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Cortex. 2015 Jun;67:122-33. doi: 10.1016/j.cortex.2015.03.011. Epub 2015 Apr 1.

Is the logopenic-variant of primary progressive aphasia a unitary disorder?

Author information

1
Faculty of Health Sciences, The University of Sydney, Lidcombe, NSW, Australia; Neuroscience Research Australia, Randwick, NSW, Australia; ARC Centre of Excellence in Cognition and its Disorders, Sydney, NSW, Australia. Electronic address: cristian.leyton@sydney.edu.au.
2
Neuroscience Research Australia, Randwick, NSW, Australia; ARC Centre of Excellence in Cognition and its Disorders, Sydney, NSW, Australia; School of Medical Sciences, The University of New South Wales, Sydney, NSW, Australia. Electronic address: j.hodges@neura.edu.au.
3
Department of Anatomical Pathology, Alfred Hospital, Melbourne, VIC, Australia. Electronic address: C.McLean@alfred.org.au.
4
Department of Pathology, Sydney Medical School, The University of Sydney, Sydney, NSW, Australia. Electronic address: jillian.kril@sydney.edu.au.
5
Neuroscience Research Australia, Randwick, NSW, Australia; ARC Centre of Excellence in Cognition and its Disorders, Sydney, NSW, Australia; School of Medical Sciences, The University of New South Wales, Sydney, NSW, Australia. Electronic address: o.piguet@neura.edu.au.
6
Faculty of Health Sciences, The University of Sydney, Lidcombe, NSW, Australia; Neuroscience Research Australia, Randwick, NSW, Australia. Electronic address: kirrie.ballard@sydney.edu.au.

Abstract

Logopenic progressive aphasia is one of the clinical presentations of primary progressive aphasia and formally defined by the co-occurrence of impaired naming and sentence repetition. Impaired naming is attributed to failure of lexical retrieval, which is a multi-staged process subserved by anatomically segregated brain regions. By dissecting the neurocognitive processes involved in impaired naming, we aimed to disentangle the clinical and neuroanatomical heterogeneity of this syndrome. Twenty-one individuals (66.7% females, age range 53-83 years) who fulfilled diagnostic criteria for logopenic variant and had at least two clinical and language assessments, 1 year apart, were recruited and matched for age, sex distribution and level of education with a healthy control sample (n = 18). All participants underwent a structural brain scan at the first visit and surface-wise statistical analysis using Freesurfer. Seventeen participants with logopenic variant underwent amyloid imaging, with 14 demonstrating high amyloid retention. Based on their performance on single-word comprehension, repetition and confrontation naming, three subgroups of logopenic cases with distinctive linguistic profiles and distribution of atrophy were identified. The first subgroup (n = 10) demonstrated pure anomia and left-sided atrophy in the posterior inferior parietal lobule and lateral temporal cortex. The second subgroup (n = 6), presented additional mild deficits in single-word comprehension, and also exhibited bilateral thinning of the fusiform gyri. The third subgroup (n = 5) showed additional impaired single-word repetition, and cortical thinning focused on the left superior temporal gyrus. The subgroups differed in the proportion of cases with high amyloid retention and in the rate of decline of naming performance over time, suggesting that neurodegeneration spreads differentially throughout regions subserving word processing. In line with previous reports, these results confirm the extensive damage to the language network and, in part, explain the clinical heterogeneity observed across logopenic cases.

KEYWORDS:

Alzheimer's disease; Anomia; Logopenic variant of primary progressive aphasia; Primary progressive aphasia

PMID:
25955499
DOI:
10.1016/j.cortex.2015.03.011
[Indexed for MEDLINE]

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