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Treating Bipolar Disorder - Kids & Teens

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Treating Bipolar Disorder - Kids & Teens

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CE credits: 1

Learning objectives: After reading this article, CE candidates will be able to:

1. Explain how the research base on pediatric bipolar disorder has evolved since 1990.

2. Understand the basic diagnostic criteria for pediatric bipolar disorder and know what tools are used to assess it.

3. List and describe the top-line pharmacological and psychosocial treatments for bipolar disorder in children and adolescents.

For more information on earning CE credit for this article, go CE Corner.

Of the nearly 11,000 articles on bipolar disorder in children and adolescents, more than 90% have been published in the last 15 years-after most practitioners were trained and licensed. Keeping up with that explosion of literature can be a challenge, says Eric Youngstrom, PhD, a professor of psychology, neuroscience and psychiatry at the University of North Carolina at Chapel Hill (UNC Chapel Hill).

"It's great to have the research," says Youngstrom, who also directs the Center for Excellence in Research and Treatment of Bipolar Disorder at UNC Chapel Hill. "But the speed of its arrival creates a challenge. How do we find and digest it? How do we learn about new tools and skills and use them?"

The rapid acceleration in research occurred after bipolar disorder was embraced by practitioners as a legitimate diagnosis for youth in the 1990s. Now, studies show that about 4% of people under 18, including children as young as 5, have the disorder, which is characterized by episodes of mania or hypomania-a slightly milder mood state-and, in most cases, depression (Van Meter, A., et al., The Journal of Clinical Psychiatry, Vol. 80, No. 3, 2019; Luby, J.L., & Navsaria, N., The Journal of Child Psychology and Psychiatry, Vol. 51, No. 4, 2010). About 3% of U.S. adults have bipolar disorder, according to the National Institute of Mental Health.

Over the past decade or so, experts across psychology and psychiatry have helped refine assessment and treatment of bipolar disorder among children and adolescents.

Researchers have also designed and tested psychosocial approaches that combine education, skill building and lifestyle modifications to help kids and parents manage the condition. Evidence to support those interventions is growing, giving hope to children and teens for a less tumultuous transition to adulthood if bipolar disorder is diagnosed and addressed early on.

"The field has come a really long way, even in the last five or 10 years, in terms of both diagnosis and treatment," says Tina Goldstein, PhD, an associate professor of psychiatry and psychology at the University of Pittsburgh. "Now, a big focus is disseminating those insights for use by practitioners in various settings."

An overlooked diagnosis

Bipolar disorder was described by modern psychiatrists as early as 1851, though practitioners long believed that mood disorders did not develop until adulthood (Mason, B.L., et al., Behavioral Sciences, Vol. 6, No. 3, 2016). That perspective began to shift in the 1980s when two researchers based at the University of California, Los Angeles (UCLA)-psychologist Michael Strober, PhD, and psychiatrist Gabrielle Carlson, MD-studied a group of 60 teenagers with depression and characterized youth bipolar disorder (Archives of General Psychiatry, Vol. 39, No. 5, 1982).

Though some clinicians were skeptical at first, most ultimately embraced the new findings-perhaps too heartily. Between 1994-95 and 2002-03, outpatient visits with a diagnosis of bipolar disorder increased 40-fold among youth (Moreno, C., et al., Archives of General Psychiatry, Vol. 64, No. 9, 2007). Working at The Ohio State University's Wexner Medical Center, one of the first clinics to specialize in diagnosing the disorder, Mary Fristad, PhD, ABPP, says only about a third of youths referred to her practice for treatment of bipolar disorder had been accurately diagnosed. Instead, many of those patients were suffering from attention-deficit hyperactivity disorder (ADHD), obsessive-compulsive disorder, autism spectrum disorder, depression, anxiety disorders or conduct disorders.

"That experience spoke to the need for better assessment tools and adequate training of clinicians to perform differential diagnosis," Fristad says.

A second wave of research soon began to fill in those gaps. Psychiatrist Barbara Geller, MD, based at Washington University in St. Louis, led the charge to characterize pediatric bipolar disorder and to establish basic diagnostic criteria (Archives of General Psychiatry, Vol. 65, No. 10, 2008). Researchers also began to develop and test treatments for pediatric populations-including mood stabilizers and antipsychotic drugs known to be effective for adults with bipolar disorder, as well as psychosocial interventions to help children and families cope with the diagnosis.

In the last five years, more specialized research has started to help practitioners better understand pediatric bipolar disorder and to differentiate it from other conditions. Psychologists have also studied patients with comorbid conditions, such as ADHD or anxiety disorders (Arnold, L.E., et al., The Journal of Child Psychology and Psychiatry, Vol. 61, No. 2, 2020). Neuroscientific methods such as fMRI and electroencephalography are also being applied to better characterize the physiological underpinnings of the disorder in children.

Diagnosing in children

The criteria used to diagnose bipolar disorder in children and adolescent populations are the same as those used for adults-fluctuations between depression, which can include extreme sadness, low energy levels, loss of pleasure and suicidal ideation, and hypomania or mania, which can involve periods of elevated mood, irritability, a decreased need for sleep, increases in goal-oriented behaviors and inflated self-esteem.

