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Olfactory dysfunction represents one of the most frequent symptoms of coronavirus disease 2019, affecting about 70 per cent of patients. However, the pathogenesis of the olfactory dysfunction in coronavirus disease 2019 has not yet been elucidated.
This report presents the radiological and histopathological findings of a patient who presented with anosmia persisting for more than three months after infection with severe acute respiratory syndrome coronavirus-2.
The biopsy demonstrated significant disruption of the olfactory epithelium. This shifts the focus away from invasion of the olfactory bulb and encourages further studies of treatments targeted at the surface epithelium.
This chapter provides an overview of the key areas of agreement and debate about workaholism, particularly its conceptualization, prevention, and treatment. The chapter integrates biomedical and health psychology perspectives with a view to challenging and advancing understanding on how to prevent people from developing a problematic relationship with work, and how best to support those experiencing the problem. The chapter begins by reviewing the conceptualization of workaholism, and then reviews the existing evidence concerning the main correlates and vulnerability factors. This discussion then leads to an exploration into alternative ways that workaholism can be theorized, in particular biopsychosocial models and critical theory of addiction. Building upon this combined theoretical perspective, the chapter ends by reviewing and speculating on different aspects of prevention and treatment according to the different stakeholders involved.
This chapter provides a brief overview of gaming disorder (GD) and its treatment. There are now over twenty different screens for assessing problematic gaming although relatively few have used nationally representative samples. The prevalence rates in these nationally representative studies have ranged from 1.2 percent to 8.5 percent depending upon country and screening instrument used. There have been a number of studies describing treatment of GD, although many of these tend not to distinguish between Internet Use Disorder and GD. In terms of treatment for GD, both psychological and pharmacological approaches have been adopted. More specifically, psychological treatment using a cognitive-behavioral framework (CBT) appears to be the most widely used. Furthermore, pharmacological treatment using opioid receptor antagonists, antidepressants, antipsychotics, opioid receptor antagonists, and psychostimulants has been reported in the literature. It is concluded that standardized and comprehensive methods of diagnosis are at present lacking, and that further research into GD is needed from clinical, epidemiological, cross-cultural, and neurobiological perspectives of GD.
The authors offer their appreciation of the astute commentaries by Scott and Pilkonis and Niedtfeld, Paret, and Schmahl regarding their chapter on borderline personality disorder. Scott and Pilkonis address some very important big picture themes regarding the conceptualization, etiology, and treatment of BPD, and Niedtfeld et al. more specifically comment on innovative research highlighting the interplay of neuroscience and psychotherapy. In this rejoinder, the authors comment on these and other issues and suggest that a developmental psychopathology framework for theory and research has promise for illuminating the nature and etiology of BPD and highlighting important directions for prevention and treatment.
This commentary expands on some key issues in the assessment, developmental psychopathology, and treatment of borderline personality disorder (BPD). The authors review evidence suggesting that BPD severity can be assessed along a continuum based on number of DSM criteria, which form a unitary dimension. However, to advance the clinical impact of alternative trait-based dimensional models of BPD, there is a need for measures and clinically validated thresholds that can inform early detection, diagnosis, and treatment planning along the full spectrum of BPD severity and at various stages of its development. They also highlight the importance of longitudinal studies examining dynamic transactional processes contributing to the onset and developmental course of BPD that have implications for individual and family-based interventions and prevention efforts. Regarding treatment, the authors emphasize the importance of addressing functional impairments in major social roles and improving interpersonal relatedness with close attachment figures as valuable means for improving emotion regulation and enhancing long-term recovery and rehabilitation from BPD. Finally, they encourage the use of assessment and analytic strategies capable of modeling idiographic dynamic processes, which may lead to the development of person-specific case conceptualization and treatment approaches.
Characterized by a combination of interpersonal, emotional, behavioral, and cognitive instability, borderline personality disorder (BPD) is a serious and often misunderstood condition. The prevalence of BPD is approximately 1.4 to 6%, with substantially higher estimates among psychiatric outpatients and inpatients. Beyond the personal costs of BPD in terms of suffering, BPD is strongly associated with functional impairment and high societal costs for mental healthcare. Clinical descriptions of BPD first appeared before the mid-twentieth century and have evolved to the present conceptualization of an overarching BPD construct represented by the key domains of emotion dysregulation, impulsivity, and interpersonal disturbance. BPD has a varying course, with many individuals achieving remission or recovery, but emotional and interpersonal vulnerabilities and functional impairments often persist for many years, even after structured treatment. The success of treatment for BPD over the past few decades, however, has countered common clinical lore that BPD patients are recalcitrant. Further, novel developments in research on the putative core vulnerabilities underlying BPD, as well as evidence that these vulnerabilities can be addressed in treatment, illuminate important future directions and hope for patients and loved ones affected by this disorder.
