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This chapter summarizes findings from structural and functional neuroimaging studies in individuals with idiopathic rapid eye movement (REM) sleep behavior disorder (iRBD). In humans, functional brain imaging has been used to evaluate the neural mechanisms and structures that regulate REM sleep. Dysfunction of the REM sleep atonia network forms the neuropathological basis for RBD. In humans, iRBD is diagnosed when a patient with videopolysomnographic confirmation of REM sleep without atonia has no evidence of a neurological disease or other possible causes. The chapter summarizes the neuroimaging abnormalities that have been identified in Parkinson disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA). Several neuroimaging studies have evaluated the morphological and functional state of the substantia nigra in iRBD. These studies have evaluated the echogenicity of the substantia nigra with transcranial sonography (TCS) and the nigrostriatal dopaminergic system with functional imaging.
This chapter discusses recent structural neuroimaging studies that address the regions of interest in the proposed anterior limbic network model. Given the predominance of MRI in structural imaging of psychiatric disorders, the chapter also focuses on this imaging modality. First, longitudinal studies are needed to clarify how brain structures change within individual patients, with particular regard to the corresponding course of illness. Second, more sophisticated measures, such as diffusion tensor imaging (DTI) tractography or shape analyses, may more consistently define the subtle structural abnormalities that are likely in bipolar disorder and that may be missed with less-specific measures. Third, studies in young patients are critical given the typical adolescent onset of bipolar disorder and early course progression. Finally, integrating structural imaging with functional and neurochemical are the only ways to move morphometric imaging from high-priced and sophisticated phrenology to a better understanding of the neural basis of bipolar disorder.
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