The Diagnostic and Statistical Manual of Mental Disorders (DSM-V) distinguishes three subcategories of the disorder. Bipolar I is characterized by cycles of episodic major depression and full mania with impairment. Bipolar II involves major depression alternating with briefer and less-impairing periods of hypomania. Two other categories-"other specified bipolar and related disorder" and cyclothymic disorder-describe people with shorter manic or depressive episodes or episodes that fall one or two symptoms short of the full syndrome criteria.

But these disorders can look different in children, who may have more rapidly cycling moods and more "mixed" periods, characterized by simultaneous mania and depression, so experts say specialized assessment tools are needed.

"One of the challenges both in assessing and treating bipolar disorder in kids is that some of the symptoms can look a lot like extreme versions of normal child or adolescent behaviors," says Anna Van Meter, PhD, an assistant professor at New York-based health-care provider Northwell Health's Feinstein Institutes for Medical Research.

Clinicians who assess children and adolescents for bipolar disorder typically start with a symptom checklist, then they conduct a clinical interview that evaluates risk factors-such as a family history of the disorder-and draws on semi-structured interviewing tools such as the Kiddie Schedule for Affective Disorders and Schizophrenia for School Aged Children (Hunt, J.I., et al., Journal of Child and Adolescent Psychopharmacology, Vol. 15, No. 6, 2005).

In fact, clinicians can diagnose bipolar disorder in children more accurately when they ask the children, their teachers and their caregivers to fill out empirically validated questionnaires that ask about mood, energy levels and other factors, Youngstrom and Van Meter found in a metaanalysis (Youngstrom, E.A., et al., Archives of Scientific Psychology, Vol. 3, No. 1, 2015). These scales are available for free on the learning community Wikiversity and at EffectiveChildTherapy.org, supported by APA's Div. 53 (Society of Clinical Child and Adolescent Psychology).

"Improving our accuracy is important because on average, individuals with bipolar disorder will go about 10 years from initially seeking mental health services to receiving a bipolar disorder diagnosis," Van Meter says.

Early intervention

Even before a patient experiences manic and depressive episodes that warrant a bipolar disorder diagnosis, early intervention may hold promise to alter the condition's course for those at risk of developing it. Working with teens who had a first-degree family history of bipolar disorder but no existing mood disorder diagnosis, Goldstein tested Interpersonal and Social Rhythm Therapy (IPSRT), an educational and skill-based approach that aims to help individuals with bipolar disorder establish and maintain regular daily routines to help stabilize their moods. In a small randomized trial, she found that IPSRT helped teens establish more regular sleep-wake cycles, which appeared to mediate mood fluctuations (Goldstein, T.R., et al., Journal of Affective Disorders, Vol. 235, 2018).

Psychologist David Miklowitz, PhD, a professor of psychiatry at UCLA's Semel Institute for Neuroscience and Human Behavior, tested family-focused therapy (FFT), a psychosocial intervention that includes psychoeducation and skill training on communication and problem-solving for youth and their family members. In a three-site randomized trial involving children and teens who had mood instability and a family history of bipolar disorder, his group found that FFT elongated the intervals of wellness between mood episodes and reduced both depressive episodes and suicidal ideation (JAMA Psychiatry, Vol. 77, No. 5, 2020).

"We can't erase bipolar disorder, but we may see a milder course of the illness and lower levels of suicidality when we intervene at an early stage," Miklowitz says.

Increasingly, psychologists and psychiatrists are relying on "risk calculators" to determine who might be a good candidate for such early interventions. Goldstein helped develop one such tool for youth with a family history, which uses information about a child's age, mood and other factors to determine the likelihood that they will develop bipolar disorder (Hafeman, D.M., et al., JAMA Psychiatry, Vol. 74, No. 8, 2017).

"Clinicians anywhere can plug in patient data online, then use the calculator to make decisions with a family about early intervention and treatment options," she says.

Psychologists are also testing ways that technology can help young patients who have already received a diagnosis. Last year, Van Meter launched a study to describe the "digital phenotype" of bipolar disorder in adolescents by quantifying digital markers of their behavior. By passively monitoring teens' smartphones, she obtains estimates of their weekly schedules, physical activity, screen time and degree of social interaction-some of the factors clinicians expect to change before a manic or depressive episode occurs.

"My hope is that we can use this type of monitoring to prospectively identify when a patient is becoming symptomatic so that we can intervene to prevent a full relapse," says Van Meter.

Digital monitoring is also less burdensome for patients than self-reporting and may provide a more accurate snapshot of behavior, she adds. Teenagers and their caregivers complete informed consent for passive monitoring, which logs data about how a phone is used but does not monitor the content of messages or who the participant contacts.

Treatment options

For most cases of pediatric bipolar disorder, the American Academy of Child and Adolescent Psychiatry recommends a combination of medication and psychotherapy ("Practice Parameter for the Assessment and Treatment of Children and Adolescents With Bipolar Disorder," Journal of the American Academy of Child and Adolescent Psychiatry, Vol. 46, No. 1, 2007).

Mood stabilizers and antipsychotic drugs, which have been used for decades to treat bipolar disorder in adults, are also effective in pediatric populations. "In most cases, medication helps stabilize kids so that they can participate effectively in psychotherapy, which then helps with longer-term symptom management and coping strategies," says Amy West, PhD, an associate professor of clinical pediatrics and psychology at Children's Hospital Los Angeles and the University of Southern California's Keck School of Medicine. "I see the two as working in concert."

