MDNews - San Antonio

September 2012

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++++++++++++++ + + ++++++++++++++ IMAGING Alzheimer's Disease The Role of the +++ +++ Radiologist in By Barry J. Menick, M.D. "TRUTH DOES NOT BECOME MORE TRUE BY VIRTUE OF THE FACT THAT THE ENTIRE WORLD AGREES WITH IT, NOR LESS SO EVEN IF THE WHOLE WORLD DISAGREES WITH IT." —MAIMONIDES, THE GUIDE FOR THE PERPLEXED Barry J. Menick, M.D. T HIS YEAR, I had the good for- tune to attend the 50th Annual Meeting of the American Society of Neuroradiology and the 6th Annual Meeting of the American Society of Functional Neuroradiology. My objec- tive was to focus on Alzheimer's disease. According to the 2012 annual report released by the Alzheimer's Association, 5.4 million Americans are living with Alzheimer's disease. One in eight older Americans has the disease. It is the sixth-leading cause of death in the United States. More than 15 million Americans provide unpaid care valued at $210 billion for patients with Alzheimer's disease and other dementias. Payments for care are estimated to be $200 billion in the United States in 2012. Tremendous resources have been dedicated to the pathophysiology, diag- nosis and treatment of this disease, with mixed results. It is disappointing there 10 | San Antonio MD NEWS ■ MDNEWS.COM is no prevention, cure or treatment that will slow the ultimate progression of the disease. Those of us in the medical profession, however, need to stay focused on our individual roles in the care of these patients and their families. Our role is to diagnose Alzheimer's disease as quickly and as accurately as possible. The radiologist's toolkit now includes exciting new diagnostic imaging tools that are available today at South Texas Radiology Imaging Centers (STRIC). Brain imaging can identify three bio- markers associated with the predementia form of Alzheimer's disease: neurodegen- eration (identified via magnetic resonance imaging), hypometabolism (identified via FDG-PET) and fibrillar amyloid deposition (identified via amyloid positron emission tomography). Fluoroscopically guided lumbar puncture can be performed to identify the CSF biomarkers of tau protein elevation and beta-amyloid depression. Patients with normal cognition and one of these biomarkers are classified as "at risk with Alzheimer's disease pathology" or as having "preclinical Alzheimer's disease." Patients with mild symptoms and one of these biomarkers are classified as having "prodromal Alzheimer's disease" or "mild cognitive impairment due to Alzheimer's disease." Patients with clini- cal dementia and Alzheimer's phenotype are classified as having "Alzheimer's disease dementia." Early diagnosis is essential to initiate appropriate medical therapy to preserve functional status and allow time to facilitate life planning and relationship preservation. Magnetic resonance imaging (MRI) is the indispensable imaging modality of modern neuroradiology. Even the most experienced radiologists, however, will have difficulty characterizing the degree of cortical volume loss or ventricular enlargement in older patients due to vari- ability. Quantitative CSF flow MRI can be used to obtain stroke volume through the cerebral aqueduct. This objective measure can identify patients with normal pressure hydrocephalus whose symptoms, includ- ing dementia, may respond to shunting. The medial temporal lobe, the locus of early Alzheimer's pathology, is particu- larly difficult to characterize due to its complexity and small size. Fortunately, U.S. Food and Drug Administration (FDA)-approved MRI software enables us to objectively quantify hippocampal volumes and compare them to a normal database. This volumetric analysis is available at all STRIC MRI sites. While atrophy on MRI is the imaging manifestation of the neurodegeneration biomarker, a negative MRI study does not exclude the presence of Alzheimer's pathology. In fact, amyloid plaque can begin to accumulate in the brain 10 years or more before symptom onset. Brain positron emission tomography (PET) generates images of f luorine uptake proportional to cortical glucose metabolism. Hypometabolism (a result of synaptic dysfunction and neuronal

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