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Under the influence of the novel coronavirus epidemic, some negative social events, such as separation of family or friends and home isolation have increased. These events can cause negative emotion experiences similar to physical pain, thus they are called social pain. Placebo effect refers to the positive response to the inert treatment with no specific therapeutic properties, which has been shown to be one of the effective ways to alleviate social pain. Studies have shown that the dorsolateral prefrontal cortex (DLPFC) plays a key role in placebo effect. Therefore, this study aimed to explore whether activating DLPFC by using transcranial magnetic stimulation (TMS) could improve the ability of placebo effects to regulate social pain. Besides, we also combined neuroimaging and neuromodulation techniques to provide bidirectional evidence for the role of the DLPFC on placebo effects. We recruited a total of 100 participants to finish the task of negative emotional rating of the social exclusion images. Among them, 50 participants were stimulated by TMS at the right DLPFC (rDLPFC), while the others were assigned to the sham group. This study contained two independent variables. The between-subject variable was TMS group (rDLPFC-activated group or sham group) and the within-subject variable was placebo type (no-placebo and placebo). All participants received nasal spray in two blocks. In the no-placebo condition, participants were instructed that they would receive a saline nasal spray which helped to improve physiological readings;in placebo block, participants were told to administrate an intranasal fluoxetine spray (saline nasal spray in fact) that could reduce unpleasantness within 10 minutes. To strengthen the expectation of intranasal fluoxetine, participants viewed a professional introduction to fluoxetine's clinical and academic usage including downregulating negative emotion, such as fear, anxiety, and disgust. Participants who received the placebo block first would be reminded that fluoxetine's effect was over before the next block to reduce the carry-over for the following block. Self-reported negative emotional and electroencephalogram data were recorded. There was a significant two-way interaction of TMS group and placebo type. Results showed that compared with the sham group, participants in the rDLPFC-activated group reported less negative emotional feeling and had a lower amplitude of the late positive potential (LPP) in placebo condition, a component that reflects the emotional intensity, suggesting that activating rDLPFC can improve the ability of placebo effect to regulate social pain. The above finding suggested that activating DLPFC can improve the placebo effect of regulating negative emotion. Moreover, this study is the first attempt to investigate the enhancement of placebo effects by using TMS on emotion regulation. The findings not only support the critical role of DLPFC on placebo effect using neuroimaging and neuromodulation techniques, but also provide a potential brain target for treating emotional regulation deficits in patients with psychiatric disorders. © 2023 WANG Mei.
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The proceedings contain 40 papers. The topics discussed include: sex, bugs microwave attacks: how bad science, mating insects psychogenic illness created an international incident with Cuba;Covid-19 and neuropsychiatry;clinical update on delirium;fibromyalgia and myalgic encephalomyelitis/ chronic fatigue syndrome (ME/CFS): an interoceptive predictive coding model of pain and fatigue expression;when the spark goes out: the neurology of apathy and motivation;is subjective cognitive decline (SCD) a better marker of susceptibility to functional cognitive disorder (FCD) than to neurodegeneration?: the caerphilly prospective study;temporal and spectral dynamics of reward and risk processing in the amygdala revealed with stereo-EEG recordings in epilepsy;a systematic review of extra-motor symptom evaluation in clinical trials for amyotrophic lateral sclerosis;and stimulation of the ventrolateral prefrontal cortex speeds up evidence accumulation in conflictual-uncertain environments.
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It has been proven that mRNA vaccines are highly effective against the COVID-19 outbreak, and low prevalence of side effects has been shown. However, there are still many gaps in our understanding of the biology and biosafety of nucleic acids as components of lipid nanoparticles (LNPs) most often used as a system for inctracellular delivery of mRNA-based vaccines. It is known that LNPs cause severe injection site inflammation, have broad biodistribution profiles, and are found in multiple tissues of the body, including the brain, after administration. The role of new medications with such pharmacokinetics in inflammation developing in inaccessible organs is poorly understood. The study was aimed to assess the effects of various doses of mRNA-LNP expressing the reporter protein (0, 5, 10, and 20 microg of mRNA encoding the firefly luciferase) on the expression of neuroinflammation markers (Tnfalpha, Il1beta, Gfap, Aif1) in the prefrontal cortex and hypothalamus of laboratory animals 4, 8, and 30 h after the intramuscular injection of LNP nanoemulsion. It was shown that mRNA-LNP vaccines in a dose of 10-20 microg of mRNA could enhance Aif1 expression in the hypothalamus 8 h after vaccination, however, no such differences were observed after 30 h. It was found that the Gfap, l11beta, Tnfalpha expression levels in the hypothalamus observed at different times in the experimental groups were different. According to the results, mRNA-LNPs administered by the parenteral route can stimulate temporary activation of microglia in certain time intervals in the dose-dependent and site specific manner.Copyright © 2022 Pirogov Russian National Research Medical University. All rights reserved.
