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Progressive non-fluent aphasia is associated with hypometabolism centred on the left anterior insula
Authors:
Nestor, P.J., GRAHAM, N.L., Fryer, T.D., Williams, G.B., PATTERSON, K. & HODGES, J.R.
Reference:
Brain, 126(11), 2406-2418
Year of publication:
2003
CBU number:
5588
Abstract:
Progressive non-fluent aphasia (PNFA) is a syndrome in which patients lose the ability to communicate fluently in the context of relative preservation of single word comprehension and non-linguistic cognitive abilities. Neuroimaging in case studies with PNFA has failed to identify a consistent neural substrate for the language disorder. In this study of a group of patients (N=10) whose presenting complaint was progressive dysfluency, resting cerebral metabolism was measured using 18fluorodeoxyglucose-positron emission tomography (FDG-PET) and analysed with the technique of statistical parametric mapping (SPM). Regional atrophy was assessed with voxel-based morphometry (VBM). Seven patients had a ‘pure’ PNFA syndrome, while the remaining three had additional features of a more pervasive dementia. Compared to controls, the patients showed hypometabolism in several regions that, most notably, included the left anterior insula/frontal operculare region. The VBM analysis revealed only one small area of atrophy in the left peri-Sylvian region. The PNFA group was then contrasted to a group with Alxheimer’s disease (N=10) whose clinical profile did not include non-fluent aphasic features. In this analysis, the only persisting hypometabolic region was that centred over the left anterior insula. VBM did not identify any regional differences in atrophy between PNFA and AD. A third analysis comparing the pute PNFA cases (N=7) to controls, yielded similar results to that of the whole group, suggesting that these cases were also at risk of a more generalised dementia a finding borne out in subsequent follow-up of two cases to date. In light of current theories of fluent language production, the findings offer anatomical evidence that the breakdown in fluency is due to a motor articulatory planning deficit (speech apraxia) combined with a variable degree of agrammatism.
