Psykisk ohälsa bland äldre har ökat i samhället och är ett relativt outforskat ämne. Cirka 22 % av populationen som led av psykisk ohälsa eller beteendestörningar under 2019 var del av Sveriges äldre befolkning. Detta resulterar i ett ökat behov av stöd till äldre med psykisk ohälsa. Den här studien kommer genom en kvalitativ ansats samt semistrukturerade intervjuer med nio enhetschefer inom äldreomsorgen, utforska stödet samt alternativa utvecklingsbehov för äldre med psykisk ohälsa. Syftet med studien är att beskriva enhetschefers inom äldreomsorgens erfarenheter av stödet erbjudet av statliga verksamheter som finns för äldre personer med psykisk ohälsa. Studiens resultat påvisar en brist av kompetens kring äldre med psykisk ohälsa. Sammanfattningsvis framkom det i slutsatsen att bättre samverkan mellan verksamheterna och en högre personaltäthet behövs för att bättre kunna utforma ett stöd som tillmötesgår deras behov. / The occurrence of mental illness amongst the elderly has increased and is a relatively unexplored subject. About 22% of the Swedish population that suffered from mental illness or behavioural disorders in 2019 was elderly. This study will use a qualitative method and semi structured interviews with nine different unit managers within the elderly care, to explore the support for this target group. The purpose of the study is to describe the managers within elderly care's experiences with support for elderly with mental illness. The study’s results show a lack of competence about elderly with mental illness. The conclusion showed collaboration between the operating agencies and a higher staffing density is needed in order to better design a support that fills their needs.

Der erste Teil der vorliegenden Arbeit ist ein Review über die unterschiedlichen Studien aus den letzten zwanzig Jahren, die sich mit der Thematik: psychische Komorbidität bei (Brust-) Krebs auseinandersetzen. Die thematische Auseinandersetzung erfolgte zum Großteil in Form von Querschnittstudien. Das Fortbestehen der psychischen Komorbidität über Monate oder auch Jahre, nach dem Zeitpunkt der Diagnosestellung, ist erst in jüngster Zeit in das Blickfeld der Wissenschaft gerückt. Der zweite Teil der Arbeit beschäftigt sich mit der Untersuchung verschiedener soziodemographischer und krankheitsspezifischer Faktoren und deren Einfluß auf die psychische Komorbidität. Die untersuchte Patientinnengruppe sind Frauen mit Brustkrebs. Das verwendete Screeninginstrument ist die Hospital Anxiety and Depression Scale (HADS). Die Identifizierung der soziodemographischen und krankheitsspezifischen Faktoren, die psychische Komorbidität beeinflussen, ist ein noch junges Forschungsgebiet. Die Identifikation dieser Faktoren ist wichtig für die Erkrankten, um Chronifizierungsprozesse seelischen Leiden vorzubeugen. Das Ziel sollte sein, die psychische Komorbidität frühzeitig zu erkennen und zu behandeln. Dadurch kann die Lebensqualität der Frauen mit Brustkrebs gesteigert werden. Durch Fragebögen beispielsweise, als sekundär präventive Maßnahme, kann die psychische Komorbidität frühzeitig erkannt und therapiert werden. Ein zusätzlicher und nicht unerheblicher Aspekt ist dabei eine mögliche Kostenersparnis im Gesundheitswesen.

The prevailing utility, and indeed necessity, of clinical staging models applied in considerations of neuropsychiatric disease progressions is discussed from the perspectives of schizophrenia spectrum disorders and affective disorders, cannabis in schizopsychotic disorder, incidences of affect and psychosis, staging disorders in aging and the indices and prevalence of apathy. There would appear to be a strong current consensus that the pursuit of clinical staging of these and other brain disease states has contributed a systematic conceptual instrument to facilitate the better understanding, diagnosis, prognosis and treatment as derived from a multitude of genetic predispositions, symptoms and syndromes, early-onset and prodromal phases, recurrences and relapses, that have complicated the situation of the patient. Through a staging determination of the disorder, elements of diagnosis will describe the progression of symptoms/syndromes through pre-onset, prodromal, first-episode, recurrences and relapses, and treatment resistance thereby facilitating the eventual prognosis, intervention alternatives and treatment. This approach varies from observations of individuals at early stages of development (infancy, childhood, adolescece) to early middle age, in the case of diseases expressed through the aging processes. Essentially, the major contribution of the staging model may lie in the early identification, diagnosis, and treatments of disorders that afflict the brain and central nervous system.

