Search

Background: Over the last decades, brain surgery became a more frequently applied treatment for temporal lobe epilepsy (TLE). Despite its success, several studies found de-novo post-operative psychiatric symptoms in TLE surgery patients. Cognitive behavioural therapy is effective to treat brain healthy psychiatric patients but might not be translatable to patients with resections in emotion regulating networks as these areas seem to be essentially involved in successful psychotherapeutic treatment. Methods: Here we report the case of a female patient with medically refractory medial temporal lobe epilepsy resulting in left anterior temporal lobectomy at age 35. Post operation she did not show adequate fearful response but at the same time manifested symptoms of a severe panic disorder. We investigated if this patient, despite lesions in emotion-behaviour brain circuits, can benefit from cognitive behavioural therapy. Results: The intervention, customized to the specific resources and difficulties of the patient, was effective in stopping panic attacks and improving social functioning. Conclusions: This case shows that MTL brain surgery patients may benefit from CBT and demonstrates the important and if yet still somewhat mysterious role of the amygdala in emotion regulation processes. [ABSTRACT FROM AUTHOR]

Chronic stress is generally accepted as the main risk factor in the development of cognitive decline; however, the underlying mechanisms remain unclear. Previous data have demonstrated that the levels of homocysteine (Hcy) are significantly elevated in the plasma of stressed animals, which suggests that Hcy is associated with stress and cognitive decline. To test this hypothesis, we analyzed the cognitive function, plasma concentrations of Hcy, and brain-derived neurotropic factor (BDNF) levels in rats undergoing chronic unpredicted mild stress (CUMS). The results showed that decreased cognitive behavioral performance and decreased BDNF transcription and protein expression were correlated with hyperhomocysteinemia (HHcy) levels in stressed rats. Diet-induced HHcy mimicked the cognitive decline and BDNF downregulation in the same manner as CUMS, while Hcy reduction (by means of vitamin B complex supplements) alleviated the cognitive deficits and BDNF reduction in CUMS rats. Furthermore, we also found that both stress and HHcy disturbed the DNA methylation process in the brain and induced DNA hypermethylation in the BDNF promoter. In contrast, control of Hcy blocked BDNF promoter methylation and upregulated BDNF levels in the brain. These results imply the possibility of a causal role of Hcy in stress-induced cognitive decline. We also used ten-eleven translocation (TET1), an enzyme that induces DNA demethylation, to verify the involvement of Hcy and DNA methylation in the regulation of BDNF expression and the development of stress-related cognitive decline. The data showed that TET1-expressing viral injection into the hippocampus inhibited BDNF promoter methylation and significantly mitigated the cognitive decline in HHcy rats. Taken together, novel evidence from the present study suggests that Hcy is likely involved in chronic stress-induced BDNF reduction and related cognitive deficits. In addition, the negative side-effects of HHcy may be associated with Hcy-induced DNA hypermethylation in the BDNF promoter. The results also suggest the possibility of Hcy as a target for therapy and the potential value of vitamin B intake in preventing stress-induced cognitive decline. [ABSTRACT FROM AUTHOR]

The cerebrospinal fluid (CSF) space is convoluted. CSF flow oscillates with a net flow from the ventricles towards the cerebral and spinal subarachnoid space. This flow is influenced by heartbeats, breath, head or body movements as well as the activity of the ciliated epithelium of the plexus and ventricular ependyma. The shape of the CSF space and the CSF flow preclude rapid equilibration of cells, proteins and smaller compounds between the different parts of the compartment. In this review including reinterpretation of previously published data we illustrate, how anatomical and (patho)physiological conditions can influence routine CSF analysis. Equilibration of the components of the CSF depends on the size of the molecule or particle, e.g., lactate is distributed in the CSF more homogeneously than proteins or cells. The concentrations of blood-derived compounds usually increase from the ventricles to the lumbar CSF space, whereas the concentrations of brain-derived compounds usually decrease. Under special conditions, in particular when distribution is impaired, the rostro-caudal gradient of blood-derived compounds can be reversed. In the last century, several researchers attempted to define typical CSF findings for the diagnosis of several inflammatory diseases based on routine parameters. Because of the high spatial and temporal variations, findings considered typical of certain CNS diseases often are absent in parts of or even in the entire CSF compartment. In CNS infections, identification of the pathogen by culture, antigen detection or molecular methods is essential for diagnosis. [ABSTRACT FROM AUTHOR]

Background and objective: Cervical spondylosis (CS) is often accompanied by persistent cervical pain, and psychological complications including depression and anxiety, which aggravate pain. Past studies have revealed brain alterations in chronic pain patients. However, the cortical mechanism for NSAID (non-steroidal anti-inflammatory drug) responders relative to non-responders is still lacking. Therefore, we aimed to investigate the brain functional differences between responders to NSAID relative to non-responders using amplitude of low-frequency fluctuation (ALFF) and dynamic functional connectivity variance (DFCV). To our knowledge, our study is the first to investigate the DFCV in CS patients. Materials and methods: We first explored the differences in psychological inventories in CS patients who respond to NSAID vs non-responders. The voxel-wise ALFF was calculated and compared between CS patients and healthy controls. The ALFF within the resultant clusters were extracted and compared between responders and non-responders. DFCV among the resulting clusters was compared in responders vs non-responders. Results: We found that (1) compared to responders, non-responders exhibited higher levels of anxiety and depression; (2) relative to healthy controls, CS patients exhibited altered ALFF within the middle cingulate cortice (MCC), cerebellum, and middle frontal gyrus (MFG); (3) moreover, compared with responders, non-responders exhibited lower ALFF within MCC; furthermore, non-responders also exhibited increased DFCV between MCC and cerebellum, and between MCC and MFG. Conclusion: Our data indicate that psychological comorbidities (e.g., anxiety) influence response to NSAID in CS patients. Relative to NSAID responders, non-responders had altered MCC function, which may be associated with anxiety in CS patients. [ABSTRACT FROM AUTHOR]

