Dataset Information

How the speed of word finding depends on ventral tract integrity in primary progressive aphasia.

ABSTRACT: Primary progressive aphasia (PPA) is a clinical neurodegenerative syndrome with word finding problems as a core clinical symptom. Many aspects of word finding have been clarified in psycholinguistics using picture naming and a picture-word interference (PWI) paradigm, which emulates naming under contextual noise. However, little is known about how word finding depends on white-matter tract integrity, in particular, the atrophy of tracts located ventrally to the Sylvian fissure. To elucidate this question, we examined word finding in individuals with PPA and healthy controls employing PWI, tractography, and computer simulations using the WEAVER++ model of word finding. Twenty-three individuals with PPA and twenty healthy controls named pictures in two noise conditions. Mixed-effects modelling was performed on naming accuracy and reaction time (RT) and fixel-based tractography analyses were conducted to assess the relation between ventral white-matter integrity and naming performance. Naming RTs were longer for individuals with PPA compared to controls and, critically, individuals with PPA showed a larger noise effect compared to controls. Moreover, this difference in noise effect was differentially related to tract integrity. Whereas the noise effect did not depend much on tract integrity in controls, a lower tract integrity was related to a smaller noise effect in individuals with PPA. Computer simulations supported an explanation of this paradoxical finding in terms of reduced propagation of noise when tract integrity is low. By using multimodal analyses, our study indicates the significance of the ventral pathway for naming and the importance of RT measurement in the clinical assessment of PPA.

SUBMITTER: Janssen N

PROVIDER: S-EPMC7586239 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

How the speed of word finding depends on ventral tract integrity in primary progressive aphasia.

Janssen Nikki N Roelofs Ardi A Mangnus Margot M Sierpowska Joanna J Kessels Roy P C RPC Piai Vitória V

NeuroImage. Clinical 20200929

Primary progressive aphasia (PPA) is a clinical neurodegenerative syndrome with word finding problems as a core clinical symptom. Many aspects of word finding have been clarified in psycholinguistics using picture naming and a picture-word interference (PWI) paradigm, which emulates naming under contextual noise. However, little is known about how word finding depends on white-matter tract integrity, in particular, the atrophy of tracts located ventrally to the Sylvian fissure. To elucidate this ...[more]

PMID: 33395954

Similar Datasets

Project description:BackgroundA subset of patients with the nonfluent variant of primary progressive aphasia (PPA) exhibit concomitant single-word comprehension problems, constituting a 'mixed variant' phenotype. This phenotype is rare and currently not fully characterized. The aim of this study was twofold: to assess the prevalence and nature of single-word comprehension problems in the nonfluent variant and to study multimodal imaging characteristics of atrophy, tau, and amyloid burden associated with this mixed phenotype.MethodsA consecutive memory-clinic recruited series of 20 PPA patients (12 nonfluent, five semantic, and three logopenic variants) were studied on neurolinguistic and neuropsychological domains relative to 64 cognitively intact healthy older control subjects. The neuroimaging battery included high-resolution volumetric magnetic resonance imaging processed with voxel-based morphometry, and positron emission tomography with the tau-tracer [18F]-THK5351 and amyloid-tracer [11C]-Pittsburgh Compound B.ResultsSeven out of 12 subjects who had been classified a priori with nonfluent variant PPA showed deficits on conventional single-word comprehension tasks along with speech apraxia and agrammatism, corresponding to a mixed variant phenotype. These mixed variant cases included three females and four males, with a mean age at onset of 65 years (range 44-77 years). Object knowledge and object recognition were additionally affected, although less severely compared with the semantic variant. The mixed variant was characterized by a distributed atrophy pattern in frontal and temporoparietal regions. A more focal pattern of elevated [18F]-THK5351 binding was present in the supplementary motor area, the left premotor cortex, midbrain, and basal ganglia. This pattern was closely similar to that seen in pure nonfluent variant PPA. At the individual patient level, elevated [18F]-THK5351 binding in the supplementary motor area and premotor cortex was present in six out of seven mixed variant cases and in five and four of these cases, respectively, in the thalamus and midbrain. Amyloid biomarker positivity was present in two out of seven mixed variant cases, compared with none of the five pure nonfluent cases.ConclusionsA substantial proportion of PPA patients with speech apraxia and agrammatism also have single-word comprehension deficits. At the neurobiological level, the mixed variant shows a high degree of similarity with the pure nonfluent variant of PPA.Trial registrationEudraCT, 2014-002976-10 . Registered on 13-01-2015.