The Charles Bonnet syndrome is characterized by the occurrence of visual hallucinations in elderly people, but without any mental disorders. Two clinical cases are described. An etiological and physiopathological theory is proposed, based on vascular pathology, lack of visual stimulation and a psychodynamic component.
This brief essay reviews the chapter by William Bechtel which explores the optimal conceptual framework with which to understand the etiology of psychiatric disorders. Bechtel’s tentative answer to that question -- altered functioning of a network of control mechanisms – is then taken on a road test and applied to three current etiologic theories for psychiatric illness – two for schizophrenia and one for panic disorder. While they do not all fit perfectly within Bechtel’s framework, its application provides useful insights into the nature of the explanations current extant in the field.
Several observational studies have investigated the association of insomnia with psychiatric disorders. Such studies yielded mixed results, and whether these associations are causal remains unclear. Thus, we aimed to identify the causal relationships between insomnia and five major psychiatric disorders.
The analysis was implemented with six genome-wide association studies; one for insomnia and five for psychiatric disorders (attention-deficit/hyperactivity disorder, autism spectrum disorder, major depressive disorder, schizophrenia, and bipolar disorder). A heterogeneity in dependent instrument (HEIDI) approach was used to remove the pleiotropic instruments, Mendelian randomization (MR)-Egger regression was adopted to test the validity of the screened instruments, and bidirectional generalized summary data-based MR was performed to estimate the causal relationships between insomnia and these major psychiatric disorders.
We observed significant causal effects of insomnia on the risk of autism spectrum disorder and bipolar disorder, with odds ratios of 1.739 (95% confidence interval: 1.217–2.486, p = 0.002) and 1.786 (95% confidence interval: 1.396–2.285, p = 4.02 × 10−6), respectively. There was no convincing evidence of reverse causality for insomnia with these two disorders (p = 0.945 and 0.546, respectively). When insomnia was considered as either the exposure or outcome variable, causal estimates for the remaining three psychiatric disorders were not significant.
Our results suggest a causal role of insomnia in autism spectrum disorder and bipolar disorder. Future disease models should include insomnia as a factor for these two disorders to develop effective interventions. More detailed mechanism studies may also be inspired by this causal inference.
This study used repeated measures data to identify developmental profiles of elevated risk for ADHD (i.e., six or more inattentive and/or hyperactive-impulsive symptoms), with an interest in the age at which ADHD risk first emerged. Risk factors that were measured across the first 3 years of life were used to predict profile membership. Participants included 1,173 children who were drawn from the Family Life Project, an ongoing longitudinal study of children's development in low-income, nonmetropolitan communities. Four heuristic profiles of ADHD risk were identified. Approximately two thirds of children never exhibited elevated risk for ADHD. The remaining children were characterized by early childhood onset and persistent risk (5%), early childhood limited risk (10%), and middle childhood onset risk (19%). Pregnancy and delivery complications and harsh-intrusive caregiving behaviors operated as general risk for all ADHD profiles. Parental history of ADHD was uniquely predictive of early onset and persistent ADHD risk, and low primary caregiver education was uniquely predictive of early childhood limited ADHD risk. Results are discussed with respect to how changes to the age of onset criterion for ADHD in DSM5 may affect etiological research and the need for developmental models of ADHD that inform ADHD symptom persistence and desistance.
