Early Interventions for Psychosis

Morris B. Goldman, MD; Marko Mihailovic, MA, LCPC; Philip G. Janicak, MD

Curr Psychiatr. 2021;20(10):13, 24-31.

Introduction

Neuroscience research over the past half century has failed to significantly advance the treatment of severe mental illness.^[1,2] Hence, evidence that a longer duration of untreated psychosis (DUP) aggravates—and early intervention with medication and social supports ameliorates—the long-term adverse consequences of psychotic disorders generated a great deal of interest.^[3,4] This knowledge led to the development of diverse early intervention services worldwide aimed at this putative “critical window.” It raised the possibility that appropriate interventions could prevent the long-term disability that makes chronic psychosis one of the most debilitating disorders.^[5,6] However, even beyond the varied cultural and economic confounds, it is difficult to assess, compare, and optimize program effectiveness.^[7] Obstacles include paucity of sufficiently powered, well-designed randomized controlled trials (RCTs), the absence of diagnostic biomarkers or other prognostic indicators to better account for the inherent heterogeneity in the population and associated outcomes, and the absence of modifiable risk factors that can guide interventions and provide intermediate outcomes.^[4,8,9,10]

To better appreciate these issues, it is important to distinguish whether a program is designed to prevent psychosis, or to mitigate the effects of psychosis. Two models include the:

Prevention model, which focuses on young individuals who are not yet overtly psychotic but at high risk
First-episode recovery model, which focuses on those who have experienced a first episode of psychosis (FEP) but have not yet developed a chronic disorder.

Both models share long-term goals and are hampered by many of the same issues summarized above. They both deviate markedly from the standard medical model by including psychosocial services designed to promote restoration of a self-defined trajectory to greater independence.^{[11,12,13,14]} The 2 differ, however, in the challenges they must overcome to produce their sample populations and establish effective interventions.^[10,15,16]

In this article, we provide a succinct overview of these issues and a set of recommendations based on a “strength-based” approach. This approach focuses on finding common ground between patients, their support system, and the treatment team in the service of empowering patients to resume responsibility for transition to adulthood.

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Next Section

Biomarkers and modifiable risk factors^{[4,9,10,41,43]} are at the core of personalized medicine and its ultimate objective (ie, theragnostics). This is the ability to identify the correct intervention for a disorder based on a biomarker of the illness.^[10,36] The inability to identify biomarkers of severe mental illness is multifactorial but in part may be attributable to “looking in all the wrong places.”^[41] By focusing on neural processes that generate psychiatric symptomatology, investigators are assuming they can bridge the “mind gap”^[1] and specifically distinguish between pathological, compensatory, or collateral measures of poorly characterized limbic neural functions.^[41]

It may be more productive to identify a pathological process within the limbic system that produces a medical condition as well as the mental disorder. If one can isolate the pathologic limbic circuit activity responsible for a medical condition, one may be able to reproduce this in animal models and determine whether analogous processes contribute to the core features of the mental illness. Characterization of the aberrant neural circuit in animal models also could yield targets for future therapies. For example, episodic water intoxication in a discrete subset of patients with schizophrenia^[44] appears to arise from a stress diathesis produced by anterior hippocampal pathology that disrupts regulation of antidiuretic hormone, oxytocin, and hypothalamic-pituitary-adrenal axis secretion. These patients also exhibit psychogenic polydipsia that may be a consequence of the same hippocampal pathology that disrupts ventral striatal and lateral hypothalamic circuits. These circuits, in turn, also modulate motivated behaviors and cognitive processes likely relevant to psychosis.^[45]

Table. A strength-based approach to early interventions for psychosis
Recommendation	Example	Source
Avoid divisive aspects of the medical model	“You must take medication”	Dixon et al³⁵(2018)
Seek common ground with the patient	“What are you interested in?”	Dixon et al¹² (2016)
Commit to helping the patient reach their goals	“Let’s think about next steps”	Tindall et al¹¹ (2020)
Identify needed skills and barriers to achievement	“Can you read a book?”	Dixon et al¹² (2016)
Consider long-acting injectable antipsychotics	“I believe the shot may reduce tension by getting your parents off your back”	Kane et al³⁷ (2020)
Look to clozapine after first failed antipsychotic	“It’s hard to pay attention in class when you can’t ignore the voices”	Morrison et al³⁸ (2020)
Anticipate problems and solutions	“Would you be willing to meet with a nutritionist and join an exercise group?”	Chen et al³⁹(2021)
Maintain a noncritical attitude toward failure	“What have we learned?”	Tindall et al¹¹ (2020)
Consider EIS (if available) or other resources	“There is a local program you and your family may want to check out”	Early Assessment and Support Alliance⁴⁶ (2021)
Consider attempting to re-create key EIS elements	“I know a therapist and counselor who may help you find a job you like”	Dixon et al³⁵ (2018)

EIS: early intervention services

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Early Interventions for Psychosis

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