Hangzhou Seventh Peoples Hospital

Studies using animal models have shown that depression affects the stability of the microbiota, but the actual structure and composition in patients with major depressive disorder (MDD) are not well understood. Here, we analyzed fecal samples from 46 patients with depression (29 active-MDD and 17 responded-MDD) and 30 healthy controls (HCs). High-throughput pyrosequencing showed that, according to the Shannon index, increased fecal bacterial α-diversity was found in the active-MDD (A-MDD) vs. the HC group but not in the responded-MDD (R-MDD) vs. the HC group. Bacteroidetes, Proteobacteria, and Actinobacteria strongly increased in level, whereas that of Firmicutes was significantly reduced in the A-MDD and R-MDD groups compared with the HC group. Despite profound interindividual variability, levels of several predominant genera were significantly different between the MDD and HC groups. Most notably, the MDD groups had increased levels of Enterobacteriaceae and Alistipes but reduced levels of Faecalibacterium. A negative correlation was observed between Faecalibacterium and the severity of depressive symptoms. These findings enable a better understanding of changes in the fecal microbiota composition in such patients, showing either a predominance of some potentially harmful bacterial groups or a reduction in beneficial bacterial genera. Further studies are warranted to elucidate the temporal and causal relationships between gut microbiota and depression and to evaluate the suitability of the microbiome as a biomarker.

OBJECTIVE: The aim of this study was to examine the reliability and validation of the 9-item Patient Health Questionnaire (PHQ-9) for late-life depression in Chinese primary care. METHODS: In the primary care clinics (PCCs) of Hangzhou city, we recruited 364 older patients (aged ≥ 60) for the PHQ-9 screening. Then 77 of them were further interviewed with Structured Clinical Interview for DSM Disorders (SCID) for the diagnosis of major depression in late life. Statistic strategies for the feasibility, reliability, validity, and receiver operating characteristic curve were performed. RESULTS: The mean administration time was 7.5 min, and the Cronbach's α was 0.91. The optimal cut-off score of PHQ-9 ≥ 9 revealed a sensitivity of 0.86, specificity of 0.77, and positive likelihood ratio of 5.73. The area under the curve (AUC) in this study was 0.92 (SD = 0.02, 95% CI 0.88-0.96). The PHQ-2 also revealed good sensitivity (0.84) and specificity (0.90) at the cut-off point ≥ 3. CONCLUSIONS: The PHQ-9 performs well and has acceptable psychometric properties for screening of patients with late-life depression in Chinese primary care settings.

Aberrant topological organization of whole-brain networks has been inconsistently reported in studies of patients with major depressive disorder (MDD), reflecting limited sample sizes. To address this issue, we utilized a big data sample of MDD patients from the REST-meta-MDD Project, including 821 MDD patients and 765 normal controls (NCs) from 16 sites. Using the Dosenbach 160 node atlas, we examined whole-brain functional networks and extracted topological features (e.g., global and local efficiency, nodal efficiency, and degree) using graph theory-based methods. Linear mixed-effect models were used for group comparisons to control for site variability; robustness of results was confirmed (e.g., multiple topological parameters, different node definitions, and several head motion control strategies were applied). We found decreased global and local efficiency in patients with MDD compared to NCs. At the nodal level, patients with MDD were characterized by decreased nodal degrees in the somatomotor network (SMN), dorsal attention network (DAN) and visual network (VN) and decreased nodal efficiency in the default mode network (DMN), SMN, DAN, and VN. These topological differences were mostly driven by recurrent MDD patients, rather than first-episode drug naive (FEDN) patients with MDD. In this highly powered multisite study, we observed disrupted topological architecture of functional brain networks in MDD, suggesting both locally and globally decreased efficiency in brain networks.

Autism spectrum disorder (ASD) is a prevalent and complex neurodevelopmental disorder which has strong genetic basis. Despite the rapidly rising incidence of autism, little is known about its aetiology, risk factors, and disease progression. There are currently neither validated biomarkers for diagnostic screening nor specific medication for autism. Over the last two decades, there have been remarkable advances in genetics, with hundreds of genes identified and validated as being associated with a high risk for autism. The convergence of neuroscience methods is becoming more widely recognized for its significance in elucidating the pathological mechanisms of autism. Efforts have been devoted to exploring the behavioural functions, key pathological mechanisms and potential treatments of autism. Here, as we highlight in this review, emerging evidence shows that signal transduction molecular events are involved in pathological processes such as transcription, translation, synaptic transmission, epigenetics and immunoinflammatory responses. This involvement has important implications for the discovery of precise molecular targets for autism. Moreover, we review recent insights into the mechanisms and clinical implications of signal transduction in autism from molecular, cellular, neural circuit, and neurobehavioural aspects. Finally, the challenges and future perspectives are discussed with regard to novel strategies predicated on the biological features of autism.

