Psychiatry and Clinical Neurosciences最新文献

{"title":"The effects of potentially traumatic events on the recovery from pre-existing anxiety and depression symptomatology and the risk of PTSD.","authors":"Peter G van der Velden, Carlo Contino, Lonneke Lenferink, Marcel Das, Lutz Wittmann","doi":"10.1111/pcn.13725","DOIUrl":"https://doi.org/10.1111/pcn.13725","url":null,"abstract":"<p><strong>Aim: </strong>The extent to which recent potentially traumatic events (PTEs) hinder the recovery from pre-existing mental health problems is largely unknown. The same applies to the extent to which non-recovery from pre-existing mental health problems increases the risk of posttraumatic stress disorder (PTSD). The aim of the present study is to gain insight in these effects.</p><p><strong>Methods: </strong>Data were extracted from six annual surveys of the Dutch population-based Victims in Modern Society (VICTIMS) study. Of the adult respondents who participated in two subsequent surveys (labeled T1 and T2, n = 6942), those with severe anxiety and depression symptoms (ADS) at T1 (n = 487) were selected. We distinguished respondents exposed to PTEs (PTE-group, n = 162) and not exposed to PTEs (comparison group, n = 325) between T1 and T2. We applied five indicators of recovery [based on the Reliable Change Index (RCI), degrees of symptom reduction, and the cut-off score at T2]. Differences in the recovery from ADS and probable PTSD at T2 were examined using multivariate logistic regression.</p><p><strong>Results: </strong>The PTE group less often recovered from severe ADS between T1 and T2 than the comparison group according to all five indicators of recovery, while controlling for 11 different variables (0.40 ≤ adjusted OR's ≤ 0.66). Those in the PTE group who did not recover, considerably more often suffered from probable PTSD at T2 (63%-82%) than those who did recover (0%-29%; 8.96 ≤ adjusted OR ≤ 26.33).</p><p><strong>Conclusion: </strong>Recent potentially traumatic events hinder the recovery from pre-existing anxiety and depression symptomatology and thereby increase the risk of probable PTSD.</p>","PeriodicalId":20938,"journal":{"name":"Psychiatry and Clinical Neurosciences","volume":null,"pages":null},"PeriodicalIF":5.0,"publicationDate":"2024-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142005126","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The status of MRI databases across the world focused on psychiatric and neurological disorders.","authors":"Saori C Tanaka, Kiyoto Kasai, Yasumasa Okamoto, Shinsuke Koike, Takuya Hayashi, Ayumu Yamashita, Okito Yamashita, Tom Johnstone, Franco Pestilli, Kenji Doya, Go Okada, Hotaka Shinzato, Eri Itai, Yuji Takahara, Akihiro Takamiya, Motoaki Nakamura, Takashi Itahashi, Ryuta Aoki, Yukiaki Koizumi, Masaaki Shimizu, Jun Miyata, Shuraku Son, Morio Aki, Naohiro Okada, Susumu Morita, Nobukatsu Sawamoto, Mitsunari Abe, Yuki Oi, Kazuaki Sajima, Koji Kamagata, Masakazu Hirose, Yohei Aoshima, Sayo Hamatani, Nobuhiro Nohara, Misako Funaba, Tomomi Noda, Kana Inoue, Jinichi Hirano, Masaru Mimura, Hidehiko Takahashi, Nobutaka Hattori, Atsushi Sekiguchi, Mitsuo Kawato, Takashi Hanakawa","doi":"10.1111/pcn.13717","DOIUrl":"https://doi.org/10.1111/pcn.13717","url":null,"abstract":"<p><p>Neuroimaging databases for neuro-psychiatric disorders enable researchers to implement data-driven research approaches by providing access to rich data that can be used to study disease, build and validate machine learning models, and even redefine disease spectra. The importance of sharing large, multi-center, multi-disorder databases has gradually been recognized in order to truly translate brain imaging knowledge into real-world clinical practice. Here, we review MRI databases that share data globally to serve multiple psychiatric or neurological disorders. We found 42 datasets consisting of 23,293 samples from patients with psychiatry and neurological disorders and healthy controls; 1245 samples from mood disorders (major depressive disorder and bipolar disorder), 2015 samples from developmental disorders (autism spectrum disorder, attention-deficit hyperactivity disorder), 675 samples from schizophrenia, 1194 samples from Parkinson's disease, 5865 samples from dementia (including Alzheimer's disease), We recognize that large, multi-center databases should include governance processes that allow data to be shared across national boundaries. Addressing technical and regulatory issues of existing databases can lead to better design and implementation and improve data access for the research community. The current trend toward the development of shareable MRI databases will contribute to a better understanding of the pathophysiology, diagnosis and assessment, and development of early interventions for neuropsychiatric disorders.