Functional connectivity of the default mode network (DMN) during rest has been shown to be different among adults with Mild Cognitive Impairment (MCI) relative to aged-matched individuals without MCI and is predictive of transition to dementia. Post-traumatic stress disorder (PTSD) is also associated with aberrant connectivity of the DMN. Prior work from this group has demonstrated a higher rate of MCI and PTSD among World Trade Center (WTC) responders relative to the general population. The current study sought to investigate the main and interactive effects of MCI and PTSD on DMN functioning. Based on prior work, we hypothesized that MCI, but not PTSD, would predict aberrant connectivity in the DMN.

99 WTC responders aged 44–65 stratified by MCI status (yes/no) and PTSD status (yes/no) and matched for age in years, sex (male vs. female), race (white, black, and other), and educational attainment (high school or less, some college / technical school, and university degree), and occupation on September 11, 2001 (law enforcement vs. other) underwent fMRI using a 3T Siemens Biograph MR scanner. A single 10-minute continuous functional MR sequence was acquired while participants were at rest with their eyes open. Group-level analyses were conducted using SPM-12, with correction for multiple comparisons using AFNI's 3dClustSim. Based on this threshold, the number of comparisons in our imaging volume, and the smoothness of our imaging data as measured by 3dFWHMx-acf, a minimum cluster size of 1134 voxels was required to have a corrected p . .05 with 2-sided thresholding. Spherical 3 mm seeds were placed in the dorsal (4, -50, 26) and ventral (4, -60, 46) posterior cingulate cortex (PCC).

Individuals with PTSD demonstrated significantly less connectivity of the dorsal posterior cingulate cortex (PCC) with medial insula (T = 5.21), subthalamic nucleus (T = 4.66), and postcentral gyrus (T = 3.81). There was no difference found in this study for connectivity between groups stratified by MCI status. There were no significant results for the ventral PCC seed.

Contrary to hypotheses that were driven by a study of cortical thickness in WTC responders, the impact of PTSD appears to outweigh the impact of MCI on dorsal DMN connectivity among WTC responders stratified by PTSD and MCI status. This study is limited by several issues, including low number of female and minority participants, relatively small group cell sizes (n = 23–27 per cell), a brief resting state sequence (10 minutes), and lack of a non-WTC control group. Importantly, responders are a unique population so generalizability to other populations may be limited. Individuals in the current study are now being followed longitudinally to relate baseline resting state functional connectivity with cognitive changes and changes in connectivity over a four-year period.

Major depressive disorder is characterized by a high risk of relapse. We aimed to compare the prophylactic effects of different antidepressant medicines (ADMs).

PubMed, Cochrane Central Register of Controlled Trials, Embase and the Web of Science were searched on 4 July 2019. A pooled analysis of parametric survival curves was performed using a Bayesian framework. The main outcomes were hazard ratios (HRs), relapse-free survival and mean relapse-free months.

Forty randomized controlled trials were included. The 1-year relapse-free survival for ADM (76%) was significantly better than that for placebo (56%). Most of the relapse difference (86.5%) occurred in the first 6 months. Most HRs were not constant over time. Proof of benefit after 6 months of follow-up was not established partially because of small differences between the drug and placebo after 6 months. Almost all studies used an ‘enriched’ randomized discontinuation design, which may explain the high relapse rates in the first 6 months after randomization.

The superiority of ADM v. placebo was mainly attributed to the difference in relapse rates that occurred in the first 6 months. Our analysis provided evidence that the prophylactic efficacy was not constant over time. A beneficial effect was observed, but the prevention of new episodes after 6 months was questionable. These findings may have implications for clinical practice.

Ventilation-associated changes in blood carbon dioxide levels are associated with various physiological changes in infants undergoing surgery. Studies on the effects of mechanical ventilation on cerebral haemodynamics especially for infants with CHD are scarce.

This study was done to compare the changes in regional cerebral oxygen saturation and cerebral blood flow velocity when the end-tidal carbon dioxide partial pressure changed during different minute ventilation settings in infants undergoing ventricular septal defect repair.