But many parents express concern about their child or teen using such medications. Antipsychotics, for instance, can cause metabolic disturbances that may result in weight gain and an increased risk for Type 2 diabetes (Harrison, J.N., et al., Journal of Pediatric Health Care, Vol. 26, No. 2, 2012). Miklowitz says more work is needed to establish guidelines for when psychotherapy alone is sufficient to treat bipolar disorder.

At the same time, families that do include medication in a child's treatment may not be getting its full benefit. In a three-month study of teens taking psychotropic drugs for bipolar disorder, Goldstein monitored medication adherence using Bluetooth-equipped pillboxes (Journal of Child and Adolescent Psychopharmacology, Vol. 26, No. 10, 2016).

"What we learned was really distressing. Almost half the time, kids were not taking their medications as prescribed," she says. "But the patients, parents and psychiatrists all reported more than 90% medication adherence."

To address that gap, Goldstein designed a brief intervention that uses motivational interviewing techniques to better understand kids' feelings about taking mood-stabilizing medications, as well as how to stimulate behavior change. She found that the intervention improved adherence compared with a control group (Journal of Affective Disorders, Vol. 265, 2020). The intervention can even be delivered by a nurse or peer educator without a background in mental health, she says.

Psychologists have also been instrumental in developing psychosocial interventions for bipolar disorder to equip kids and families with the tools and information they need to function well. Three popular evidence-based interventions all focus on education, skill building and lifestyle shifts-such as establishing regular sleep-wake cycles, often key for achieving remission-among children and family members.

"We know that the family system is really important for maintaining youth stability following a bipolar diagnosis, so these interventions tend to focus on helping families create a new normal," says West.

FFT, the intervention Miklowitz developed, works with adolescents who have bipolar disorder and their family members to recognize symptoms of the condition and develop a plan for managing manic and depressive episodes. It also helps parents reduce their own stress and expressed emotion. Eight randomized controlled trials have shown that FFT, when delivered in combination with mood-stabilizing medications, reduces symptom severity and relapse in both adolescents and adults with bipolar disorder (Miklowitz, D.J., & Chung, B., Family Process, Vol. 55, No. 3, 2016).

Along with psychiatrist Mani Pavuluri, MD, West developed and tested an intervention known as RAINBOW, which targets children ages 7 to 13 and their families ("RAINBOW: A Child- and Family-Focused Cognitive-Behavioral Treatment for Pediatric Bipolar Disorder, Clinician Guide," Oxford University Press, 2017). Its 12 sessions focus on education about the nature of the disorder, skill building to help kids regulate their emotions, and coping and parenting strategies for caregivers, such as the importance of creating routines. It incorporates cognitive-behavioral therapy, interpersonal psychotherapy and mindfulness-based approaches.

Using a group therapy format, Fristad also developed a widely used psychosocial treatment program, Multifamily Psychoeducational Psychotherapy (MF-PEP), for children and adolescents with mood disorders (Archives of General Psychiatry, Vol. 66, No. 9, 2009). Psychoeducation, a primary component of MF-PEP, teaches parents strategies for managing manic and depressive episodes, as well as how to navigate school and health systems to best support their child (Fristad, M.A., Development and Psychopathology, Vol. 18, No. 4, 2006).

"You can be a great parent, but that doesn't mean you automatically know what to do if your child is suddenly suicidal or is experiencing a manic episode," Fristad says.

Alternative treatments

Researchers are also exploring other interventions for bipolar disorder to help practitioners manage special cases, such as patients with high levels of suicidality or those who don't respond well to medications.

Goldstein adapted a model of dialectical behavior therapy for youth with bipolar disorder, finding that it decreased suicidal ideation compared with typical psychosocial treatment for the condition in a small randomized trial (Journal of Child and Adolescent Psychopharmacology, Vol. 25, No. 2, 2015). She is working to replicate those findings in a larger sample.

Nutritional interventions also show promise for treating bipolar disorder. Fristad has tested the use of broad-spectrum nutrients for children not taking mood stabilizers or antipsychotic medications, with promising results (The Journal of Alternative and Complementary Medicine, Vol. 18, No. 7, 2012). In a randomized controlled trial, she also found that dietary supplementation with omega-3 fatty acids can help reduce both manic and depressive symptoms and improve executive functioning (Journal of Child and Adolescent Psychopharmacology, Vol. 25, No. 10, 2015; The Journal of Child Psychology and Psychiatry, Vol. 59, No. 6, 2018).

But even the top-line pharmacological, psychosocial and lifestyle interventions only help 50% to 60% of pediatric bipolar patients, says West.

"There's a lot of room for improvement in terms of translating our findings into better assessments and treatments," she says.

For example, research on the neural underpinnings of bipolar disorder should directly inform the development of psychological interventions, West says. In addition, research to optimize the match between a child and a given course of treatment could speed up progress and ultimately improve patient outcomes, says Goldstein.

Most important, new findings and best practices for treating bipolar disorder in children and adolescents need to reach private practice and community settings to help the broadest patient population.