Abstract Ketamine, an N -methyl- d -aspartate receptor (NMDAR) antagonist 1 , has revolutionized the treatment of depression because of its potent, rapid and sustained antidepressant effects 2–4 . Although the elimination half-life of ketamine is only 13 min in mice 5 , its antidepressant activities can last for at least 24 h 6–9 . This large discrepancy poses an interesting basic biological question and has strong clinical implications. Here we demonstrate that after a single systemic injection, ketamine continues to suppress burst firing and block NMDARs in the lateral habenula (LHb) for up to 24 h. This long inhibition of NMDARs is not due to endocytosis but depends on the use-dependent trapping of ketamine in NMDARs. The rate of untrapping is regulated by neural activity. Harnessing the dynamic equilibrium of ketamine–NMDAR interactions by activating the LHb and opening local NMDARs at different plasma ketamine concentrations, we were able to either shorten or prolong the antidepressant effects of ketamine in vivo. These results provide new insights into the causal mechanisms of the sustained antidepressant effects of ketamine. The ability to modulate the duration of ketamine action based on the biophysical properties of ketamine–NMDAR interactions opens up new opportunities for the therapeutic use of ketamine.

Despite a growing neuroimaging literature on the pathophysiology of major depressive disorder (MDD), reproducible findings are lacking, probably reflecting mostly small sample sizes and heterogeneity in analytic approaches. To address these issues, the Depression Imaging REsearch ConsorTium (DIRECT) was launched. The REST-meta-MDD project, pooling 2428 functional brain images processed with a standardized pipeline across all participating sites, has been the first effort from DIRECT. In this review, we present an overview of the motivations, rationale, and principal findings of the studies so far from the REST-meta-MDD project. Findings from the first round of analyses of the pooled repository have included alterations in functional connectivity within the default mode network, in whole-brain topological properties, in dynamic features, and in functional lateralization. These well-powered exploratory observations have also provided the basis for future longitudinal hypothesis-driven research. Following these fruitful explorations, DIRECT has proceeded to its second stage of data sharing that seeks to examine ethnicity in brain alterations in MDD by extending the exclusive Chinese original sample to other ethnic groups through international collaborations. A state-of-the-art, surface-based preprocessing pipeline has also been introduced to improve sensitivity. Functional images from patients with bipolar disorder and schizophrenia will be included to identify shared and unique abnormalities across diagnosis boundaries. In addition, large-scale longitudinal studies targeting brain network alterations following antidepressant treatment, aggregation of diffusion tensor images, and the development of functional magnetic resonance imaging-guided neuromodulation approaches are underway. Through these endeavours, we hope to accelerate the translation of functional neuroimaging findings to clinical use, such as evaluating longitudinal effects of antidepressant medications and developing individualized neuromodulation targets, while building an open repository for the scientific community.

BACKGROUND: Convergent studies have highlighted the dysfunction of the amygdala, prefrontal cortex and hippocampus in post-traumatic stress disorder (PTSD). However, only a few studies have investigated the functional connectivity between brain regions in PTSD patients during the resting state, which may improve our understanding of the neuropathophysiology of PTSD. The aim of this study was to investigate patterns of whole-brain functional connectivity in treatment-naive PTSD patients without co-morbid conditions who experienced the 8.0-magnitude earthquake in the Sichuan province of China. METHOD: A total of 72 PTSD patients and 86 trauma-exposed non-PTSD controls participated in the resting-state functional magnetic resonance imaging study. All these subjects were recruited from the disaster zone of the 2008 Sichuan earthquake. Functional connectivities between 90 paired brain regions in PTSD patients were compared with those in trauma-exposed non-PTSD controls. Furthermore, Pearson correlation analysis was performed between significantly abnormal connectivities in PTSD patients and their clinician-administered PTSD scale (CAPS) scores. RESULTS: Compared with non-PTSD controls, PTSD patients showed weaker positive connectivities between the middle prefrontal cortex (mPFC) and the amygdala, hippocampus, parahippocampal gyrus and rectus, as well as between the inferior orbitofrontal cortex and the hippocampus. In addition, PTSD patients showed stronger negative connectivity between the posterior cingulate cortex (PCC) and the insula. The CAPS scores in PTSD patients correlated negatively with the connectivity between the amygdala and the mPFC. CONCLUSIONS: PTSD patients showed abnormalities in whole-brain functional connectivity, primarily affecting the connectivities between the mPFC and limbic system, and connectivity between the PCC and insula.