Thus, a subset of patients with late-onset panic disorder may subsequently develop not only Parkinson's disease but also DLB. Dear editor, Lewy body disease (LBD) encompasses two clinicopathological syndromes associated with Lewy bodies (LB): Parkinson's disease and dementia with Lewy bodies (DLB).[1] Both disorders share prodromal symptoms such as anxiety and rapid eye movement (REM) sleep behavior disorder (RBD), which precede the disorders by years or decades before the clinical criteria are fulfilled. Panic disorder preceding the onset of Parkinson's disease and DLB have been reported.[[2], [4]] However, our report is the first case of autopsy-confirmed DLB with late-onset panic disorder as the initial presentation. [Extracted from the article]

Copyright of Praktické Lékárenství is the property of SOLEN sro and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Hemodialysis patients require spiritual care due to their spiritual distress. This study aimed to investigate the effect of spiritual care on spiritual experiences of hemodialysis patients. This randomized controlled trial was conducted in 2017 at hemodialysis departments of Baqiyatallah and Cham ran hospitals in Tehran. The volunteer patients were selected by available sampling according to the inclusion criteria. Participants were randomly assigned to intervention and control groups. Interventions were performed in the educational-supportive nursing system according to the patients' self-care ability. Eight individual counseling sessions, 15–45 min, face-to-face, during dialysis, once a week were implemented for intervention group. Developing the relationship with God, self, people and nature were the main goals of care. Daily spiritual experience questionnaire was completed by patients before and three months after the intervention. There was no significant difference in the spiritual experience score of the intervention (75.20 ± 9.14) and control group (76.63 ± 10.03), before the intervention (P = 0.523). There was a statistically significant difference between the intervention (82.93 ± 5.69) and the control group score (77.24 ± 12.09) three months after the intervention (P < 0.0001). Due to the need for holistic and community-oriented care and the positive effect of this study, the use of the Sound Heart Model is recommended for Muslim patients. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to test the hypothesis that the relationship between glutamic acid decarboxylase (GAD) 1 gene methylation and severity of clinical symptoms of panic disorder (PD) is mediated by the effect of GAD1 gene methylation on gray matter volume (GMV) and the effect of GMV on PD. Methods: Panic disorder (n = 24) patients were recruited consecutively from the Affiliated Brain Hospital of Nanjing Medical University through outpatient and public advertising, eligible healthy controls (HCs) (n = 22) were recruited from public advertising. We compared GMV and GAD1 gene methylation in PD and HCs to estimate the differences, and on the basis of the relationship between gray matter volumes and GAD1 gene methylation in PD patients was evaluated, the role of GMV as a mediator of GAD1 gene methylation and PD clinical symptoms was analyzed. Results: Panic disorder patients had significantly lower methylation in the GAD1 promoter region on Cytosine-phosphate-guanine (CPG) 7 than HCs (t = 2.380, p = 0.021). Pearson correlation analysis found a significant negative association between cg171674146 (cg12) site and clinical severity (n = 24, r = −0.456, p = 0.025). Compared to HCs, patients with PD had decreased gray matter volumes in several brain regions, which were also associated with PD severity. Left postcentral gyrus (PoCG) GMV mediated the association between cg12 methylation and PD severity, and there was a significant mediation effect of right angular gyrus (ANG) gray matter volumes on the relationship between cg12 methylation and PD severity. Limitation: No direct results can be derived for methylation patterns in different brain regions; the study is cross-sectional; relatively small size. [ABSTRACT FROM AUTHOR]

Background: Extensive studies put forward the association between Alzheimer's disease (AD) and psychiatric disorders; however, it remains unclear whether these associations are causal.Objective: We aimed to assess the potential causal relationship between major psychiatric disorders and AD.Methods: A bidirectional two-sample Mendelian randomization (MR) was applied to evaluate potential causality between five psychiatric disorders and AD by selecting the single-nucleotide polymorphisms from the genome-wide association studies as instrumental variables. Inverse-variance weighted (IVW) method was used as the main analyzing approach to estimate possible causal effects, alternative methods including MR-Egger, the MR pleiotropy residual sum and outlier, and leave-one-out analysis method were implemented as sensitivity analyzing approaches to ensure the robustness of results.Results: All forward and reverse MR analyses consistently suggested absent causal relations between psychiatric disorders and AD risk [forward IVW: ORADHD, 1.030, 95% CI, 0.908-1.168, p = 0.674; ORanxiety disorders, 0.904, 95% CI, 0.722-1.131, p = 0.377; ORASD, 0.973, 95% CI, 0.746-1.272, p = 0.846; ORBIP, 1.033, 95% CI, 0.925-1.153, p = 0.564; and ORschizophrenia, 1.039, 95% CI, 0.986-1.095, p = 0.156; reverse IVW: ORADHD, 0.993, 95% CI, 0.954-1.034, p = 0.746; ORanxiety disorders, 1.000, 95% CI, 0.999-1.000, p = 0.898; ORASD, 1.001, 95% CI, 0.962-1.042, p = 0.949; ORBIP, 0.997, 95% CI, 0.966-1.028, p = 0.831; and ORschizophrenia, 1.013, 95% CI, 0.978-1.051, p = 0.466].Conclusion: There is no significant evidence supporting the causal association between the five major psychiatric disorders and AD. [ABSTRACT FROM AUTHOR]

Depressive disorder is the most prevalent affective disorder today. Depressive disorder has been linked to changes in the white matter. White matter changes in depressive disorder could be a result of impaired cerebral blood flow (CBF) and CBF self-regulation, impaired blood-brain barrier function, inflammatory factors, genes and environmental factors. Additionally, white matter changes in patients with depression are associated with clinical variables such as differential diagnosis, severity, treatment effect, and efficacy assessment. This review discusses the characteristics, possible mechanisms, clinical relevance, and potential treatment of white matter alterations caused by depressive disorders. [ABSTRACT FROM AUTHOR]

