| BackgroundDepression is a common neuropsychiatry disease with high incidence and negative health effects in old adult. Firstly, with the age going on, the ability of anti-pressure for the brain declines. Secondly, chronic diseases like hypertension, diabetes are very common in the old people. All of which cause the high prevalence of depression in these persons. However, the clinical manifestations in the late life depression are atypical. They often express anxiety, agitate and feel uncomfortable while the young depression persons often feel down. What’s more, late life depression often had cognitive impairment. They often can not express their discomfort appropriately. As a consequence, they were often looked over by their families or misdiagnosed.The cognitive impairment in late life depression is still even if effective antidepressant treatments. Information preceding disorder, executive dysfunction and memory disorder were the most common cognitive disorders in late life depression. Research found that people had poor effect for the antidepressant drugs if they had accompanied with executive dysfunction. Furthermore, late life depression with executive dysfunction will have higher risk of dementia in the later time. Executive function includes three main aspects:task switching, working memory refresh, and inhibitory control. The inhibitory control is the core aspect of the executive function.Event related potential is a kind of evoke potential which records from the scalp. As its high temporal resolution, it can time-locked reflect the electrophysiological change of the cognitive proceeding in the brain. In the visual Go/NoGo ERP studies, two components of the event-related potentials have consistently been associated with inhibition control:the N2 and P3. The N2 is a negative deflection which occurs between 150 and 300 ms after stimulus onset. It is assumed to reflect top-down inhibition of a pre-response motor programmer. It also reflects competition between execution and inhibition of a motor action. Meanwhile, it reflects the early stage processing in the inhibition control. The declining N2 amplitude reflects the attenuating inhibition control while the raising N2 amplitude reflects the enhancing inhibition control, especially its early stage. P3 is a large positive deflection, which is generated about 300-500 ms after stimulus presentation. The amplitude of the P3 is thought to reflect cognitive and motor inhibition. In particular, it is often associated with a later stage of inhibition control such as evaluation of successful inhibition and termination of the inhibition process. The declining P3 amplitude reflects the attenuating inhibition control while the raising P3 amplitude reflects the enhancing inhibition control, especially its later stage.Research in inhibitory control in depression found that the depression patients in young had declining N2 and P3 amplitude in their depression state. However, the amplitudes recovered after antidepressant treatments. What’s more, the amplitude and latency of the P3 recovered absolutely. But in late life depression, some research found the N2 and P3 amplitude declined and P3 latency prolonged. Meanwhile, the N2 amplitude was relevant with the severity of depression. While some research found that the N2 amplitude raised and P3 amplitude declined in these patients. In addition, the P3 amplitude was relevant with the severity of depression. As we know, depression is also known as pseudo dementia. In other words, the severity of depression can influence the cognitive function. So what about the inhibitory control in remitted late life depression?Objection:1. To explore the executive function in the remitted late life depression.2. To explore the event-related potentials---inhibitory control in remitted late life depression and provide the electrophysiology evidence for the executive dysfunction in these patients.3. To explore which stage of the inhibitory control impairment in the remitted late life depression.MethodSeventeen remitted late life depression patients were consecutively recruited from clinic and inpatient of Guangzhou Brain Hospital from July-2015 to January-2016. The controls were recruited from Guangzhou communities. We collected the age, sex, years of education, medications and so on.Neuropsychological evaluation:mini-mental state (MMSE) examination, which evaluated the global cognitive; Hamilton Depression Scale (HAMD), which evaluated the severity of depression. Trail Making Test (TMT) and Stroop color words Test (CWT), which evaluated the executive function. In addition, we also calculated the Interference Effects, which reflected inhibitory control.Stimulus presentation:We used the E-Prime to present the stimulus. Upright or down equilateral triangular figures were used as the stimuli, which were black on a white background and with a viewing distance of 75 cm. The stimulus size was 7cm horizontal by 6.06cm height. Stimulus was presented one by one. Participants were instructed to press the space key with the left or right index finger as fast as possible for upright triangle (Go), but withheld their response when shown down triangular (Nogo). The experiment consisted of 400 stimuli presented pseudo randomly with equal probability on the screen. The duration of the stimulus was 50ms and the inter-trial-interval was set at 950 ms. It took about 10 min for completing the task.EEG recording:In order to ensure the participants completing the task better, we conducted the EEG recording in quiet, comfortable, sound insulation, dimly lit, temperature appropriate Brain cognitive