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000136134 0247_ $$2doi$$a10.1002/mds.23318
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000136134 0247_ $$2ISSN$$a1531-8257
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000136134 037__ $$aDZNE-2020-02456
000136134 041__ $$aEnglish
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000136134 1001_ $$0P:(DE-HGF)0$$aMinnerop, Martina$$b0$$eCorresponding author
000136134 245__ $$aCallosal tissue loss in multiple system atrophy--a one-year follow-up study.
000136134 260__ $$aNew York, NY$$bWiley$$c2010
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000136134 520__ $$aMultiple system atrophy (MSA) is a neurodegenerative disease not only affecting the basal ganglia, brainstem, cerebellum, and intermediolateral cell columns of the spinal cord but also the cerebral cortex. Clinically, cerebellar (MSA-C) and parkinsonian variants of MSA (MSA-P) are distinguished. We investigated 14 MSA patients (10 MSA-C, 4 MSA-P, men: 7, women: 7; age: 61.1 ± 3.3 years) and 14 matched controls (men: 7, women: 7; age: 58.6 ± 5.1 years) with voxel-based morphometry (VBM) to analyze gray and white matter differences both at baseline and at follow-up, 1 year later. Baseline comparisons between patients and controls confirmed significantly less gray matter in MSA in the cerebellum and cerebral cortex, and significantly less white matter in the cerebellar peduncles and brainstem. Comparisons of tissue-loss profiles (i.e., baseline versus follow-up) between patients and controls, revealed white matter reduction in MSA along the middle cerebellar peduncles, reflecting degeneration of the ponto-cerebellar tract as a particularly prominent and progressive morphological alteration in MSA. Comparisons between baseline and follow-up, separately performed in patients and controls, revealed additional white matter reduction in MSA along the corpus callosum at follow-up. This was replicated through additional shape-based analyses indicating a reduced callosal thickness in the anterior and posterior midbody, extending posteriorly into the isthmus. Callosal atrophy may possibly reflect a disease-specific pattern of neurodegeneration and cortical atrophy, fitting well with the predominant impairment of motor functions in the MSA patients.
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000136134 650_2 $$2MeSH$$aAged
000136134 650_2 $$2MeSH$$aAtrophy: pathology
000136134 650_2 $$2MeSH$$aBrain Stem: pathology
000136134 650_2 $$2MeSH$$aCerebellum: pathology
000136134 650_2 $$2MeSH$$aCorpus Callosum: pathology
000136134 650_2 $$2MeSH$$aFemale
000136134 650_2 $$2MeSH$$aFollow-Up Studies
000136134 650_2 $$2MeSH$$aHumans
000136134 650_2 $$2MeSH$$aImage Processing, Computer-Assisted
000136134 650_2 $$2MeSH$$aMagnetic Resonance Imaging
000136134 650_2 $$2MeSH$$aMale
000136134 650_2 $$2MeSH$$aMiddle Aged
000136134 650_2 $$2MeSH$$aMultiple System Atrophy: pathology
000136134 7001_ $$0P:(DE-HGF)0$$aLüders, Eileen$$b1
000136134 7001_ $$0P:(DE-HGF)0$$aSpecht, Karsten$$b2
000136134 7001_ $$0P:(DE-HGF)0$$aRuhlmann, Jürgen$$b3
000136134 7001_ $$0P:(DE-HGF)0$$aSchimke, Nicole$$b4
000136134 7001_ $$0P:(DE-HGF)0$$aThompson, Paul M$$b5
000136134 7001_ $$0P:(DE-HGF)0$$aChou, Yi Y$$b6
000136134 7001_ $$0P:(DE-HGF)0$$aToga, Arthur W$$b7
000136134 7001_ $$0P:(DE-HGF)0$$aAbele, Michael$$b8
000136134 7001_ $$0P:(DE-HGF)0$$aWüllner, Ullrich$$b9
000136134 7001_ $$0P:(DE-2719)2810314$$aKlockgether, Thomas$$b10$$eLast author
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000136134 773__ $$0PERI:(DE-600)2041249-6$$a10.1002/mds.23318$$gVol. 25, no. 15, p. 2613 - 2620$$n15$$p2613-2620$$q25:15<2613 - 2620$$tMovement disorders$$v25$$x0885-3185$$y2010
000136134 8567_ $$2Pubmed Central$$uhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC2989455
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