American Psychiatric Association

This column describes 3 mechanisms of therapeutic action in the treatment of mental and substance use disorders. These mechanisms include biomedical interventions, dyadic interventions, and interventions involving transdyadic social learning. Combining mechanisms of action offers the potential to augment treatment response. Intermediate levels of care (Intensive Outpatient Programs, Partial Hospital Programs, and Residential Treatment Centers) are generally designed to provide treatment combining all 3 mechanisms of therapeutic action in the service of helping patients better use outpatient treatment to pursue recovery.

Abstract Psychiatric diagnoses are based on consensus and are not related to pathophysiology, leading to confusion in treatment and in basic and clinical psychiatric research. The pathology of mood disorders arises from the intrinsic function and interactions between key neural circuits of the triple network. These circuits are the central executive network composed of the dorsolateral prefrontal cortex and posterior parietal cortex; the default mode network consisting of the dorsal medial prefrontal cortex, posterior cingulate/precuneus and angular gyrus and the salience network made up of the anterior insula, dorsal anterior cingulate cortex associated with subcortical limbic nodes including the amygdala. In this work, we develop a formal model using nonlinear dynamics and network theory, which captures the dynamic interactions of these three brain networks, allowing us to illustrate how various mood disorders can arise. Recurrent circuit dynamics are modeled on the physio-dynamics of a single neural component and is dependent on a balance of total input (feedforward and feedback) and the sensitivity of activation of its neural components. We use the average percentage of maximal firing rate frequency as a measure of network activity over long periods, which corresponds to fMRI activity.While the circuits function at moderate rates in euthymia, depressive symptoms are due to hypoactivity of the CEN and SN and hyperactivity of the DMN. Mania arises from a hyperactive SN with hypofunction of the CEN and moderate to high activity of the DMN. Functional abnormalities arise from genetic or epigenetic changes, affecting either the weight of neural interconnections or the sensitivity of activation of neurons comprising the network. Decreased excitation in unipolar depressive states is caused by diminished dendritic branches and decreased density of AMPA and NMDA receptors or a decrease in glutamate released by presynaptic neurons. All bipolar states result from heightened neural sensitivity due to altered sodium, calcium, or potassium channel conductance. Our formal model of mood disorders is consistent with fMRI studies, genetic research, as well as preclinical and clinical studies.

The author describes her struggle with depression and borderline personality disorder, self-harm, and suicidality. She first reviews the long years during which she did not respond to any of the numerous antidepressant medications that were prescribed. She then describes how she finally achieved healing and good functioning as a result of long-term caring psychotherapy in the context of a strong therapeutic relationship in combination with medications that were found to be effective for her symptoms.

BackgroundOlanzapine toxicity is reported to be a rare but specific phenomenon characterized by rapid fluctuations between somnolence and agitation, which has been referred to as “agitation despite sedation.” A similar phenomenon is observed as an adverse reaction of the long-acting injectable olanzapine formulation, which has been referred to as “delirium/sedation syndrome.”Case presentationThis case report describes a 48-year-old man diagnosed with schizophrenia who experienced rapid fluctuations between somnolence and agitation during a cross-titration of olanzapine to clozapine. The patient had normal serum levels of both medications and the symptoms resolved with the discontinuation of olanzapine.ConclusionRapid fluctuations in mental status between somnolence and agitation are not clearly described among other antipsychotics, and it is possible that this phenomenon may be specific to olanzapine. The findings of this case report suggested that this phenomenon was likely the result of the oversaturation of (H1) and (M1) receptors.

The dearth of child and adolescent mental health services (CAMHS) is a global problem. Integrating CAMHS in primary care has been offered as a solution. We sampled integrated care perspectives from colleagues around the world. Our findings include various models of integrated care namely: the stepped care model in Australia; shared care in the United Kingdom (UK) and Spain; school-based collaborative care in Qatar, Singapore and the state of Texas in the US; collaborative care in Canada, Brazil, US, and Uruguay; coordinated care in the US; and, developing collaborative care models in low-resource settings, like Kenya and Micronesia. These findings provide insights into training initiatives necessary to build CAMHS workforce capacity using integrated care models, each with the ultimate goal of improving access to care. Despite variations and progress in implementing integrated care models internationally, common challenges exist: funding within complex healthcare systems, limited training mechanisms, and geopolitical/policy issues. Supportive healthcare policy, robust training initiatives, ongoing quality improvement and measurement of outcomes across programs would provide data-driven support for the expansion of integrated care and ensure its sustainability.