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Poster E12, Friday, November 10, 10:00 – 11:15 am, Harborview and Loch Raven Ballrooms

Measuring an Individual's Semantic Storage Loss due to Temporal Lobe Damage

Carlos Roncero1, Jim Nikelski1, Stephan Probst1, Alex Theil1, Howard Chertkow1;1Lady Davis Institute, Jewish General Hospital

Objectives: Developing a simple means of semantic syndrome classification with anatomic validation is now clinically important given the correlation between Primary Progressive aphasia (PPA) subgroups and molecular pathology. Anomia is a cognitive sign in both Alzheimer Disease(AD) and Frontotemporal dementia (FTD). Past group comparisons (e.g., Lambon-Ralph & Jefferies, 2004) have suggested that anomia is often caused by either an underlying executive impairment that impedes retrieving the object name from memory (seen in frontal or parietal lesions due to cerebrovascular disease or the logopenic variant of Primary Progressive aphasia), or a loss of storage of the concept itself from semantic memory (more seen in the semantic variant of Primary Progressive aphasia, where damage localizes to temporal pole region). We wished to validate a simple approach to distinguishing these syndromes at the individual patient level. Methods: Following the literature, an approach to patient classification was developed focussing on three characteristics of the syndrome of semantic storage loss: 1) naming scores are unrelated to a subject’s executive function, 2) subjects fail to retrieve object names even when cues are given, and 3) they fail to correctly recognize concepts even when executive requirements are lowered. Tests requiring thirty minutes total time were developed to operationalize these characteristics. Scores were combined to produce an omnibus semantic memory storage loss score for each participant, with a higher score indicating increasing evidence of semantic storage loss. Semantic storage loss stores were assessed with raters blind to clinical diagnosis or neuropsychology results. FDG-PET with regional semi-quantitative assessment of hypometabolism was carried out on all subjects. Extensive complementary neuropsychological evaluation was also carried out. Results: Twenty subjects with anomia (14 FTD patients and 6 AD patients with PPA logopenic variety) were tested. Xx Subjects scored over 26 (indicating evidence of semantic storage loss) while xx subjects scored below 15 (no semantic storage loss). Subsequent analyses found that these scores correlated strongly with: (a) presence of left and right anterior temporal lobe damage on FDG-PET; (b) whether anomia in a participant was demonstrably due to executive impairment or concept loss on extended neuropsychological testing. This correlation held both for the FTD and the AD subjects. Conclusion: It is possible to classify patients with anomia and predict FDG-PET localization at an individual level in terms of semantic syndromes, using a 30 minute omnibus semantic memory storage loss score. Underlying cause of the anomia and its localization may be important factors to consider in non-invasive neuromodulation therapy for anomia.

Topic Area: Methods

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