"The need is so high, and unfortunately it takes time for evidence-based practices to permeate the field," West says. "We need to do a better job of preparing practitioners to understand pediatric bipolar disorder and to feel comfortable diagnosing and treating it."

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Treating bipolar disorder in kids and teens

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CE credits: 1 Learning objectives: After reading this article, CE candidates will be able to: Explain how the research base on pediatric bipolar disorder has evolved since 1990. Understand the basic diagnostic criteria for pediatric bipolar disorder and know what tools are used to assess it.

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Instructions: This is a screening measure to help you determine whether you might have an eating disorder that needs professional attention. This screening measure is not designed to make a diagnosis of an eating disorder or take the place of a professional consultation. Please fill out the form below as accurately, honestly and completely as possible. There are no right or wrong answers. All of your responses are confidential.

Sample Code:

Part A: Complete the following questions:

1) Birth Date 2) Gender: Male Female

3) Height

4) Current Weight (lbs.): 5) Highest Weight (excluding pregnancy):

6) Lowest Adult Weight: 7) Ideal Weight:

Part B: Check a response for each of the following statements:

Always:

Usually:

Often:

Some
times:

Rarely:

Never:

1.

I Am terrified about being overweight.

2.

I Avoid eating when I am hungry.

3.

I Find myself preoccupied with food.

4.

I Have gone on eating binges where I feel that I may not be able to stop.

5.

I Cut my food into small pieces.

6.

I Aware of the calorie content of foods that I eat.

7.

I Particularly avoid food with a high carbohydrate content (i.e. bread, rice, potatoes, etc.)

8.

I Feel that others would prefer if I ate more.

9.

I Vomit after I have eaten.

10.

I Feel extremely guilty after eating.

11.

I Am occupied with a desire to be thinner.

12.

I Think about burning up calories when I exercise.

13.

I Other people think that I am too thin.

14.

I Am preoccupied with the thought of having fat on my body.

15.

I Take longer than others to eat my meals.

16.

I Avoid foods with sugar in them.

17.

I Eat diet foods.

18.

I Feel that food controls my life.

19.

I Display self-control around food.

20.

I Feel that others pressure me to eat.

21.

I Give too much time and thought to food.

22.

I Feel uncomfortable after eating sweets.

23.

I Engage in dieting behavior.

24.

I Like my stomach to be empty.

25.

I Have the impulse to vomit after meals.

26.

I Enjoy trying new rich foods.

| | | | | | |

Part C: Behavioral Questions:

In the past 6 months have you:

Never

Once a month or less

2-3 times a month

Once a week

2-6 times a week

Once a day or more

A.

Gone on eating binges where you feel that you may not be able to stop?*

B.

Ever made yourself sick (vomited) to control your weight or shape?

C.

Ever used laxatives, diet pills or diuretics (water pills) to control your weight or shape?

D.

Exercised more than 60 minutes a day to lose or to control your weight?

E.

Lost 20 pounds or more in the past 6 months

YES

NO

F.

Have you ever been treated for an eating disorder?

YES

NO

*Defined as eating much more than most people would under the same circumstances and feeling that eating is out of control.

© Copyright: EAT-26: (Garner et al. 1982, Psychological Medicine, 12, 871-878); adapted by D. Garner with permission.

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Eat-26 - EAT-26: Eating Attitudes Test & Eating Disorder Testing

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Abstract

Objective

Although eating disorders are common psychiatric disorders that usually onset during adolescence, few evidence-based treatments for this age group have been identified. A critical review of treatments used for Anorexia Nervosa (AN) and Bulimia Nervosa (BN) and related conditions (EDNOS) is provided that summarizes the rationale for the treatments, evidence of effectiveness available, and outcomes.

Method

Critical review of published randomized clinical trials (RCTs).

Results

There are only seven published RCTs of psychotherapy for AN in adolescents with a total of 480 subjects. There are only two published RCTs for outpatient psychotherapy for adolescent BN with a total of 165 subjects. There are no published RCTs examining medications for adolescent AN or BN. For adolescent AN, Family-Based Treatment (FBT) is the treatment with the most evidence supporting its use. Three RCTs suggest that FBT is superior to individual therapy at the end of treatment; however, at follow-up differences between individual and family approaches are generally reduced. For adolescent BN, one study found no differences between Cognitive Behavioral Therapy and FBT at the end of treatment or follow-up, while the other found FBT superior to individual therapy.

Conclusions

Although the evidence remains limited, FBT appears to be the first line treatment for adolescent AN. There is little evidence to support a specific treatment for adolescent BN. There is a need for additional studies of treatment of child and adolescent eating disorders. New treatments studies may build on current evidence as well as examine new approaches based on novel findings in the neurosciences about cognitive and emotional processes in eating disorders.

Keywords: Anorexia Nervosa, Bulimia Nervosa, Treatment, Review, Adolescents

Introduction

Both of the classic eating disorders (Anorexia Nervosa and Bulimia Nervosa) onset during the adolescent years. Anorexia Nervosa (AN) has an incidence rate of 0.48-0.7% among adolescent females between 15-19 years of age with almost all cases beginning before the age of 25 ( Hoek and Hoeken, 2003; van Son et al., 2006). Bulimia Nervosa (BN) has an incidence of 1-2% in the adolescent population while clinically significant bulimic behaviors occur in an additional 2-3%. Binge eating and purging behaviors usually begin during middle adolescence ( Stice and Agras, 1998). Many cases of AN and BN in children and adolescents are diagnosed as Eating Disorder Not Otherwise Specified (EDNOS) because DSM criteria are not developmentally sensitive and based on more chronic adult presentations of these disorders ( Workgroup, 2007).