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The monoamine hypothesis of depression has dominated treatment for decades, but for some with treatment-resistant depression, alternative approaches are needed. This article discusses some of the other mechanisms involved in depression and how novel treatments could address these.Copyright © 2023 Wiley Interface Ltd.
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Background: Prolonged cognitive deficits ("brain fog") following COVID19 infection (long-COVID) are common and debilitating, yet there are currently no approved treatments. Cognitive impairment particularly targets the working memory and executive functions of the prefrontal cortex (PFC). The PFC has unusual neurotransmission and neuromodulation that render it vulnerable to stressors, and basic research has identified mechanisms that protect PFC connections. Based on the basic neuroscience data, we tried a combined open label treatment to bolster prefrontal function: the alpha2A-adrenoceptor agonist, guanfacine, which strengthens prefrontal connectivity, and the anti-oxidant, N- acetylcysteine (NAC), which protects mitochondria and reduces kynurenic acid blockade of NMDA receptors. Case report: Twelve patients with "brain fog" including difficulties in executive functions were treated with guanfacine (1mg, PO bedtime for the first month, increased to 2mg after 1 month, if well-tolerated) and 600 mg NAC daily. Guanfacine+NAC improved cognitive abilities in eight of the twelve patients;four patients discontinued therapy, two for unspecified reasons and two due to hypotension and/or dizziness, common side effects of guanfacine. Those who stayed on guanfacine+NAC reported improved working memory, concentration, and executive functions, including a resumption of normal workloads. One patient briefly stopped taking guanfacine due to a hypotensive episode and reported a return of cognitive deficits that abated with resumed guanfacine treatment. Conclusion(s): Although placebo-controlled trials will be needed to more rigorously demonstrate efficacy, as these agents have established safety, they may be immediately helpful in treating the large number of patients suffering from prolonged cognitive deficits following COVID19 infection.Copyright © 2022 The Author(s)
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Background: Despite the acute infection's remission, COVID-19 is associated with clinically severe residual symptoms (i.e., post-COVID-19 syndrome). One of the most prevalent and incapacitating symptoms of the syndrome is fatigue, accompanied by cognitive impairment. Very few therapy options are effective for post-acute SARS-Cov-2 sequelae (PASC). There is a possibility that non-invasive brain stimulation methods could become successful and convenient treatment options for post-acute and chronic COVID-19. There are already the first clinical results for the use of transcranial direct current stimulation (tDCS) in the therapy of PASC. Our goal was to study the potential tDCS effect on cognitive impairment in patients with PASC. Method(s): We present a four-week, double-blind, randomized, placebo-controlled, parallel study with a 4-week active dorsolateral prefrontal cortex (DLPFC) tDCS (20 tDCS applications;anode on the F3;2 mA, 30 min/tDCS session). Patients were evaluated with tests measuring attention (digit span forward), working memory (digit span backward), and psychomotor speed (digit symbol substitution test) at baseline, after two weeks, and at the end of four weeks of treatment. The tests were chosen according to previous studies on the assessment of cognitive function in patients after COVID-19. Result(s): 15 out of 34 enrolled patients were included in Intention-to-treat (ITT) analysis. The treatment groups did not differ in age, gender, and baseline cognitive tests. There wasn't a significant difference in cognitive tests results between active DLPFC tDCS and sham tDCS after four weeks. However, the study is still in progress and the results will be updated. No major side effects were observed during and after the treatment. Supported by grant No. NU22-D-133 of the MH CR. Research Category and Technology and Methods Clinical Research: 9. Transcranial Direct Current Stimulation (tDCS) Keywords: cognitive symptoms, post-acute sequelae of SARS-Cov-2, transcranial direct current stimulation, dorsolateral prefrontal cortexCopyright © 2023
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Introduction: The amygdala plays an important role in stress responses and stress-related psychiatric disorders. It is possible that amygdala connectivity may be a neurobiological vulnerability marker for stress responses or stress-related psychiatric disorders and will be useful to precisely identify the vulnerable individuals before stress happens. However, little is known about the relationship between amygdala connectivity and subsequent stress responses. The current study investigated whether amygdala connectivity measured before experiencing stress is a predisposing neural feature of subsequent stress responses while individuals face an emergent and unexpected event like the COVID-19 outbreak. Methods: Data collected before the COVID-19 pandemic from an established fMRI cohort who lived in the pandemic center in China (Hubei) during the COVID-19 outbreak were used to investigate the relationship between amygdala connectivity and stress responses during and after the pandemic in 2020. The amygdala connectivity was measured with resting-state functional connectivity (rsFC) and effective connectivity. Results: We found the rsFC of the right amygdala with the dorsomedial prefrontal cortex (dmPFC) was negatively correlated with the stress responses at the first survey during the COVID-19 outbreak, and the rsFC between the right amygdala and bilateral superior frontal gyri (partially overlapped with the dmPFC) was correlated with SBSC at the second survey. Dynamic causal modeling suggested that the self-connection of the right amygdala was negatively correlated with stress responses during the pandemic. Discussion: Our findings expand our understanding about the role of amygdala in stress responses and stress-related psychiatric disorders and suggest that amygdala connectivity is a predisposing neural feature of subsequent stress responses.