</p>","PeriodicalId":20938,"journal":{"name":"Psychiatry and Clinical Neurosciences","volume":null,"pages":null},"PeriodicalIF":5.0,"publicationDate":"2024-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142005127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serum cortisol and neuroticism for post-traumatic stress disorder over 2 years in patients with physical injuries.","authors":"Jae-Min Kim, Hee-Ju Kang, Ju-Wan Kim, Hyunseok Jang, Jung-Chul Kim, Byung Jo Chun, Ju-Yeon Lee, Sung-Wan Kim, Il-Seon Shin","doi":"10.1111/pcn.13718","DOIUrl":"https://doi.org/10.1111/pcn.13718","url":null,"abstract":"<p><strong>Aim: </strong>This study aimed to explore the relationships between serum cortisol levels, personality traits, and the development of Post-Traumatic Stress Disorder (PTSD) over 2 years among individuals with physical injuries.</p><p><strong>Methods: </strong>Participants were consecutively recruited from a trauma center and followed prospectively for 2 years. At baseline, serum cortisol levels were measured, and personality traits were categorized into five dimensions (Extraversion, Agreeableness, Conscientiousness, Neuroticism, and Openness), using the Big Five Inventory-10. The diagnosis of PTSD during follow-up (at 3, 6, 12, and 24 months post-injury) was determined using the Clinician-Administered PTSD Scale for DSM-5. Binary and multinomial logistic regression analyses were conducted to examine the interactions between cortisol levels, personality traits, and PTSD development.</p><p><strong>Results: </strong>Among 923 patients analyzed, 112 (12.1%) were diagnosed with PTSD at some point during the study period, with prevalence rates decreasing from 8.8% at 3 months to 3.7% at 24 months post-injury. Direct associations between cortisol levels or personality traits and PTSD were not observed. However, a significant interaction between lower cortisol levels and higher Neuroticism in relation to PTSD risk was identified, especially during the early follow-up periods (3 to 6 months), but this association waned from the 12-month follow-up onward.</p><p><strong>Conclusion: </strong>Our findings reveal Neuroticism-dependent associations between serum cortisol levels and PTSD development, exhibiting temporal variations. These results suggest that PTSD development may be influenced by a complex, time-sensitive interplay of biological and psychosocial factors, underscoring the importance of considering individual differences in stress reactivity and personality in PTSD research and treatment.</p>","PeriodicalId":20938,"journal":{"name":"Psychiatry and Clinical Neurosciences","volume":null,"pages":null},"PeriodicalIF":5.0,"publicationDate":"2024-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141898117","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Worry: A key player in psychopathology after acquired brain injury?","authors":"Jai Carmichael, Jennie Ponsford","doi":"10.1111/pcn.13689","DOIUrl":"https://doi.org/10.1111/pcn.13689","url":null,"abstract":"","PeriodicalId":20938,"journal":{"name":"Psychiatry and Clinical Neurosciences","volume":null,"pages":null},"PeriodicalIF":5.0,"publicationDate":"2024-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141898118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardiovascular disease, and major depression: Study on both diseases and serum brain-derived neurotrophic factor (BDNF).","authors":"Reiji Yoshimura","doi":"10.1111/pcn.13678","DOIUrl":"10.1111/pcn.13678","url":null,"abstract":"","PeriodicalId":20938,"journal":{"name":"Psychiatry and Clinical Neurosciences","volume":null,"pages":null},"PeriodicalIF":5.