A total of 67 patients less than 1 year old with ventricular septal defect were enrolled, and 65 patients (age: 6.7 ± 3.4 months, weight: 6.4 ± 1.5 kg) were studied. After anaesthesia induction and endotracheal intubation, the same mechanical ventilation mode (The fraction of inspired oxygen was 50%, and the inspiratory-to-expiratory ratio was 1:1.5.) was adopted. The end-tidal carbon dioxide partial pressure of 30 mmHg (T1), 35 mmHg (T2), 40 mmHg (T3), or 45 mmHg (T4) were obtained, respectively, by adjusting tidal volume and respiratory rate. Minute ventilation per kilogram was calculated by the formula: minute ventilation per kilogram = tidal volume * respiratory rate/kg. Regional cerebral oxygen saturation was monitored by real-time near-infrared spectroscopy. Cerebral blood flow velocity (systolic flow velocity, end-diastolic flow velocity, and mean flow velocity), pulsatility index, and resistance index were measured intermittently by transcranial Doppler. Systolic pressure, diastolic pressure, stroke volume index, and cardiac index were recorded using the pressure recording analytical method.

As the end-tidal carbon dioxide partial pressure increased from 30 to 45 mmHg, regional cerebral oxygen saturation increased significantly from 69 ± 5% to 79 ± 4% (p < 0.001). Cerebral blood flow velocity (systolic flow velocity, end-diastolic flow velocity, and mean flow velocity) increased linearly, while pulsatility index and resistance index decreased linearly from T1 (systolic flow velocity, 84 ± 19 cm/second; end-diastolic flow velocity, 14 ± 4 cm/second; mean flow velocity, 36 ± 10 cm/second; pulsatility index, 2.13 ± 0.59; resistance index, 0.84 ± 0.12) to T4 (systolic flow velocity, 113 ± 22 cm/second; end-diastolic flow velocity, 31 ± 6 cm/second; mean flow velocity, 58 ± 11 cm/second; pulsatility index, 1.44 ± 0.34; resistance index, 0.72 ± 0.07) (p < 0.001). There were significant differences in changes of systolic flow velocity, end-diastolic flow velocity, mean flow velocity, pulsatility index, and resistance index as the end-tidal carbon dioxide partial pressure increased from 30 to 45 mmHg between subgroups of infants ≤6 and infants >6 months, while the changes of regional cerebral oxygen saturation between subgroups were not statistically different. Regional cerebral oxygen saturation and cerebral blood flow velocity (systolic flow velocity, end-diastolic flow velocity, and mean flow velocity) were negatively correlated with minute ventilation per kilogram (r = −0.538, r = −0.379, r = −0.504, r = −0.505, p < 0.001). Pulsatility index and resistance index were positively related to minute ventilation per kilogram (r = 0.464, r = 0.439, p < 0.001). The diastolic pressure was significantly reduced from T1 (41 ± 7 mmHg) to T4 (37 ± 6 mmHg) (p < 0.001). There were no significant differences in systolic pressure, stroke volume index, and cardiac index with the change of end-tidal carbon dioxide partial pressure from T1 to T4 (p = 0.063, p = 0.382, p = 0.165, p > 0.05).

A relative low minute ventilation strategy increases regional cerebral oxygen saturation and cerebral blood flow, which may improve cerebral oxygenation and brain perfusion in infants undergoing ventricular septal defect repair.

Altered heart rate variability (HRV), an index of autonomic nervous system function, has been reported in generalized anxiety disorder (GAD), but the results have been mixed. Thus, the present study, using a large sample size and better methodology, aims to examine whether GAD is associated with impaired HRV, both at rest and in response to posture challenges.

In total, 1832 participants were recruited in this study, consisting of 682 patients with GAD (including 326 drug- and comorbidity-free GAD patients) and 1150 healthy controls. Short-term HRV was measured during the supine-standing-supine test (5-min per position). Propensity score matching (PSM), a relatively novel method, was used to control for potential confounders.

After PSM algorithm, drug- and comorbidity-free GAD patients had reductions in resting (baseline) high-frequency power (HF), an index for parasympathetic modulation, and increases in the low-frequency/HF ratio (LF/HF), an index for sympathovagal balance as compared to matched controls. Furthermore, the responses of HF and LF/HF to posture changes were all attenuated when compared with matched controls. Effect sizes, given by Cohen's d, for resting HF and HF reactivity were 0.42 and 0.36–0.42, respectively.

GAD is associated with altered sympathovagal balance, characterized by attenuation in both resting vagal modulation and vagal reactivity, with an almost medium effect size (Cohen's d ≈ 0.4), regardless of medication use or comorbidity status.