Studies of early life stress (ELS) demonstrate the long-lasting effects of acute and chronic stress on developmental trajectories. Such experiences can become biologically consolidated, creating individual vulnerability to psychological and psychiatric issues later in life. The hippocampus, amygdala, and the medial prefrontal cortex are all important limbic structures involved in the processes that undermine mental health. Hyperarousal of the sympathetic nervous system with sustained allostatic load along the Hypothalamic Pituitary Adrenal (HPA) axis and its connections has been theorized as the basis for adult psychopathology following early childhood trauma. In this review we synthesize current understandings and hypotheses concerning the neurobiological link between childhood trauma, the HPA axis, and adult psychiatric illness. We examine the mechanisms at play in the brain of the developing child and discuss how adverse environmental stimuli may become biologically incorporated into the structure and function of the adult brain via a discussion of the neurosequential model of development, sensitive periods and plasticity. The HPA connections and brain areas implicated in ELS and psychopathology are also explored. In a targeted review of HPA activation in mood and psychotic disorders, cortisol is generally elevated across mood and psychotic disorders. However, in bipolar disorder and psychosis patients with previous early life stress, blunted cortisol responses are found to awakening, psychological stressors and physiological manipulation compared to patients without previous early life stress. These attenuated responses occur in bipolar and psychosis patients on a background of increased cortisol turnover. Although cortisol measures are generally raised in depression, the evidence for a different HPA activation profile in those with early life stress is inconclusive. Further research is needed to explore the stress responses commonalities between bipolar disorder and psychosis in those patients with early life stress. [ABSTRACT FROM AUTHOR]

Objective: The objectives of this study are to identify patterns of anxiety symptomology over time among patients with systemic lupus erythematosus (SLE) and to assess the longitudinal relationship between SLE disease activity and anxiety symptomology. Methods: Longitudinal data from 139 patients with American College of Rheumatology or Systemic Lupus International Collborating Clinic (SLICC)‐classified SLE were analyzed. Anxiety symptomology was assessed using the Patient‐Reported Outcomes Measurement Information System (PROMIS) Emotional Distress: Anxiety Short Form 8a. SLE disease activity was measured using the Systemic Lupus Erythematosus Disease Activity Index (SLEDAI)‐2000 (S2K) and S2K Responder Index 50 (S2K RI‐50). Group‐based trajectory modeling (GBTM) identified longitudinal trajectories of anxiety symptomology. The relationship between disease activity and anxiety over time was assessed using multilevel linear regressions. Results: The mean patient age was 40.2 years (standard deviation [SD], 12.7); 90.6% were female, and 56.1% were of Black race. All patients had at least three PROMIS anxiety scores over an average of 30.9 months (SD, 13.0). GBTM identified four trajectories of anxiety symptomology, labeled as the following: low (LA), average (AA), moderate (MA), and high anxiety (HA). Black patients were 2.47 (95% confidence interval: 1.19‐5.12) times as likely as White patients to be classified into the MA or HA groups compared with the LA or AA groups. On multivariable analysis, active SLE disease was not significantly associated with anxiety over time (P = 0.19). Conclusion: Anxiety trajectories remained stable over time, and racial differences in anxiety severity were observed. SLE disease activity was not longitudinally associated with anxiety after controlling for depression and other factors. Further understanding of the factors that contribute to the persistence of anxiety among individuals with SLE is necessary. [ABSTRACT FROM AUTHOR]

Adult neurogenesis is the creation of new neurons which integrate into the existing neural circuit of the adult brain. Recent evidence suggests that adult hippocampal neurogenesis (AHN) persists throughout life in mammals, including humans. These newborn neurons have been implicated to have a crucial role in brain functions such as learning and memory. Importantly, studies have also found that hippocampal neurogenesis is impaired in neurodegenerative and neuropsychiatric diseases. Alzheimer’s disease (AD) is one of the most common forms of dementia affecting millions of people. Cognitive dysfunction is a common symptom of AD patients and progressive memory loss has been attributed to the degeneration of the hippocampus. Therefore, there has been growing interest in identifying how hippocampal neurogenesis is affected in AD. However, the link between cognitive decline and changes in hippocampal neurogenesis in AD is poorly understood. In this review, we summarized the recent literature on AHN and its impairments in AD. [ABSTRACT FROM AUTHOR]

Copyright of Revista de Psiquiatría Infanto-Juvenil is the property of Asociacion Espanola de Psiquiatria del Nino y el Adolescente (AEPNyA) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Saúde e Pesquisa is the property of Saude e Pesquisa and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Purpose: It is known that the diagnosis of breast cancer often causes anxiety and depression. Radiotherapy of the breast as an obligatory part of a breast-conserving treatment concept can markedly increase these psychological symptoms in many, but not all patients. In this clinical observational study, we aimed at identifying cognitive, health-related and social factors that may either enhance or reduce the emergence of anxiety and depression. Methods: Using a longitudinal study design with 25 women (mean age: 52.9 years; SD = 10.6; age range 29–70 years) with a first diagnosis of nonmetastatic breast cancer, measures of anxiety, depression, situational emotional states, intelligence, and aspects of social frameworks were assessed before, during, and after radiotherapy of the breast. At 4 time-points, standard and self-constructed questionnaires were used to assess the course of anxiety and depressive symptoms across the radiotherapy intervention. Results: We found that anxiety is highest immediately before the start of radiation therapy, while the anxiety level was lowest on the day that therapy was completed. Anxiety and depression were enhanced in women with a lifetime history of chronic diseases at all time points of measurement. Moreover, women with high intelligence and low social support had stronger symptoms of depression than women with low intelligence and a stable family background at some time points of measurement. The degree of anxiety was neither related to intelligence nor to social support. Conclusion: For the first time, we demonstrate empirical pilot data on cognitive and social modulators of anxiety and depression in women with breast cancer over the course of radiotherapy. Our results may help to optimize clinical procedures and thereby reduce symptoms of anxiety and depression in these patients. [ABSTRACT FROM AUTHOR]

