Search

Research criteria for the diagnosis of prodromal dementia with Lewy bodies (DLB) include three clinical subtypes: mild cognitive impairment with Lewy bodies (MCI‐LB), delirium‐onset prodromal DLB, and psychiatric‐onset prodromal DLB. Late‐onset psychiatric manifestations are at a higher risk of developing dementia, but its relation to prodromal DLB remains unclear. In addition to the risk of severe antipsychotic hypersensitivity reactions, accurate discrimination from non‐DLB cases is important due to the potential differences in management and prognosis. This article aims to review a rapidly evolving psychiatric topic and outline clinical pictures of psychiatric‐onset prodromal DLB, including the proposed biomarker findings of MCI‐LB: polysomnography‐confirmed rapid eye movement sleep behaviour disorder, cardiac [123I]metaiodobenzylguanidine scintigraphy, and striatal dopamine transporter imaging. We first reviewed clinical pictures of patients with autopsy‐confirmed DLB. Regarding clinical reports, we focused on the patients who predominantly presented with psychiatric manifestations and subsequently developed DLB. Thereafter, we reviewed clinical studies regarding the diagnostic applications of the proposed biomarkers to patients with late‐onset psychiatric disorders. Clinical presentations were mainly late‐onset depression and psychosis; however, other clinical manifestations were also reported. Psychotropic medications before a DLB diagnosis may cause extrapyramidal signs, and potentially influences the proposed biomarker findings. These risks complicate clinical manifestation interpretation during the management of psychiatric symptoms. Longitudinal follow‐up studies with standardised evaluations until conversion to DLB are needed to investigate the temporal trajectories of core features and proposed biomarker findings. In patients with late‐onset psychiatric disorders, identification of patients with psychiatric‐onset prodromal DLB provides the opportunity to better understanding the distinct prognostic subgroup that is at great risk of incident dementia. Advances in the establishment of direct biomarkers for the detection of pathological α‐synuclein may encourage reorganising the phenotypic variability of prodromal DLB. [ABSTRACT FROM AUTHOR]

In the article, the authors discuss their study of outpatients at the Shiga Medical Centre in Japan to examine the prevalence of core clinical features and other neuropsychiatric symptoms in dementia with Lewy bodies (DLB). Among the features and symptoms are parkinsonism, hallucinations, and recurrent sleep talking. Also cited are the supportive features of DLB like depression and anxiety.

A case study is presented of a 68-year-old woman who used to see human faces on the ceiling as she lay at night before falling asleep. She was suspected of having rapid eye movement sleep behavior disorder and dementia with Lewy bodies; mini-mental state examination score showed 29/30; audio and video monitoring showed overnight polysomnography. She is still being diagnosed of pareidolic illusions of a patient with suspected late-onset, sleep-related epilepsy.

Dementia with Lewy bodies ( DLB) is defined pathologically as neurodegeneration associated with Lewy bodies ( LB). LB-related symptoms, including olfactory dysfunction, dysautonomia, and mood and sleep disorders, are increasingly recognized as clinical signs that enable the early detection of DLB, because these symptoms often antedate dementia by years or even decades. It remains unknown if the clinical history of LB-related symptoms is sufficient for the prodromal state of DLB 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 DLB. The timing of LB-related symptoms that preceded or followed relative to the onset of memory loss was calculated. LB-related symptoms were present in 79 of 90 patients (87.8%) with probable DLB 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-demented patients with a clinical history of LB-related symptoms in our memory clinic. All four patients showed reduced cardiac [123 I]-metaiodobenzylguanidine levels. Moreover, [18 F]fluoro-D-glucose positron emission tomography scans revealed glucose hypometabolism in the occipital cortex in two patients. One patient converted to probable DLB with the development of parkinsonism 2 years after major depression was diagnosed. Based on a clinical history of LB-related symptoms, we propose a conceptual framework to identify these symptomatic but non-demented individuals that led us to suspect the underlying pathophysiology of Lewy body disease. Further prospective study is warranted to determine the clinical significance of LB-related symptoms in non-demented patients. [ABSTRACT FROM AUTHOR]