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141420652","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Habenular volume changes after venlafaxine treatment in patients with major depression.","authors":"Josselin Etienne, Alexandre Boutigny, Denis J David, Eric Deflesselle, Florence Gressier, Laurent Becquemont, Emmanuelle Corruble, Romain Colle","doi":"10.1111/pcn.13684","DOIUrl":"10.1111/pcn.13684","url":null,"abstract":"<p><strong>Background: </strong>Habenula, a hub brain region controlling monoaminergic brain center, has been implicated in major depressive disorder (MDD) and as a possible target of antidepressant response. Nevertheless, the effect of antidepressant drug treatment on habenular volumes remains unknown. The objective of the present research was to study habenular volume change after antidepressant treatment in patients with MDD, and assess whether it is associated with clinical improvement.</p><p><strong>Methods: </strong>Fifty patients with a current major depressive episode (MDE) in the context of MDD, and antidepressant-free for at least 1 month, were assessed for habenula volume (3T MRI with manual segmentation) before and after a 3 months sequence of venlafaxine antidepressant treatment.</p><p><strong>Results: </strong>A 2.3% significant increase in total habenular volume (absolute volume: P = 0.0013; relative volume: P = 0.0055) and a 3.3% significant increase in left habenular volume (absolute volume: P = 0.00080; relative volume: P = 0.0028) were observed. A significant greater variation was observed in male patients (4.8%) compared to female patients. No association was observed between habenular volume changes and response and remission. Some habenula volume changes were associated with improvement of olfactory pleasantness.</p><p><strong>Conclusion: </strong>Habenular volumes increased after 3 months of venlafaxine treatment in depressed patients. Further studies should assess whether cell proliferation and density or dendritic structure variations are implied in these volume changes.</p>","PeriodicalId":20938,"journal":{"name":"Psychiatry and Clinical Neurosciences","volume":null,"pages":null},"PeriodicalIF":5.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141311514","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metacognition as a window into subjective affective experience.","authors":"Cody A Cushing, Hakwan Lau, Stefan G Hofmann, Joseph E LeDoux, Vincent Taschereau-Dumouchel","doi":"10.1111/pcn.13683","DOIUrl":"10.1111/pcn.13683","url":null,"abstract":"<p><p>When patients seek professional help for mental disorders, they often do so because of troubling subjective affective experiences. While these subjective states are at the center of the patient's symptomatology, scientific tools for studying them and their cognitive antecedents are limited. Here, we explore the use of concepts and analytic tools from the science of consciousness, a field of research that has faced similar challenges in having to develop robust empirical methods for addressing a phenomenon that has been considered difficult to pin down experimentally. One important strand is the operationalization of some relevant processes in terms of metacognition and confidence ratings, which can be rigorously studied in both humans and animals. By assessing subjective experience with similar approaches, we hope to develop new scientific approaches for studying affective processes and promoting psychological resilience in the face of debilitating emotional experiences.</p>","PeriodicalId":20938,"journal":{"name":"Psychiatry and Clinical Neurosciences","volume":null,"pages":null},"PeriodicalIF":5.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141331566","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of synaptic density and cognitive performance in temporal lobe epilepsy: Humans and animals PET imaging study with [¹⁸F]SynVesT-1.","authors":"Ling Xiao, Shijun Xiang, Chen Chen, Haoyue Zhu, Ming Zhou, Yongxiang Tang, Li Feng, Shuo Hu","doi":"10.1111/pcn.13682","DOIUrl":"10.1111/pcn.13682","url":null,"abstract":"<p><strong>Aim: </strong>Cognitive impairment is a common comorbidity in individuals with temporal lobe epilepsy (TLE), yet the underlying mechanisms remain unknown. This study explored the putative association between in vivo synaptic loss and cognitive outcomes in TLE patients by PET imaging of synaptic vesicle glycoprotein 2A (SV2A).