Recent neuroimaging studies have identified alterations in activity and connectivity among many brain regions as potential biomarkers for panic disorder. However, the functional connectome of panic disorder is not well understood. Therefore, a graph-theoretical approach was applied in this study to construct functional networks of patients and healthy controls in order to discover topological changes in panic disorder. 31 patients and 33 age and sex matched healthy controls underwent resting-state functional magnetic resonance imaging. Brain networks for each participant were structured using nodes from the Anatomical Automatic Labeling template and edges from connectivity matrices. Then, topological organizations of networks were calculated. Network-based statistical analysis was conducted, and global and nodal properties were compared between patients and controls. Unlike controls, patients with panic disorder displayed a small-world network. Patients also revealed decreased nodal efficiency in right superior frontal gyrus (SFG), middle frontal gyrus (MFG), right superior temporal gyrus (STG), and left middle temporal gyrus (MTG). Decreased functional connectivity was found in panic disorder between right MTG and extensive temporal regions. Among these disrupted regions, the decreased nodal efficiency of SFG showed a positive correlation with clinical symptoms while nodal betweenness centrality in angular gyrus showed a negative correlation. Our results indicated decreased function of global and regional information transmission in panic disorder and emphasized the role of temporal regions in its pathology. [ABSTRACT FROM AUTHOR]

Background: Mental illness represents a major global burden of disease worldwide. It has been hypothesised that individuals with mental illness have greater blood pressure fluctuations that lead to increased cardiovascular risk and target organ damage. This systematic review aims to (i) investigate the association between mental illness and blood pressure variability (BPV) and (ii) describe methods of BPV measurements and analysis which may affect pattern and degree of variability.Methods: Four electronic databases were searched from inception until 2020. The quality assessment was performed using STROBE criteria. Studies were included if they investigated BPV (including either frequency or time domain analysis) in individuals with mental illness (particularly anxiety/generalised anxiety disorder, depression/major depressive disorder, panic disorder and hostility) and without hypertension. Two authors independently screened titles, abstracts and full texts. A third author resolved any disagreements.Results: Twelve studies met the inclusion criteria. Three studies measured short-term BPV, two measured long-term BPV and seven measured ultra-short-term BPV. All studies related to short-term BPV using ambulatory and home blood pressure monitoring found a higher BPV in individuals with depression or panic disorder. The two studies measuring long-term BPV were limited to the older population and found mixed results. Mental illness is significantly associated with an increased BPV in younger and middle-aged adults. All studies of ultra-short-term BPV using standard cardiac autonomic assessment; non-invasive continuous finger blood pressure and heart rate signals found significant association between BPV and mental illness. A mixed result related to degree of tilt during tilt assessment and between controlled and spontaneous breathing were observed in patients with psychological state.Conclusions: Current review found that people with mental illness is significantly associated with an increased BPV regardless of age. Since mental illness can contribute to the deterioration of autonomic function (HRV, BPV), early therapeutic intervention in mental illness may prevent diseases associated with autonomic dysregulation and reduce the likelihood of negative cardiac outcomes. Therefore, these findings may have important implications for patients' future physical health and well-being, highlighting the need for comprehensive cardiovascular risk reduction. [ABSTRACT FROM AUTHOR]

Anxiety disorders are complex diseases, and often co-occur with depression. It is as yet unclear if a common neural circuit controls anxiety-related behaviors in both anxiety-alone and comorbid conditions. Here, utilizing the chronic social defeat stress (CSDS) paradigm that induces singular or combined anxiety- and depressive-like phenotypes in mice, we show that a ventral tegmental area (VTA) dopamine circuit projecting to the basolateral amygdala (BLA) selectively controls anxiety- but not depression-like behaviors. Using circuit-dissecting ex vivo electrophysiology and in vivo fiber photometry approaches, we establish that expression of anxiety-like, but not depressive-like, phenotypes are negatively correlated with VTA → BLA dopamine neuron activity. Further, our optogenetic studies demonstrate a causal link between such neuronal activity and anxiety-like behaviors. Overall, these data establish a functional role for VTA → BLA dopamine neurons in bi-directionally controlling anxiety-related behaviors not only in anxiety-alone, but also in anxiety-depressive comorbid conditions in mice. Anxiety and depression are highly comorbid, yet the distinct or shared neurobiological correlates of anxiety remain elusive. Here, Morel et al. define that the midbrain projection to the basolateral amygdala control anxiety but not depression. [ABSTRACT FROM AUTHOR]

Individuals' social contexts are broadly recognized to impact both their psychology and neurobiology. These effects are observed in people and in nonhuman animals who are the subjects for comparative and translational science. The social contexts in which monkeys are reared have long been recognized to have significant impacts on affective processing. Yet, the social contexts in which monkeys live as adults are often ignored and could have important consequences for interpreting findings, particularly those related to biopsychiatry and behavioral neuroscience studies. The extant nonhuman primate neuropsychological literature has historically tested individually-housed monkeys, creating a critical need to understand how social context might impact the outcomes of such experiments. We evaluated affective responding in adult rhesus monkeys living in four different social contexts using two classic threat processing tasks—a test of responsivity to objects and a test of responsivity to an unfamiliar human. These tasks have been commonly used in behavioral neuroscience for decades. Relative to monkeys with full access to a social partner, individually-housed monkeys had blunted reactivity to threat and monkeys who had limited contact with their partner were more reactive to some threatening stimuli. These results indicate that monkeys' social housing contexts impact affective reactivity and point to the potential need to reconsider inferences drawn from prior studies in which the impacts of social context have not been considered. [ABSTRACT FROM AUTHOR]