Abstract Major depressive disorder (MDD) is a complex state-dependent psychiatric illness for which biomarkers linking psychophysical, biochemical, and psychopathological changes remain yet elusive, though. Earlier studies demonstrate reduced GABA in lower-order occipital cortex in acute MDD leaving open its validity and significance for higher-order visual perception, though. The goal of our study is to fill that gap by combining psychophysical investigation of visual perception with measurement of GABA concentration in middle temporal visual area (hMT+) in acute depressed MDD. Psychophysically, we observe a highly specific deficit in visual surround motion suppression in a large sample of acute MDD subjects which, importantly, correlates with symptom severity. Both visual deficit and its relation to symptom severity are replicated in the smaller MDD sample that received MRS. Using high-field 7T proton Magnetic resonance spectroscopy ( 1 H-MRS), acute MDD subjects exhibit decreased GABA concentration in visual MT+ which, unlike in healthy subjects, no longer correlates with their visual motion performance, i.e., impaired SI. In sum, our combined psychophysical-biochemical study demonstrates an important role of reduced occipital GABA for altered visual perception and psychopathological symptoms in acute MDD. Bridging the gap from the biochemical level of occipital GABA over visual-perceptual changes to psychopathological symptoms, our findings point to the importance of the occipital cortex in acute depressed MDD including its role as candidate biomarker.

OBJECTIVE: The key principle of motor imagery (MI) decoding for electroencephalogram (EEG)-based Brain-Computer Interface (BCI) is to extract task-discriminative features from spectral, spatial, and temporal domains jointly and efficiently, whereas limited, noisy, and non-stationary EEG samples challenge the advanced design of decoding algorithms. METHODS: Inspired by the concept of cross-frequency coupling and its correlation with different behavioral tasks, this paper proposes a lightweight Interactive Frequency Convolutional Neural Network (IFNet) to explore cross-frequency interactions for enhancing representation of MI characteristics. IFNet first extracts spectro-spatial features in low and high-frequency bands, respectively. Then the interplay between the two bands is learned using an element-wise addition operation followed by temporal average pooling. Combined with repeated trial augmentation as a regularizer, IFNet yields spectro-spatio-temporally robust features for the final MI classification. We conduct extensive experiments on two benchmark datasets: the BCI competition IV 2a (BCIC-IV-2a) dataset and the OpenBMI dataset. RESULTS: Compared with state-of-the-art MI decoding algorithms, IFNet achieves significantly superior classification performance on both datasets while improving the winner's result in BCIC-IV-2a by 11%. Moreover, by conducting sensitivity analysis on decision windows, we show IFNet attains the best trade-off between decoding speed and accuracy. Detailed analysis and visualization verify IFNet can capture the coupling across frequency bands along with the known MI signatures. CONCLUSION: We demonstrate the effectiveness and superiority of the proposed IFNet for MI decoding. SIGNIFICANCE: This study suggests IFNet holds promise for rapid response and accurate control in MI-BCI applications.

Eye-tracking studies in young children with autism spectrum disorder (ASD) have shown a visual attention preference for geometric patterns when viewing paired dynamic social images (DSIs) and dynamic geometric images (DGIs). In the present study, eye-tracking of two different paired presentations of DSIs and DGIs was monitored in a group of 13 children aged 4 to 6 years with ASD and 20 chronologically age-matched typically developing children (TDC). The results indicated that compared with the control group, children with ASD attended significantly less to DSIs showing two or more children playing than to similar DSIs showing a single child. Visual attention preference in 4- to 6-year-old children with ASDs, therefore, appears to be modulated by the type of visual stimuli.