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Background: Transcranial direct current stimulation (tDCS) is effective in the man-agement of patients with depression and anxiety. However, it is not known if it is effective in the case of anxiety and depression following SARS-CoV2 and NeuroCOVID-19 infection. The aim of this study was to determine the efficacy of stimulating the brain with the use of a tDCS protocol ameliorated by a functional neuromarker, and here based on HBI methodology to reduce anxiety and depression following SARS-CoV2 infection and NeuroCOVID-19 contraction.Case study: A 47-year-old patient manifested severe anxiety and depression following a stroke following SARS-CoV2 infection and Neuro-COVID-19 contraction. The anxiety and depression were diagnosed using the HAD-Scale (Zigmond, Snaith 1983). A score of 8 to 10 is broad ly accepted as indicating mild symptoms, a score between 11-16 suggests moderate anxiety or depression, and a score of 16 or more indicates severe anxiety or depressive symptoms. The patient received anodal tDCS to the left DLPFC using two different applica-tion protocols. Initially, a stimulation session of 2 milliamperes (mA) intensity for 20 minutes was administered every working day for 2 weeks. After 3 weeks, she subsequently received 7 daily sessions of periodic stimulations of an intensity of 2 mA for 13 minutes each with 20 minutes inter-session intervals for 1 week. It was found that tDCS delivered via the dorsolateral prefrontal cortex (DLPFC) was effective in the reduction of post-stroke anxiety and depression following SARS-CoV2 infection and NeuroCOVID-19 contraction. Immediately follow-ing the final session of the initial protocol of stimulation, the Had Score was reduced for anxiety from 18 to 6 points, and for depression from 17 to 5 points and the symptoms disappeared.Conclusions: The HBI methodology allowed for the detection of a functional neu-romarker of anxiety and depression and the development of a tDCS protocol. It was found that tDCS delivered via the dorsolateral pre-frontal cortex (DLPFC) was effective in the reduction of post-stroke anxiety and depression following SARS-CoV2 infection and Neu-roCOVID-19 contraction.
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Background: Genome-wide association studies have found many genetic risk variants associated with Alzheimer's disease (AD). However, how these risk variants affect deeper phenotypes such as disease progression and immune response remains elusive. Also, our understanding of cellular and molecular mechanisms from disease SNPs to various phenotypes is still limited. To address these problems, we performed an integrative multi-omics analysis of genotype, transcriptomics, and epigenomics for revealing gene regulatory mechanisms from disease variants to AD phenotypes. Method(s): First, given population gene expression data of a cohort, we construct and cluster its gene co-expression network to identify modules for various AD phenotypes. Next, we predict transcription factors (TFs) regulating co-expressed genes and SNPs interrupting TF binding sites on regulatory elements. Finally, we construct a gene regulatory network (GRN) linking SNPs, interrupted TFs, and regulatory elements to target genes and modules for AD phenotypes. This network provides systematic insights into gene regulatory mechanisms from SNPs to phenotypes. We looked at our GRNs relating to genes from shared AD-Covid pathways (e.g. NFKB Pathway) and used machine learning to prioritize those genes for predicting Covid-19 severity. Result(s): Our analysis predicted cross-region-conserved and region-specific GRNs in 3 regions Hippocampus, Dorsolateral Prefrontal Cortex (DLPFC), Lateral Temporal Lobe (LTL). For instance, SNPs rs13404184 and rs61068452 disrupt SPI1 binding and regulation of INPP5D in Hippocampus and LTL. While rs4802200 disrupts E2F7 regulation of KCNN4 (belongs to AD LTL module), rs117863556 interrupts REST regulation of GAB2 in DLPFC. Further, we used Covid-19 as a proxy for immune dysregulation to identify possible regulatory mechanisms for AD neuroimmunology. Decision Curve Analysis suggest our AD-Covid genes along with linked SNPs (that outperform known genes) can be potential novel biomarkers for neuroimmunology. Finally, our results are open-source available as a comprehensive AD functional genomic map, providing deeper mechanistic understanding of the interplay among multi-omics, regions, gene functions, phenotypes. Conclusion(s): Our pipeline predicts how non-coding risk SNPs may be associated with changes in regulation and subsequent expression of genes associated with different phenotypes and pathways in AD. Moreover, we flagged 51 potential AD-neuroinflammatory risk genes, which may be early biomarkers as neuroinflammation may begin decades before clinical onset. Copyright © 2022 the Alzheimer's Association.
