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E1349. Discerning Dementias and Movement Disorders: From Pathophysiology to a Picture
Authors
  1. Aleksandra Augustynowicz; Mount Auburn Hospital
  2. Caitlin Connolly; Mount Auburn Hospital
Background
There are many causes of cognitive impairment, and clinical history/exam are not always sufficient for diagnosis. Prognosis for these conditions is generally poor, and early treatment can improve outcomes. Therefore, the use of imaging to aid in diagnosis is increasing, and it is crucial to recognize the patterns associated with each disease. Structural imaging is first-line to exclude secondary causes of dementia or movement disorders such as ischemia or masses. Nuclear medicine imaging can elucidate underlying pathologic processes, for example, the accumulation of abnormal proteins such as amyloid beta and tau leading to cell death.

Educational Goals / Teaching Points
This exhibit discusses the disease processes of common dementias and movement disorders, reviews pertinent neuroanatomy, and highlights imaging options and characteristics of each condition.

Key Anatomic/Physiologic Issues and Imaging Findings/Techniques
Alzheimer’s disease (AD) is the most common neurodegenerative disease and affects 10% of individuals over 65 years old. Patients suffer word-finding difficulties, short-term memory loss, and loss of spatial orientation. The pathophysiology is linked to accumulation of amyloid ?? plaques and ?? aggregates, leading to cortical loss in the mesial temporal, temporal, parietal, precuneus, and posterior cingulate gyrus regions. Before this loss is perceptible on structural imaging, it can be observed on positron emission tomography (PET) with (18)F-fluoro-deoxy-glucose (FDG), as hypometabolism in these areas. On single-photon emission computed tomography (SPECT) perfusion imaging, perfusion abnormalities follow the abnormalities seen on FDG-PET, with hypoperfusion in the posterior temporal and parietal cortices, precuneus, and posterior cingulate gyrus. PET agents such as 18F-florbetapir bind to neurofibrillary plaques in the cortex of AD patients, aiding diagnosis. Lewy Body dementia (LBD) is the second most common neurodegenerative disorder after AD. Misfolded ??-synuclein proteins damage dopaminergic neurons and cause cognitive decline, visual hallucinations, constipation, vomiting, and gastroparesis. On FDG-PET, there is hypometabolism in the frontotemporal cortex, posterior parietotemporal cortex, and occipital cortex. Additionally, patients with LBD have decreased uptake of I-123 Ioflupane, which binds the dopamine transporter in the basal ganglia, on SPECT imaging—a pattern characteristic of parkinsonian disorders. Parkinson’s Disease (PD) affects approximately 60,000 Americans yearly, causing mood or cognitive disturbances, resting tremor, rigidity, bradykinesia, and postural instability. Because PD is characterized by a loss of dopaminergic synapses, I-123 Ioflupane SPECT imaging demonstrates loss of uptake in the putamen. Other less common neurodegenerative disorders also have recognizable patterns on PET imaging, which helps with diagnosis.

Conclusion
The pathophysiology of the most common neurodegenerative disorders can be directly visualized as distinct patterns on PET and SPECT with targeted radiotracers. Early diagnosis and treatment of these conditions can improve prognosis, and nuclear medicine imaging can help attain this goal.