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Childhood adversities (CAs) predict heightened risks of posttraumatic stress disorder (PTSD) and major depressive episode (MDE) among people exposed to adult traumatic events. Identifying which CAs put individuals at greatest risk for these adverse posttraumatic neuropsychiatric sequelae (APNS) is important for targeting prevention interventions.
Methods
Data came from n = 999 patients ages 18–75 presenting to 29 U.S. emergency departments after a motor vehicle collision (MVC) and followed for 3 months, the amount of time traditionally used to define chronic PTSD, in the Advancing Understanding of Recovery After Trauma (AURORA) study. Six CA types were self-reported at baseline: physical abuse, sexual abuse, emotional abuse, physical neglect, emotional neglect and bullying. Both dichotomous measures of ever experiencing each CA type and numeric measures of exposure frequency were included in the analysis. Risk ratios (RRs) of these CA measures as well as complex interactions among these measures were examined as predictors of APNS 3 months post-MVC. APNS was defined as meeting self-reported criteria for either PTSD based on the PTSD Checklist for DSM-5 and/or MDE based on the PROMIS Depression Short-Form 8b. We controlled for pre-MVC lifetime histories of PTSD and MDE. We also examined mediating effects through peritraumatic symptoms assessed in the emergency department and PTSD and MDE assessed in 2-week and 8-week follow-up surveys. Analyses were carried out with robust Poisson regression models.
Results
Most participants (90.9%) reported at least rarely having experienced some CA. Ever experiencing each CA other than emotional neglect was univariably associated with 3-month APNS (RRs = 1.31–1.60). Each CA frequency was also univariably associated with 3-month APNS (RRs = 1.65–2.45). In multivariable models, joint associations of CAs with 3-month APNS were additive, with frequency of emotional abuse (RR = 2.03; 95% CI = 1.43–2.87) and bullying (RR = 1.44; 95% CI = 0.99–2.10) being the strongest predictors. Control variable analyses found that these associations were largely explained by pre-MVC histories of PTSD and MDE.
Conclusions
Although individuals who experience frequent emotional abuse and bullying in childhood have a heightened risk of experiencing APNS after an adult MVC, these associations are largely mediated by prior histories of PTSD and MDE.
Major depressive disorder (MDD) was previously associated with negative affective biases. Evidence from larger population-based studies, however, is lacking, including whether biases normalise with remission. We investigated associations between affective bias measures and depressive symptom severity across a large community-based sample, followed by examining differences between remitted individuals and controls.
Methods
Participants from Generation Scotland (N = 1109) completed the: (i) Bristol Emotion Recognition Task (BERT), (ii) Face Affective Go/No-go (FAGN), and (iii) Cambridge Gambling Task (CGT). Individuals were classified as MDD-current (n = 43), MDD-remitted (n = 282), or controls (n = 784). Analyses included using affective bias summary measures (primary analyses), followed by detailed emotion/condition analyses of BERT and FAGN (secondary analyses).
Results
For summary measures, the only significant finding was an association between greater symptoms and lower risk adjustment for CGT across the sample (individuals with greater symptoms were less likely to bet more, despite increasingly favourable conditions). This was no longer significant when controlling for non-affective cognition. No differences were found for remitted-MDD v. controls. Detailed analysis of BERT and FAGN indicated subtle negative biases across multiple measures of affective cognition with increasing symptom severity, that were independent of non-effective cognition [e.g. greater tendency to rate faces as angry (BERT), and lower accuracy for happy/neutral conditions (FAGN)]. Results for remitted-MDD were inconsistent.
Conclusions
This suggests the presence of subtle negative affective biases at the level of emotion/condition in association with depressive symptoms across the sample, over and above those accounted for by non-affective cognition, with no evidence for affective biases in remitted individuals.
This article is a clinical guide which discusses the “state-of-the-art” usage of the classic monoamine oxidase inhibitor (MAOI) antidepressants (phenelzine, tranylcypromine, and isocarboxazid) in modern psychiatric practice. The guide is for all clinicians, including those who may not be experienced MAOI prescribers. It discusses indications, drug-drug interactions, side-effect management, and the safety of various augmentation strategies. There is a clear and broad consensus (more than 70 international expert endorsers), based on 6 decades of experience, for the recommendations herein exposited. They are based on empirical evidence and expert opinion—this guide is presented as a new specialist-consensus standard. The guide provides practical clinical advice, and is the basis for the rational use of these drugs, particularly because it improves and updates knowledge, and corrects the various misconceptions that have hitherto been prominent in the literature, partly due to insufficient knowledge of pharmacology. The guide suggests that MAOIs should always be considered in cases of treatment-resistant depression (including those melancholic in nature), and prior to electroconvulsive therapy—while taking into account of patient preference. In selected cases, they may be considered earlier in the treatment algorithm than has previously been customary, and should not be regarded as drugs of last resort; they may prove decisively effective when many other treatments have failed. The guide clarifies key points on the concomitant use of incorrectly proscribed drugs such as methylphenidate and some tricyclic antidepressants. It also illustrates the straightforward “bridging” methods that may be used to transition simply and safely from other antidepressants to MAOIs.