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Introduction: SARS-CoV-2 is the newest beta coronavirus family member to demonstrate neuroinvasive capability in severe cases of infection. Despite much research activity in the SARS-CoV-2/COVID-19 space, the gene-level biology of this phenomenon remains poorly understood. In the present analysis, we leveraged spatial transcriptomics methodologies to examine relevant gene heterogeneity in tissue retrieved from the human prefrontal cortex. Methods: Expression profiles of genes with established relations to the SARS-CoV-2 neuroinvasion process were spatially resolved in dorsolateral prefrontal cortex tissue (N = 4). Spotplots were generated with mapping to six (6) previously defined gray matter layers. Results: Docking gene BSG, processing gene CTSB, and viral defense gene LY6E demonstrated similar spatial enrichment. Docking gene ACE2 and transmembrane series proteases involved in spike protein processing were lowly expressed across DLPFC samples. Numerous other findings were obtained. Conclusion: Efforts to spatially represent expression levels of key SARS-CoV-2 brain infiltration genes remain paltry to date. Understanding the sobering history of beta coronavirus neuroinvasion represents a weak point in viral research. Here we provide the first efforts to characterize a motley of such genes in the dorsolateral prefrontal cortex.
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BACKGROUND: There is increasing interest in identifying factors to predict posttraumatic growth (PTG), a positive psychological response following traumatic events (e.g., the COVID-19 pandemic). Grit, a psychological trait of perseverance and passion to pursue long-term goals, has emerged as a promising predictor for PTG. This study aimed to examine the functional connectivity markers of grit and the potential brain-grit mechanism in predicting PTG. METHODS: Baseline brain imaging scans and grit scale and other controlling measures were administered in 100 normal young adults before the COVID-19 pandemic, and follow-up PTG measurement was obtained during the period of community-level outbreak. Whole-brain correlation analysis and prediction analysis were used to identify the brain regions whose functional connectivity density (FCD) related to individuals' grit scores. Mediation analyses were performed to explore the mediation relation between FCD, grit and PTG. RESULTS: Grit was positively related to FCD in the right dorsolateral prefrontal cortex (DLPFC), a core hub implicated in self-regulation and reward-motivation processes. Furthermore, grit mediated the effect of right DLPFC FCD on COVID-related PTG. These results survived controlling for self-control and family socioeconomic status. LIMITATIONS: Our study is limited by only one-session neuroimaging data and self-reported behavioral measures in a sample of normal adults. CONCLUSIONS: This study indicates grit and right DLPFC FCD as neuropsychological contributors for the development of PTG. It deepens our understanding of the neural bases of grit, and may have clinical potential to develop targeted brain interventions aimed at improving grit to raise PTG and mental health during the pandemic.