The under-or misdiagnosis, and symptomatic treatment of the panic disorder (PD), despite high prevalent medical illness, is common among non-psychiatric physicians. The non-psychiatrist physician's role is vital in the care of PD as most patients initially approach general medical settings for medical help, including primary care. However, a significant proportion is undiagnosed and undergoes either unnecessary investigation, misdiagnosed, or mismanaged even among post-Coronary Artery Bypass Grafting patients, which profoundly affects the patients functioning and quality of life. This article aims to provide overviews of relevant epidemiological aspects, presenting features across medical specialties with respective diagnostic dilemmas, assessment, and management of the PD in their general medical settings, including emergency visits. Apart from psychiatrists, this will also assist non-psychiatrist physicians across all medical specialties, including general practitioners, to understand, identify, and provide the first line evidence-based pharmacotherapy and address the unmet need of patients with PD in their day-to-day busy clinical practice. This paper also provides a referral guide for non-psychiatrist physicians to refer to psychiatrists for further management after their first-line management. [ABSTRACT FROM AUTHOR]

It has been hypothesised that early-onset panic disorder (PD) may constitute a biologically distinct subtype of PD, but the few relevant data are inconclusive. We systematically explored for potential psychopathological and hormonal differences between early-onset (age at onset ≤ 27 years) versus late-onset PD, in consecutively-referred, medication-free, acutely-ill PD outpatients, moreover without comorbid mental disorders except agoraphobia (N = 54; age = 32.3 ± 7.5 years; early-onset = 27; females = 38). Hormones assessed (plasma levels) included adrenocorticotropic hormone (ACTH), cortisol and dehydroepiandrosterone sulphate (DHEAS). Psychopathological measures included panic attacks' number during last three weeks, the Agoraphobic Cognitions and the Body Sensations Questionnaires and the Hamilton Anxiety Rating Scale. Early-onset PD patients – compared to their late-onset counterparts – had longer duration of the disease. The two onset-groups demonstrated similar panic and anxiety symptoms and similar ratios of smokers/never-smokers. However, early-onset patients demonstrated significantly greater ACTH and DHEAS levels and higher (marginally significant) cortisol levels than the late-onset patients. Moreover, in the early-onset patients only, significant positive correlations emerged between ACTH levels and the severity of both panic and anxiety symptomatology. These findings suggest that the two onset-groups demonstrate significant differences in the hypothalamic-pituitary-adrenal axis functioning, at least when acutely-ill. Early-onset panic disorder (EOPD) may differ biologically from late-onset PD (LOPD). EOPD was correlated with greater adrenocorticotropic hormone (ACTH) plasma levels. EOPD was correlated with greater dehydroepiandrosterone sulphate plasma levels. In EOPD only, ACTH levels were positively correlated with panic and anxiety symptoms. [ABSTRACT FROM AUTHOR]

Across species, animals organize into social dominance hierarchies that serve to decrease aggression and facilitate survival of the group. Neuroscientists have adopted several model organisms to study dominance hierarchies in the laboratory setting, including fish, reptiles, rodents and primates. We review recent literature across species that sheds light onto how the brain represents social rank to guide socially appropriate behaviour within a dominance hierarchy. First, we discuss how the brain responds to social status signals. Then, we discuss social approach and avoidance learning mechanisms that we propose could drive rank-appropriate behaviour. Lastly, we discuss how the brain represents memories of individuals (social memory) and how this may support the maintenance of unique individual relationships within a social group. This article is part of the theme issue ‘The centennial of the pecking order: current state and future prospects for the study of dominance hierarchies’. [ABSTRACT FROM AUTHOR]

Background: From previous studies, we know the correlations of some brain metabolites with a generalized anxiety disorder (GAD) and its symptoms. The response of GAD patients to various treatments is not the same and finding the best treatment option for each patient takes a long period of time. Objective: In this study, we try to examine if there is any relationship between a special treatment option and GAD patients' response and brain metabolite correlation with anxiety level change. Material and Methods: This study is a clinical trial type of studies. We have used proton MRS (1H-MRS) with field strength of 3 Tesla to assess whether a different treatment option makes different responses based on metabolite changes. We chose 16 patients based on Hamilton's anxiety rate and a psychiatrist diagnosis. Patients were divided into two groups randomly. Each group took different treatments. Before treatment started, patients underwent MRS imaging and 8 weeks after treatment as well. Our study lacked a control group, and the results were analyzed by comparing the measured values of metabolites and clinical scores before and after treatment. Results: The NAA and Cho concentration increased after treatments and Cr concentration remained constant in both groups. Both groups showed improvements in their symptoms of anxiety and also in their clinical score rates. Sertraline group showed a more increase in NAA concentration than CBT and also a more decrease in HAMA and HAMD-17 scores. Conclusion: A simultaneously increase in NAA and Cho in both groups and a decrease in clinical anxiety levels demonstrate that NAA and Cho concentration are associated negatively with anxiety levels. In addition, both CBT and sertraline are effective in the improvement of anxiety symptoms. [ABSTRACT FROM AUTHOR]

Introduction: The postmenopausal symptoms affect the quality of life (QoL) of women. Depression and anxiety too have been associated with diminished QoL. It is known that antidepressants escitalopram and desvenlafaxine are effective in the treatment of depression and anxiety. However, to the best of our knowledge, their comparative effect on the QoL of postmenopausal women with depression and anxiety has not been studied in the Indian setup. Materials and Methods: The present study was a randomized, intention to treat, open-label trial undertaken in North India's a tertiary care teaching hospital. Postmenopausal women attending the psychiatry outpatient department and newly diagnosed with depression and anxiety were randomized in two groups to receive Tab. Escitalopram 10–20 mg and Tab. Desvenlafaxine 50–100 mg. Their QoL was assessed using the WHOQOL BREF scale at baseline, 3 weeks and 6 weeks. Results: Escitalopram was observed to be statistically better than desvenlafaxine in improving the overall QoL score of the WHOQOL-BREF scale. Individually, escitalopram significantly improved the scores of the physical health domain, psychological and environmental domains except for the social relationship domain. Desvenlafaxine significantly improved scores of all four domains. Conclusion: Escitalopram was observed to be significantly better than desvenlafaxine in improving the overall QoL scores. Both the drugs were well tolerated. [ABSTRACT FROM AUTHOR]