The mechanism of bipolar disorder is unclear. Growing evidence indicates that gut microbiota plays a pivotal role in mental disorders. This study aimed to find out changes in the gut microbiota in bipolar depression (BD) subjects following treatment with quetiapine, and evaluate their correlations with the brain and immune function. Totally 36 subjects with BD and 27 healthy controls (HCs) were recruited. The severity of depression was evaluated with the Montgomery–Asberg Depression Rating Scale (MADRS). At baseline, fecal samples were collected and analyzed by quantitative polymerase chain reaction (qPCR). T lymphocyte subsets were measured to examine immune function. Near-infrared spectroscopy (NIRS) was used to assess brain function. All BD subjects received quetiapine treatment (300 mg/d) for four weeks, following which the fecal microbiota and immune profiles were reexamined. Here, we first put forward the new concept of brain-gut coefficient of balance (B-GCB), which referred to the ratio of [oxygenated hemoglobin]/(Bifidobacteria to Enterobacteriaceae ratio), to analyze the linkage between the gut microbiota and brain function. At baseline, the CD3+ T cell proportion was positively correlated with log10 Enterobacter spp count, while the correlativity between the other bacteria and immune profiles were negative. Log10 B-GCB was positively correlated with CD3+ T cell proportion. In subjects with BD, counts of Faecalibacterium prausnitzii, Bacteroides–Prevotella group, Atopobium Cluster, Enterobacter spp and Clostridium Cluster IV were higher, while the log10 (B/E) were lower than HCs (B/E refers to Bifidobacteria to Enterobacteriaceae ratio, and represents microbial colonization resistance). After treatment, MADRS scores were reduced while the levels of Eubacterium rectale, Bifidobacteria and B/E increased. The composition of the gut microbiota and its relationship to brain function were altered in BD subjects. Quetiapine treatment was effective for depression and influenced the composition of gut microbiota in patients. Clinical trial registration: http://www.chictr.org.cn/index.aspx, identifier: ChiCTR-COC-17011401, URL: http://www.chictr.org.cn/listbycreater.aspx.

-methyl-d-aspartate receptor (NMDAR), it was not clear whether there is a selective, primary site for ketamine's antidepressant action. We found that ketamine injection in depressive-like mice specifically blocks NMDARs in lateral habenular (LHb) neurons, but not in hippocampal pyramidal neurons. This regional specificity depended on the use-dependent nature of ketamine as a channel blocker, local neural activity, and the extrasynaptic reservoir pool size of NMDARs. Activating hippocampal or inactivating LHb neurons swapped their ketamine sensitivity. Conditional knockout of NMDARs in the LHb occluded ketamine's antidepressant effects and blocked the systemic ketamine-induced elevation of serotonin and brain-derived neurotrophic factor in the hippocampus. This distinction of the primary versus secondary brain target(s) of ketamine should help with the design of more precise and efficient antidepressant treatments.

Bipolar disorder (BD) is a complex psychiatric disorder characterized by dominant symptom swings across different phases (manic, depressive, and euthymic). Different symptoms in BD such as abnormal episodic memory recall and psychomotor activity have been related to alterations in different regions, ie, hippocampus and motor cortex. How the abnormal regional distribution of neuronal activity relates to specific symptoms remains unclear, however. One possible neuronal mechanism of the relationship is the alteration of the global distribution of neuronal activity manifested in specific local regions; this can be measured as the correlation between the global signal (GS) and local regions. To understand the GS and its relationship to psychopathological symptoms, we here investigated the alteration of both GS variance and its regional topography in healthy controls and 3 phases of BD. We found that the variance of GS showed no significant difference between the 4 groups. In contrast, the GS topography was significantly altered in the different phases of BD, ie, the regions showing abnormally strong topographical GS contribution changed from hippocampus (and parahippocampus/fusiform gyrus) in depression to motor cortex in mania. Importantly, topographical GS changes in these regions correlated with psychopathological measures in both depression and mania. Taken together, our findings demonstrate the central importance of GS topography for psychopathological symptoms. This sheds lights on the neuronal mechanisms of specific psychopathological symptoms in BD, and its relevance in the relationship between global and local neuronal activities for behavior in general.

The anterior cingulate cortex (ACC) is frequently reported to have functionally distinct sub-regions that play key roles in different intrinsic networks. However, the contribution of the ACC, which is connected to several cortical areas and the limbic system, to autism is not clearly understood, although it may be involved in dysfunctions across several distinct but related functional domains. By comparing resting-state fMRI data from persons with autism and healthy controls, we sought to identify the abnormalities in the functional connectivity (FC) of ACC sub-regions in autism. The analyses found autism-related reductions in FC between the left caudal ACC and the right rolandic operculum, insula, postcentral gyrus, superior temporal gyrus, and the middle temporal gyrus. The FC (z-scores) between the left caudal ACC and the right insula was negatively correlated with the Stereotyped Behaviors and Restricted Interests scores of the autism group. These findings suggest that the caudal ACC is recruited selectively in the pathomechanism of autism.

