精神症状加速变成失智症


  【24drs.com】两篇新研究确认,神经精神症状(NPS)与轻微认知障碍(MCI)更快恶化成阿兹海默氏症(AD)有关。
  
  马里兰州巴尔的摩约翰霍普金斯大学博士候选人Sarah Forrester领导的第一篇研究明确指出,NPS和更快速恶化有关。旧金山加州大学R. Scott Mackin博士领导的第二篇研究认为,与脑部结构变化有关的慢性忧郁症状,可能会促使病情更快速转化。
  
  Forrester表示,在临床上,我们的研究让医师知道在实务上要注意哪里些人,我们可以明确地指出哪里些患者需要更多注意,高风险者可能适用一些预防策略,例如改善一般医疗状况。
  
  这些研究发表于2月版的美国老年精神病学期刊。
  
  第一篇研究中,Forrester等人探讨NPS和恶化成失智症的关联,研究对象是「Alzheimer's Disease Cooperative Study (ADCS)」研究中、540名偶发MCI的患者,追踪这些患者2年,每次访视时,使用神经精神量表问卷评估这些患者。
  
  研究者使用隐藏分类分析将MCI患者根据有无出现各种NPS而分组,他们共分成三组NPS:严重组,高燥动率(84%)、焦虑(52%)、淡漠(51%)、夜间行为(48%)、去抑制(44%);情绪组,特征是高忧郁率(41%)、焦虑(31%)、易怒(32%)、夜间行为(35%);无症状组,纳入这组是因为不到5%的患者有所有症状;每个类别的盛行率分别是7%、 37%和56%。
  
  在追踪期间,121名(22%)患者被判断已恶化成失智,419人(78%)依旧是MCI,有167人(31%)恢复到正常的认知。研究者报告指出,从MCI恶化到失智的比率,以严重组最高、情绪组居中、无症状组最低。
  
  与无症状组相比,严重组恶化成失智的风险超过2倍以上(风险比[HR]为2.69;95%信赖区间[CI]为1.12 - 2.70);情绪组恶化成失智的风险则是超过1.5倍(HR, 1.79;95% CI, 1.12 - 2.70)。
  
  Forrester等人在文章中指出,根据患者的症状资料将他们分组,可以更加了解哪里些症状会造成失智诊断之风险改变、以及缩短恶化时间。冷漠和忧郁在情绪组都很常见,这些症状可能被证明是NPS群组的一部份,最能预测恶化。
  
  他们结论表示,对那些有NPS的人,我们的结果对于及早侦测和治疗失智有所影响。因为有较多NPS和特定NPS的患者,更可能恶化成失智诊断,及早预防NPS或许有助于预防MCI和失智。
  
  第二篇研究中,Mackin博士等人检视了慢性忧郁症状对于有恶化成失智之风险者的影响。
  
  他们使用「Alzheimer's Disease Neuroimaging Initiative」的资料检视慢性忧郁症状、区域性脑萎缩和恶化成AD的关联,研究对象是94名MCI患者,其中32人有慢性忧郁症状。
  
  研究者发现,慢性忧郁症状和额叶与前扣带的皮质加速萎缩有关,已知这两个区域会受到AD影响。
  
  在3年追踪期间,38名患者(42.7%)恶化成AD,有慢性忧郁症状者的偶发AD比率高于没有慢性忧郁症状者(62.1% vs 33.3%);至于有慢性忧郁症状者,恶化变成AD的时间比没有忧郁症状者少60% (P = .008)。
  
  研究者指出,慢性忧郁症状和偶发AD之间的关联,与颞叶区的皮质萎缩率无关,和额叶区域的皮质萎缩率有关。整体看来,研究结果认为,和脑部结构改变有关的慢性忧郁症状,可能会造成MCI更快速恶化成失智。
  
  编辑评论的共同作者、宾州匹兹堡大学精神病学教授、生物工程副教授Howard Aizenstein博士表示,这两篇研究一起为更清楚说明MCI患者的情感症状提供证据。
  
  Aizenstein博士表示,即便没有失智风险之关联,依旧建议充分治疗情感症状-但是,越来越多的证据认为,这或许可降低失智风险,为考量心智健康治疗选项的患者提供更多信息。
  
  这两篇研究支持情感症状和失智风险增加之关联,但是都没有确认因果关系。因此,我们不知道是否是情感症状促成恶化为AD,也可能是潜在的神经退化变化导致情感症状和失智。不过,似乎有著因果关系,因为情感症状的多个路径会恶化认知与功能,从而加快恶化成AD,因此,缓解情感症状可能会降低失智症的风险。
  
  资料来源:http://www.24drs.com/
  
  Native link:Psychiatric Symptoms Speed Conversion to Dementia

Psychiatric Symptoms Speed Conversion to Dementia

By Megan Brooks
Medscape Medical News

Neuropsychiatric symptoms (NPS) are associated with more rapid progression from mild cognitive impairment (MCI) to Alzheimer's disease (AD), two new studies confirm.