Objective: Post-stroke cognitive impairment is common, but mechanisms and risk factors are poorly understood. Frailty may be an important risk factor for cognitive impairment after stroke. We investigated the association between pre-stroke frailty and acute post-stoke cognition. Methods: We studied consecutively admitted acute stroke patients in a single urban teaching hospital during three recruitment waves between May 2016 and December 2017. Cognition was assessed using the Mini-Montreal Cognitive Assessment (min=0; max=12). A Frailty Index was used to generate frailty scores for each patient (min=0; max=100). Clinical and demographic information were collected, including pre-stroke cognition, delirium, and stroke-severity. We conducted univariate and multiple-linear regression analyses with covariates forced in (covariates included were: age, sex, stroke severity, stroke-type, pre-stroke cognitive impairment, delirium, previous stroke/transient ischemic attack) to investigate the association between pre-stroke frailty and post-stroke cognition. Results: Complete data were available for 154 stroke patients. Mean age was 68 years (SD=11; range=32–97); 93 (60%) were male. Median mini-Montreal Cognitive Assessment score was 8 (IQR=4–12). Mean Frailty Index score was 18 (SD=11). Pre-stroke cognitive impairment was apparent in 13/154 (8%) patients. Pre-stroke frailty was significantly associated with lower post-stroke cognition (Standardized-Beta=−0.40; p<0.001) and this association was independent of covariates (Unstandardized-Beta=−0.05; p=0.005). Additional significant variables in the multiple regression model were age (Unstandardized-Beta=−0.05; p=0.002), delirium (Unstandardized-Beta=−2.81; p<0.001), pre-stroke cognitive impairment (Unstandardized-Beta=−2.28; p=0.001), and stroke-severity (Unstandardized-Beta=−0.20; p<0.001). Conclusions: Pre-stroke frailty may be a moderator of post-stroke cognition, independent of other well-established post-stroke cognitive impairment risk factors. (JINS, 2019, 25, 501–506)
Until recently, nodding syndrome (NS) was considered as a mysterious disease of unknown etiology. A link between onchocerciasis and epilepsy was suspected for a long time. However, onchocerciasis was not considered as the cause of NS because NS was believed to occur only in onchocerciasis-endemic regions in Uganda, South Sudan, and Tanzania. In October 2015, with funding from the European Research Council, the NSETHIO group launched a trans-disciplinary, multi-country research project to identify the cause of NS and to study the link between onchocerciasis and epilepsy.
We reviewed NSETHIO activities as well as all published papers, and compared project findings with results of previous research on NS.
Findings from the NSETHIO project showed that NS is only one of the clinical manifestations in the wide spectrum of onchocerciasis-associated epilepsy (OAE) that could be prevented by strengthening onchocerciasis elimination programs. NSETHIO demonstrated that OAE is an important neglected public health problem in onchocerciasis-endemic areas with no or a sub-optimally functioning onchocerciasis control strategies.
Today there is overwhelming evidence that NS together with the Nakalanga syndrome is clinical presentations of OAE, a condition that could be prevented by strengthening onchocerciasis elimination programs. While research needs to continue to elucidate the pathophysiological mechanisms causing NS, new strategies to accelerate onchocerciasis elimination coupled with community-based surveillance and treatment programs for epilepsy are urgently needed in areas of high Onchocerca volvulus transmission.
Suicide is a major global health concern. Bhutanese refugees resettled in the USA are disproportionately affected by suicide, yet little research has been conducted to identify factors contributing to this vulnerability. This study aims to investigate the issue of suicide of Bhutanese refugee communities via an in-depth qualitative, social-ecological approach.
Focus groups were conducted with 83 Bhutanese refugees (adults and children), to explore the perceived causes, and risk and protective factors for suicide, at individual, family, community, and societal levels. Audio recordings were translated and transcribed, and inductive thematic analysis conducted.
Themes identified can be situated across all levels of the social-ecological model. Individual thoughts, feelings, and behaviors are only fully understood when considering past experiences, and stressors at other levels of an individual's social ecology. Shifting dynamics and conflict within the family are pervasive and challenging. Within the community, there is a high prevalence of suicide, yet major barriers to communicating with others about distress and suicidality. At the societal level, difficulties relating to acculturation, citizenship, employment and finances, language, and literacy are influential. Two themes cut across several levels of the ecosystem: loss; and isolation, exclusion, and loneliness.
This study extends on existing research and highlights the necessity for future intervention models of suicide to move beyond an individual focus, and consider factors at all levels of refugees’ social-ecology. Simply focusing treatment at the individual level is not sufficient. Researchers and practitioners should strive for community-driven, culturally relevant, socio-ecological approaches for prevention and treatment.
Prior work has indicated both theoretical and empirical overlap between social and physical aggression. The extent to which their covariance can be explained by the same underlying genetic or environmental factors, however, remains unclear. It is also uncertain whether or how the origins of their covariance might vary across sex. The current study sought to fill these gaps in the literature.
We examined maternal and teacher reports of youth physical and social aggression in over 1000 6–10 years old (mean age = 8.02 years) twin pairs from the Michigan State University Twin Registry. We made use of the bivariate correlated factors model to clarify the origins of their association. We further tested both sex difference and no-sex difference versions of that model to determine whether there are sex differences in the association between social and physical aggression, as often assumed.
