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NEUROLOGY 2008;71:1628-1633
© 2008 American Academy of Neurology

The anatomic correlate of prosopagnosia in semantic dementia

K. A. Josephs, MST, MD, J. L. Whitwell, PhD, P. Vemuri, PhD, M. L. Senjem, BS, B. F. Boeve, MD, D. S. Knopman, MD, G. E. Smith, PhD, R. J. Ivnik, PhD, R. C. Petersen, MD, PhD and C. R. Jack, Jr, MD

From the Departments of Neurology (K.A.J., B.F.B., D.S.K., R.C.P.), Radiology Research (J.L.W., P.V., C.R.J.), Information Technology (M.L.S.), and Neuropsychiatry and Neuropsychology (G.E.S., R.J.I.), Mayo Clinic, Rochester, MN.

Address correspondence and reprint requests to Dr. Keith A. Josephs, Department of Neurology, Mayo Clinic, 200 First Street SW, Rochester, MN 55905 josephs.keith{at}mayo.edu

Objective: To determine the anatomic correlate of prosopagnosia in subjects with semantic dementia.

Methods: We identified all subjects who had been evaluated by an experienced behavioral neurologist, met criteria for semantic dementia, and had completed a volumetric head MRI scan. In all subjects, historical records were reviewed and subjects in which the presence (n = 15) or absence (n = 12) of prosopagnosia was specifically ascertained by the neurologist were identified. Voxel-based morphometry was used to assess patterns of gray matter atrophy in subjects with and without prosopagnosia compared to a group of age and gender-matched normal controls, and compared to each other.

Results: Compared to controls, both groups showed prominent temporal lobe volume loss. Those with prosopagnosia showed bilateral loss but with greater involvement of the right temporal lobe, while those without prosopagnosia showed predominantly left anterior temporal lobe loss. On direct comparison, subjects with prosopagnosia showed greater loss predominantly in the right amygdala, hippocampus, fusiform gyrus, and anterior temporal pole than those without prosopagnosia. No regions were involved to a greater degree in those without prosopagnosia, compared to those with prosopagnosia.

Conclusions: Prosopagnosia appears to be associated with volume loss of the right temporal lobe, particularly medial temporal lobe, fusiform gyrus, and anterior temporal pole, although in semantic dementia it is occurring in the context of bilateral temporal lobe volume loss.

Abbreviations: ADPR = Alzheimer’s Disease Patient Registry; ADRC = Alzheimer’s Disease Research Center; BNT = Boston Naming Test; CDR-SB = Clinical Dementia Rating score sum of boxes; DCT = discrete cosine transformation; DRS = Dementia Rating Scale; FTLD-U = frontotemporal lobar degeneration with ubiquitin-only-immunoreactive changes; FWHM = full-width at half-maximum; GM = gray matter; MMSE = Mini-Mental State Examination; MNI = Montreal Neurological Institute; SPGR = spoiled gradient echo; STMS = Short Test of Mental Status; VBM = voxel-based morphometry; WM = white matter.

K.A.J. is supported by the NIH Roadmap Multidisciplinary Clinical Research Career Development Award Grant (K12/NICHD)-HD49078. Co-authors on this study are also supported by NIH grants P50-AG16574, U01-AG06786, R01-AG11378, as well as the generous support of the Robert H. and Clarice Smith and Abigail Van Buren Alzheimer’s Disease Research Program of the Mayo Foundation, the Alexander Family Alzheimer’s Disease Research Professorship of the Mayo Foundation, and the NIH Construction Grant (NIH C06 RR018898).

Disclosure: D.S.K. has been a consultant to GE HealthCare, GlaxoSmithKline, and Myriad Pharmaceuticals, has served on a Data Safety Monitoring Board for Neurochem Pharmaceuticals, and is an investigator in a clinical trial sponsored by Elan Pharmaceuticals. B.F.B. is an investigator in a clinical trial sponsored by Myriad Pharmaceuticals. R.C.P. has been a consultant to GE Healthcare and has served on a data safety monitoring board in a clinical trial sponsored by Elan Pharmaceuticals. C.R.J. receives research support from Pfizer in the form of research grants.

Received May 23, 2008. Accepted in final form August 8, 2008.






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