The first study, led by Sarah Forrester, a doctoral candidate at Johns Hopkins University, in Baltimore, Maryland, pinpoints clusters of NPS associated with faster progression. The second study, led by R. Scott Mackin, PhD, University of California, San Francisco, suggests that chronic depressive symptoms are associated with structural brain changes that may contribute to more rapid conversion.

"Clinically," Forrester told Medscape Medical News, "our study gives clinicians an idea of who to keep an eye on in practice. We can definitively say which patients may deserve greater attention than others, and those in the higher-risk groups may be candidates for preventive measures, such as improvement in general medical health."

The studies are published in the February issue of the American Journal of Geriatric Psychiatry.

Predicting the Future

In the first study, Forrester and colleagues explored the association between NPS and progression to dementia in 540 patients with incident MCI from the Alzheimer's Disease Cooperative Study (ADCS). The patients were followed for a period of 2 years. At each visit, participants were assessed with the Neuropsychiatric Inventory Questionnaire.

The researchers used latent class analysis to classify MCI individuals into distinct subgroups on the basis of the presence or absence of different NPS. They identified three clusters of NPS: a severe cluster, marked by high rates of agitation (84%), anxiety (52%), apathy (51%), nighttime behaviors (48%), and disinhibition (44%); an affective cluster, characterized by high rates of depression (41%), anxiety (31%), irritability (32%), and nighttime behaviors (35%); and an asymptomatic cluster, labeled as such because all symptoms were endorsed by fewer than 5% of patients. The prevalence of each class was 7%, 37% and 56%, respectively.

During follow-up, 121 (22%) patients were judged to have progressed to dementia, 419 (78%) remained with MCI, and 167 (31%) reverted to normal cognition. The rate of progression from MCI to dementia was highest in the severe group, intermediate for the affective group, and lowest for the asymptomatic group, the researchers report.

Compared with the asymptomatic class, the severe class had more than twice the risk for progression to dementia (hazard ratio [HR], 2.69; 95% confidence interval [CI], 1.12 - 2.70); the affective class had more than 1.5 times the risk for progression to dementia (HR, 1.79; 95% CI, 1.12 - 2.70).

"Classifying patients based on their symptom profiles might allow a better understanding of how the addition of certain symptoms may change the risk of dementia diagnosis and shorten time to diagnosis," Forrester and colleagues note in their article.

Apathy and depression were common in both the affective and severe classes. "These symptoms may prove to be part of NPS clusters that are most predictive of progression," they write.

"Our results," they conclude, "have implications for early detection and treatment of dementia in those with NPS. Because patients with more NPS and specific NPS are more likely to progress to dementia diagnosis, preventing NPS earlier in life may be an avenue for prevention of MCI and dementia."

Brain Atrophy

In the second study, Dr Mackin and colleagues examined the role of chronic depressive symptoms in the risk for progression to dementia.

They used data from the Alzheimer's Disease Neuroimaging Initiative to characterize the relationship of chronic depressive symptoms, regional brain atrophy, and progression to AD in 94 individuals with MCI, 32 of whom had chronic depressive symptoms.

The investigators found that chronic depressive symptoms were associated with accelerated cortical atrophy in the frontal lobe and anterior cingulate, regions known to be affected by AD.

During median follow-up of 3 years, 38 participants (42.7%) progressed to AD. Incident AD was more common in those with than in those without chronic depressive symptoms (62.1% vs 33.3%). For patients with chronic depressive symptoms, the time to conversion to AD was 60% shorter than for those without depressive symptoms (P = .008).

The researchers note that the association between chronic depressive symptoms and incident AD was independent of cortical atrophy rates in the temporal regions but not of cortical atrophy rates in frontal regions. Taken together, the findings suggest that chronic depressive symptoms are associated with structural brain changes that may contribute to more rapid conversion to dementia in MCI, they conclude.

Causal Relationship "Likely"

Howard Aizenstein, MD, PhD, coauthor of an accompanying editorial, said that together, the two studies provide support for fully addressing affective symptoms in patients with MCI. Dr Aizenstein is professor of psychiatry and associate professor of bioengineering at the University of Pittsburgh, in Pennsylvania.

"Even without the link to dementia risk, full treatment of the affective symptoms would be recommended — but the accumulating evidence that this also may lower dementia risk provides additional information for patients in considering mental health treatment options," Dr Aizenstein told Medscape Medical News.

"These two studies support the association of affective symptoms with increased dementia risk. Neither study confirms causation; thus, we don't know if the affective symptoms potentiate the progression to AD. It could be that the underlying neurodegenerative changes lead to both the affective symptoms and dementia.

"However, it seems likely that there is a causal relationship, as there are multiple pathways in which affective symptoms can worsen cognition and function and thus hasten progression to AD. Thus, alleviating the affective symptoms may lower the dementia risk," he said.

The study authors and Dr. Aizenstein report no relevant financial relationships.

Am J Geriatr Psychiatry. 2016;24:105-106,117-125,126-135. Forrester et al,

    
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