The covariation between social and physical aggression was due to overlapping genetic factors and common environmental conditions. Specifically, 50–57% of the genetic factors, 74–100% of the shared environmental factors, and 28–40% of the unique environmental factors influencing physical aggression also influenced social aggression according to both mother and teacher reports. These shared etiological factors did not differ across sex.
These findings argue against the common assumption that social aggression is the ‘female version’ of male physical aggression, and instead suggest that social aggression may be best conceptualized as a form of antisocial behavior that shares developmental pathways with other manifestations of externalizing pathology.
Punitive parenting and stressful life events are associated with obsessive-compulsive symptoms (OCS). However, the lack of longitudinal, genetically-informative studies means it remains unclear whether these factors represent environmentally-mediated risks for the development of OCS.
Twins and siblings from the Genesis1219 study completed self-report questionnaires two years apart (Time 1: N = 2616, mean age = 15.0; Time 2: N = 1579, mean age = 17.0 years) assessing OCS, maternal and paternal punitive parenting, and dependent stressful life events. Multiple regression models tested cross-sectional and longitudinal associations between the putative environmental risk factors and obsessive-compulsive symptoms using: (a) individual scores; and (b) monozygotic twin difference scores. The aetiologies of significant phenotypic associations between putative risk factors and OCS were further examined using multivariate genetic models.
At a phenotypic level, maternal and paternal punitive parenting and stressful life events were all associated with OCS both cross-sectionally and longitudinally. However, only stressful life events predicted the subsequent development of OCS, after controlling for earlier symptoms. Genetic models indicated that the association between life events and change in OCS symptoms was due to both genetic (48%) and environmental (52%) influences. Overall, life events associated with change in OCS accounted for 1.2% of variation in OCS at Time 2.
Stressful life events, but not punitive parenting, predict OCS change during adolescence at a phenotypic level. This association exists above and beyond genetic confounding, consistent with the hypothesis that stressful life events play a causal role in the development of obsessive-compulsive symptoms.
Northeastern China is a region of high tick abundance, multiple tick-borne pathogens and likely human infections. The spectrum of diseases caused by tick-borne pathogens has not been objectively evaluated in this region for clinical management and for comparison with other regions globally where tick-transmitted diseases are common. Based on clinical symptoms, PCR, indirect immunofluorescent assay and (or) blood smear, we identified and described tick-borne diseases from patients with recent tick bite seen at Mudanjiang Forestry Central Hospital. From May 2010 to September 2011, 42% (75/180) of patients were diagnosed with a specific tick-borne disease, including Lyme borreliosis, tick-borne encephalitis, human granulocytic anaplasmosis, human babesiosis and spotted fever group rickettsiosis. When we compared clinical and laboratory features to identify factors that might discriminate tick-transmitted infections from those lacking that evidence, we revealed that erythema migrans and neurological manifestations were statistically significantly differently presented between those with and without documented aetiologies (P < 0.001, P = 0.003). Twelve patients (6.7%, 12/180) were co-infected with two tick-borne pathogens. We demonstrated the poor ability of clinicians to identify the specific tick-borne disease. In addition, it is necessary to develop specific laboratory assays for optimal diagnosis of tick-borne diseases.
Delirium is heterogeneous and can vary by etiology.
We sought to determine how delirium subtyped by etiology affected six-month function and cognition.
Prospective cohort study.
Tertiary care, academic medical center.
A total of 228 hospitalized patients > 65 years old were admitted from the emergency department (ED).
The modified Brief Confusion Assessment Method was used to determine delirium in the ED. Delirium etiology was determined by three trained physician reviewers using a Delirium Etiology checklist. Pre-illness and six-month function and cognition were determined using the Older American Resources and Services Activities of Daily Living (OARS ADL) questionnaire and the short-form Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE). Multiple linear regression was performed to determine if delirium etiology subtypes were associated with six-month function and cognition adjusted for baseline OARS ADL and IQCODE. Two-factor interactions were incorporated to determine pre-illness function or cognition-modified relationships between delirium subtypes and six-month function and cognition.
In patients with poorer pre-illness function only, delirium secondary to metabolic disturbance (β coefficient = −2.9 points, 95%CI: −0.3 to −5.6) and organ dysfunction (β coefficient = −4.3 points, 95%CI: −7.2 to −1.4) was significantly associated with poorer six-month function. In patients with intact cognition only, delirium secondary to central nervous system insults was significantly associated with poorer cognition (β coefficient = 0.69, 95%CI: 0.19 to 1.20).
