TY - CHAP M1 - Book, Section TI - Dementia with Lewy Bodies A1 - Seeley, William W. A1 - Tanner, Caroline M. A1 - Miller, Bruce L. A2 - Jameson, J. Larry A2 - Fauci, Anthony S. A2 - Kasper, Dennis L. A2 - Hauser, Stephen L. A2 - Longo, Dan L. A2 - Loscalzo, Joseph PY - 2018 T2 - Harrison's Principles of Internal Medicine, 20e AB - Although Lewy body disease (LBD) was once conceptualized as a disease of the substantia nigra, modern human postmortem studies with alpha-synuclein immunohistochemistry revealed that Lewy body and Lewy neurite pathology most often begins in the enteric and autonomic nervous systems before ascending through the brainstem to the substantia nigra, limbic system, and ultimately the cerebral cortex. In other individuals, disease may begin in the olfactory bulb and spread inward through olfactory system connections. These sites of onset, positioned as they are at neural interfaces with the environment, have suggested to some that a toxic environmental exposure may trigger the disease. Individual patients vary in their adherence to these general patterns, and the tempo and topology of progression dictate the clinical syndrome. Some patients with long-standing Parkinson’s disease (PD) (Chap. 427) without cognitive impairment slowly develop a dementia that is associated with visual hallucinations and fluctuating alertness. In this scenario, the term Parkinson’s disease dementia (PDD) is often used. In other patients, dementia and a neuropsychiatric syndrome precede or co-emerge with the parkinsonism, and the patient is diagnosed with dementia with Lewy bodies (DLB). SN - PB - McGraw-Hill Education CY - New York, NY Y2 - 2024/11/08 UR - accessmedicine.mhmedical.com/content.aspx?aid=1155958612 ER -