Longitudinal changes in brains of patients with fluent primary progressive aphasia

Heim, Stefan; Pieperhoff, Peter; Grande, M.; Kuijsten, Wiebke; Wellner, Barbara; Sáez, Louise Etcheverry; Schulte, Stephanie; Südmeyer, Martin; Caspers, Svenja; Minnerop, Martina; Binkofski, Ferdinand; Huber, Walter; Amunts, Katrin

doi:10.1016/j.bandl.2013.05.012

Cited by 14 publications

(9 citation statements)

References 43 publications

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“…Moreover, there are few studies that have assessed the cerebral metabolism or brain atrophy in PPA-plus phases and whether the impairment of some regions may be associated to different clinical syndromes [5][6][7][8][9][10][11].…”

Section: Introductionmentioning

confidence: 98%

Clinical course of primary progressive aphasia: clinical and FDG-PET patterns

et al. 2014

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Primary progressive aphasia (PPA) may be the onset of several neurodegenerative diseases. This study evaluates a cohort of patients with PPA to assess their progression to different clinical syndromes, associated factors that modulate this progression, and patterns of cerebral metabolism linked to different clinical evolutionary forms. Thirty-five patients meeting PPA criteria underwent a clinical and neuroimaging (18)F-Fluorodeoxyglucose PET evaluation. Survival analysis was performed using time from clinical onset to the development of a non-language symptom or deficit (PPA-plus). Cerebral metabolism was analyzed using Statistical Parametric Mapping. Patients classified into three PPA variants evolved to atypical parkinsonism, behavioral disorder and motor neuron disease in the agrammatic variant; to behavioral disorder in the semantic; and to memory impairment in the logopenic. Median time from the onset of symptoms to PPA-plus was 36 months (31-40, 95 % confidence interval). Right laterality, and years of education were associated to a lower risk of progression, while logopenic variant to a higher risk. Different regions of hypometabolism were identified in agrammatic PPA with parkinsonism, motor neuron disease and logopenic PPA-plus. Clinical course of PPA differs according to each variant. Left anterior temporal and frontal medial hypometabolism in agrammatic variant is linked to motor neuron disease and atypical parkinsonism, respectively. PPA variant, laterality and education may be associated to the risk of progression. These results suggest the possibility that clinical and imaging data could help to predict the clinical course of PPA.

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Section: Introductionmentioning

confidence: 98%

Clinical course of primary progressive aphasia: clinical and FDG-PET patterns

et al. 2014

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“…Cognitively, lvPPA, svPPA, and nfvPPA variants are characterized by core language deficits involving repetition, comprehension, and agrammatism, respectively [1]. Structural neuroimaging studies also highlight distinct, primarily left hemispheric, patterns of atrophy in temporal and frontal lobe structures, across PPA variants [1][2][3][4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Divergent Longitudinal Propagation of White Matter Degradation in Logopenic and Semantic Variants of Primary Progressive Aphasia

Leyton

Hodges

et al. 2015

JAD

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Abstract.Background: Clinico-pathological distinction of primary progressive aphasia (PPA) can be challenging at clinic presentation. In particular, cross-sectional neuroimaging signatures across the logopenic (lvPPA) and semantic (svPPA) variants are difficult to establish, with longitudinal profiles showing greater divergence. Objective: Assess longitudinal propagation of white matter degradation in lvPPA and svPPA to determine disease progression over time, and whether this reflects distinct underlying pathology. Method: A cohort of 27 patients with dementia (12 lvPPA; 15 svPPA) and 12 healthy controls were assessed at baseline and 1-year follow-up on the Addenbrooke's Cognitive Examination-Revised and Sydney Language Battery. Diffusion weighted images were collected at both time-points and analyzed for longitudinal white matter change using DTI-TK and TBSS. Results: LvPPA patients showed a significant decline in naming and repetition, over 1 year, while svPPA patients declined in naming and comprehension. Longitudinal imaging revealed widespread bilateral degradation of white matter tracts in lvPPA over a 1-year period with early involvement of the left posterior inferior longitudinal fasciculus (ILF). SvPPA demonstrated focal left lateralized white matter degradation involving the uncinate fasciculus (UF) and anterior ILF, propagating to the right UF with disease progression. Conclusions: LvPPA and svPPA cohorts showed distinct longitudinal cognitive and white matter profiles. We propose differences in multi-centric and focal white matter dysfunction in lvPPA and svPPA, respectively, reflect underlying pathological differences. The clinical relevance of white matter degradation and mechanisms underlying disease propagation are discussed.

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“…Une é tude en IRM fonctionnelle montre une hyperactivation des structures atrophié es et adjacentes, interpré té e comme le reflet d'un mé canisme de compensation permettant le maintien des performances langagiè res alors que l'activation controlaté rale n'est pas efficace [84].…”

Section: Irmunclassified

“…Le degré d'atrophie au cours du temps est, lui aussi, moindre dans ce groupe « atypique ». La mise en place de mé canismes de compensation est é voqué e avec notamment un recrutement des ré gions homolaté rales adjacentes en IRM fonctionnelle [84].…”

Section: E´volution Des Troubles Et Pronosticunclassified