AN is characterized by a restrictive eating pattern resulting in severe weight loss, amenorrhea, and distorted perceptions of body weight and shape ( APA, 1994). Associated psychopathology includes high levels of anxiety and depression, low self-esteem, and interpersonal and familial difficulties. Physical health is also severely compromised due to malnutrition. AN is arguably one of the most severe psychiatric disorders as measured by mortality and morbidity rates-the crude mortality rate is between 4 and 5%, higher than any other mental disorder with the possible exception of substance abuse ( Crow et al., 2009). Costs for AN treatment, mostly because of hospitalization treatment rivals that of schizophrenia ( Streigel-Moore et al., 2000).

BN is characterized by overvalued ideas concerning body weight and shape, dieting and disinhibited eating patterns consisting of binge eating and purging. The physical complications of bulimic behaviors include hypokalemia, esophageal tears, gastric disturbances, dehydration, orthostasis, cardiac arrhythmias, and death. Psychiatric complications include depression, personality disorders, anxiety disorders, and substance abuse disorders. Although considerable advances have been made in understanding the etiology and treatment of BN in adults, little treatment research has been conducted in adolescents with the disorder ( Mitchell et al., 2007). BN is apparently less medically concerning than AN, though recent data suggest that mortality rates can still be significant with this disorder ( Crow et al., 2009). There has been a comparative neglect of specific medical implications of the disorder and current medical criteria for emergency medical intervention are primarily designed to identify and treat the deleterious physical effects of malnutrition ( Golden et al., 2003).

The majority (about 60%) of children and adolescents with eating disorders are diagnosed as EDNOS using current DSM criteria. While it also true that most adults with eating disorders fall into the EDNOS category, the reasons for this differ between the age groups ( Fairburn and Bohn, 2005). For many children and adolescents, the main reasons for not meeting diagnostic criteria are failure to meet recommended physical thresholds, lower frequency of eating disordered behaviors or not clearly reporting specific eating related thoughts and beliefs, ( Workgroup, 2007) while in adults, the issue appears more often related to symptomatic migration and overlap between disorders over time, where about 30% of patients change from AN to BN ( Fairburn and Bohn, 2005). In addition to these issues, binge eating disorder (BED)-episodes of binge eating without efforts to purge--still falls in the EDNOS category. Prevalence rates of BED in adults are between 0.7 and 4% ( Hudson et al., 2007). Although some studies suggest BED symptoms often start in children and adolescents, prevalence rates are not well characterized in younger populations ( Marcus and Kalarchian, 2003). This review focuses on treatment of AN and BN and subthreshold cases of these disorders rather than other atypical eating disorders of childhood and adolescence. A recent review provides an excellent overview of these less common eating problems in young patients ( Bryant-Waugh et al., 2010, published on line ahead of print).

Treatments for Anorexia Nervosa

Although family therapy is commonly clinically employed for adolescents with AN, only one form of family therapy has been systematically tested to date in RCTs--that initially developed by the Maudsley group at the Institute of Psychiatry in London ( Dare and Eisler, 1997) and manualized as Family Based Treatment (FBT) ( Lock et al., 2001). The approach is theoretically agnostic as to the etiology of AN, but the rationale for the approach is based on the idea that families make accommodations in feeding their child that initially appear useful in combating AN, but these ultimately become maladaptive, disrupting both the development of the adolescent with AN, and perpetuating the behaviors that maintain the disorder ( Eisler, 2005). Treatment aims to identify and help the family modify these accommodations. FBTor the Maudsley Approach has tested in 6 randomized clinical trials with adolescents and 2 randomized clinical trials with adults with AN ( Dare et al., 2001; Eisler et al., 2000; Le Grange et al., 1992; Lock et al., 2005; Russell et al., 1987). Outcomes using the approach suggest it is effective for adolescents in the short term with 80-90% of patients with good to excellent progress and that treatment effects are maintained at longer term follow-up ( Eisler et al., 1997; Eisler et al., 2007; Le Grange and Lock, 2005; Lock et al., 2006a). In three studies comparing FBT to other treatments, FBT was found to be superior to comparison treatments ( Lock et al., in press-b; Robin et al., 1999; Russell et al., 1987). It is noteworthy, however, that some differences favoring FBT diminish at longer term follow-up, suggesting that adolescents treated using other methods could often "catch up" to those treated with FBT ( Eisler et al., 1997; Robin et al., 1999). A further study documents that FBT is as effective in a 6 month/ten session dose as a 12 month/20 session dose, suggesting that FBT can be a highly efficient treatment for most adolescent patients ( Lock et al., 2005; Lock et al., 2006a).