Racial and ethnic groups in the USA differ in the prevalence of posttraumatic stress disorder (PTSD). Recent research however has not observed consistent racial/ethnic differences in posttraumatic stress in the early aftermath of trauma, suggesting that such differences in chronic PTSD rates may be related to differences in recovery over time.
Methods
As part of the multisite, longitudinal AURORA study, we investigated racial/ethnic differences in PTSD and related outcomes within 3 months after trauma. Participants (n = 930) were recruited from emergency departments across the USA and provided periodic (2 weeks, 8 weeks, and 3 months after trauma) self-report assessments of PTSD, depression, dissociation, anxiety, and resilience. Linear models were completed to investigate racial/ethnic differences in posttraumatic dysfunction with subsequent follow-up models assessing potential effects of prior life stressors.
Results
Racial/ethnic groups did not differ in symptoms over time; however, Black participants showed reduced posttraumatic depression and anxiety symptoms overall compared to Hispanic participants and White participants. Racial/ethnic differences were not attenuated after accounting for differences in sociodemographic factors. However, racial/ethnic differences in depression and anxiety were no longer significant after accounting for greater prior trauma exposure and childhood emotional abuse in White participants.
Conclusions
The present findings suggest prior differences in previous trauma exposure partially mediate the observed racial/ethnic differences in posttraumatic depression and anxiety symptoms following a recent trauma. Our findings further demonstrate that racial/ethnic groups show similar rates of symptom recovery over time. Future work utilizing longer time-scale data is needed to elucidate potential racial/ethnic differences in long-term symptom trajectories.
Substantial progress has been made in the standardization of nomenclature for paediatric and congenital cardiac care. In 1936, Maude Abbott published her Atlas of Congenital Cardiac Disease, which was the first formal attempt to classify congenital heart disease. The International Paediatric and Congenital Cardiac Code (IPCCC) is now utilized worldwide and has most recently become the paediatric and congenital cardiac component of the Eleventh Revision of the International Classification of Diseases (ICD-11). The most recent publication of the IPCCC was in 2017. This manuscript provides an updated 2021 version of the IPCCC.
The International Society for Nomenclature of Paediatric and Congenital Heart Disease (ISNPCHD), in collaboration with the World Health Organization (WHO), developed the paediatric and congenital cardiac nomenclature that is now within the eleventh version of the International Classification of Diseases (ICD-11). This unification of IPCCC and ICD-11 is the IPCCC ICD-11 Nomenclature and is the first time that the clinical nomenclature for paediatric and congenital cardiac care and the administrative nomenclature for paediatric and congenital cardiac care are harmonized. The resultant congenital cardiac component of ICD-11 was increased from 29 congenital cardiac codes in ICD-9 and 73 congenital cardiac codes in ICD-10 to 318 codes submitted by ISNPCHD through 2018 for incorporation into ICD-11. After these 318 terms were incorporated into ICD-11 in 2018, the WHO ICD-11 team added an additional 49 terms, some of which are acceptable legacy terms from ICD-10, while others provide greater granularity than the ISNPCHD thought was originally acceptable. Thus, the total number of paediatric and congenital cardiac terms in ICD-11 is 367. In this manuscript, we describe and review the terminology, hierarchy, and definitions of the IPCCC ICD-11 Nomenclature. This article, therefore, presents a global system of nomenclature for paediatric and congenital cardiac care that unifies clinical and administrative nomenclature.
The members of ISNPCHD realize that the nomenclature published in this manuscript will continue to evolve. The version of the IPCCC that was published in 2017 has evolved and changed, and it is now replaced by this 2021 version. In the future, ISNPCHD will again publish updated versions of IPCCC, as IPCCC continues to evolve.
Research using fMRI indicates that sustained limbic activity is linked to processing negative words and self-reported rumination in currently depressed individuals. It is unknown whether this is also present in remitted depressed individuals. We tested the hypothesis that a tendency to ruminate constitutes a trait for depression by using a standard covert fMRI emotional task face in previously and never depressed volunteers and postulated that high rumination scores would correlate with activity in brain areas previously associated with depression.
Methods:
37 controls (25 female) and 30 remitted depressed (RD, 22 female) were enrolled. Volunteers completed the Ruminative Responses Scale (RRS) and underwent fMRI scanning using a standard covert fMRI emotional task faces. Significance level was set at p < 0.05 (FWE).
