We use cookies to distinguish you from other users and to provide you with a better experience on our websites. Close this message to accept cookies or find out how to manage your cookie settings.
To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure no-reply@cambridge.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
This chapter focuses on the observations that variations in adrenal steroid levels, particularly cortisol, contribute to psychopathology and major depression in particular. The associations are complex due to clinical heterogeneity together with physiological and genetic variations, influencing corticoid production, function and activation by environmental adversities. There is evidence that genetic differences in adrenal function, the impact of chronic early adversity, excess corticoid production or exogenous corticoids each contribute to the risk of depression, delay in clinical recovery and relapse. Further, psychiatric illnesses, mainly but not exclusively depression, may induce changes in corticoid activity. Elevated corticoids can affect psychological function, in particular reduced memory acuity for recall of and emotional responses to life experiences.
Childhood adversity is one of the strongest predictors of adolescent mental illness. Therefore, it is critical that the mechanisms that aid resilient functioning in individuals exposed to childhood adversity are better understood. Here, we examined whether resilient functioning was related to structural brain network topology. We quantified resilient functioning at the individual level as psychosocial functioning adjusted for the severity of childhood adversity in a large sample of adolescents (N = 2406, aged 14–24). Next, we examined nodal degree (the number of connections that brain regions have in a network) using brain-wide cortical thickness measures in a representative subset (N = 275) using a sliding window approach. We found that higher resilient functioning was associated with lower nodal degree of multiple regions including the dorsolateral prefrontal cortex, the medial prefrontal cortex, and the posterior superior temporal sulcus (z > 1.645). During adolescence, decreases in nodal degree are thought to reflect a normative developmental process that is part of the extensive remodeling of structural brain network topology. Prior findings in this sample showed that decreased nodal degree was associated with age, as such our findings of negative associations between nodal degree and resilient functioning may therefore potentially resemble a more mature structural network configuration in individuals with higher resilient functioning.
We want to emphasise the importance of psychoeducation (PE) as an active intervention in clinical BPI practice. As noted already, PE was originally considered as a passive aid to medical treatments rather than an active therapeutic agent. For example, it is highly likely that PE enhances adherence and collaborative working in any intervention through explaining the implications of treatment to the patient. This is undoubtedly a useful mediating process but in BPI practice we want the therapist to utilise PE from the perspective that it acts as a therapeutic change element of treatment. For BPI practice, PE is the conversational delivery vehicle for information about how to understand mental states, engage in adaptive activities and habilitate and use new understandings and strategies to promote well-being and resilience in the face of future adversities. Whilst the focus is directly on the adolescent, such PE can also be delivered to important others such as family, carers and teachers, with the consent of the YP.
This chapter describes the clinical methods that most likely make the best use of the clinical tools described in Chapters 3 and 6. First, we describe the three BPI domains of psychoeducation, social and personal prescribing and habilitation that constitute the framework of BPI.
The Notion That The Teenage Years Have Any Particular Value In Social, Cultural Or Biological Terms Does Not Appear In Any Literature Until The Fifteenth Century. Before Then, Received Wisdom Was That Infancy And Childhood Were Followed By Adulthood And All That Goes With Being A Grown-Up Individual In Any Society. The Word ‘Adolescence’ Came From The Latin Word Adolescere, Meaning ‘To Grow Up Or To Grow Into Maturity’. Although Ongoing Maturation During The Teenage Years Is Clearly Suggested, There Appears To Be No Formal Adoption Of The Concept In Any Society Until The Early Twentieth Century. In 1904 The First President Of The American Psychological Association, Greville Stanley Hall, Was Credited With Coining The Term ‘Adolescence’. In His Study Entitled Adolescence, He Described This New Developmental Phase, Which He Hypothesised Came About Due To Social Changes. Some Of This Hypothesis Resonates Clearly With Today’S Viewpoints, Although Much Is Also Now Known To Be Incorrect.
In the previous chapter we outlined a brief history of psychotherapies since the medieval period and noted that we are now in a scientific phase that is particularly focused on establishing valid clinical effects for talking cures.
In Chapters 5 and 6 we outlined the BPI framework together with clinical principles and methods. In Chapters 7 and 8 we translate these into practical BPI practice. You will have read about the concepts and techniques in prior chapters but now you get the chance to consider them through the clinical practice lens. These two chapters can serve as clinical guides and underpin the clinical manual and protocol that was used in the IMPACT study.
We have noted that, in our view, when undertaking any psychotherapy there should be supervision and reflective practice throughout one’s career. Senior therapists can be as much in need of discussions about their cases as newly qualified practitioners. Until we have much improved our understanding of what intervention works for which patient and how, we recommend supervision as a key clinical tool in learning the skills and techniques of BPI. Of course, we do not yet know which of these tips is responsible for clinical effectiveness. Therefore, regular fortnightly supervision with a senior, more experienced colleague is sound practice. Table 9.1 describes key general components that should activate a discussion with your supervisor.
