3 research outputs found
Improving the Accuracy of DaT Scan Interpretation: a retrospective study to identify variables that standardize the review of DaT scans for idiopathic Parkinson’s disease
Introduction: Until recently, the diagnosis of Parkinson’s disease (PD) has been based solely on clinical observation. The DaT scan is a tool that allows clinicians to visualize areas of neurodegeneration in PD and can help guide diagnosis. However, there is a discordance between clinical judgement and interpretation of DaT scans. In this study, we aim to improve the utility of DaT scans in the diagnosis of PD by identifying factors that can lead to a misdiagnosis and determine which image findings predict a clinical syndrome of parkinsonism.
Methods: We will conduct a retrospective chart review to analyze DaT scans of 100 patients clinically diagnosed with PD. We will calculate the initial SN/SP/PPV/NPV for diagnoses based clinically compared to scan. We will then blindly review and reclassify all scans as definitely abnormal, definitely normal, or indeterminate. We will then recalculate a revised SN/SP/PPV/NPV to see if these values changed following reanalysis. From the discordant scans, we will attempt to identify factors that can further assist in interpreting DaT scans.
Results: Patients have been identified and we are in the process of extracting data. We anticipate that after systematic, careful re-review, the specificity of DaT scans will be higher, due to improvement in identifying positive scans.
Discussion: Imaging can be costly and cumbersome for patients and clinicians alike. Currently, DaT scans do not offer an improved accuracy in diagnosis over clinical judgement. If the interpretation of DaT scans can be optimized, they will be of greater utility to both patients and physicians
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Differential regulation of the Drosophila sleep homeostat by circadian and arousal inputs.
One output arm of the sleep homeostat in Drosophila appears to be a group of neurons with projections to the dorsal fan-shaped body (dFB neurons) of the central complex in the brain. However, neurons that regulate the sleep homeostat remain poorly understood. Using neurogenetic approaches combined with Ca2+ imaging, we characterized synaptic connections between dFB neurons and distinct sets of upstream sleep-regulatory neurons. One group of the sleep-promoting upstream neurons is a set of circadian pacemaker neurons that activates dFB neurons via direct glutaminergic excitatory synaptic connections. Opposing this population, a group of arousal-promoting neurons downregulates dFB axonal output with dopamine. Co-activating these two inputs leads to frequent shifts between sleep and wake states. We also show that dFB neurons release the neurotransmitter GABA and inhibit octopaminergic arousal neurons. We propose that dFB neurons integrate synaptic inputs from distinct sets of upstream sleep-promoting circadian clock neurons, and arousal neurons