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While visuospatial deficits are well-characterized cognitive sequelae of right hemisphere (RH) stroke, apraxic deficits in RH stroke remain poorly understood. Likewise, very little is known about the association between apraxic and visuospatial deficits in RH stroke or about the putative common or differential pathophysiology underlying these deficits. Therefore, we examined the behavioural and lesion patterns of apraxic deficits (pantomime of object use and bucco-facial imitation) and visuospatial deficits (line bisection and letter cancellation tasks) in 50 sub-acute RH stroke patients. Using principal component analysis (PCA), we characterized the relationship between the two deficits. We hypothesized that any interaction of these neuropsychological measures may be influenced by the demands of ego-centric/space-based and/or allo-centric/object-based processing. Contralesional visuospatial deficits were common in our clinically representative patient sample, affecting more than half of RH stroke patients. Furthermore, about one-third of all patients demonstrated apraxic deficits. PCA revealed that pantomiming and the imitation of bucco-facial gestures loaded clearly on a first component (PCA1), while letter cancellation loaded heavily on a second component (PCA2). For line bisection, overall mean deviation loaded on PCA1, while the difference between the mean deviations in contra- versus ipsilesional space loaded on PCA2. These results suggest that PCA1 represents allo-centric/object-based processing and PCA2 ego-centric/space-based processing. This interpretation was corroborated by the statistical lesion analyses with the component scores. Data suggest that disturbed allo-centric/object-based processing contributes to apraxic pantomime and imitation deficits in (sub-acute) RH stroke.
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http://dx.doi.org/10.1111/jnp.12191 | DOI Listing |
Neurology
December 2024
From the Multimodal Neuroimaging Group, Department of Nuclear Medicine (G.N.B., E.J., K.G., A.D.), Department of Psychiatry (F.J.), Department of Neurology (O.A.O., E.K., P.H.W.), Medical Faculty and University Hospital of Cologne, University of Cologne; Molecular Organization of the Brain (G.N.B., A.D.), Institute for Neuroscience and Medicine II, Research Center Juelich; German Center for Neurodegenerative Diseases (F.J.), Bonn/Cologne, Germany; Institute for Translational Research (S.O.B.), and Department of Family Medicine (S.O.B.), Texas College of Osteopathic Medicine, University of North Texas Health Science Center, Fort Worth; and Cognitive Neuroscience (P.H.W.), Institute for Neuroscience and Medicine (INM-3), Research Center Juelich, Germany.
Background And Objectives: Apraxia is a frequently observed symptom in Alzheimer disease (AD), but the causal pathomechanism underlying this dysfunction is not well understood. Previous studies have demonstrated associations between various cognitive dysfunctions in AD and cortical tau deposition in specific brain areas, suggesting a causal relationship. Thus, we hypothesized that specific regional patterns of tau pathology in praxis-related brain regions may be associated with apraxic deficits in AD.
View Article and Find Full Text PDFNeurosci Biobehav Rev
July 2024
Université de Franche-Comté, UMR INSERM 1322, LINC, Besançon F-25000, France; Maison des Sciences de l'Homme et de l'Environnement (UAR 3124), Besançon, France; Unité de Neurologie Vasculaire, CHU Besançon, France. Electronic address:
Limb apraxia is a motor disorder frequently observed following a stroke. Apraxic deficits are classically assessed with four tasks: tool use, pantomime of tool use, imitation, and gesture understanding. These tasks are supported by several cognitive processes represented in a left-lateralized brain network including inferior frontal gyrus, inferior parietal lobe (IPL), and lateral occipito-temporal cortex (LOTC).
View Article and Find Full Text PDFObjectives: Apraxia is a core feature of Alzheimer's disease, but the pathomechanism of this characteristic symptom is not well understood. Here, we systematically investigated apraxia profiles in a well-defined group of patients with Alzheimer's disease (AD; N=32) who additionally underwent PET imaging with the second-generation tau PET tracer [18F]PI-2620. We hypothesized that specific patterns of tau pathology might be related to apraxic deficits.
View Article and Find Full Text PDFClin Neuropsychol
February 2024
Department of Psychology, Sapienza Università di Roma, Rome, Italy.
To identify the cortical and subcortical distribution of atrophy and the disorganization of white matter bundles underlying the apraxic disorders in a patient with corticobasal degeneration (CBD). Patient underwent appropriate neuropsychological tasks aimed at identifying the nature of the apraxic disorder and morphometric structural MRI with whole-brain voxel-wise analysis. Progressive limbkinetic apraxia (LKA) with onset in the right upper limb with subsequent extension to the limbs, trunk, orofacial district, and eye movements was documented, associated with element of ideomotor apraxia (IMA).
View Article and Find Full Text PDFFront Neurol
July 2023
Department of Psychology, University of California, Berkeley, Berkeley, CA, United States.
Introduction: Apraxia of speech (AOS) is a motor speech disorder impairing the coordination of complex articulatory movements needed to produce speech. AOS typically co-occurs with a non-fluent aphasia, or language disorder, making it challenging to determine the specific brain structures that cause AOS. Cases of pure AOS without aphasia are rare but offer the best window into the neural correlates that support articulatory planning.
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