electrophysiology laboratory. The electroencephalography (EEG) was recorded from 64-channel array (10/20 system) with linked nose reference. The electrooculogram (EOG) was recorded with two pairs of electrodes, one placed above and below the left eye, and the other placed 1cm from the bilateral lateral canthi. The electrode impedances were kept below 5KΩ throughout the experiment. The EEG was amplified by a NeuroScan SyAmp2 EEG/ERPs with a band pass of 0.01-200 Hz and sampled at a rate of 1000 Hz.Offline data analysis:We used the SCAN4.5 software to conduct the offline data analysis. First, we browsed the entire recording and delete the clear artifact. Second, we removed the eye power with the traditional way. Third, The EEG was segmented into the epoch. Forth, baseline corrected to the mean amplitude 200 ms before the stimulus. Fifth, the ERPs data were digitally low-pass filtered to eliminating 50HZ interference. Sixth, contaminated with artifacts greater than ±100μV were rejected before averaging. At last, the artifact-free EEG epochs with response for Go and Nogo conditions were averaged respectively and at least 100 trials were available for each subject and condition. We used the peakdetection to define the N2 and P3. The N2 was define as the most negative peak in the 150-300 ms time window after stimulus onset.The P3 was define as the most positive peak in the 300-500 ms time window after stimulus onset.Statistical analyses:All analysis were conducted using SPSS 17.0。(1)Normal distribution clinical, neuropsychological and behavioral data (i.e MMSE and reaction time, and error rate) were analyzed using independent-samples t test. Skewed distribution data use Mann-Whitney U test. Qualitative data like sex was tested by chi square test. P<0.05 as statistic significance.(2) ERPs component analysis:The main components were N2 and P3. The N2 was define as the most negative peak in the 150-300 ms time window after stimulus onset.The P3 was define as the most positive peak in the 300-500 ms time window after stimulus onset. Three-way RMANOVA of N2 and P3 were calculated for between-group comparisons with factors of the Group (Patients and Controls), condition (Go and Nogo) and Electrode site (FZ, CZ, PZ). The Greenhouse-Geisser corrections were adopted where appropriate. P<0.05 as statistic significance.(3) We selected the Electrode site FZ as representative. The correlation between the Nogo-N2 amplitude and neuropsychological data MMSE, SIE Time consuming and SIE Correct number were assessed by calculating Pearson correlation. The correlation between the Nogo-N2 amplitude and TMT Interference effect was assessed by calculating Spearman’s rank correlation coefficient. P<0.05 as statistic significance.Result1. The score of HAMD was significant difference between remitted late life depression and controls ((4.5(0,6),0(0,6), p=0.015).2. Neuropsychological results between remitted late life depression and controls:There were statistic significance in overall cognitive assessment MMSE, Stroop-B Time consuming, Stroop-C Time consuming and Stroop-C Correct number between remitted late life depression and controls(24.59±4.01,27.35±1.66,p=0.014; 44.75±10.77,34.29±7.752,p=0.003,109.50±47.53,68.18±7.39, p=0.001, 38.44±6.30,46.71±1.69,p<0.001). In addition, there were statistically significant in the SIE Time consuming and SIE Correct number between them (64.75±40.10, 33.88±9.16,p=0.004,10.50±5.92,2.59±1.58,p<0.001). In the TMT-A and TMT-B, they were also significant difference (61.19±20.17,45.65±13.33, p=0.013, 80.81±30.51,52.53±11.84, p=0.001). What’s more, there were also significant difference in TMT Interference effect (14(1,73),5.5(0,17),p=0.014)3. Behavior result between remitted late life depression and controlsThere were statistic significance in the commission rate between remitted late life depression and controls (79.11±17.48,93.59±7.68,p=0.004)4. The ERP results between remitted late life depression and controlsFor the N2 amplitude, the repeated measure variance analysis (groupxcondition×Electrode site 2×2×3) show:The main effect in group, condition and Electrode site were significant difference(F(1,32)=137.90, P<0.001, F(1,32)=84.11,P<0.001, F(2,64)=36.79, P<0.001). There were not significant interaction of groupxcondition or group×electrode(F(1,32)=0.118, P=0.734, F(2,64)= 1.841, P=0.167). For the N2 latency, the repeated measure variance analysis (groupxcondition×Electrode site 2x2x3) show:The main effect in group was significant difference (F (1,32)=7.027, P=0.012). For the P3 amplitude and latency, the repeated measure variance analyses (groupxcondition×Electrode site 2x2x3) show that there were not significant.5. Correlation:there was not significant difference between the Nogo-N2 amplitude and MMSE and TMT Interference effect (P=0.896, P=0.631). There were significant difference between the Nogo-N2 amplitude and SIE Time consuming and SIE Correct number (R=0.631, P=0.007,R=0.542,P=0.025)Conclusion:1. Remitted late life depression have executive dysfunction.2. Abnormal early conflict monitoring (inhibitory control processing disorder within 150-300ms time window) while normal later conflict monitoring (inhibitory control processing within 300-500ms time window) in remitted late life depression. The result provides electrophysiological evidence that executive dysfunction in remitted late life depression.3.the amplitude of Nogo-N2 have correlation with SIE Time consuming and SIE Correct number, which provides electrophysiological evidence that executive dysfunction in remitted late life depression. |
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