</p><p><strong>Methods: </strong>We enrolled 16 TLE patients and 10 cognitively normal controls. All participants underwent SV2A PET imaging using [¹⁸F]SynVesT-1 and cognitive assessment. Lithium chloride-pilocarpine-induced rats with status epilepticus (n = 20) and controls (n = 6) rats received levetiracetam (LEV, specifically binds to SV2A), valproic acid (VPA), or saline for 14 days. Then, synaptic density was quantified by [¹⁸F]SynVesT-1 micro-PET/CT. The novel object recognition and Morris water maze tests evaluated TLE-related cognitive function. SV2A expression was examined and confirmed by immunohistochemistry.</p><p><strong>Results: </strong>Temporal lobe epilepsy patients showed significantly reduced synaptic density in hippocampus, which was associated with cognitive performance. In the rat model of TLE, the expression of SV2A and synaptic density decreased consistently in a wider range of brain regions, including the entorhinal cortex, insula, hippocampus, amygdala, thalamus, and cortex. We treated TLE animal models with LEV or VPA to explore whether synaptic loss contributes to cognitive deficits. It was found that LEV significantly exerted protective effects against brain synaptic deficits and cognitive impairment.</p><p><strong>Conclusion: </strong>This is the first study to link synaptic loss to cognitive deficits in TLE, suggesting [¹⁸F]SynVesT-1 PET could be a promising biomarker for monitoring synaptic loss and cognitive dysfunction. LEV might help reverse synaptic deficits and ameliorate learning and memory impairments in TLE patients.</p>","PeriodicalId":20938,"journal":{"name":"Psychiatry and Clinical Neurosciences","volume":null,"pages":null},"PeriodicalIF":5.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141158109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Distinct biological property of tau in tau-first cognitive proteinopathy: Evidence by longitudinal clinical neuroimaging profiles and compared with late-onset Alzheimer disease.","authors":"Hsin-I Chang, Chi-Wei Huang, Shu-Hua Huang, Shih-Wei Hsu, Kun-Ju Lin, Tsung-Ying Ho, Hsiu-Chuan Wu, Chiung-Chih Chang","doi":"10.1111/pcn.13680","DOIUrl":"10.1111/pcn.13680","url":null,"abstract":"<p><strong>Background: </strong>Tau-first cognitive proteinopathy (TCP) denotes a clinical phenotype of Alzheimer disease (AD) showing Florzolotau(18F) positron emission tomography (PET) positivity but a negative amyloid status.</p><p><strong>Aim: </strong>We explored the biological property of tau using longitudinal cognitive and neuroimaging data in TCP and compared with late-onset AD (LOAD).</p><p><strong>Method: </strong>We enrolled 56 patients with LOAD, 34 patients with TCP, and 26 cognitive unimpaired controls. All of the participants had historical data of 2 to 4 three-dimensional T1 images and 2 to 6 annual cognitive evaluations over a follow-up period of 7 years. Tau topography was measured using Florzolotau(18F) PET. In the LOAD and TCP groups, we constructed tau or gray matter clusters covarying with the cognitive measurements. We used mediator analysis to explore the regional tau load as predictor, gray matter partitions as mediators, and significant cognitive test scores as outcomes. Longitudinal cognitive decline and cortical thickness degeneration pattern were analyzed using a linear mixed-effects model.</p><p><strong>Results: </strong>The TCP group had longitudinal declines in nonexecutive domains. The deterministic factor predicting the short-term memory score in TCP was the hippocampal volume and not directly via the medial and lateral temporal tau load. These features formed the conceptual differences with LOAD.</p><p><strong>Discussion: </strong>The biological properties of tau and the longitudinal cognitive-imaging trajectory support the conceptual distinction between TCP and LOAD. TCP represents one specific entity featuring salient short-term memory impairment, declines in nonexecutive domains, a slower gray matter degenerative pattern, and a restricted impact of tau.</p>","PeriodicalId":20938,"journal":{"name":"Psychiatry and Clinical Neurosciences","volume":null,"pages":null},"PeriodicalIF":5.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141306712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PCN Art Brut Series No. 40, Artwork Description.","authors":"Kenjiro Hosaka","doi":"10.1111/pcn.13719","DOIUrl":"https://doi.org/10.1111/pcn.13719","url":null,"abstract":"","PeriodicalId":20938,"journal":{"name":"Psychiatry and Clinical Neurosciences","volume":null,"pages":null},"PeriodicalIF":5.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141890045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}