RESUMO
BACKGROUND: While there are mental health treatment programs for children and young people in secure settings (i.e., secure treatment programs) in many countries, there is a lack of transparency and consistency across these that causes confusion for stakeholders and challenges for the design and delivery of high-quality, evidence-based programs. This systematic review addresses two questions: What do mental health treatment programs for children and young people in secure community settings look like across jurisdictions? What is the evidence underlying the various components of these programs? METHODS: Twelve databases were searched in November 2021: CINAHL, EMBASE, MEDLINE, PsycINFO, PubMed, Scopus, Science Direct, Academic Search Complete, Psychology and Behavioral Sciences Collection, Google Scholar, OpenDOAR, and GreyLit.org. To be included, publications had to be empirical literature or a report on mental health treatment within a secure setting for people under the age of 25; contain pre-identified keywords; be based on a research or evaluation study conducted since 2000; and be assessed as low risk of bias using an adaptation of the Critical Appraisal Skills Programme qualitative research checklist. The systematic review included 63 publications. Data were collected and analyzed in NVivo qualitative software using a coding framework. RESULTS: There are secure treatment programs in Australia, Belgium, Canada, New Zealand, the Netherlands, England and Wales, Scotland, and the United States. Although there are inconsistencies across programs in terms of the systems in which they are embedded, client profiles, treatments provided, and lengths of stays, most share commonalities in their governance, definitions, designs, and intended outcomes. CONCLUSIONS: The commonalities across secure treatment programs appear to stem from them being designed around a need for treatment that includes a mental disorder, symptom severity and salience involving significant risk of harm to self and/or others, and a proportionality of the risks and benefits of treatment. Most share a common logic; however, the evidence suggested that this logic may not to lead to sustained outcomes. Policymakers, service providers, and researchers could use the offered recommendations to ensure the provision of high-quality secure treatment programming to children and young people with serious and complex mental health needs.
RESUMO
An excitatory-inhibitory neurotransmitter dysbalance has been suggested in pathogenesis of panic disorder. The neuropeptide S (NPS) system has been implicated in modulating GABA and glutamate neurotransmission in animal models and to genetically drive altered fear circuit function and an increased risk of panic disorder in humans. Probing a multi-level imaging genetic risk model of panic, in the present magnetic resonance spectroscopy (MRS) study brain glutamate+glutamine (Glx) levels in the bilateral anterior cingulate cortex (ACC) during a pharmacological cholecystokinin tetrapeptide (CCK-4) panic challenge were assessed depending on the functional neuropeptide S receptor gene (NPSR1) rs324981 A/T variant in a final sample of 35 healthy male subjects. The subjective panic response (Panic Symptom Scale; PSS) as well as cortisol and ACTH levels were ascertained throughout the experiment. CCK-4 injection was followed by a strong panic response. A significant time×genotype interaction was detected (p=.008), with significantly lower ACC Glx/Cr levels in T allele carriers as compared to AA homozygotes 5min after injection (p=.003). CCK-4 induced significant HPA axis stimulation, but no effect of genotype was discerned. The present pilot data suggests NPSR1 gene variation to modulate Glx levels in the ACC during acute states of stress and anxiety, with blunted, i.e. possibly maladaptive ACC glutamatergic reactivity in T risk allele carriers. Our results underline the notion of a genetically driven rapid and dynamic response mechanism in the neural regulation of human anxiety and further strengthen the emerging role of the NPS system in anxiety.