Substance abuse is a frequent comorbid condition with other psychiatric disorders including schizophrenia and depression. These disorders may share a common substrate at the neurotransmitter or neurocircuit level. One candidate is hypofunction of the glutamate system. Several lines of evidence suggest that N-methyl-D-aspartate (NMDA) receptors may hypofunction in schizophrenia. Thus, NMDA receptor antagonists are schizophrenogenic; postmortem and imaging results point to reduced NMDA receptor function in schizophrenic brains; a number of genes that have been linked to schizophrenia code for proteins that influence NMDA function; and there is preliminary evidence that pro-NMDA drugs may be therapeutic in the treatment of schizophrenia. One of the most effective therapeutics for the treatment of substance abuse in schizophrenic people is clozapine, and clozapine may act at the glycine modulatory site to enhance NMDA receptor function. This preliminary line of evidence may link schizophrenia and drug abuse to a common neurochemical base, subnormal NMDA receptor function. People with schizophrenia and drug abusers similarly show deficits in tasks known to be sensitive to ventromedial prefrontal cortical damage, and both groups show decreased activation in the ventral striatum during reward anticipation in functional magnetic resonance imaging studies. These observations implicate common prefrontal cortical-striatal circuits and their modulation by hippocampal projections in schizophrenia and substance abuse. Withdrawal from substance abuse and depression both have been linked to changes in the function of several neurotransmitters including serotonin, dopamine and glutamate. These findings suggest possible common substrates and novel therapeutic approaches. Further studies are needed to fully characterize the neurocircuits and transmitters involved in various psychiatric disorders and their possible common elements in comorbid drug abuse.

Psychiatric disorders may co-occur in the same individual. These include, for example, substance abuse or obsessive-compulsive disorder with schizophrenia, and movement disorders or epilepsy with affective dysfunctional states. Medications may produce iatrogenic effects, for example cognitive impairments that co-occur with the residual symptoms of the primary disorder being treated. The observation of comorbid disorders in some cases may reflect diagnostic overlap. Impulsivity, impulsiveness or impulsive behaviour is implicated in a range of diagnostic conditions including substance abuse, affective disorder and obsessive-compulsive disorder. These observations suggest a need to re-evaluate established diagnostic criteria and disorder definitions, focusing instead on symptoms and symptom-profiles.

The neuronal substrates underlying aspects of comorbidity in brain disease states may be described over psychiatric and neurologic conditions that include affective disorders, cognitive disorders, schizophrenia, obsessive-compulsive disorder, substance abuse disorders as well as the neurodegenerative disorders. Regional and circuitry analyses of biogenic amine systems that are implicated in neural and behavioural pathologies are elucidated using neuroimaging, electrophysiological, neurochemical, neuropharmacological and neurobehavioural methods that present demonstrations of the neuropathological phenomena, such as behavioural sensitisation, cognitive impairments, maladaptive reactions to environmental stress and serious motor deficits. Considerations of neuronal alterations that may or may not be associated with behavioural abnormalities examine differentially the implications of discrete areas within brains that have been assigned functional significance; in the case of the frontal lobes, differential deficits of ventromedial and dorsolateral prefrontal cortex may be associated with different aspects of cognition, affect, remission or response to medication thereby imparting a varying aspect to any investigation of comorbidity.

No description available.

No description available.

