Brain diffusion‐weighted imaging in Friedreich's ataxia
Identifieur interne : 001778 ( Main/Exploration ); précédent : 001777; suivant : 001779Brain diffusion‐weighted imaging in Friedreich's ataxia
Auteurs : Giovanni Rizzo [Italie] ; Caterina Tonon [Italie] ; Maria Lucia Valentino [Italie] ; David Manners [Italie] ; Filippo Fortuna [Italie] ; Cinzia Gellera [Italie] ; Antonella Pini [Italie] ; Alessandro Ghezzo [Italie] ; Agostino Baruzzi [Italie] ; Claudia Testa [Italie] ; Emil Malucelli [Italie] ; Bruno Barbiroli [Italie] ; Valerio Carelli [Italie] ; Raffaele Lodi [Italie]Source :
- Movement Disorders [ 0885-3185 ] ; 2011-03.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Adolescent, Adult, Brain (pathology), Brain Mapping, Diffusion Magnetic Resonance Imaging (methods), Disability Evaluation, Encephalon, Female, Friedreich Ataxia (diagnosis), Friedreich Ataxia (genetics), Friedreich Ataxia (metabolism), Friedreich Ataxia (physiopathology), Friedreich ataxia, Friedreich's ataxia, Humans, Image Processing, Computer-Assisted, MRI, Male, Nervous system diseases, Nuclear magnetic resonance imaging, Regression Analysis, Reproducibility of Results, Retrospective Studies, Young Adult, diffusion‐weighted imaging.
- MESH :
- diagnosis : Friedreich Ataxia.
- genetics : Friedreich Ataxia.
- metabolism : Friedreich Ataxia.
- methods : Diffusion Magnetic Resonance Imaging.
- pathology : Brain.
- physiopathology : Friedreich Ataxia.
- Adolescent, Adult, Brain Mapping, Disability Evaluation, Female, Humans, Image Processing, Computer-Assisted, Male, Regression Analysis, Reproducibility of Results, Retrospective Studies, Young Adult.
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
Affiliations:
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<term>Adult</term>
<term>Brain (pathology)</term>
<term>Brain Mapping</term>
<term>Diffusion Magnetic Resonance Imaging (methods)</term>
<term>Disability Evaluation</term>
<term>Encephalon</term>
<term>Female</term>
<term>Friedreich Ataxia (diagnosis)</term>
<term>Friedreich Ataxia (genetics)</term>
<term>Friedreich Ataxia (metabolism)</term>
<term>Friedreich Ataxia (physiopathology)</term>
<term>Friedreich ataxia</term>
<term>Friedreich's ataxia</term>
<term>Humans</term>
<term>Image Processing, Computer-Assisted</term>
<term>MRI</term>
<term>Male</term>
<term>Nervous system diseases</term>
<term>Nuclear magnetic resonance imaging</term>
<term>Regression Analysis</term>
<term>Reproducibility of Results</term>
<term>Retrospective Studies</term>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Friedreich Ataxia</term>
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<keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Diffusion Magnetic Resonance Imaging</term>
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<term>Disability Evaluation</term>
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<term>Humans</term>
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<term>Male</term>
<term>Regression Analysis</term>
<term>Reproducibility of Results</term>
<term>Retrospective Studies</term>
<term>Young Adult</term>
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<term>Hérédodégénérescence spinocérébelleuse de Friedreich</term>
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<front><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>
</front>
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<name sortKey="Barbiroli, Bruno" sort="Barbiroli, Bruno" uniqKey="Barbiroli B" first="Bruno" last="Barbiroli">Bruno Barbiroli</name>
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