The Ser9Gly polymorphism in dopamine D3 receptor gene (DRD3) was considered an important factor in the pathogenesis of schizophrenia. Allele and genotype frequencies of this polymorphism were studied in different ethnic groups of schizophrenic patients. However, the results have been inconclusive.

To determine whether the DRD3 Ser9Gly polymorphism is associated with schizophrenia or influences its psychopathological symptoms in Han Chinese population.

We recruited 256 schizophrenic patients and 285 normal controls matched for gender, age and ethnicity. Pretreatment psychotic symptoms were evaluated with the Positive and Negative Symptom Scale (PANSS) in 128 acutely exacerbated schizophrenic in-patients. Genotyping of Ser9Gly polymorphism was performed with a polymerase chain reaction restriction fragment length polymorphism method and reconfirmed by a direct sequencing technique.

No significant difference was found between either patients with schizophrenia or with more homogeneous schizophrenic subgroups and healthy controls in genotype distributions and allele frequencies for the DRD3 Ser9Gly polymorphism. Similarly, DRD3 Ser9Gly genotype differences failed to reach significance in PANSS global, positive, negative and general symptoms scores. There is a trend (P = 0.064) towards higher PANSS positive symptoms scores in subjects carrying the Gly/Gly genotype.

This study does not support the role of DRD3 Ser9Gly polymorphism in increasing genetic risk for schizophrenia in Han Chinese population. Still, there is a possibility that the DRD3 Ser9Gly variant may reflect genetic variation of severity of positive symptoms in acutely exacerbated schizophrenia. Further studies are warranted to investigate the effect of the DRD3 Ser9Gly polymorphism in relation to longer time course of schizophrenia, including treatment response to antipsychotics.

Altered cardiac autonomic function has been proposed in schizophrenia, but the results are mixed. Therefore, analyses with larger sample sizes and better methodology are needed.

To examine whether acute schizophrenia is associated with cardiac autonomic dysfunction, 314 unmedicated patients with acute schizophrenia and 409 healthy volunteers, aged 18–65 years, were recruited for a case–control analysis. The severity of schizophrenia symptoms was assessed with the Positive and Negative Syndrome Scale. Cardiac autonomic function was evaluated by measuring heart rate variability (HRV) parameters during the supine–standing–supine test. Frequency-domain indices of HRV were obtained.

Unmedicated patients with acute schizophrenia consistently exhibited reduced mean RR interval and HRV levels in a supine rest and standing position compared with healthy volunteers. The severity of psychopathology, in particular positive symptoms, was negatively correlated with cardiac vagal control.

These data suggest that acute schizophrenia is accompanied by cardiac autonomic dysregulation. In view of the higher risk for cardiac complications in these patients, one might also consider the antipsychotic treatment in favour of improving cardiac autonomic modulation. Further studies using larger patient groups and controlled therapeutics may better understand the influence of antipsychotic treatment on cardiac autonomic regulation in schizophrenia.

Cardiac autonomic dysregulation has been reported in major depressive disorder (MDD), but scarce studies investigated that in fully remitted MDD.

To examine cardiac autonomic function in remitted MDD, 470 unmedicated individuals with a diagnosis of MDD earlier in life and 462 healthy volunteers, aged 18–65 years, were recruited for a case–control analysis. Cardiac autonomic function was evaluated by measuring heart rate variability (HRV) parameters. Frequency-domain indices of HRV were obtained. The obtained results were evaluated in association with personality traits assessed by the Tridimensional Personality Questionnaire.

In patients with remitted MDD, no differences in RR intervals and all frequency-domain indices of HRV could be detected as compared with controls. Stratified analyses by the presence of a history of suicide ideation (the SI+ vs. the SI-subgroup) revealed decreased cardiac vagal control in the SI+ subgroup. The correlation analysis revealed an inverse relation between HRV levels and the harm avoidance score (which has been suggested to be associated with serotonergic activity), mainly attributable to the robust association in the SI+ subgroup.

Our study shows that cardiac autonomic dysregulation is not shown in remitted MDD patients as a whole but is limited to the subgroup of remitted MDD patients with a history of suicidal ideation. In view of the higher risk for cardiac complications in these vulnerable individuals, one might consider the treatment to restore their autonomic function.