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      Functional brain imaging in the dementias: role in early detection, differential diagnosis, and longitudinal studies.

      European Journal of Nuclear Medicine and Molecular Imaging
      Alzheimer Disease, diagnosis, radionuclide imaging, Brain, anatomy & histology, Dementia, Diagnosis, Differential, Diagnostic Imaging, methods, Humans, Magnetic Resonance Imaging, Magnetic Resonance Spectroscopy, Reproducibility of Results, Risk Assessment, Sensitivity and Specificity, Tomography, Emission-Computed, Tomography, Emission-Computed, Single-Photon

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          Abstract

          This review considers the role of functional brain imaging techniques in the dementias. The substantial assistance that especially single-photon emission tomography and positron emission tomography can play in the initial diagnosis of dementia and in the differential diagnosis of the specific dementing disorder is discussed. These techniques alone essentially match the sensitivity and specificity of clinical diagnoses in distinguishing Alzheimer's dementia (AD) from age-matched controls, from frontal lobe dementia and vascular dementia, and even from Lewy body dementia. Newer analytic techniques such as voxel-based correlational analyses and discriminant function analyses enhance the power of such differential diagnoses. Functional brain imaging techniques can also significantly assist in patient screening for clinical trials. The correlation of the observed deficits with specific patterns of cognitive abnormalities permits enhanced patient management and treatment planning and improved longitudinal assessment of outcome. It is also noteworthy that the classic abnormalities of temporoparietal and posterior cingulate hypoperfusion or hypometabolism appear to be present prior to symptom onset. These abnormalities predict progression to AD in the presence of the earliest of symptoms, and are present even in cognitively normal but at-risk subjects, with a severity proportional to the risk status. Even greater predictive ability for progression to AD is obtained by combining measures of perfusion or metabolism with risk factors, tau protein levels, hippocampal N-Acetyl aspartate concentrations, or hippocampal volume measures.

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