement Disorder Society</accessCondition>
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<recordContentSource>WILEY</recordContentSource>
<recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin>
</recordInfo>
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<serie></serie>
</istex>
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