Importance: The genetic basis of bipolar disorder (BD) in Han Chinese individuals is not fully understood. Objective: To explore the genetic basis of BD in the Han Chinese population. Design, Setting, and Participants: A genome-wide association study (GWAS), followed by independent replication, was conducted to identify BD risk loci in Han Chinese individuals. Individuals with BD were diagnosed based on DSM-IV criteria and had no history of schizophrenia, mental retardation, or substance dependence; individuals without any personal or family history of mental illnesses, including BD, were included as control participants. In total, discovery samples from 1822 patients and 4650 control participants passed quality control for the GWAS analysis. Replication analyses of samples from 958 patients and 2050 control participants were conducted. Summary statistics from the European Psychiatric Genomics Consortium 2 (PGC2) BD GWAS (20 352 cases and 31 358 controls) were used for the trans-ancestry genetic correlation analysis, polygenetic risk score analysis, and meta-analysis to compare BD genetic risk between Han Chinese and European individuals. The study was performed in February 2020. Main Outcomes and Measures: Single-nucleotide variations with P < 5.00 × 10-8 were considered to show genome-wide significance of statistical association. Results: The Han Chinese discovery GWAS sample included 1822 cases (mean [SD] age, 35.43 [14.12] years; 838 [46%] male) and 4650 controls (mean [SD] age, 27.48 [5.97] years; 2465 [53%] male), and the replication sample included 958 cases (mean [SD] age, 37.82 [15.54] years; 412 [43%] male) and 2050 controls (mean [SD] age, 27.50 [6.00] years; 1189 [58%] male). A novel BD risk locus in Han Chinese individuals was found near the gene encoding transmembrane protein 108 (TMEM108, rs9863544; P = 2.49 × 10-8; odds ratio [OR], 0.650; 95% CI, 0.559-0.756), which is required for dendritic spine development and glutamatergic transmission in the dentate gyrus. Trans-ancestry genetic correlation estimation (ρge = 0.652, SE = 0.106; P = 7.30 × 10-10) and polygenetic risk score analyses (maximum liability-scaled Nagelkerke pseudo R2 = 1.27%; P = 1.30 × 10-19) showed evidence of shared BD genetic risk between Han Chinese and European populations, and meta-analysis identified 2 new GWAS risk loci near VRK2 (rs41335055; P = 4.98 × 10-9; OR, 0.849; 95% CI, 0.804-0.897) and RHEBL1 (rs7969091; P = 3.12 × 10-8; OR, 0.932; 95% CI, 0.909-0.956). Conclusions and Relevance: This GWAS study identified several loci and genes involved in the heritable risk of BD, providing insights into its genetic architecture and biological basis.

Localization of epileptogenic zone currently requires prolonged intracranial recordings to capture seizure, which may take days to weeks. The authors developed a novel method to identify the seizure onset zone (SOZ) and predict seizure outcome using short-time resting-state stereotacticelectroencephalography (SEEG) data. In a cohort of 27 drug-resistant epilepsy patients, the authors estimated the information flow via directional connectivity and inferred the excitation-inhibition ratio from the 1/f power slope. They hypothesized that the antagonism of information flow at multiple frequencies between SOZ and non-SOZ underlying the relatively stable epilepsy resting state could be related to the disrupted excitation-inhibition balance. They found flatter 1/f power slope in non-SOZ regions compared to the SOZ, with dominant information flow from non-SOZ to SOZ regions. Greater differences in resting-state information flow between SOZ and non-SOZ regions are associated with favorable seizure outcome. By integrating a balanced random forest model with resting-state connectivity, their method localized the SOZ with an accuracy of 88% and predicted the seizure outcome with an accuracy of 92% using clinically determined SOZ. Overall, this study suggests that brief resting-state SEEG data can significantly facilitate the identification of SOZ and may eventually predict seizure outcomes without requiring long-term ictal recordings.