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COVID-19 , Posttraumatic Growth, Psychological , Young Adult , Humans , Dorsolateral Prefrontal Cortex , Prefrontal Cortex , Pandemics , Magnetic Resonance Imaging/methods , BrainABSTRACT
ARNSTEN, A.F.T., M.K.P. Joyce and A.C. Roberts. The Aversive Lens: Stress effects on the prefrontal-cingulate cortical pathways that regulate emotion. NEUROSCI BIOBEHAV REV XXX-XXX, 2022. The symptoms of major-depressive-disorder include psychic pain and anhedonia, i.e. seeing the world through an "aversive lens". The neurobiology underlying this shift in worldview is emerging. Here these data are reviewed, focusing on how activation of subgenual cingulate (BA25) induces an "aversive lens", and how higher prefrontal cortical (PFC) areas (BA46/10/32) provide top-down regulation of BA25 but are weakened by excessive dopamine and norepinephrine release during stress exposure, and dendritic spine loss with chronic stress exposure. These changes may generate an attractor state, which maintains the brain under the control of BA25, requiring medication or neuromodulatory treatments to return connectivity to a more flexible state. In line with this hypothesis, effective anti-depressant treatments reduce the activity of BA25 and restore top-down regulation by higher circuits, e.g. as seen with SSRI medications, ketamine, deep brain stimulation of BA25, or rTMS to strengthen dorsolateral PFC. This research has special relevance in an era of chronic stress caused by the COVID19 pandemic, political unrest and threat of climate change.
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COVID-19 , Depressive Disorder, Major , Humans , Brain , Emotions/physiology , Prefrontal Cortex/physiology , Depressive Disorder, Major/therapyABSTRACT
Background: There is growing evidence to support the view that a variety of neurologi-cal, neurocognitive and neuropsychiatric sequelae occur following SARS-CoV-2 infection and NeuroCovid 19. Furthermore, scholars report that various syndromes, including Parkinson's disease (PD), can develop within a short period of time following on from COVID-19. Although the mechanism of this phenomenon is not fully understood and it is not known whether this is in fact an acceleration of the development of PD already 'smouldering' in the body or related to a viral infection, these patients need rehabilitation assistance. Recently, as adjuvant therapy, transcranial direct current stimulation (tDCS) has been shown to improve the motor and non-motor function of patients with Parkinson's disease (PD), including neurocogni-tive impairment and therefore potentially change their quality of life. The aim of this article is to show the effectiveness of tDCS in the treatment of the patient with newly diagnosed Parkinson's disease after infection with the SARS-CoV-2 virus and the contracting of NeuroCovid 19, and equally developing long COVID. The motivation would be to help other patients with a similar situation during the COVID-19 pandemic. Case study: A 62-year-old man, an academic Art Teacher, was infected with SARS-CoV-2 and contracted NeuroCOVID-19 on November 11, 2021. Initially, he lost his sense of smell (anosmia), of taste (ageusia), developed hea-daches, and dizziness. After 10 days of illness, the patient developed se-vere, level two infextion (according to Wise 2020), and he was hospitalized, sedated and mechanically ventilated for 30 days. After discharge from hos-pital, the patient was still weak with different symptoms. Four months later he was diagnosed with long COVID and also the neurodegenerative disease PD (according to the DSM-5 criteria). He received levodopa the-rapy, and was referred to the Reintegration and Training Center of the Polish Neuropsychological Society for further treatment. The functional neuromar-ker, that is hypoactivation of the left dorsolateral prefrontal cortex (DLPFC), obtained with the use of QEEG/ERPs was helpful in choosing the approp-riate tDCS protocol. Neurostimulation with the use of anodal tDCS over these area of the brain was administered systematically for 20 days. He also received individual sessions of art therapy for 20 day. After the treatment the patient improved and returned to his previous work as a university art tea-cher. The proposed anodal tDCS over the left dorsolateral prefrontal cortex (DLPFC), in combination with goal-oriented individual art therapy, offered to the patient, was effective in the reduction of all his syndromes. Conclusions: ERPs can be useful in the diagnosis and treatment of patients following infection by SARS-CoV-2 who contracted COVID-19, developed long COVID and additionally PD. It allows for the detection of the functional neuromarker of PD (e.g., hypoactivation of the dorsolateral prefrontal cortex, DLPFC) and enabled the choosing of a proper tDCS protocol with the anode over these region of the brain, and also the selection of effective neurostimulation. The proposed protocol of tDCS tailored by the neuromarker offered to our patient, was effective in the reduction of longCOVID symptoms as well as early PD symptoms.
