Abstract Introduction: Postpartum psychosis is one of the severest psychiatric disorders to occur in the postpartum period. If it requires a woman’s admission, a psychiatric mother baby unit is recommended, where care will focus on the mother’s health, the mother-baby dyad, and their next of kin. To date, few studies have examined nursing interventions for patients with postpartum psychosis. Aim: Identifying nursing interventions used at a psychiatric mother baby unit, when a patient is hospitalized with postpartum psychosis. Method: A qualitative design using thematic analysis. Data was collected using semi-structured interviews (N=13) with expert nurses working at such a unit. Results: The analysis identified three themes: 1. Treatment of the mental disorder, which involves interventions to improve the mother’s mental and physical wellbeing; 2. Care for the mother-baby dyad, which involves interventions intended to promote safe interactions between mother and baby; and 3. Care for the partner, which involves interventions to improve the partner’s wellbeing. Discussion: Overall, within each of these themes, nurses described the urgency to tailor interventions to the needs of the patient, baby and partner. Implications to practice: Our comprehensive description of interventions can be used for the improvement of nursing care for patients hospitalized with postpartum psychosis.
The aim of this study is to obtain insight, from a patient's perspective, into the results and essential components of treatment in specialist settings for so-called ‘difficult’ patients in mental health care. In cases where usual hospital treatment is not successful, a temporary transfer to another, specialist hospital may provide a solution. We investigated which aspects of specialist treatment available to ‘difficult’ patients are perceived as essential by the patients and what are the results of this treatment in their perception. A qualitative research design based on the Grounded Theory method was used. To generate data, 14 semi-structured interviews were held with 12 patients who were admitted to a specialist hospital in the Netherlands. Almost all respondents rated the results of the specialist treatment as positive. The therapeutic climate was perceived as extremely strict, with a strong focus on structure, cooperation and safety. This approach had a stabilizing effect on the patients, even at times when they were not motivated. Most patients developed a motivation for change, marked by a growing and more explicit determination of their future goals. We concluded that a highly structured treatment environment aimed at patient stabilization is helpful to most ‘difficult’ patients.
"Background: Victimization is highly prevalent in individuals with mild intellectual disability (MID) or borderline intellectual functioning (BIF) and is an important risk factor for mental health problems and violent behavior. Not much is known, however, about victimization history in women with MID-BIF admitted to forensic mental health care. Aims: The aim of this multicenter study is to gain insight into victimization histories and mental health problems of female forensic psychiatric patients with MID-BIF. Methods: File data were analyzed of 126 women with MID-BIF who have been admitted to one of five Dutch forensic psychiatric hospitals between 1990 and 2014 and compared to data of 76 female patients with average or above intellectual functioning and to a matched sample of 31 male patients with MID-BIF. Results: All forensic paients had high rates of victimization, but women with MID-BIF showed an even higher prevalence of victimization during both childhood and adulthood and more complex psychopathology compared to female patients without MID-BIF. Compared to male forensic patients with MID-BIF, women with MID-BIF were more often victim of sexual abuse during childhood. During adulthood, the victimization rate in these women was more than three times higher than in men. Conclusions: Victimization is a salient factor in female forensic patients with MID-BIF and more gender-responsive trauma-focused treatment is needed."
Huntington’s disease (HD) and various spinocerebellar ataxias (SCA) are autosomal dominantly inherited neurodegenerative disorders caused by a CAG repeat expansion in the disease-related gene1. The impact of HD and SCA on families and individuals is enormous and far reaching, as patients typically display first symptoms during midlife. HD is characterized by unwanted choreatic movements, behavioral and psychiatric disturbances and dementia. SCAs are mainly characterized by ataxia but also other symptoms including cognitive deficits, similarly affecting quality of life and leading to disability. These problems worsen as the disease progresses and affected individuals are no longer able to work, drive, or care for themselves. It places an enormous burden on their family and caregivers, and patients will require intensive nursing home care when disease progresses, and lifespan is reduced. Although the clinical and pathological phenotypes are distinct for each CAG repeat expansion disorder, it is thought that similar molecular mechanisms underlie the effect of expanded CAG repeats in different genes. The predicted Age of Onset (AO) for both HD, SCA1 and SCA3 (and 5 other CAG-repeat diseases) is based on the polyQ expansion, but the CAG/polyQ determines the AO only for 50% (see figure below). A large variety on AO is observed, especially for the most common range between 40 and 50 repeats11,12. Large differences in onset, especially in the range 40-50 CAGs not only imply that current individual predictions for AO are imprecise (affecting important life decisions that patients need to make and also hampering assessment of potential onset-delaying intervention) but also do offer optimism that (patient-related) factors exist that can delay the onset of disease.To address both items, we need to generate a better model, based on patient-derived cells that generates parameters that not only mirror the CAG-repeat length dependency of these diseases, but that also better predicts inter-patient variations in disease susceptibility and effectiveness of interventions. Hereto, we will use a staggered project design as explained in 5.1, in which we first will determine which cellular and molecular determinants (referred to as landscapes) in isogenic iPSC models are associated with increased CAG repeat lengths using deep-learning algorithms (DLA) (WP1). Hereto, we will use a well characterized control cell line in which we modify the CAG repeat length in the endogenous ataxin-1, Ataxin-3 and Huntingtin gene from wildtype Q repeats to intermediate to adult onset and juvenile polyQ repeats. We will next expand the model with cells from the 3 (SCA1, SCA3, and HD) existing and new cohorts of early-onset, adult-onset and late-onset/intermediate repeat patients for which, besides accurate AO information, also clinical parameters (MRI scans, liquor markers etc) will be (made) available. This will be used for validation and to fine-tune the molecular landscapes (again using DLA) towards the best prediction of individual patient related clinical markers and AO (WP3). The same models and (most relevant) landscapes will also be used for evaluations of novel mutant protein lowering strategies as will emerge from WP4.This overall development process of landscape prediction is an iterative process that involves (a) data processing (WP5) (b) unsupervised data exploration and dimensionality reduction to find patterns in data and create “labels” for similarity and (c) development of data supervised Deep Learning (DL) models for landscape prediction based on the labels from previous step. Each iteration starts with data that is generated and deployed according to FAIR principles, and the developed deep learning system will be instrumental to connect these WPs. Insights in algorithm sensitivity from the predictive models will form the basis for discussion with field experts on the distinction and phenotypic consequences. While full development of accurate diagnostics might go beyond the timespan of the 5 year project, ideally our final landscapes can be used for new genetic counselling: when somebody is positive for the gene, can we use his/her cells, feed it into the generated cell-based model and better predict the AO and severity? While this will answer questions from clinicians and patient communities, it will also generate new ones, which is why we will study the ethical implications of such improved diagnostics in advance (WP6).