Results:
With RRS score controlled for RD showed reduced subcortical and limbic activity to sad and fearful faces compared to controls. Correlations between RRS scores and neural activity in all participants and control participants alone were very limited. However, in RD, RRS score was negatively correlated with neural response to happy faces and positively correlated with neural response to sad and fearful faces, in cortical and limbic regions associated with depression (hippocampus, thalamus, caudate, insula and cingulate gyrus).
Conclusion:
The results suggest that reduced limbic activity is associated with remission, possibly as a maintenance mechanism. However, within the remitted group the more ruminative participants show greater response in these areas to negative stimuli, and less to positive stimuli. This could be a neurobiological marker for risk of relapse
Research using fMRI indicates that sustained limbic activity is linked to processing negative words and self-reported rumination in currently depressed individuals. It is unknown whether this is also present in remitted depressed individuals. We tested the hypothesis that a tendency to ruminate constitutes a trait for depression by using a standard covert fMRI emotional task face in previously and never depressed volunteers and postulated that high rumination scores would correlate with activity in brain areas previously associated with depression.
Methods:
37 controls (25 female) and 30 remitted depressed (RD, 22 female) were enrolled. Volunteers completed the Ruminative Responses Scale (RRS) and underwent fMRI scanning using a standard covert fMRI emotional task faces. Significance level was set at p < 0.05 (FWE).
Results:
With RRS score controlled for RD showed reduced subcortical and limbic activity to sad and fearful faces compared to controls. Correlations between RRS scores and neural activity in all participants and control participants alone were very limited. However, in RD, RRS score was negatively correlated with neural response to happy faces and positively correlated with neural response to sad and fearful faces, in cortical and limbic regions associated with depression (hippocampus, thalamus, caudate, insula and cingulate gyrus).
Conclusion:
The results suggest that reduced limbic activity is associated with remission, possibly as a maintenance mechanism. However, within the remitted group the more ruminative participants show greater response in these areas to negative stimuli, and less to positive stimuli. This could be a neurobiological marker for risk of relapse.
There is increasing evidence for a neurobiological basis of antisocial personality disorder (ASPD), includinggenetic liability, aberrant serotonergic function, neuropsychological deficits and structural and functional brain abnormalities. However, few functional brain imaging studies have been conducted using tasks of clinically relevant functions such as impulse control and reinforcement processing. Here we report on a study investigating the neural basis of behavioural inhibition and reward sensitivity in ASPD using functional magnetic resonance imaging (fMRI).
Methods
17 medication-free male individuals with DSM IV ASPD and 14 healthy controls were included. All subjects were screened for Axis I pathology and substance misuse. Scanner tasks included two block design tasks: one Go/No-Go task and one reward task. Scanning was carried out on a 1.5T Phillips system. Whole brain coverage was achieved using 40 axial slices with 3.5mm spacing a TR of 5 seconds. Data were analysed using SPM5 using random effects models.
Results
Results of the Go/No-Go task confirmed brain activation previously described in the processing of impulse inhibition, namely in the orbitofrontal and dorsolateral prefrontal cortex and the anterior cingulate, and these were enhanced in the PD group. The reward task was associated with BOLD response changes in the reward network in both groups. However, these BOLD responses were reduced in the ASPD group, particularly in prefrontal areas.
Conclusions
Our results further support the notion of prefrontal dysfunction in ASPD. However, contrary to previous studies suggesting “hypofrontality” in this disorder, we found task specific increased and decreased BOLD responses.
In this volume,experts from a range of disciplines use a variety of perspectives, notably those of public health, criminology, ecology, and developmental psychology, to review research on the causes of youth violence in the nation's schools and communities and on school-based interventions that have prevented or reduced it. They describe and evaluate strategies for the prevention and treatment of violence that go beyond punishment and incarceration. The volume offers a strategy for the problem of youth violence, arguing that the most effective interventions use a comprehensive, multi-disciplinary approach and take into account differences in stages of individual development and involvement in overlapping social contexts, families, peer groups, schools and neighborhoods. This book can be used profitably by school teachers and administrators, scholars, policy makers, and those who work with young people at risk, as well as by the general reader who is concerned with current social problems.