Project description:As an example of complex auditory signal processing, the analysis of accented speech is potentially vulnerable in the progressive aphasias. However, the brain basis of accent processing and the effects of neurodegenerative disease on this processing are not well understood. Here we undertook a detailed neuropsychological study of a patient, AA with progressive nonfluent aphasia, in whom agnosia for accents was a prominent clinical feature. We designed a battery to assess AA's ability to process accents in relation to other complex auditory signals. AA's performance was compared with a cohort of 12 healthy age and gender matched control participants and with a second patient, PA, who had semantic dementia with phonagnosia and prosopagnosia but no reported difficulties with accent processing. Relative to healthy controls, the patients showed distinct profiles of accent agnosia. AA showed markedly impaired ability to distinguish change in an individual's accent despite being able to discriminate phonemes and voices (apperceptive accent agnosia); and in addition, a severe deficit of accent identification. In contrast, PA was able to perceive changes in accents, phonemes and voices normally, but showed a relatively mild deficit of accent identification (associative accent agnosia). Both patients showed deficits of voice and environmental sound identification, however PA showed an additional deficit of face identification whereas AA was able to identify (though not name) faces normally. These profiles suggest that AA has conjoint (or interacting) deficits involving both apperceptive and semantic processing of accents, while PA has a primary semantic (associative) deficit affecting accents along with other kinds of auditory objects and extending beyond the auditory modality. Brain MRI revealed left peri-Sylvian atrophy in case AA and relatively focal asymmetric (predominantly right sided) temporal lobe atrophy in case PA. These cases provide further evidence for the fractionation of brain mechanisms for complex sound analysis, and for the stratification of progressive aphasia syndromes according to the signature of nonverbal auditory deficits they produce.

Project description:ObjectiveTo automatically extract and quantify specific disease biomarkers of prosody from the acoustic properties of speech in patients with primary progressive aphasia.MethodsWe analyzed speech samples from 59 progressive aphasic patients (non-fluent/agrammatic = 15, semantic = 21, logopenic = 23; ages 50-85 years) and 31 matched healthy controls (ages 54-89 years). Using a novel, automated speech analysis protocol, we extracted acoustic measurements of prosody, including fundamental frequency and speech and silent pause durations, and compared these between groups. We then examined their relationships with clinical tests, gray matter atrophy, and cerebrospinal fluid analytes.ResultsWe found a narrowed range of fundamental frequency in patients with non-fluent/agrammatic variant aphasia (mean 3.86 ± 1.15 semitones) compared with healthy controls (6.06 ± 1.95 semitones; P < 0.001) and patients with semantic variant aphasia (6.12 ± 1.77 semitones; P = 0.001). Mean pause rate was significantly increased in the non-fluent/agrammatic group (mean 61.4 ± 20.8 pauses per minute) and the logopenic group (58.7 ± 16.4 pauses per minute) compared to controls. In an exploratory analysis, narrowed fundamental frequency range was associated with atrophy in the left inferior frontal cortex. Cerebrospinal level of phosphorylated tau was associated with an acoustic classifier combining fundamental frequency range and pause rate (r = 0.58, P = 0.007). Receiver operating characteristic analysis with this combined classifier distinguished non-fluent/agrammatic speakers from healthy controls (AUC = 0.94) and from semantic variant patients (AUC = 0.86).InterpretationRestricted fundamental frequency range and increased pause rate are characteristic markers of speech in non-fluent/agrammatic primary progressive aphasia. These can be extracted with automated speech analysis and are associated with left inferior frontal atrophy and cerebrospinal phosphorylated tau level.

Dataset Information

How the speed of word finding depends on ventral tract integrity in primary progressive aphasia.

Publications

How the speed of word finding depends on ventral tract integrity in primary progressive aphasia.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets