Frontotemporal dementia and early Alzheimer disease: differentiation with frontal lobe H-1 MR spectroscopy.
OBJECTIVE
To evaluate cerebral biochemical abnormalities in patients with frontotemporal dementia and Alzheimer disease and to determine whether proton (hydrogen-1) magnetic resonance (MR) spectroscopy can help differentiate among these two patient groups and healthy (control) subjects.


METHODS
MR imaging and H-1 MR spectroscopy were performed in 14 patients with frontotemporal dementia, 12 with probable Alzheimer disease (Alzheimer), and 11 healthy (control) elderly subjects. Spectra were acquired from midfrontal and temporoparietal gray matter with a double spin-echo sequence (repetition time, 3,000 msec; echo time, 30 msec). Results were expressed in metabolite concentrations corrected for the presence of cerebrospinal fluid.


RESULTS
In frontotemporal dementia patients, the frontal lobe showed reduced N-acetyl compounds (-28%) and glutamate plus glutamine (-16%), suggestive of neuron loss, and increased myo-inositol (MI) (+19%), suggestive of increased glial content. In three frontotemporal dementia patients, a lactate peak was present in the frontal lobe. In Alzheimer patients, no statistically significant abnormalities were observed in the frontal region, but MI was elevated (+8%) in the temporoparietal region. With use of linear discriminant analysis of MR spectroscopy data alone, 92% of the frontotemporal dementia patients were correctly differentiated from the Alzheimer patients and control subjects. The overall accuracy for discrimination among all three groups was 84%.


CONCLUSIONS
H-1 MR spectroscopy demonstrated biochemical abnormalities in patients with frontotemporal dementia and aided differentiation between patients with frontotemporal dementia and Alzheimer disease.
Ernst
T
T
Department of Radiology, Harbor-UCLA Medical Center, University of California at Los Angeles School of Medicine, Torrance 90502, USA.
Chang
L
L
Melchor
R
R
Mehringer
C M
CM
D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000134:cerebrospinal fluid / Q000175:diagnosis* / Q000378:metabolism; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000378:metabolism; D003704:Dementia / Q000134:cerebrospinal fluid / Q000175:diagnosis* / Q000378:metabolism; D016002:Discriminant Analysis; D005260:Female; D005625:Frontal Lobe / Q000378:metabolism / Q000473:pathology*; D018698:Glutamic Acid / Q000378:metabolism; D005973:Glutamine / Q000378:metabolism; D006801:Humans; D006859:Hydrogen; D007294:Inositol / Q000378:metabolism; D007773:Lactates / Q000378:metabolism; D016014:Linear Models; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D008875:Middle Aged; D009410:Nerve Degeneration; D009457:Neuroglia / Q000473:pathology; D009474:Neurons / Q000473:pathology; D010296:Parietal Lobe / Q000378:metabolism / Q000473:pathology; D011522:Protons; D012680:Sensitivity and Specificity; D013702:Temporal Lobe / Q000378:metabolism / Q000473:pathology*
D007773:Lactates; D011522:Protons; D005973:Glutamine; D001224:Aspartic Acid; D018698:Glutamic Acid; D007294:Inositol; D006859:Hydrogen; C000179:N-acetylaspartate