The mineral in bones and teeth is an impure form of hydroxylapatite (HAP), the principal impurity being 2—5 wt.% carbonate. This mineral dissolves during remodelling of bone and also in dental caries as a result of the action of acids produced by osteoclasts and by bacteria, respectively. In enamel, demineralization proceeds with preferential loss of carbonate relative to phosphate. Surprisingly, in the early stages, the demineralization is subsurface. In order to facilitate the understanding of physical chemical aspects of these processes, we have undertaken studies of demineralization in model systems. We give three examples here. The first two used scanning microradiography in which the specimen is stepped across a 10—30 μm diameter X-ray beam. Intensity measurements allow calculation of the mineral mass per unit area in the X-ray path through the specimen. In the first experiment, porous HAP sections were separated from a reservoir of acidic buffer by a column initially filled with water (the diffusion length) and scanned with the X-ray beam perpendicular to the axis of the diffusion length. The rate of total loss of mineral along each profile was calculated from the scans. The rate of demineralization fell as the diffusion length increased. We believe the explanation is that the rate-controlling step is the diffusion of dissolved HAP away from the solid to the buffer reservoir. In the second experiment, demineralizing solution and water were pumped alternately, for equal lengths of time, past blocks of porous HAP or enamel. The X-ray beam was perpendicular to the exposed surface. As the rate of switching between solutions decreased, the mean rate of demineralization also fell. We propose that this effect is due to retention of acid in the pores of the HAP during the time when water flows, allowing further demineralization to take place during this time. The third study used X-ray microtomography, a form of 3D microscopy, to study the loss of mineral in compacted carbonate apatite powders. The powders were packed in six 10 mm internal diameter acrylic cylinders to a depth of 4 mm (after pressing). One end was covered with a porous polyethylene disc and each tube placed in acidic buffer for 70 days. Periodic examination by microtomography showed the development of subsurface demineralization. Infrared spectroscopy of the dissected-out surface layers showed preferential loss of carbonate over phosphate by comparison with deeper layers. Rietveld analysis of X-ray powder diffraction data showed changes in the crystallographic structures of the apatites between the initial and dissected-out apatite.
The Arizona Department of Health Services identified unusually high levels of influenza activity and severe complications during the 2015–2016 influenza season leading to concerns about potential increased disease severity compared with prior seasons. We estimated state-level burden and severity to compare across three seasons using multiple data sources for community-level illness, hospitalisation and death. Severity ratios were calculated as the number of hospitalisations or deaths per community case. Community influenza-like illness rates, hospitalisation rates and mortality rates in 2015–2016 were higher than the previous two seasons. However, ratios of severe disease to community illness were similar. Arizona experienced overall increased disease burden in 2015–2016, but not increased severity compared with prior seasons. Timely estimates of state-specific burden and severity are potentially feasible and may provide important information during seemingly unusual influenza seasons or pandemic situations.
A high proportion of patients with remitted major depressive disorder (MDD) will experience recurring episodes, whilst some develop resilience and remain in recovery. The neural basis of resilience to recurrence is elusive. Abnormal resting-state connectivity of the subgenual cingulate cortex (sgACC) was previously found in cross-sectional studies of MDD, suggesting its potential pathophysiological importance. The current study aimed to investigate whether resting-state connectivity to a left sgACC seed region distinguishes resilient patients from those developing recurring episodes.
Method
A total of 47 medication-free remitted MDD patients and 38 healthy controls underwent resting-state functional magnetic resonance imaging (fMRI) at baseline. Over 14 months, 30 patients remained resilient whilst 17 experienced a recurring episode.
Results
Attenuated interhemispheric left-to-right sgACC connectivity distinguished the resilient from the recurring-episode and control groups and was not correlated with residual depressive symptoms.
Conclusions
The current study revealed a neural signature of resilience to recurrence in MDD and thereby elucidates the role of compensatory adaptation in sgACC networks.
Gamma-ray burst host galaxies are deficient in molecular gas, and show anomalous metal-poor regions close to GRB positions. Using recent Australia Telescope Compact Array (ATCA) Hi observations we show that they have substantial atomic gas reservoirs. This suggests that star formation in these galaxies may be fuelled by recent inflow of metal-poor atomic gas. While this process is debated, it can happen in low-metallicity gas near the onset of star formation because gas cooling (necessary for star formation) is faster than the Hi-to-H2 conversion.
The incidence of papillary thyroid cancer is rising, with an increase in the number of microcarcinomas being discovered. There is controversy in the literature regarding the optimal management of these tumours. This study aimed to review our institution's experience with the presentation and management of papillary thyroid microcarcinoma.
Methods:
Retrospective analysis from the Sydney Head and Neck Cancer Institute, from 1987 to 2009.
Results:
A total of 228 patients were analysed. Papillary thyroid microcarcinomas were discovered incidentally in 116 (50.9 per cent) patients and non-incidentally in the remaining 112 (49.1 per cent) patients. Amongst the non-incidental group, 11.6 per cent of patients presented with lateral cervical lymph node involvement. Non-incidental microcarcinomas were significantly associated with younger age (<45 years) (p = 0.007) and larger tumours (5–10 mm) (p < 0.001). Only four patients in the incidental group suffered recurrent disease (locoregional). No patient developed distant metastatic disease or died during follow up.
Conclusion:
Papillary thyroid microcarcinomas present both incidentally and non-incidentally, with equal prevalence. Non-incidental tumours not infrequently present with cervical lymph node disease. The patient outcome is generally excellent.