Taomoto Daiki, Nishio Yoshiyuki, Hidaka Yousuke, Kanemoto Hideki, Takahashi Shun, Ikeda Manabu
Department of Psychiatry, Osaka University Graduate School of Medicine, Suita, Osaka, Japan.
Department of Behavioral Neurology and Neuropsychiatry, United Graduate School of Child Development, Osaka University, Suita, Osaka, Japan.
Clin Park Relat Disord. 2024 Nov 21;11:100289. doi: 10.1016/j.prdoa.2024.100289. eCollection 2024.
Delirium-onset prodromal Lewy body disease (LBD) has been proposed as one of the primary phenotypes of prodromal stages of LBD. The detailed clinical features and biomarker profiles of delirium-onset prodromal LBD have not been well characterized.
Five consecutive cases of delirium-onset prodromal LBD were documented. The diagnosis of prodromal LBD was made based on neuroimaging biomarkers, including dopamine transporter single-photon emission computed tomography (SPECT), cardiac I-metaiodobenzylguanidine scintigraphy, and/or brain perfusion SPECT, as well as clinical findings in the post-delirium follow-up periods.
In all cases, one or more of the core or supportive clinical features of dementia with Lewy bodies, including rapid eye movement sleep behavior disorder, minor hallucinations, hyposmia, or autonomic dysfunction, were present prior to the onset of delirium. The precipitating factors for delirium were diverse, including surgery, radiation therapy, chemotherapy, and infection. The duration of delirium was prolonged for several months in two cases, whereas it was resolved within a few weeks in the other cases. In most cases, persistent mild cognitive or behavioral symptoms were observed, which were improved with donepezil.
Our observations suggest that delirium-onset prodromal LBD may represent the later stages of the prodromal LBD rather than its initial stages. It is possible that delirium in the prodromal stages of LBD may represent subthreshold cognitive fluctuations that are transformed into clinically detectable states by a variety of precipitating factors.
谵妄起病的前驱期路易体病（LBD）已被提出作为LBD前驱期的主要表型之一。谵妄起病的前驱期LBD的详细临床特征和生物标志物谱尚未得到很好的描述。
记录了连续5例谵妄起病的前驱期LBD病例。前驱期LBD的诊断基于神经影像学生物标志物，包括多巴胺转运体单光子发射计算机断层扫描（SPECT）、心脏碘-间位碘代苄胍闪烁扫描和/或脑灌注SPECT，以及谵妄后随访期的临床发现。
在所有病例中，在谵妄发作之前均存在一种或多种路易体痴呆的核心或支持性临床特征，包括快速眼动睡眠行为障碍、轻微幻觉、嗅觉减退或自主神经功能障碍。谵妄的诱发因素多种多样，包括手术、放射治疗、化疗和感染。2例谵妄持续时间延长数月，而其他病例在数周内得到缓解。在大多数病例中，观察到持续的轻度认知或行为症状，使用多奈哌齐后有所改善。
我们的观察结果表明，谵妄起病的前驱期LBD可能代表前驱期LBD的后期阶段而非初始阶段。LBD前驱期的谵妄可能代表阈下认知波动，其通过多种诱发因素转变为临床可检测状态。