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Background: There is a growing interest in airway inflammation and mental health. Recent genetic and epidemiological evidence supports an association between PTSD and asthma however, contributory immune mediators/mechanisms are unclear. Recent work from our group employs mouse aeroallergen, house dust mite (HDM) models to examine the role of severe asthma linked inflammatory T helper cells, Th17 and interleukin 17 (IL-17A) in regulating PTSD-relevant behaviors. Methods: A combination of behavioral, immunological, transgenic and transcriptomic approaches were used. 1) BALBc-C5a receptor treatment that shifts Th2 mild asthma phenotype to Th17/IL17a expansion and robust airway inflammation;2) IL-17a receptor knockout mice and 3) RNAseq transcriptomics of cortical and blood brain barrier compromised area, subfornical organ (SFO) tissue was performed. Fear conditioning and extinction was assessed as a PTSD-relevant behavior. Results: Induction of Th17/IL-17 in the BALBc/anti-C5aR1 treated mice resulted in compromised fear extinction and increased fear reinstatement. Absence of IL-17 signaling in IL17Ra deficient mice attenuated HDM effects on fear extinction. Preliminary evidence suggests a potential of the SFO in translating HDM effects to the medial prefrontal cortex, an area regulating fear extinction. Transcriptomic analyses revealed modulation of immune T cell-targeted signaling pathways within the SFO in mice with Th17A expansion. Conclusion: Overall, our work provides novel insights on mechanisms by which mediators of severe airway inflammation, Th17/IL17A regulate fear memory of relevance to PTSD. Beyond asthma-PTSD, our findings have relevant implications for other pulmonary (e.g. COVID-19) and autoimmune inflammatory conditions and mental health.
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Background: Catatonia, a motor dysregulation syndrome with behavioral components, has undergone many conceptual changes since its inception as a syndrome by Kahlbaum in 1874. Prevalence of catatonia in consultation-liaison services is approximately 5.5 percent in patients aged 65 and older.1 Stuporous catatonia is most common, but catatonia may present in excited or malignant subtypes. Together, the subtypes have over 40 documented signs and symptoms, making catatonia difficult to diagnose and appropriately treat.2 Catatonia involves hyperactivation of the orbitofrontal cortex (OFC) and ventromedial prefrontal cortex. GABA, NMDA, and dopamine have been implicated. GABA-A agonism by benzodiazepines improve catatonia by normalizing OFC activity.3 Case: A 66-year-old male with schizophrenia was admitted to a medical unit for failure to thrive after not eating for three days. He had not taken his medications for 2 weeks including chlorpromazine, quetiapine, oxcarbazepine, and clonazepam. Upon psychiatric consult, the patient exhibited staring, grimacing, echopraxia, and negativism. He was diagnosed with stuporous catatonia. 30 minutes after lorazepam challenge (2 milligram intravenous lorazepam), the patient was moving, conversing, and eating. After second dose of lorazepam, the patient became difficult to redirect, displaying stereotypy, verbigeration, and hitting. Additional doses of lorazepam were unsuccessful in breaking excited catatonia. History revealed previous catatonic episodes, including nine months prior when the patient was admitted to a gero-psychiatric unit. He initially presented in stuporous state, normalized with lorazepam, then transitioned to excited state. He received 16 milligrams of lorazepam in 24 hours without successful termination of excited catatonia. Lorazepam in combination with carbamazepine, clozapine, or valproic acid was unsuccessful. Catatonia was successfully treated with 10 sessions of electroconvulsive therapy (ECT) with lorazepam, clozapine, and valproic acid. Maintenance ECT was not continued because of the COVID pandemic, and the patient was admitted to a state facility after regression. Discussion: Catatonia is often encountered on consultation-liaison services in general hospital settings. We observed conversion of stuporous catatonia to excited catatonia after administration of lorazepam. This treatment-resistant catatonia ultimately required ECT. No reported cases of stuporous catatonia transitioning to excited catatonia were found on thorough literature review. Recognition of this conversion may be difficult and may require development of a catatonia scale that clearly identifies the presenting subtype. This is a challenge;clinical signs are not mutually exclusive among subtypes. This patient’s clinical course may provide insight into the identification of treatment-resistant catatonia, and accurate identification is necessary to allow for timely escalation of treatment. References: 1. Solmi M, et al. Prevalence of catatonia and its moderators in clinical samples: Results from a meta-analysis and meta-regression analysis. Schizophrenia Bulletin. 2017;44(5):1133–50. 2. Fink M, Taylor MA. The catatonia syndrome. Archives of General Psychiatry. 009;66(11):1173. 3. Ellul P, Choucha W. Neurobiological approach of Catatonia and Treatment Perspectives. Frontiers in Psychiatry. 2015;6.
