Abstract：
Objective: To review the literature on the neurobiological mechanisms of obsessive-compulsive symptoms (OCS) in people with dementia.
Data Sources: MEDLINE/PubMed, CENTRAL, and PsycNet databases were searched from inception to March 2023.
Study Selection: Original studies of any methodology with newly published data on the neurobiological underpinnings of OCS in patients with dementia, regardless of patient age or comorbidity and publication year, were included. The following search terms were used: (Obses* OR compul* OR OCD) AND (cognitive de* OR cognitive dysfunction OR cognitive disfunction OR dementia).
Data Extraction: Individual study data were extracted onto a piloted extractions sheet.
Results: Patients with dementia and OCS were reported to have atrophy and hypoperfusion of frontal, temporal, striatal, and limbic structures. Serotonergic agents may be efficacious in reducing OCS. One randomized controlled trial of paroxetine in behavioral symptoms of dementia did not show efficacy. Evidence of dopaminergic dysfunction is too sparse to draw conclusions. Microglia dysfunction mediates obsessive-compulsive-like symptoms. Mutations of microtubule-associated protein τ may increase the risk of OCS. Cognitive self-consciousness and obsessive-compulsive-related cognitions may mediate OCS in old age. Dysfunction of the processing of one class of stimuli may increase the salience of other classes of stimuli, leading to OCS.
Conclusions: Frontal lobe hypometabolism and temporal lobe atrophy and hypometabolism are unexpected given previous research in obsessive compulsive disorder. Serotonergic agents have encouraging efficacy in case reports but require more specific research.
Prim Care Companion CNS Disord 2024;26(3):23r03689.
Author affiliations are listed at the end of this article.
Data Sources: MEDLINE/PubMed, CENTRAL, and PsycNet databases were searched from inception to March 2023.
Study Selection: Original studies of any methodology with newly published data on the neurobiological underpinnings of OCS in patients with dementia, regardless of patient age or comorbidity and publication year, were included. The following search terms were used: (Obses* OR compul* OR OCD) AND (cognitive de* OR cognitive dysfunction OR cognitive disfunction OR dementia).
Data Extraction: Individual study data were extracted onto a piloted extractions sheet.
Results: Patients with dementia and OCS were reported to have atrophy and hypoperfusion of frontal, temporal, striatal, and limbic structures. Serotonergic agents may be efficacious in reducing OCS. One randomized controlled trial of paroxetine in behavioral symptoms of dementia did not show efficacy. Evidence of dopaminergic dysfunction is too sparse to draw conclusions. Microglia dysfunction mediates obsessive-compulsive-like symptoms. Mutations of microtubule-associated protein τ may increase the risk of OCS. Cognitive self-consciousness and obsessive-compulsive-related cognitions may mediate OCS in old age. Dysfunction of the processing of one class of stimuli may increase the salience of other classes of stimuli, leading to OCS.
Conclusions: Frontal lobe hypometabolism and temporal lobe atrophy and hypometabolism are unexpected given previous research in obsessive compulsive disorder. Serotonergic agents have encouraging efficacy in case reports but require more specific research.
Prim Care Companion CNS Disord 2024;26(3):23r03689.
Author affiliations are listed at the end of this article.
摘要：
目的:回顾有关痴呆患者强迫症状(OCS)神经生物学机制的文献。
数据源：MEDLINE/PubMed,中部,和PsycNet数据库从开始到2023年3月进行了搜索。
研究选择：对任何方法的原始研究，以及新发表的关于痴呆患者OCS神经生物学基础的数据，无论患者年龄或合并症和出版年份，包括在内。使用以下搜索词：（Obses*ORcompul*OROCD）和（认知障碍*或认知功能障碍或认知障碍或痴呆）。
数据提取：将个体研究数据提取到试点提取表上。
结果：据报道，痴呆和OCS患者的额叶萎缩和灌注不足，temporal,纹状体,和边缘结构。5-羟色胺能药物可有效减少OCS。一项帕罗西汀治疗痴呆行为症状的随机对照试验未显示疗效。多巴胺能功能障碍的证据太稀少，无法得出结论。小胶质细胞功能障碍介导强迫样症状。微管相关蛋白τ的突变可能会增加OCS的风险。认知自我意识和强迫症相关认知可能介导老年OCS。一类刺激的处理功能障碍可能会增加其他类刺激的显著性，导致OCS。
结论：鉴于先前对强迫症的研究，额叶代谢低下和颞叶萎缩和代谢低下是出乎意料的。血清素能药物在病例报告中具有令人鼓舞的疗效，但需要更具体的研究。
PrimCareCompanionCNSDisord2024；26（3）：23r03689。
本文末尾列出了作者从属关系。
数据源：MEDLINE/PubMed,中部,和PsycNet数据库从开始到2023年3月进行了搜索。
研究选择：对任何方法的原始研究，以及新发表的关于痴呆患者OCS神经生物学基础的数据，无论患者年龄或合并症和出版年份，包括在内。使用以下搜索词：（Obses*ORcompul*OROCD）和（认知障碍*或认知功能障碍或认知障碍或痴呆）。
数据提取：将个体研究数据提取到试点提取表上。
结果：据报道，痴呆和OCS患者的额叶萎缩和灌注不足，temporal,纹状体,和边缘结构。5-羟色胺能药物可有效减少OCS。一项帕罗西汀治疗痴呆行为症状的随机对照试验未显示疗效。多巴胺能功能障碍的证据太稀少，无法得出结论。小胶质细胞功能障碍介导强迫样症状。微管相关蛋白τ的突变可能会增加OCS的风险。认知自我意识和强迫症相关认知可能介导老年OCS。一类刺激的处理功能障碍可能会增加其他类刺激的显著性，导致OCS。
结论：鉴于先前对强迫症的研究，额叶代谢低下和颞叶萎缩和代谢低下是出乎意料的。血清素能药物在病例报告中具有令人鼓舞的疗效，但需要更具体的研究。
PrimCareCompanionCNSDisord2024；26（3）：23r03689。
本文末尾列出了作者从属关系。
