Objective To evaluate the efficacy of eszopiclone for patients with acute insomnia and the impact of premedication with eszopiclone on sleep structure of patients with acute insomnia.Methods In an open-label,self-control trial was conducted at Changzheng Hospital Sleep Centers,and patients (n =32) with acute insomnia (12 men,20 women; mean age,36.2 years) were administered eszopiclone 3 mg for three consecutive nights.Sleep was monitored via polysomnography.The insomnia severity index (ISI),and mini-mental state examination (MMSE) were used to assess the degree of insomnia and impact of drugs on cognitive function during the day.Results Eszopiclone can shorten sleep latency ( before treatment:(52.92 ± 11.71 ) min,after treatment:(28.2 ± 10.11 ) min; t =-4.376,P ＜0.01 ),prolong total sleep time(before treatment:(365.22 ±30.13) min,after treatment:(429.18 ±26.93 ) min; t =4.102,P ＜ 0.01 ),decrease wake up times( before treatment:( 5.00 ± 1.92 ) times,after treatment:( 2.73 ± 0.91 )times; t =- 4.592,P ＜ 0.01 ),improve sleep efficiency ( before treatment:72.69％ ± 6.32％,after treatment:82.67％ ± 4.16％ ; t =3.371,P ＜ 0.01 ),reduce awake time ( before treatment:( 88.51 ±17.48) min,after treatment:(65.93 ±21.l0)min; t =-4.592,P ＜0.01 ),decrease light sleep ( NREM1 period) the percentage of time ( before treatment:12.54％ ± 2.10％,after treatment:7.30％ ± 2.90％ ;t=-3.155,P ＜ 0.01 ),and increase the percentage of slow wave sleep (before treatment:8.03％ ±5.37％,after treatment:9.31％ ±5.29％; t =4.228,P ＜0.01).No effect was observed on the percentage of NERM2 period (t =0.731,P ＞0.05) and REM period (t =-0.813,P ＞0.05).Eszopiclone can improve the quality of subjective assessment of sleep ( ISI score decreased,t =- 2.551,P ＜ 0.05) and has no significant effect on cognitive function on first the morning after patients taking the medication.Conclusion Eszopiclone can positively regulate the sleep structure in patients with acute insomnia and improve subjective assessment of sleep quality.It is safe and has no significant effect on cognitive function.

Mild cognitive impairment (MCI), as a nosological entity referring to elderly people with MCI but without dementia, was proposed as a warning signal of dementia occurrence and a novel therapeutic target. MCI clinical criteria and diagnostic procedure from the MCI Working Group of the European Alzheimer's Disease Consortium (EADC) may better reflect the heterogeneity of MCI syndrome. Beijing United Study Group on MCI funded by the Capital Foundation of Medical Developments (CFMD) proposed the guiding principles of clinical research on MCI. The diagnostic methods include clinical, neuropsychological, functional, neuroimaging and genetic measures. The diagnostic procedure includes three stages. Firstly, MCI syndrome must be defined, which should correspond to: (1) cognitive complaints coming from the patients or their families; (2) reporting of a relative decline in cognitive functioning during the past year by the patient or informant; (3) cognitive disorders evidenced by clinical evaluation; (4) activities of daily living preserved and complex instrumental functions either intact or minimally impaired; and (5) absence of dementia. Secondly, subtypes of MCI have to be recognized as amnestic MCI (aMCI), single non-memory MCI (snmMCI) and multiple-domains MCI (mdMCI). Finally, the subtype causes could be identified commonly as Alzheimer disease (AD), vascular dementia (VaD), and other degenerative diseases such as frontal-temporal dementia (FTD), Lewy body disease (LBD), semantic dementia (SM), as well as trauma, infection, toxicity and nutrition deficiency. The recommended special tests include serum vitamin B12 and folic acid, plasma insulin, insulin-degrading enzyme, Abeta40, Abeta42, inflammatory factors. Computed tomography (or preferentially magnetic resonance imaging, when available) is mandatory. As measurable therapeutic outcomes, the primary outcome should be the probability of progression to dementia, the secondary outcomes should be cognition and function, and the supplement outcome should be the syndrome defined by traditional Chinese medicine. And for APOE epsilon4 carrier, influence of the carrier status on progression rate to dementia and the effect of treatment should be evaluated.

In order to provide the "guiding principles of clinical research on mild cognitive impairment (MCI) (protocol)" edited by Beijing United Study Group on MCI of the Capital Foundation of Medical Developments (CFMD) with evidence support, clinical criteria, subtypes, inclusion and exclusion of MCI, and use of rating scales were reviewed. The authors suggested that MCI clinical criteria and new diagnosis procedure from the MCI Working Group of the European Alzheimer's disease Consortium (EADC) may better reflect the heterogeneity of MCI syndrome. Diagnostic rating scales including Clinical Dementia Rating (CDR), Global Deterioration Scale (GDS), Alzheimer's Disease Assessment Scale-cognitive subscale (ADAS-cog) and Instrumental Activities of Daily Living (IADL) are very useful in definition of MCI but can not replace its clinical criteria. Absence of major repercussions on daily life in patients with MCI was emphasized, but the patients may have minimal impairment in complex IADL. According to their previous research, the authors concluded that highly recommendable neuropsychological scales with cut-off scores in the screening of MCI cases should include Mini-Mental State Examination (MMSE), logistic memory test such as Delayed Story Recall (DSR), executive function test such as Clock Draw Test (CDT), language test such as Verbal Category Fluency Test (VCFT), etc. And finally, the detection of biological and neuroimaging changes, including atrophy in hippocampus or medial temporal lobe in patients with MCI, was introduced.