Despite the larger evidence base for FBT, probably the most commonly used therapy for adolescent AN is an individually-based approach that is psychodynamically informed and developmentally tailored. The rationale for the approach is that AN is a maladaptive strategy to manage the developmental challenges of adolescence through avoidance of emotion, a concrete focus on maintaining a pre-pubescent body, and ambivalence about separation and individuation from parents. Treatment includes encouraging the patient to gain weight and to eat normally as a way for increasing self-control and mastery. This approach maps well onto many theoretical ideas that adolescents with AN develop symptoms because they feel out of control and/or are over controlled and prevented from developing into normal adolescents by their parents. The approach was initially called Ego-Oriented Individual Therapy (EOIT), but has been described in more clinical detail in a published brief manualized form called Adolescent Focused Therapy (AFT) ( Fitzpatrick et al., in press; Robin et al., 1999). Evidence about the usefulness EOIT/AFT is limited at this time to two RCTs that compared this treatment to either FBT or a treatment closely modeled FBT (Behavioral Family Systems Therapy).( Robin, 2003; Robin et al., 1999) In the first study, participants did well in both treatments, though weight and menstrual return was greater in FBT. EOIT/AFT was also compared to FBT in a larger RCT with 121 adolescents with AN ( Lock et al., in press-b) with results similar to those found in the Robin et al study (1999) suggesting that AFT was effective and helpful to patients.

Cognitive Behavioral Therapy (CBT) is suggested to be useful for adolescent AN ( Cooper and Stewart, 2008). The rationale for the approach is that the patient with AN has distorted thoughts about shape and weight and an over valuation of thinness ( Pike et al., 2004). These lead in turn to severe dieting and over exercise to lose weight. CBT for AN addresses these behavioral and distorted thoughts through normalizing eating patterns, monitoring food intake through food logs, collaborative problem solving, behavioral experiments, and cognitive restructuring. Adaptations of CBT for adolescents include involvement of parents, use of real time monitoring, and attention to interpersonal dilemmas within an expanded model of CBT ( Cooper and Stewart, 2008). While some evidence support CBT for adolescents with BN only one RCT study has examined CBT in adolescents with AN ( Gowers et al., 2007). This study compared CBT to hospital treatment and usual care. The sample included 167 adolescent females, and no differences were found between the three groups at end of treatment or follow-up, except that CBT was the most cost-effective ( Byford et al., 2007).

Nutritional advice and counseling is often recommended in the treatment of eating disorders. However, evidence of the usefulness of this approach is not available for adolescents. In adults, one study of 30 AN patients, those that those that received nutritional counseling gained more weight than those in psychological treatment, while those who received psychological treatment improved more on measures of psychological change ( Hall and Crisp, 1987). In the other published study, CBT was compared to nutritional counseling. Patients randomized to CBT recovered at significantly greater rates (17%) compared to nutritional therapy (0%) ( Pike et al., 2004). Despite the limited support for dietary advice, it is commonly used and may be useful for some adolescents with AN. However, there are also concerns that some types of dietary counseling may be deleterious in younger patients because diet plans and dietary regimens can sometimes worsen eating and weight preoccupations and obsessions. In addition, these types of plans can also undermine parental authority when using an approach where parents are expected to make dietary decisions (e.g. FBT).

Treatment for AN often includes treatment in inpatient, residential, or day programs. However, studies of the effectiveness of such treatment programs for AN are limited. The available data suggest that hospital treatment for adolescent AN is not more effective on average than outpatient treatment. In a recent study examining this issue, an adolescent population was randomized to hospital treatment, CBT, or treatment as usual (TAU). Those treated in hospital received an average of 15.2 weeks of hospital treatment on a specialized eating disorder service ( Gowers et al., 2007). Outcomes at the end of treatment and follow-up suggested that hospitalized patients did no better than those who received outpatient care. Other forms of treatment, residential care, day programs, and other intensive professional treatment programs have not been systematically studied. Thus, the usefulness of hospitalization for the majority of adolescents with AN is doubtful especially as such treatment may lead to unnecessary separation from family and friends and exposure to more intractable patients with AN. It remains unclear for whom and when these intensive type programs should be utilized.

Medication studies for adolescents with AN are limited and results to date are not promising ( Couturier and Lock, 2007; Crow et al., 2008). Although medications in most psychotropic medication classes have been studied in small case series or trials in adults, none of them consistently demonstrate systematic effectiveness. There was enthusiasm for the potential for SSRIs (e.g., fluoxetine) as possibly useful to prevent weight loss after acute weight restoration, but a large study now suggests that this is not likely ( Walsh et al., 2006). Also, atypical antipsychotics, because of their propensity to lead to weight gain as well as their anxiolytic properties, have been considered potentially useful. Data from a few small adult studies of adults with AN using Olanzapine are inconsistent as to the benefits of this medications on weight gain or related psychosocial variables with some suggesting benefit, while others do not ( Bissada et al., 2008; Brambilla et al., 2007). Smaller case series studies in adolescent samples reach a similar conclusion, though systemic studies are pending.( Broachie et al., 2003) A recent report examining risperidone (mean dose 3mg for a median duration of 9 weeks) in 41 adolescents with AN being treated in a milieu based treatment program found no specific benefit to this adding medication in adolescent AN on any measure of weight or psychological variables ( Hagman et al., 2009). Using medications for co-morbid conditions (anxiety disorder, depression) appears to be useful in some cases, though waiting until moderate weight regain has been accomplished makes both treatment targets and treatment effects more specific and effective.