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OVERVIEW OF EVENTS 10:30 am Opening of Meeting 10:45 am Opening Remarks - Dr. Jeff Daskalakis, CCNP President 10:50 am Introduction - Dr. Cecilia Flores, CCNP Vice-President 11:00 am CCNP 2020 Young Investigator Award Presentation Caroline Ménard, PhD, Department of Psychiatry & Neuroscience, Université Laval: "Sex-specific vascular alterations and biomarkers underlie stress responses in mice mirrored in human depression" 11:50 am CCNP Next Generation Awardee Andrea H. Pantoja Urban, MSc, Integrated Program in Neuroscience, McGill University: "Short and long-term effects of social defeat stress in adolescent female mice" 12:05 pm CCNP Next Generation Awardee Orna Issler, PhD, Department of Neuroscience, Mount Sinai:"The sex-specific role for long noncoding RNAs in depression: from genome-wide patterns to behavioral readout" 12:20 pm Lunch/Break 12:50 pm CCNP 2020 Heinz Lehmann Award Presentation Martin Alda, MD, FRCPC, Department of Psychiatry, Dalhousie University: "Personalized long-term treatment of bipolar disorder" 1:40 pm CCNP Next Generation Awardee Mikaela K Dimick, BA, Centre for Youth Bipolar Disorder, Centre for Addiction and Mental Health: "Cerebral blood flow and core mood symptoms in youth bipolar disorder: evidence for region-symptom specificity" 1:55 pm CCNP Next Generation Awardee Sneha Chenji, PhD, Department of Psychiatry & Pediatrics, University of Calgary: "The effect of rTMS treatment on cortico-striatal-thalamo-cortical (CSTC) circuit connectivity in Tourette's syndrome: a pilot study" 2:10 pm Break 2:20 pm CCNP 2020 Innovations in Neuropsychopharmacology Award Presentation Jeffrey Meyer, MD, PhD, FRCPC, Department of Psychiatry, University of Toronto: "Imaging markers of gliosis and monoamine oxidase in major depressive disorder: implications for personalized prevention and treatment" 3:10 pm CCNP Next Generation Awardee Jasmine D. Cakmak, MSc, Neuroscience, Western University: "The functional and structural consequences of aberrant microglial activity in major depressive disorder" 3:25 pm CCNP Next Generation Awardee Kayla D. Stone, PhD, Department of Psychiatry, University of Calgary: "Dorsolateral prefrontal cortex neurometabolite concentrations in pediatric mild traumatic brain injury" 3:40 pm Break 3:50 pm Keynote Speaker Rémi Quirion, OC, CQ, PhD, FRSC, Chief Scientist of Quebec, Ministry of Economy & Innovation: "A less well travelled road: from neuroscientist to chief scientist and then came COVID-19" 4:50 pm Closing Remarks - Dr. Cecilia Flores, CCNP Vice President Acknowledgments: In keeping with CMA guidelines, program content and selection of speakers are the responsibility of the planning committee. Methods: Here, we characterized the enduring changes in histone modifications in the NAcc of mice exposed to chronic social defeat stress (CSDS), a validated model for the study of depression-like behaviours that separates mouse populations into susceptible (SUS) and resilient (RES) based on a social interaction test (SIT). Tissue from the NAcc of control, SUS, and RES mice was collected either 24 hours or 4 weeks after the SIT and processed for histone profiling via mass spectrometry. From the Department of Psychiatry, University of Alberta, Edmonton, AB, Canada (Yap, Luki, S. Hanstock, Lirette, Zhaoa, Aitchison, Le Melledo);the Department of Medical Genetics, University of Alberta, Edmonton, AB, Canada (Aitchison);the Neuroscience and Mental Health Institute, University of Alberta, Edmonton, AB, Canada (Aitchison);the Edmonton Mood and Anxiety Disorders Program, University of Alberta Hospital, Edmonton, AB, Canada (Aitchison);the Department of Biomedical Engineering, University of Alberta, Edmonton, AB, Canada (C. Hanstock, Seres);and the Royal Alexandra Hospital, Edmonton, AB, Canada (Shandro).
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Conservation and executive function (EF) are important early childhood skills;however, knowledge about their relationship is scarce. Hence, in this study, this relationship is investigated, and a comparison is conducted between the Piagetian conservation and EF tasks to obtain the total hemoglobin (mMmm) for the left and right brain activity in the prefrontal cortex of children, using a functional near-infrared spectroscopy. As a case study, a survey was conducted in the home of a four-year-old child (boy) in Japan in 2020. His home was selected as the primary place of investigation owing to the spread of the coronavirus disease 2019 infection. The researcher was an expert in pedagogy and psychology. The following hypothesis could be formulated from the case studies analyzed herein: From the viewpoint of the brain activity in the prefrontal cortex, there may be a link between the conservation of quantity and EF. The preservation of quantity is closely related to mathematics education. This hypothesis can thus expand the scope of research and practice in the fields of psychology, education, and mathematics education. Furthermore, the results may help psychologists, psychiatrists, teachers, parents, and others involved in the development of children sublate the value of their concept of conservation and improve their support methods.