Bipolar spectrum disorders (BSDs) and substance use disorders (SUDs) are highly co-occurring and both are associated with dysfunction in neural networks that mediate reward processing and motivated behavior. Furthermore, despite their high comorbidity rate, limited research into their shared neural mechanisms or potential prospective risk factors exists. This study attempted to elucidate common neural pathways for these disorders, and adds to the small but growing literature on possible prospective predictors of these disorders. We employed a task-based functional magnetic resonance imaging (fMRI) study to examine regions-of-interest (ventral striatum [VS], orbitofrontal cortex [OFC], ventromedial prefrontal cortex [vmPFC], dorsolateral prefrontal cortex [dlPFC]) and connectivity (VS-OFC, VS-vmPFC, vmPFC-dlPFC) analyses to examine neural reward processing as potential predictors of future substance and mood symptoms, and to explore differences among groups of participants with and without BSDs and SUDs. Results from this study provided evidence that blunted activation in the VS and dlPFC and greater negative connectivity between the vmPFC and dlPFC, key reward and control circuits, is implicated in prospective substance use. However, we did not find evidence to support our hypothesis that reward-related neural responses predict BSD symptoms or could differentiate individuals with co-occurring BSDs and SUDs from healthy volunteers. The study highlights the importance of larger, longitudinal studies to more fully probe neurodevelopmental trajectories in mood, substance, and related disorders. We also conducted an extensive review of the neural reward literature in BSDs and SUDs to understand possible pre-existent mechanisms. Results of the review provided support for an equifinality/multifinality perspective in that similar neural reward processing dysfunctions can lead to both BSDs and SUDs and different neural reward processing abnormalities can lead to a single outcome (e.g., SUDs). Taken together, results from the dissertation address an important gap in the literature on BSD-SUD comorbidity, suggest possible shared mechanisms that predispose to both disorders, and provide a backdrop for future work in this area to inform more theoretically-targeted interventions and prevention. / Psychology

Non-suicidal self-injury (NSSI), defined as the deliberate damaging or destruction of body tissue without intent to die, are common behaviors amongst youth. Although prior work has shown heightened response to negative outcomes and dampened response to positive outcomes across multiple methods, including behavioral and physiological measures, little is known about the neural processes involved in NSSI. This study examined associations between NSSI engagement and responsivity to rewards and losses in youth with and without a lifetime engagement in NSSI. We employed a task-based functional magnetic resonance imaging (fMRI) study to examine differences between regions of interest (ROIs; ventral and dorsal striatum [VS, DS], anterior cingulate cortex [ACC], orbitofrontal cortex [OFC], ventrolateral and ventromedial prefrontal cortex [vlPFC; vmPFC], and insula) and whole-brain connectivity (utilizing bilateral DS, mPFC, and insula seed ROIs) in youth with and without NSSI. We used two reward tasks, in order to examine differences between groups across domains of reward (i.e., monetary and social). Additionally, we examined the specificity of the associations by controlling for dimensional levels of related psychopathology (i.e., aggression and depression). Results from the current study found that NSSI was associated with decreased activation following monetary gains in all ROIs. Further, these differences remained significant when controlling for comorbid psychopathology, including symptoms of aggression and depression. Finally, exploratory connectivity analyses found that NSSI was associated with differential connectivity between regions including the DS, vmPFC, insula, parietal operculum cortex, supramarginal gyrus, cerebellum, and central opercular cortex. Weakened connectivity between these regions could suggest deficits in inhibitory control of emotions in individuals with NSSI, as well as dysfunction in pain processing in individuals with NSSI, whereby these individuals experience pain as more salient or rewarding than individuals without NSSI. Although results did not support our hypotheses, findings suggest disrupted reward processes in youth with NSSI, contributing to our understanding of the role that reward processes may play in NSSI, in the engagement and reinforcement of these behaviors. We also conducted an extensive systematic review of the studies indexing neural structure and function in NSSI, summarizing the literature on the neurobiological correlates of several psychological processes implicated in NSSI engagement, including emotion processes, pain processes, executive processes, social processes, and reward processes. Results of the review highlighted the neural regions most consistently associated with NSSI, including the amygdala, insula, frontal, prefrontal, and orbitofrontal cortices, and the anterior cingulate, dorsal striatum, and ventral striatum. Additionally, data showed that NSSI is associated with greater emotional responses in negative situations, poorer down-regulation of negative emotions, and poorer inhibitory control over impulsive behaviors. Overall, findings suggest that NSSI is associated with maladaptive coping, and that this down-regulation of negative emotion resulting from NSSI may be experienced as rewarding and may serve to reinforce engagement in these behaviors. Finally, this review highlighted the importance of standardizing the methods of indexing neural structure and function in NSSI, specifically in terms of how NSSI is categorized, which comorbid disorders are examined, and how neuroimaging data are collected and analyzed, so that research in this area is comparable and reproducible. / Psychology