Bulimia Nervosa

CBT is considered the first line treatment for BN in adults. Treatment targets normalizing eating patterns through the use of food diaries and behavioral experiment and supports cognitive change through problem solving and cognitive restructuring. In adults with BN, CBT has been the subject of many RCTs and has been shown to be superior to all treatments to which it has been compared at the end of treatment. CBT been adapted for adolescents and manualized then subsequently used in a case series of adolescents with BN which found abstinence rates (30-40%) similar to those in adult studies ( Lock, 2005). Only one RCT compared guided self-help CBT to FBT for BN in adolescents and found outcomes at the end of treatment and follow-up similar for both groups, but CBT was more cost-effective ( Schmidt et al., 2007). A small case series from the Maudsley group suggested that FBT might be useful for adolescent BN ( Dodge et al., 1995). One RCT examining FBT-BN compared it to a non-specific individual supportive psychotherapy (SPT) ( Le Grange et al., 2007). FBT was superior to SPT in terms of abstinence rates of binge eating and/or purging at the end of treatment and at follow-up. Overall improvement was similar to that reported in adults treated with CBT with abstinence rates at 6 month follow-up about 30%.

Medications are sometimes recommended for treating BN. Antidepressants in particular have been examined in variety of adult studies in BN ( Mitchell et al., 2007). Antidepressants are useful and effective for adult BN, though doses were generally higher than usually prescribed for depression and the effect appears to be related to suppressing binge episodes rather than though altering mood. Only one small case series has demonstrated the acceptability and possible benefit of antidepressants (fluoxetine) for adolescent BN, but that was in the context of an inpatient multidisciplinary treatment program ( Kotler et al., 2003).

Treatment for those children and adolescents who are diagnosed with EDNOS but who do not meet some of the frequency, duration, or self-report weight and shape concerns for AN and BN, should likely be treated using approaches with evidence of effectiveness for the full-syndrome ( Le Grange et al., in press; Lock et al., 2006b). Some of the RCTs evaluating treatments for AN and BN in adolescents included sub-threshold participants lending support to the idea that these treatments will be effective for this EDNOS group ( Le Grange et al., 2007; Lock et al., 2005). In addition, some data suggest that family treatment (FBT) is useful for patients with AN symptoms that are present in patients under the age of 12 years ( Lock et al., 2006b). A range of treatments have been shown to be useful for adults with Binge Eating Disorder (BED) (currently an EDNOS diagnosis in DSM IV), including CBT, Interpersonal Psychotherapy, and medications for decreasing binge eating, but these treatments had little effect on obesity associated with BED ( Grilo et al., 2005; McElroy et al., 2003; Peterson et al., 2009; Safer et al., in press; Wilfley et al., 2002).

New Treatment Directions Based on Translating Findings from the Neurosciences

Although some progress has been made in the last decade generating systematic evidence about effective treatments for AN and BN in adolescents, many patients do not respond completely to these treatments. New directions in treatment research are being organized around new findings from the neurosciences and other clinical paradigms. For example, in the area of neuropsychology, studies of cognitive process in eating disorders suggest treatment of these processes might be a useful adjunctive treatment ( Treasure, 2007). Studies of adults with AN have identified two common neurocognitive processing inefficiencies in the population: cognitive inflexibility (set-shifting) and weak central coherence ( Roberts et al., 2005). Recent studies also suggest that similar cognitive flexibility difficulties and weak central coherence problems are present in adolescents with acute AN. ( Fitzpatrick et al., 2009). Further, neuroimaging studies suggest that a biological substrate may underlie this inflexible cognitive style ( Zastrow et al., 2009). Weak central coherence-an overly detailed focus to the neglect of the big picture( Lopez et al., 2008a; Lopez et al., 2008b) is found in other psychiatric populations, including OCD and autism spectrum disorders, disorders which sometimes occur co-morbidly with AN. An over focus on detail could support many of the obsessive preoccupation common to AN including calorie counting, weight and body checking, dietary content detail, and related behaviors and obsessive thoughts ( Treasure, 2007).

Treatment of inefficient cognitive processes through cognitive remediation therapy (CRT) has been used in brain injury, schizophrenia, and OCD and found to be useful in improving cognitive processes ( Buhlman, 2006; Lindenmayer et al., 2008; Wykes and Reader, 2005). Limited data suggest that the same may be true treating cognitive inefficiencies in adult AN ( Tchanturia et al., 2007). CRT consists of cognitive exercises that enhance cognitive flexibility including variation on "switching" tasks (i.e., Stroop, Simon task, illusion) and central coherence tasks which challenge the patient to succinctly describe the "main idea" of a piece of writing or provide an outline of the topics in a longer piece. These tasks are deliberately not focused on eating or weight, but are an opportunity to explore how thinking more flexibly and seeing the bigger picture apply to the general life circumstances of the patient. The use of CRT in the context of eating disorders, is seen as an adjunctive treatment-either to increase motivation, increase the ability to use other treatments, or to enhance maintenance of learning from other treatments-not as a stand alone treatment. In the context of adolescents with eating disorders, the idea of addressing cognitive process is particularly compelling, because adolescent brains are more flexible, undergoing major change anatomical and functional development, and therefore early intervention to improve cognitive processes may have life long benefits that could help prevent relapse, decrease the development of related psychiatric disorders, and improve cognitive functioning overall.

