Diffusion Tensor Imaging in Idiopathic Parkinson's Disease and Multisystem Atrophy (Parkinsonian Type)

Cnyrim, C.; Kupsch, Andreas; Ebersbach, Georg; Hoffmann, Karl‐Titus

doi:10.1159/000348512

Cited by 19 publications

(7 citation statements)

References 43 publications

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“…In addition, FAt values were increased in the putamen and caudate, and increased fractional anisotropy in grey matter regions could be a signal of gliosis (Budde et al, 2011). Although altered diffusion has been reported consistently in the putamen of MSA (Seppi et al, 2003;Kanazawa et al, 2004;Schocke et al, 2004;Nicoletti et al, 2006;Ito et al, 2007;Kö llensperger et al, 2007;Chung et al, 2009;Pellecchia et al, 2009;Tsukamoto et al, 2012;Baudrexel et al, 2013;Umemura et al, 2013;Cnyrim et al, 2014), the microstructural composition of the other basal ganglia nuclei is less clear, results are more variable, and STN has not been a focus of previous research. Correlation analyses revealed a significant positive relation across disease groups between total MDS-UPDRS-III and FAt values in the putamen, lobule V of the cerebellum, and cerebellar vermis.…”

Section: Discussionmentioning

confidence: 99%

“…In PSP, diffusion studies using a single tensor model have reported lower fractional anisotropy values and higher axial diffusivity, radial diffusivity, mean diffusivity, and apparent diffusion coefficient in the superior cerebellar peduncle (Blain et al, 2006;Nicoletti et al, 2008;Knake et al, 2010;Whitwell et al, 2011;Saini et al, 2012;Tsukamoto et al, 2012;Agosta et al, 2014;Tessitore et al, 2014;Worker et al, 2014). In MSA, studies using a single tensor model have found lower fractional anisotropy values and higher axial diffusivity, radial diffusivity, mean diffusivity, and apparent diffusion coefficient in the middle cerebellar peduncle (Shiga et al, 2005;Blain et al, 2006;Nicoletti et al, 2006Nicoletti et al, , 2013Paviour et al, 2007;Chung et al, 2009;Pellecchia et al, 2009;Tha et al, 2010;Tsukamoto et al, 2012;Worker et al, 2014), lower fractional anisotropy, higher apparent diffusion coefficient, and higher trace (D) values in the putamen (Schocke et al, 2004;Nicoletti et al, 2006;Ito et al, 2007;Kö llensperger et al, 2007;Chung et al, 2009;Pellecchia et al, 2009;Tsukamoto et al, 2012;Umemura et al, 2013;Cnyrim et al, 2014), and higher mean diffusivity in the cerebellar hemispheres (Nicoletti et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

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Free-water imaging in Parkinson’s disease and atypical parkinsonism

Planetta

Ofori

Pasternak

et al. 2015

Brain

166

195

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Conventional single tensor diffusion analysis models have provided mixed findings in the substantia nigra of Parkinson's disease, but recent work using a bi-tensor analysis model has shown more promising results. Using a bi-tensor model, free-water values were found to be increased in the posterior substantia nigra of Parkinson's disease compared with controls at a single site and in a multi-site cohort. Further, free-water increased longitudinally over 1 year in the posterior substantia nigra of Parkinson's disease. Here, we test the hypothesis that other parkinsonian disorders such as multiple system atrophy and progressive supranuclear palsy have elevated free-water in the substantia nigra. Equally important, however, is whether the bi-tensor diffusion model is able to detect alterations in other brain regions beyond the substantia nigra in Parkinson's disease, multiple system atrophy, and progressive supranuclear palsy and to accurately distinguish between these diseases. Free-water and free-water-corrected fractional anisotropy maps were compared across 72 individuals in the basal ganglia, midbrain, thalamus, dentate nucleus, cerebellar peduncles, cerebellar vermis and lobules V and VI, and corpus callosum. Compared with controls, free-water was increased in the anterior and posterior substantia nigra of Parkinson's disease, multiple system atrophy, and progressive supranuclear palsy. Despite no other changes in Parkinson's disease, we observed elevated free-water in all regions except the dentate nucleus, subthalamic nucleus, and corpus callosum of multiple system atrophy, and in all regions examined for progressive supranuclear palsy. Compared with controls, free-water-corrected fractional anisotropy values were increased for multiple system atrophy in the putamen and caudate, and increased for progressive supranuclear palsy in the putamen, caudate, thalamus, and vermis, and decreased in the superior cerebellar peduncle and corpus callosum. For all disease group comparisons, the support vector machine 10-fold cross-validation area under the curve was between 0.93-1.00 and there was high sensitivity and specificity. The regions and diffusion measures selected by the model varied across comparisons and are consistent with pathological studies. In conclusion, the current study used a novel bi-tensor diffusion analysis model to indicate that all forms of parkinsonism had elevated free-water in the substantia nigra. Beyond the substantia nigra, both multiple system atrophy and progressive supranuclear palsy, but not Parkinson's disease, showed a broad network of elevated free-water and altered free-water corrected fractional anisotropy that included the basal ganglia, thalamus, and cerebellum. These findings may be helpful in the differential diagnosis of parkinsonian disorders, and thereby facilitate the development and assessment of targeted therapies.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Free-water imaging in Parkinson’s disease and atypical parkinsonism