In Chapter 1 we described the emergence of the concept of adolescence in the early twentieth century and how it represented a new and developmentally sensitive period of ongoing mental maturation. We also noted that the talking cures were fast gaining a foothold in developed societies and adolescents were beginning to be a focus of these interventions, this being due to the clear-cut increases in mental health difficulties and emergent mental illnesses in the second decade of life. The theories and techniques of the psychotherapies were, until the 1970s, relatively uninfluenced by the emergence of the concept of adolescence and its implications for mind-brain maturation. This implies that very little of what we know about adolescents and their mental states has been taken into account when devising a talking treatment for young people.
Brief psychosocial intervention was first used as a non-manualised reference treatment for depressed adolescents receiving the antidepressant fluoxetine with or without CBT. Both the treatment groups received the forerunner of BPI, specialist clinical care, as their general clinical support. The surprise was that CBT provided no added value over fluoxetine and specialist clinical care by the end of the study, which was only a short-term outcome of some 28 weeks [1]. This was the first finding that specialist clinical care provided by psychiatrists and mental health nurses to depressed adolescents may be as clinically effective as specialised psychological treatments such as CBT.
An interesting consequence of this study was to ask: what exactly did the therapists do when delivering specialist clinical care and how was it delivered?
The highest incidence for clinical depressions is during adolescence. Furthermore, mental health illnesses that recur over the life-course begin in young people. 70% of all mental health emerge before thirty years of age. Almost all interventions for young people have been first developed for and targeted at adults. Here for the first time is a talking therapy (BPI), that has been developed for, and with, adolescents. After thirty years of clinical experience with mentally ill adolescents and two major randomised controlled trials of treatment, the authors reveal a brief psychosocial intervention that is as effective as CBT for adolescents with depression with and without comorbid anxiety and conduct disorder. BPI can be taught to mental health practitioners in sixteen hours and they can immediately start delivery of care. After a six-month supervision, new BPI practitioners offer an evidence based and NICE approved treatment in their usual clinical practice.
Impulsive and compulsive problem behaviours are associated with a variety of mental disorders. Latent phenotyping indicates the expression of impulsive and compulsive problem behaviours is predominantly governed by a transdiagnostic ‘disinhibition’ phenotype. In a cohort of 117 individuals, recruited as part of the Neuroscience in Psychiatry Network (NSPN), we examined how brain functional connectome and network properties relate to disinhibition. Reduced functional connectivity within a subnetwork of frontal (especially right inferior frontal gyrus), occipital and parietal regions was linked to disinhibition. Findings provide insights into neurobiological pathways underlying the emergence of impulsive and compulsive disorders.
Nonsuicidal self-injury (NSSI) is prevalent among adolescents and research is needed to clarify the mechanisms which contribute to the behavior. Here, the authors relate behavioral neurocognitive measures of impulsivity and compulsivity to repetitive and sporadic NSSI in a community sample of adolescents.
Methods
Computerized laboratory tasks (Affective Go/No-Go, Cambridge Gambling Task, and Probabilistic Reversal Task) were used to evaluate cognitive performance. Participants were adolescents aged 15 to 17 with (n = 50) and without (n = 190) NSSI history, sampled from the ROOTS project which recruited adolescents from secondary schools in Cambridgeshire, UK. NSSI was categorized as sporadic (1-3 instances per year) or repetitive (4 or more instances per year). Analyses were carried out in a series of linear and negative binomial regressions, controlling for age, gender, intelligence, and recent depressive symptoms.
Results
Adolescents with lifetime NSSI, and repetitive NSSI specifically, made significantly more perseverative errors on the Probabilistic Reversal Task and exhibited significantly lower quality of decision making on the Cambridge Gambling Task compared to no-NSSI controls. Those with sporadic NSSI did not significantly differ from no-NSSI controls on task performance. NSSI was not associated with behavioral measures of impulsivity.
Conclusions
Repetitive NSSI is associated with increased behavioral compulsivity and disadvantageous decision making, but not with behavioral impulsivity. Future research should continue to investigate how neurocognitive phenotypes contribute to the onset and maintenance of NSSI, and determine whether compulsivity and addictive features of NSSI are potential targets for treatment.
Childhood adversity (CA) increases the risk of subsequent mental health problems. Adolescent social support (from family and/or friends) reduces the risk of mental health problems after CA. However, the mechanisms of this effect remain unclear, and we speculate that they are manifested on neurodevelopmental levels. Therefore, we investigated whether family and/or friendship support at ages 14 and 17 function as intermediate variables for the relationship between CA before age 11 and affective or neural responses to social rejection feedback at age 18. We studied 55 adolescents with normative mental health at age 18 (26 with CA and therefore considered “resilient”), from a longitudinal cohort. Participants underwent a Social Feedback Task in the magnetic resonance imaging scanner. Social rejection feedback activated the dorsal anterior cingulate cortex and the left anterior insula. CA did not predict affective or neural responses to social rejection at age 18. Yet, CA predicted better friendships at age 14 and age 18, when adolescents with and without CA had comparable mood levels. Thus, adolescents with CA and normative mood levels have more adolescent friendship support and seem to have normal mood and neural responses to social rejection.