Background: Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a multisystem medical condition with heterogeneous symptom expression. Currently, there is no effective cure or treatment for the standard care of patients. A variety of ME/CFS symptoms can be linked to the vital life functions of the brainstem, the lower extension of the brain best known as the hub relaying information back and forth between the cerebral cortex and various parts of the body. Objective/Methods: Over the past decade, Magnetic Resonance Imaging (MRI) studies have emerged to understand ME/CFS with interesting findings, but there has lacked a synthesized evaluation of what has been found thus far regarding the involvement of the brainstem. We conducted this study to review and evaluate the recent MRI findings via a literature search of the MEDLINE database, from which 11 studies met the eligibility criteria. Findings: Data showed that MRI studies frequently reported structural changes in the white and gray matter. Abnormalities of the functional connectivity within the brainstem and with other brain regions have also been found. The studies have suggested possible mechanisms including astrocyte dysfunction, cerebral perfusion impairment, impaired nerve conduction, and neuroinflammation involving the brainstem, which may at least partially explain a substantial portion of the ME/CFS symptoms and their heterogeneous presentations in individual patients. Conclusions: This review draws research attention to the role of the brainstem in ME/CFS, helping enlighten future work to uncover the pathologies and mechanisms of this complex medical condition, for improved management and patient care. [ABSTRACT FROM AUTHOR]

Evidence for a single underlying factor structure of posttraumatic stress disorder (PTSD) in children remains elusive. We assessed the underlying factor structure of the Child PTSD Symptom Scale through exploratory (EFA) and confirmatory factor analyses (CFA) in 570 survivors of the 2015 Gorkha earthquake in Nepal. The EFA suggests that the three-factor DSM-IV model fit these data best. The CFA suggests that while the DSM-IV model adequately fit these data, the four-factor King model fit them better. There was no evidence of differential item functioning by age or gender, and internal consistency of the scale was high. PTSD (overall or by factor) was not correlated with functional impairment. Inconsistent psychometric results across contexts and methodologies suggest that our current theoretical conceptualizations and empirical models of posttraumatic stress are lacking. Future studies must both document the instrument properties to assure internal validity and cross-study comparisons and, bolstered by increased psychometric data and analyses, rework theoretical models of PTSD with improved cross-cultural validity. [ABSTRACT FROM AUTHOR]

This study was conducted to evaluate the effect of maternal exposure to TiO2 nanoparticles on the pain response in offspring mice. 30 female mice with a mean ± SD weight of 30 ± 5 g were randomly divided into three groups: the control group (group 1) received only the basal diet; the sham group (group 2) received saline plus as a carrier (100 μL/mice) subcutaneously on days 3, 7, 10, and 14 post-mating; and the test group (group 3) received 100 μL/mice TNPs subcutaneously on days 3, 7, 10, and 14 post-mating. Offspring were divided into 6 groups 21 days after birth and underwent formalin test. Blood samples were taken to evaluate possible oxidative changes in total antioxidant capacity (TAC) and malondialdehyde (MDA). Exposure to TNPs significantly (p < 0.05) decreased pain perception. Except for a significant difference between the sham group and the control group, MDA and TAC were not significantly different among the studied groups. Injection of TNPs to pregnant mice would affect the pain perception in their offspring. This may be attributable to the ability of these particles to pass through the placenta to produce free radicals. [ABSTRACT FROM AUTHOR]

Copyright of JBES: Brazilian Journal of Health Economics / Jornal Brasileiro de Economia da Saúde is the property of JBES: Brazilian Journal of Health Economics and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Treatment-resistant depression (TRD) complicates the management of major depression (MD). The underlying biology of TRD involves interplay between genetic propensity and chronic and/or early life adversity. By combining a genetic animal model of MD and post-weaning social isolation rearing (SIR), we sought to produce an animal that displays more severe depressive- and social anxiety-like manifestations resistant to standard antidepressant treatment. Flinders Sensitive Line (FSL) pups were social or isolation reared from weaning [postnatal day (PND) 21], receiving fluoxetine (FLX) from PND 63 (10 mg/kg × 14 days), and compared to Sprague Dawley (SD) controls. Depressive-, anxiety-like, and social behaviour were assessed from PND 72 in the forced swim test (FST) and social interaction test (SIT). Post-mortem cortico-hippocampal norepinephrine (NE), serotonin (5-HT), and dopamine (DA), as well as plasma interleukin 6 (IL-6), tumour necrosis factor alpha (TNF-α), corticosterone (CORT), and dopamine-beta-hydroxylase (DBH) levels were assayed. FSL rats displayed significant cortico-hippocampal monoamine disturbances, and depressive- and social anxiety-like behaviour, the latter two reversed by FLX. SIR-exposed FSL rats exhibited significant immobility in the FST and social impairment which were, respectively, worsened by or resistant to FLX. In SIR-exposed FSL rats, FLX significantly raised depleted NE and 5-HT, significantly decreased DBH and caused a large effect size increase in DA and decrease in CORT and TNF-α. Concluding, SIR-exposed FSL rats display depressive- and social anxiety-like symptoms that are resistant to, or worsened by, FLX, with reduced plasma DBH and suppressed cortico-hippocampal 5-HT, NE and DA, all variably altered by FLX. Exposure of a genetic animal model of MD to post-weaning SIR results in a more intractable depressive-like phenotype as well as changes in TRD-related biomarkers, that are resistant to traditional antidepressant treatment. Given the relative absence of validated animal models of TRD, these findings are especially promising and warrant study, especially further predictive validation. [ABSTRACT FROM AUTHOR]