Planetta

Ofori

Pasternak

et al. 2015

Brain

166

195

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“…In quantitative MRI studies, the bilateral R2* increase in putamen best separated MSA-P patients from PD [ 422 ], consistent with susceptibility weighted imaging results demonstrating higher iron deposition in putamen versus PD [ 423 ]. DTI allows differentiation between PD and MSA-P, the latter showing higher values of the apparent diffusion coefficient in the inner capsule, corona radiata, and lateral periputaminal white matter [ 424 ] and other pathological differences between MSA-P and PD [ 425 ]. Combined use of diffusion ratios, magnetic susceptibility values/quantitative susceptibility mapping allowed differentiation of MSA-P and MSA-C from other parkinsonian syndromes, with sensitivities and specificities of 81–100% [ 425a ].…”

Section: Clinical Diagnostic Criteriamentioning

confidence: 99%

Multiple System Atrophy: An Oligodendroglioneural Synucleinopathy1

Jellinger¹

2018

JAD

151

142

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Multiple system atrophy (MSA) is an orphan, fatal, adult-onset neurodegenerative disorder of uncertain etiology that is clinically characterized by various combinations of parkinsonism, cerebellar, autonomic, and motor dysfunction. MSA is an α-synucleinopathy with specific glioneuronal degeneration involving striatonigral, olivopontocerebellar, and autonomic nervous systems but also other parts of the central and peripheral nervous systems. The major clinical variants correlate with the morphologic phenotypes of striatonigral degeneration (MSA-P) and olivopontocerebellar atrophy (MSA-C). While our knowledge of the molecular pathogenesis of this devastating disease is still incomplete, updated consensus criteria and combined fluid and imaging biomarkers have increased its diagnostic accuracy. The neuropathologic hallmark of this unique proteinopathy is the deposition of aberrant α-synuclein in both glia (mainly oligodendroglia) and neurons forming glial and neuronal cytoplasmic inclusions that cause cell dysfunction and demise. In addition, there is widespread demyelination, the pathogenesis of which is not fully understood. The pathogenesis of MSA is characterized by propagation of misfolded α-synuclein from neurons to oligodendroglia and cell-to-cell spreading in a “prion-like” manner, oxidative stress, proteasomal and mitochondrial dysfunction, dysregulation of myelin lipids, decreased neurotrophic factors, neuroinflammation, and energy failure. The combination of these mechanisms finally results in a system-specific pattern of neurodegeneration and a multisystem involvement that are specific for MSA. Despite several pharmacological approaches in MSA models, addressing these pathogenic mechanisms, no effective neuroprotective nor disease-modifying therapeutic strategies are currently available. Multidisciplinary research to elucidate the genetic and molecular background of the deleterious cycle of noxious processes, to develop reliable biomarkers and targets for effective treatment of this hitherto incurable disorder is urgently needed.

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“…In a recent meta-analysis [13], the authors concluded that DTI may be a promising paraclinical biomarker in neurodegenerative parkinsonian syndromes and may have a future role in differential diagnosis [14]. DTI has previously been applied to PSP and has demonstrated diffusivity abnormalities in frontoparietal/frontotemporo-occipital connections and the corpus callosum (CC) [15].…”

Section: Introductionmentioning

confidence: 99%

Frontal Corpus Callosum Alterations in Progressive Supranuclear Palsy but Not in Parkinson's Disease

et al. 2014

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Background: Frontal lobe involvement is considered a clinical and magnetic resonance imaging (MRI) feature in later stages of progressive supranuclear palsy (PSP). Objective: Diffusion tensor imaging (DTI) was used to investigate the integrity of frontal pathways in PSP and Parkinson's disease (PD) patients. Methods: DTI and 3-D MRI were performed in 15 PSP patients (parkinsonism subtype: n = 8; Richardson subtype: n = 7), 15 PD patients, and 18 matched controls. DTI analysis was performed in order to identify differences along frontal white matter structures including the corpus callosum (CC) and was complemented by atlas-based volumetry and planimetry. Results: Significantly reduced regional fractional anisotropy was observed for PSP patients versus controls and PSP versus PD patients, respectively, in frontal areas including the area II of the CC and bilaterally in the callosal radiation. The DTI findings correlated with frontal lobe volumes. These differences were not observed between PD patients and controls. Conclusion: DTI identified a PSP-associated microstructural alteration pattern in the frontal lobes and in the CC area II including the corresponding bilateral callosal radiation tracts that could not be identified in both control samples, supporting the prominent PSP-associated frontal involvement as a potential neuroimaging marker.

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Diffusion Tensor Imaging in Idiopathic Parkinson's Disease and Multisystem Atrophy (Parkinsonian Type)

Cited by 19 publications

References 43 publications

Free-water imaging in Parkinson’s disease and atypical parkinsonism

Free-water imaging in Parkinson’s disease and atypical parkinsonism

Multiple System Atrophy: An Oligodendroglioneural Synucleinopathy1

Frontal Corpus Callosum Alterations in Progressive Supranuclear Palsy but Not in Parkinson's Disease

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