Anomic aphasia is characterized by good comprehension and non-word repetition but poor naming. Two sub-types of deficits might be hypothesized: faulty access to preserved phonological representations or preserved access to impaired representations. Phonological errors may occur only when representations are impaired or in post-lexical deficits (conduction aphasia). We analysed the incidence of phonological naming errors of 30 individuals, 25 with anomic aphasia based on poor naming but good repetition and comprehension, and five with conduction aphasia based on poor naming and poor repetition. Individuals with anomic aphasia produced very few phonological errors compared to individuals with conduction aphasia (0-19.1% versus 42-66%). However, six individuals with anomia produced more than 11% phonological errors, suggesting two patterns of deficit: either impaired lexical representations or impaired access to them. The lack of phonological errors in most individuals with anomic aphasia suggests that access to the phonological output lexicon is semantically, not phonologically driven.
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http://dx.doi.org/10.1080/02643294.2023.2208745 | DOI Listing |
Neuropsychologia
January 2025
Faculty of Psychology and Educational Sciences, University of Geneva, 40 Boulevard du Pont d'Arve, 1205 Geneva, Switzerland. Electronic address:
Background: Word production difficulty is one of the most common and persisting symptoms in people suffering from aphasia (i.e., anomia).
View Article and Find Full Text PDFCogn Behav Neurol
January 2025
Department of Health Care, Mitsui Memorial Hospital, Tokyo, Japan.
Here we report the case of an individual who developed proper- and common-name anomia with no category specificity, alexia with agraphia for kanji (Japanese morphograms), and mild verbal and semantic memory impairment after unilateral herpes simplex encephalitis. Although their common-name anomia, alexia with agraphia, and semantic memory impairment resolved within 2 years, this individual continued to experience proper-name anomia and verbal memory impairment. Encephalitic damage was limited to the left anterior temporal lobe (ATL), amygdala, hippocampus, and parahippocampal gyrus, sparing the mid-fusiform and posterior inferior temporal gyri.
View Article and Find Full Text PDFSci Rep
December 2024
Department of Zoology, University of São Paulo, São Paulo, SP, Brazil.
Animals have evolved numerous mechanisms to perceive and interact with the environment that can be translated into different sensory modalities. However, the genomic and phenotypic features that support sensory functions remain enigmatic for many invertebrates, such as bivalves, an ecologically and economically important taxonomic group. No repertoire of sensory genes has been characterized in bivalves, representing a significant knowledge gap in molluscan sensory biology.
View Article and Find Full Text PDFEur J Phys Rehabil Med
December 2024
Laboratory of Neuropsychology, Department of Neurorehabilitation Sciences, IRCCS Istituto Auxologico Italiano, Milan, Italy.
Background: The defective spoken output of persons with aphasia has anomia as a main clinical manifestation. Improving anomia is therefore a main goal of any language treatment.
Aim: This study assessed the effectiveness of a novel, 2-week, rehabilitation protocol (PHOLEXSEM), focused on PHonological, SEmantic, and LExical deficits, aiming at improving lexical retrieval, and, generally, spoken output.
J Alzheimers Dis
December 2024
Innovation Center for Neurological Disorders, Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, China.
Background: Although Boston Naming Test has been thoroughly validated at a global level, there is limited assessment of item-level properties using modern psychometric methods.
Objective: This study aimed to investigate the construct validity and item-level properties of the color-picture version of Boston Naming Test (CP-BNT) in a Chinese cohort with neurodegenerative diseases.
Methods: This retrospective study included 424 participants, consisting of 118 normal controls, 152 with Alzheimer's disease, 101 with primary progressive aphasia, and 53 with other neurodegenerative diseases.
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