Delirium is heterogeneous and different etiologies may have different prognostic implications. Furthermore, the effect of these delirium etiologies on outcome may be dependent on the patient's pre-illness functional status and cognition.
Social aggression is a form of antisocial behavior in which social relationships and social status are used to damage reputations and inflict emotional harm on others. Despite extensive research examining the prevalence and consequences of social aggression, only a few studies have examined its genetic–environmental etiology, with markedly inconsistent results.
We estimated the etiology of social aggression using the nuclear twin family (NTF) model. Maternal-report, paternal-report, and teacher-report data were collected for twin social aggression (N = 1030 pairs). We also examined the data using the classical twin (CT) model to evaluate whether its strict assumptions may have biased previous heritability estimates.
The best-fitting NTF model for all informants was the ASFE model, indicating that additive genetic, sibling environmental, familial environmental, and non-shared environmental influences significantly contribute to the etiology of social aggression in middle childhood. However, the best-fitting CT model varied across informants, ranging from AE and ACE to CE. Specific heritability estimates for both NTF and CT models also varied across informants such that teacher reports indicated greater genetic influences and father reports indicated greater shared environmental influences.
Although the specific NTF parameter estimates varied across informants, social aggression generally emerged as largely additive genetic (A = 0.15–0.77) and sibling environmental (S = 0.42–0.72) in origin. Such findings not only highlight an important role for individual genetic risk in the etiology of social aggression, but also raise important questions regarding the role of the environment.
This article focuses on the consolidation of naval hygiene practices during the Victorian era, a period of profound medical change that coincided with the fleet’s transition from sail to steam. The ironclads of the mid- to late- nineteenth century offered ample opportunities to improve preventive medicine at sea, and surgeons capitalised on new steam technologies to provide cleaner, dryer, and airier surroundings below decks. Such efforts reflected the sanitarian idealism of naval medicine in this period, inherited from the eighteenth-century pioneers of the discipline. Yet, despite the scientific thrust of Victorian naval medicine, with its emphasis on collecting measurements and collating statistics, consensus about the causes of disease eluded practitioners. It proved almost impossible to eradicate sickness at sea, and the enclosed nature of naval vessels showed the limitations – rather than the promise – of attempting to enforce absolute environmental controls. Nonetheless, sanitarian ideology prevailed throughout the steam age, and the hygienic reforms enacted throughout the fleet showed some of the same successes that attended the public health movement on land. It was thus despite shifting ideas about disease and new methods of investigation that naval medicine remained wedded to its sanitarian roots until the close of the nineteenth century.
HIV-positive individuals are at significantly increased risk of depression. In low- and middle-income countries, depression is frequently under-detected, hampered by a lack of data regarding available screening tools. The 5-item World Health Organization Well-Being Index (WHO-5) is widely used to screen for depression, yet its validity in African adults with HIV has yet to be examined.
In this cross-sectional study, we enrolled HIV-positive adults presenting to an outpatient HIV clinic in Mwanza, Tanzania. Patients were administered the Patient Health Questionnaires (PHQ)-2/9 and WHO-5 questionnaires. The rate of positive screens was calculated. Fisher's exact test and Pearson's correlation coefficients between PHQ-2/9 and WHO-5 scores were calculated.
We enrolled 72 HIV-positive adults: rates of positive depression screen were 62.5%, 77.8%, and 47.2% according to PHQ-2, PHQ-9, and WHO-5, respectively. PHQ and WHO results for depression were significantly associated (Fisher's exact test: PHQ-2 v. WHO-5, p = 0.028; PHQ-9 v. WHO-5, p = 0.002). The level of correlation between PHQ and WHO results for depression was moderate (Pearson's correlation coefficient: PHQ-2 v. WHO-5 −0.3289; PHQ-9 v. WHO-5 −0.4463).Per Mantel–Haenszel analysis, screening results were significantly more concordant among patients in the following strata: men, age >40, Sukuma ethnicity, Christian, unmarried, self-employed, at least primary school education completed, and higher than the median income level.
WHO-5 scores correlated well with those of the PHQ-9, suggesting that the WHO-5 represents a valid screening tool. The concordance of PHQ-9 and WHO-5 results was poorer in marginalized socioeconomic groups. Positive depression screens were exceedingly common among HIV-positive Tanzanian adults according to all three questionnaires.