Brain oscillations underlie the function of our brains, dictating how we both think and react to the world around us. The synchronous activity of neurons generates these rhythms, which allow different parts of the brain to communicate and orchestrate responses to internal and external stimuli. Perturbations of cognitive rhythms and the underlying oscillator neurons that synchronize different parts of the brain contribute to the pathophysiology of diseases including Alzheimer's disease, (AD), Parkinson's disease (PD), epilepsy and other diseases of rhythm that have been studied extensively by Gyorgy Buzsaki. In this review, we discuss how neurologists manipulate brain oscillations with neuromodulation to treat diseases and how this can be leveraged to improve cognition and pathology underlying AD. While multiple modalities of neuromodulation are currently clinically indicated for some disorders, nothing is yet approved for improving memory in AD. Recent investigations into novel methods of neuromodulation show potential for improving cognition in memory disorders. Here, we demonstrate that neuronal stimulation using audiovisual sensory stimulation that generated 40‐HZ gamma waves reduced AD‐specific pathology and improved performance in behavioural tests in mouse models of AD, making this new mode of neuromodulation a promising new avenue for developing a new therapeutic intervention for the treatment of dementia. [ABSTRACT FROM AUTHOR]

Background: Lamotrigine (LMT) is a phenyltriazine derivative that was originally described as an antiepileptic drug.Objective: This literature review aims to evaluate the clinical epidemiological profile, pathological mechanisms, and management of lamotrigine-associated movement disorders.Methods: Relevant reports in six databases were identified and assessed by two reviewers without language restriction. Reports that the individuals only developed tremor or ataxia after LMT use were not included.Results: In total 48 reports of 108 cases from 19 countries were assessed. The movement disorders associated with LMT found were 29 tics, 21 dyskinesias, 14 myoclonus, 13 parkinsonism, 10 dystonia, and 1 stuttering. The not clearly defined cases included 10 akathisia, 4 myoclonus, 4 cerebellar syndromes, 1 hypertonia, 1 dyskinesia, and an unknown number of dystonia cases. The mean reported age was 33.34 years (range: 1.574 years). The male was the predominant sex and the most common LMT indication was epilepsy. The mean LMT-dose at the movement disorder onset was 228 mg. The time from LMT start to the onset of movement disorder was within 6 months in 81%. The time from LMT withdrawal to complete recovery was within 1 month in 83%. The most common management was LMT withdrawal.Conclusions: In the literature, the majority of the cases did not give a clear picture of the individual, and the times of movement disorder onset and recovery are not described. We believe that before withdrawal LMT, a dose adjustment based on the benefits and adverse events with careful evaluation case-by-case can be done. [ABSTRACT FROM AUTHOR]

Objective: Data regarding the potential association between the outcome of psychotherapy of panic disorder (PD) and biological parameters are few. In 21 (16 females) consecutively referred, medication-free, acutely ill PD outpatients, without comorbidities, except agoraphobia, we systematically explored for potential neuroendocrine and clinical correlates of response to a brief cognitive behavior therapy (CBT). Methods: Cortisol and adrenocorticotropic hormone (ACTH) basal plasma levels were measured. Measures of psychopathology: (a) Symptom Checklist–90-Revised (SCL-90-R), (b) Clinical Global Impressions-Improvement (CGI-I) Scale, (c) Agoraphobic Cognitions Questionnaire (ACQ), and (d) Mobility Inventory (MI)-alone subscale. Results: Nonresponders to CBT (CGI-I >2; N = 6) – as compared to the responders (CGI-I ≤2; N = 15) – demonstrated significantly higher cortisol and ACTH basal plasma concentrations. These differences were much stronger when only female patients (nonresponders = 4; responders = 12) were taken into consideration. Regarding psychopathology, nonresponders to CBT suffered from more severe agoraphobia (MI-alone) at baseline. On the contrary, more intense manifestations of anger (SCL-90-R) at baseline were associated with a better treatment outcome. Response to CBT was associated with significant reductions in all SCL-90-R subscales, more pronounced for "phobic anxiety" and "anxiety" subscales. Conclusions: This study suggests that in acutely ill, medication-free PD patients, response to CBT may be associated with certain hormonal and clinical parameters at baseline. [ABSTRACT FROM AUTHOR]

Objective: Disturbed regulation of vigilance in the wake state seems to play a key role in the development of mental disorders. It is assumed that hyperactivity in adult ADHD is an attempt to increase a general low vigilance level via external stimulation in order to avoid drowsiness. For depression, the avoidance of stimulation is interpreted as a reaction to a tonic increased vigilance state. Although ADHD is assumed to start during childhood, this vigilance model has been barely tested with children diagnosed for ADHD so far. Methods: Resting-state EEG (8 min) measures from two groups of children diagnosed with either ADHD [ N = 76 (16 female, 60 male), age: (mean/SD) 118/33 months] or depression [ N = 94 (73 female, 21 male), age: 184/23 months] were analyzed. Using the VIGALL toolbox, EEG patterns of vigilance level, and regulation were derived and compared between both groups. In correlation analysis, the relations between vigilance measures, attentional test performance (alertness and inhibition), and mental health symptoms were analyzed. Results: Children with ADHD differed from children with most prominent depressive symptoms in brain arousal regulation and level, but EEG vigilance was not related to behavior problems and not related to the attentional test performance. Brain arousal was dependent on the age of the participant in the whole sample; younger children showed lower vigilance stages than teenagers; this effect was not present when analyzed separately for each diagnostic group. EEG assessment time and received medication had no effect on the EEG vigilance. Discussion: Although based on a small sample, this explorative research revealed that EEG vigilance level is different between children with ADHD and with depression. Moreover, even the standard procedure of the clinical routine EEG (resting state) can be used to differentiate brain arousal states between participants with ADHD and depression. Because routine EEG is not specialized to vigilance assessment, it may not be sufficiently sensitive to find vigilance–symptomatology associations. Further research should address developmental changes in EEG measurements in children and use bigger samples of participants within the same age range. [ABSTRACT FROM AUTHOR]