BACKGROUND: Neuroimaging studies have proved that hippocampus relate to the deficient of memory in patients with post-traumatic stress disorder (PTSD). Many studies in healthy subjects also shown that insular cortex (IC) be involved in the declarative memory. This study was designed to investigate whether insular cortex is involved in declarative memory deficits in patients with PTSD. METHODS: Twelve subjects with PTSD and 12 subjects without PTSD victims underwent functional magnetic resonance imaging and magnetic resonance imaging. All subjects performed encoding and retrieval memory tasks during the fMRI session. Voxel-based morphometry method was used to analyze gray-matter volume, and the Statistical Parametric Mapping (SPM2) was used to analyze activated brain areas when performing tasks. RESULTS: Grey matter volume was significantly reduced bilaterally in the insular cortex of PTSD subjects than non-PTSD. PTSD group also had lower level of activation in insular cortex when performing word encoding and retrieval tasks than non-PTSD group. CONCLUSION: The study provides evidence on structural and function abnormalities of the insular cortex in patients with PTSD. Reduced grey-matter volume in insular cortex may be associated with declarative memory deficits in patients with PTSD.

Major depressive disorder (MDD) is a globally prevalent and highly disabling disease characterized by dysfunction of large-scale brain networks. Previous studies have found that static functional connectivity is not sufficient to reflect the complicated and time-varying properties of the brain. The underlying dynamic interactions between brain functional networks of MDD remain largely unknown, and it is also unclear whether neuroimaging-based dynamic properties are sufficiently robust to discriminate individuals with MDD from healthy controls since the diagnosis of MDD mainly depends on symptom-based criteria evaluated by clinical observation. Resting-state functional magnetic resonance imaging (fMRI) data of 221 MDD patients and 215 healthy controls were shared by REST-meta-MDD consortium. We investigated the spatial-temporal dynamics of MDD using co-activation pattern analysis and made individual diagnoses using support vector machine (SVM). We found that MDD patients exhibited aberrant dynamic properties (such as dwell time, occurrence rate, transition probability, and entropy of Markov trajectories) in some transient networks including subcortical network (SCN), activated default mode network (DMN), de-activated SCN-cerebellum network, a joint network, activated attention network (ATN), and de-activated DMN-ATN, where some dynamic properties were indicative of depressive symptoms. The trajectories of other networks to deactivated DMN-ATN were more accessible in MDD patients. Subgroup analyses also showed subtle dynamic changes in first-episode drug-naïve (FEDN) MDD patients. Finally, SVM achieved preferable accuracies of 84.69%, 76.77%, and 88.10% in discriminating patients with MDD, FEDN MDD, and recurrent MDD from healthy controls with their dynamic metrics. Our findings reveal that MDD is characterized by aberrant dynamic fluctuations of brain network and the feasibility of discriminating MDD patients using dynamic properties, which provide novel insights into the neural mechanism of MDD.

BACKGROUND: During the COVID-19, community mental health care workers (CMHWs) faced much heavier workloads, which make them vulnerable to mental problems. AIM: This study aims to investigate coronavirus disease-related occupational stress and its single and cumulative effect on mental health and self-efficacy among CMHWs. METHODS: A quick-response online cross-sectional survey WA conducted during the coronavirus disease outbreak. A total of 536 CMHWs were recruited in March 2020, in China. Demographics, occupational stress, depression, anxiety, positive and negative emotions, and self-efficacy were collected. Logistic regression analysis was employed to test the single and cumulative effect of occupational stress on mental health and self-efficacy. RESULTS: CMHWs did not show high level of depression or anxiety in this study. Those who provided service for suspected people who were quarantined reported higher risk of depression and anxiety. Staying out for more than 3 days was a risk factor of depression while cleaning/sterilising streets or communities was a protective factor of depression. Those who received psychiatric training showed higher positive emotion and self-efficacy, and providing psychological assistance online increased the self-efficacy. CMHWs with two different types of work had 0.996 times more risk of depression than those with only one type of work. CONCLUSION: The potential cumulative effect of occupation stress suggested that reasonable job assignment and organisational support are necessary safeguards for CMHWs.

OBJECTIVE: To explore hippocampal structural abnormalities in fire victims with recent-onset posttraumatic stress disorder (PTSD). METHOD: We compared 12 patients with recent-onset PTSD diagnosed according to DSM-IV criteria 6 to 8 months after a major fire with 12 individuals without PTSD who were victims of the same fire accident. Voxel-based morphometry (VBM) and magnetic resonance spectroscopy (MRS) were combined to examine hippocampal structural abnormalities in patients with recent-onset PTSD. RESULTS: Results of VBM showed that the grey matter density of the left hippocampus was lower in the group with PTSD than it was in the group without PTSD. Results of MRS showed that the ratio of N-acetyl asparate and creatine in the left hippocampus was significantly lower in patients with PTSD than in control subjects. CONCLUSION: Patients with recent-onset PTSD had hippocampal structural abnormalities.