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It remains unknown if the clinical history of\n                    <jats:styled-content style=\"fixed-case\">LB<\/jats:styled-content>\n                    \u2010related symptoms is sufficient for the prodromal state of\n                    <jats:styled-content style=\"fixed-case\">DLB<\/jats:styled-content>\n                    to be suspected in memory clinics. We retrospectively investigated the clinical courses, including olfactory dysfunction, dysautonomia, depression, and rapid eye movement sleep behaviour disorder, of 90 patients with probable\n                    <jats:styled-content style=\"fixed-case\">DLB<\/jats:styled-content>\n                    . The timing of\n                    <jats:styled-content style=\"fixed-case\">LB<\/jats:styled-content>\n                    \u2010related symptoms that preceded or followed relative to the onset of memory loss was calculated.\n                    <jats:styled-content style=\"fixed-case\">LB<\/jats:styled-content>\n                    \u2010related symptoms were present in 79 of 90 patients (87.8%) with probable\n                    <jats:styled-content style=\"fixed-case\">DLB<\/jats:styled-content>\n                    before or at the time of memory loss onset. These symptoms preceded the onset of memory loss between 1.2 and 9.3 years. We also report on four non\u2010demented patients with a clinical history of\n                    <jats:styled-content style=\"fixed-case\">LB<\/jats:styled-content>\n                    \u2010related symptoms in our memory clinic. All four patients showed reduced cardiac [\n                    <jats:sup>123<\/jats:sup>\n                    <jats:styled-content style=\"fixed-case\">I<\/jats:styled-content>\n                    ]\u2010metaiodobenzylguanidine levels. Moreover, [\n                    <jats:sup>18<\/jats:sup>\n                    <jats:styled-content style=\"fixed-case\">F<\/jats:styled-content>\n                    ]fluoro\u2010D\u2010glucose positron emission tomography scans revealed glucose hypometabolism in the occipital cortex in two patients. One patient converted to probable\n                    <jats:styled-content style=\"fixed-case\">DLB<\/jats:styled-content>\n                    with the development of parkinsonism 2 years after major depression was diagnosed. Based on a clinical history of\n                    <jats:styled-content style=\"fixed-case\">LB<\/jats:styled-content>\n                    \u2010related symptoms, we propose a conceptual framework to identify these symptomatic but non\u2010demented individuals that led us to suspect the underlying pathophysiology of\n                    <jats:styled-content style=\"fixed-case\">L<\/jats:styled-content>\n                    ewy body disease. Further prospective study is warranted to determine the clinical significance of\n                    <jats:styled-content style=\"fixed-case\">LB<\/jats:styled-content>\n                    \u2010related symptoms in non\u2010demented patients.\n                  <\/jats:p>","DOI":"10.1111\/psyg.12005","type":"journal-article","created":{"date-parts":[[2013,6,12]],"date-time":"2013-06-12T03:49:48Z","timestamp":1371008988000},"page":"128-138","source":"Crossref","is-referenced-by-count":98,"title":["Dementia with\n                    <scp>L<\/scp>\n                    ewy bodies: early diagnostic challenges"],"prefix":"10.1111","volume":"13","author":[{"given":"Hiroshige","family":"Fujishiro","sequence":"first","affiliation":[{"name":"PET\/CT Dementia Research Center Juntendo Tokyo Koto Geriatric Medical Center"},{"name":"Department of Psychiatry Juntendo University School of Medicine  Tokyo 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