Objectives: More than 40 drugs are available to treat affective disorders. Individual selection of the optimal drug and dose is required to attain the highest possible efficacy and acceptable tolerability for every patient. Methods: This review, which includes more than 500 articles selected by 30 experts, combines relevant knowledge on studies investigating the pharmacokinetics, pharmacodynamics and pharmacogenetics of 33 antidepressant drugs and of 4 drugs approved for augmentation in cases of insufficient response to antidepressant monotherapy. Such studies typically measure drug concentrations in blood (i.e. therapeutic drug monitoring) and genotype relevant genetic polymorphisms of enzymes, transporters or receptors involved in drug metabolism or mechanism of action. Imaging studies, primarily positron emission tomography that relates drug concentrations in blood and radioligand binding, are considered to quantify target structure occupancy by the antidepressant drugs in vivo. Results: Evidence is given that in vivo imaging, therapeutic drug monitoring and genotyping and/or phenotyping of drug metabolising enzymes should be an integral part in the development of any new antidepressant drug. Conclusions: To guide antidepressant drug therapy in everyday practice, there are multiple indications such as uncertain adherence, polypharmacy, nonresponse and/or adverse reactions under therapeutically recommended doses, where therapeutic drug monitoring and cytochrome P450 genotyping and/or phenotyping should be applied as valid tools of precision medicine. [ABSTRACT FROM AUTHOR]

Background and Aim: Multiple Sclerosis (MS) is among the most prevalent chronic and progressive neurological diseases with high simultaneity. MS is associated with some psychological conditions, such as depression and anxiety. Thus, we examined depression and anxiety in individuals with MS in this review study. Methods and Materials/Patients: We conducted this study using a systematic review method relying on the search from January 2010 to December 2020. Accordingly, we searched the following keywords: "multiple sclerosis, MS, psychiatric issues, psychological disorders, psychological problems, anxiety, mental health, quality of life, and depression" in 4 online databases (PsycNET, PubMed, Scopus, and Magiran). Ultimately, we selected 14 comprehensive papers that quantitatively and qualitatively examined psychiatric disorders in patients with MS. Results: A total of 14 studies were analyzed that included 27106 patients with MS. The results achieved by the analytical studies explained that depression and anxiety are significantly higher in patients with MS, compared with the healthy population. The prevalence of depression and anxiety in MS patients was reported to be heterogeneous. Conclusion: Data related to a large number of patients with MS presented a high prevalence of depression and anxiety in them; however, not separating the symptoms from the disorder can be misleading. Consequently, it is recommended to conduct further research to precisely assess the prevalence of depression and anxiety in these patients. It is required that future studies consider the further use of clinical interviews instead of self-reported questionnaires, using sample selection methods, and providing a complete report of patients' demographic, and clinical information. [ABSTRACT FROM AUTHOR]

The respiratory system reacts instantaneously to intrinsic and extrinsic inputs. This adaptability results in significant fluctuations in breathing parameters, such as respiratory rate, tidal volume, and inspiratory flow profiles. Breathing variability is influenced by several conditions, including sleep, various pulmonary diseases, hypoxia, and anxiety disorders. Recent studies have suggested that weaning failure during mechanical ventilation may be predicted by low respiratory variability. This review describes methods for quantifying breathing variability, summarises the conditions and comorbidities that affect breathing variability, and discusses the potential implications of breathing variability for anaesthesia and intensive care. [ABSTRACT FROM AUTHOR]

The hippocampus is one of the most challenging brain regions for proton MR spectroscopy (MRS) applications. Moreover, quantification of J‐coupled species such as myo‐inositol (m‐Ins) and glutamate + glutamine (Glx) is affected by the presence of macromolecular background. While long echo time (TE) MRS eliminates the macromolecules, it also decreases the m‐Ins and Glx signal and, as a result, these metabolites are studied mainly with short TE. Here, we investigate the feasibility of reproducibly measuring their concentrations at a long TE of 120 ms, using a semi‐adiabatic localization by adiabatic selective refocusing (sLASER) sequence, as this sequence was recently recommended as a standard for clinical MRS. Gradient offset‐independent adiabatic refocusing pulses were implemented, and an optimal long TE for the detection of m‐Ins and Glx was determined using the T2 relaxation times of macromolecules. Metabolite concentrations and their coefficients of variation (CVs) were obtained for a 3.4‐mL voxel centered on the left hippocampus on 3‐T MR systems at two different sites with three healthy subjects (aged 32.5 ± 10.2 years [mean ± standard deviation]) per site, with each subject scanned over two sessions, and with each session comprising three scans. Concentrations of m‐Ins, choline, creatine, Glx and N‐acetyl‐aspartate were 5.4 ± 1.5, 1.7 ± 0.2, 5.8 ± 0.3, 11.6 ± 1.2 and 5.9 ± 0.4 mM (mean ± standard deviation), respectively. Their respective mean within‐session CVs were 14.5% ± 5.9%, 6.5% ± 5.3%, 6.0% ± 3.4%, 10.6% ± 6.2% and 3.5% ± 1.4%, and their mean within‐subject CVs were 17.8% ± 18.2%, 7.5% ± 6.3%, 7.4% ± 6.4%, 12.4% ± 5.3% and 4.8% ± 3.0%. The between‐subject CVs were 25.0%, 12.3%, 5.3%, 10.7% and 6.4%, respectively. Hippocampal long‐TE sLASER single voxel spectroscopy can provide macromolecule‐independent assessment of all major metabolites including Glx and m‐Ins. [ABSTRACT FROM AUTHOR]