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The aim of the study was to present the rare co-occurring radiological findings of a child presenting with acute disseminated encephalomyelitis (ADEM) with a spinal cord and prefrontal cortex involvement after coronavirus disease 2019 (COVID-19) illness. The patient, who had COVID-19 a few weeks earlier, presented with progressive weakness in the right upper and lower extremities. Neurological examination of the patient was performed, and cranial magnetic resonance imaging (MRI) was taken on the same day. Serum severe acute respiratory syndrome coronavirus immunoglobulin M antibody testing was positive. MRI of the brain parenchyma and thoracic spine revealed fluid-attenuated inversion recovery and T2-weighted hyperintense lesions. Additionally, mild contrast enhancement was observed in both the prefrontal cortexes. The patient was discharged 10 days later with complete clinical recovery. Unlike other post-COVID-19 ADEM cases presenting in the literature, prefrontal cortex involvement makes our case rare.
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Objective: We report the approach and initial outcomes for two patients with Post-Acute Sequelae of SARS-CoV-2 (PASC) seen at our clinical transcranial direct current stimulation (tDCS) telehealth service at NYU Langone Health. Background: PASC is the syndrome of persisting (>1 month) symptoms following COVID-19 illness, which often include fatigue, cognitive dysfunction, pain, and emotional disturbance, and can lead to significant reductions in levels of daily functioning and quality of life. As the numbers of individuals who recover from COVID-19 continue to rise world-wide, there is a critical need for therapeutic interventions for this patient population. tDCS has potential for therapeutic targeting of these PASC symptoms, with the advantage of portable and wearable devices for home-based access. Design/Methods: Patients were a 42 and 57-year-old women with PASC seen 7 and 9 months following their acute COVID-19 illness. Each daily tDCS session was delivered at-home via a video visit for 30 minutes x 2.0 mA using a left anodal dorsolateral prefrontal cortex montage. Stimulation was paired with physical exercise, online adaptive computerized cognitive training, and guided mindfulness meditation, individualized to each patient. Sessions were delivered 3-5 days per week. Clinical neuropsychological evaluation was completed before and after the intervention, and we developed a symptom inventory based on the full range of PASC symptoms reported in the literature (Assessment of PASC;A-PASC) to measure treatment outcomes. Results: The patients experienced significant improvements across cognitive, emotional, physical, and functional domains, and both returned to work and resumed most of their daily activities following the intervention. Conclusions: tDCS can be delivered as a teleintervention warranting its evaluation as an accessible and scalable treatment option for PASC. Further study and clinical trials of PASC are warranted.
ABSTRACT
Background: The addictive use of digital games is a rising phenomenon, especially in adolescents and under the COVID-19 pandemic (Paschke et al., 2021). A better understanding of the new International Classification of Diseases, 11th Revision (ICD-11) diagnosis gaming disorder (GD) is urgently needed. Imaging studies report alterations in cognitive control, affective and motor regions in affected adolescents (Schettler et al., 2022). At the same time, they show deficits in self-rated emotion regulation. Objectives: The study aimed to investigate the neural correlates of emotional dysregulation in adolescents with GD and neural alterations under therapy at the very first time. Methods: In a functional magnetic resonance imaging study, 20 inpatients and outpatients with GD and 20 healthy peers were examined (aged 12-18 years) at two measurement points with a 12-week interval. Within the interval, patients received therapy as described by Wendt et al. (2021). The cognitive-reappraisal paradigm of Ochsner et al. (2004) was applied to measure emotion regulation abilities. Findings: First interim analyses revealed a positive linear relationship between the severity of initial addiction symptoms and activity changes within the dorsolateral prefrontal cortex - a brain region related to top-down emotion regulation. This relationship decreased over the 12 weeks but only in the patients group. Conclusion: Adolescents with GD seem to show higher cognitive-control effort when dealing with negative emotions which could be addressed by therapy. Data collection will be completed in December 2021. Therefore, results of high novelty and clinical relevance will be presented to the scientific community for the very first time.