Depression and anxiety in vascular dementia: an update.

IF 4
Kurt A Jellinger
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Abstract

Depression with a prevalence between 20% and 86% and anxiety with a prevalence up to 72% most frequently coexist with vascular dementia (VaD) and reciprocally increase disease risks. Both psychopathological disorders are usually more frequent and more severe in patients with VaD than in those with Alzheimer disease (AD). Although there is a significant association between depression and all-cause dementia, VaD with depression has more comorbidities and higher mortality than without depression. A history of depression prior to dementia is more common than in AD, while its pre-disease state is a matter of discussion. Although the diagnosis of depression related to cerebrovascular disorders is based on the criteria of DSM-V, VaD/depression has been suggested to be a distinct subtype differing from late-life depression and major depressive disorder, whereas others reported broadly similar depressive symptom profiles across VaD, AD, and AD plus VaD. Depression in the course of VaD, which is frequently underdiagnosed and undertreated, has been related to a variety of pathogenic mechanisms, in particular cerebral small vessel disease (CSVD), cerebral white matter lesions, damage to fronto-subcortical brain circuits, neuroinflammation, impaired neurotrophic support, and imbalance of neurotransmitter/kynurenine pathways. Multimarkers, like high CSVD and white matter hyperintensity burden, the presence of visible perivascular spaces, inflammatory markers, neurofilament light chain levels, and other biomarkers may support clinical diagnosis of VaD/depression. Treatment planning should consider a modest response to antidepressants, while treatment of vascular and metabolic comorbidities may provide promising targets for its prevention and treatment. Electroconvulsive therapy and transcranial direct current stimulation as augmentation treatment of an adequate pharmacotherapy are potential strategies in the management of VaD/depression that is known to be often unresponsive to antidepressants only. However, their effectiveness needs further investigation to assess which interventions are appropriate and effective in clinical practice.

血管性痴呆患者的抑郁和焦虑:最新进展。
抑郁症(患病率在20%至86%之间)和焦虑症(患病率高达72%)最常与血管性痴呆(VaD)共存,并相互增加疾病风险。这两种精神病理障碍在VaD患者中通常比阿尔茨海默病(AD)患者更频繁和更严重。尽管抑郁症和全因痴呆之间存在显著关联,但VaD合并抑郁症的合并症和死亡率高于无抑郁症的VaD。痴呆症之前的抑郁史比阿尔茨海默病更常见,而其病前状态是一个值得讨论的问题。尽管与脑血管疾病相关的抑郁症的诊断是基于DSM-V的标准,但VaD/抑郁症已被认为是不同于晚年抑郁症和重度抑郁症的一种明显亚型,而其他研究报告的VaD、AD和AD + VaD的抑郁症状特征大致相似。VaD过程中的抑郁,经常被误诊和治疗不足,与多种致病机制有关,特别是脑小血管疾病(CSVD)、脑白质病变、额皮质下脑回路损伤、神经炎症、神经营养支持受损和神经递质/犬尿氨酸通路失衡。多标志物,如高CSVD和白质高负荷、可见血管周围间隙、炎症标志物、神经丝轻链水平和其他生物标志物的存在可能支持VaD/抑郁症的临床诊断。治疗计划应考虑对抗抑郁药物的适度反应,而血管和代谢合并症的治疗可能为其预防和治疗提供有希望的目标。电惊厥治疗和经颅直流电刺激作为适当药物治疗的增强治疗是治疗VaD/抑郁症的潜在策略,已知仅对抗抑郁药无反应。然而,它们的有效性需要进一步调查,以评估哪些干预措施在临床实践中是适当和有效的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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