Emotion regulation studies may also provide an avenue for treatment development for eating disorders. Increasing evidence has targeted difficulties in self-regulatory behaviors, ( Marsh et al., 2009b) broadly defined, and emotion regulation skills, in particular ( Steiger and Bruce, 2007; Whiteside et al., 2007) as risk factors in the development of BN. Self-regulatory skills are linked to frontal-lobe development during adolescence and young adulthood, consistent with age of onset of BN symptomology ( Meyer et al., in press; Steiger and Bruce, 2007; Steiger et al., 2001; Whiteside et al., 2007). Recent fMRI studies suggest that both adult and adolescent BN subjects display difficulties in cognitive inhibition tasks (i.e., they are more impulsive) ( Lock et al., submitted-a; Marsh et al., 2009a; Marsh et al., 2009b). Dialectical Behavioral Therapy (DBT) might be useful for treating such dysregulation as it relates to binge eating and purging. DBT has shown some usefulness in adult BED and BN ( Safer et al., 2007).

Although current psychopharmacologic interventions for eating disorders are not particularly encouraging, converging evidence from and neurotransmitter and imaging studies confirms abnormalities in both seronergic and dopaminergic neurotransmitter systems for which future medications may be useful. In addition, while data about the usefulness of medications for core symptoms of AN and BN may be less impressive, medications targeting other symptoms, including depression, anxiety, and OCD may improve eating related outcomes.

There is considerable recent interest in developing and evaluating a broader and more comprehensive approach to CBT called CBT-E (enhanced) for eating disorders because many patients with other psychological problems in addition to BN do not respond to the focused version of CBT initially studied. Fairburn has recently published a version of this CBT-E that is expanded to include modules to address perfectionism, mood, interpersonal problems and low self-esteem that may be applicable to patients with all types of eating disorders ( Fairburn et al., 2008). A recent RCT for adult BN patients suggests that for the subset that experiences these additional problems, CBT-E is more effective than standard CBT ( Fairburn et al., 2009). It is possible this broader focus might be helpful for younger patients who often present with similar related psychological and interpersonal concerns.

Research limitations and challenges

As this review highlights, evidence for effective treatments for adolescents with AN and BN is limited. There are few studies, most are small in scale, and many problems with design are present. Studies also utilize a range of different measures of outcome, and are under controlled. Among the major problems that impede progress is the limited base of clinical researchers in the field of child and adolescent eating disorders. Although AN and BN are disorders that onset in the adolescent years, most research to date has taken place with adult populations often with chronic disorders. There are few research centers or primary investigators that focus on this population who are child focused. As a result, diagnostic criteria, studies, treatments, assessment, and outcomes are focused on an older population. Although funding for eating disorder research is a stated priority of the US National Institute of Health, few studies focus on children and adolescents, and few laboratories are supported sufficiently to train investigators with an interest in this younger population.

Nonetheless, there are a number of current studies that may provide important new evidence to guide clinical practice. A large multi-site study comparing FBT to Systemic Family Therapy (SFT) ( Pote, 2003) for adolescent AN is underway with the aim of recruiting160 subjects from 6 intervention sites. This study should help clarify what specific role families play in treating adolescent AN. Another study, based at Westmead Children's Hospital in Australia is evaluating the role of FBT in decreasing the need for inpatient weight restoration by comparing treatment response using FBT after a brief medical hospitalization compared to FBT after full weight restoration. A study examining the benefits of FBT in subsyndromal AN (ENDOS) is underway at Mount Sinai in New York; while examination of FBT compared to family education groups is being conducted at Duke University. Other formats of FBT, including a multi-family group (MFG) model for adolescent AN is being completed in the UK. MFG may be particularly useful for more treatment resistant patients by providing support to parents who are stymied in their efforts to promote weight gain ( Dare and Eisler, 2000). A clinical trial evaluating the usefulness of CRT in older adolescents and adults with AN is also currently recruiting subjects at Stanford University. In addition, data from Fairburn et al on the usefulness of CBT-E for AN patients may be available soon.

For adolescent BN, a study is now underway comparing CBT, FBT, and Supportive Individual Therapy at the University of Chicago and Stanford University. This is the first study to compare a standard form CBT adapted for adolescents to FBT for this age group and only the third treatment study focused on adolescents with BN. Other studies addressing the benefit of other types of psychotherapy and the role of medications in adolescent BN are needed.

In addition to addressing the substantial gaps in our knowledge base about effective treatments, training and dissemination of effective treatments for eating disorders is limited. Few programs offer focused training for treating this population and fewer still provide training in any evidenced based interventions. As a result, mental health providers often feel under skilled in treating this population and refer to the specialty centers with inpatient and day hospital programs rather than treat them in their own practices. The interventions currently available require training and psychotherapy skills, but the ability to evaluate and treat these common adolescent mental health problems need to be more readily available in local communities.

​

Table 1

STUDY

Eating Disorder

TYPE TREATMENT

N

AGE

(Mean)

OUTCOMES
(Morgan-Russell Modified
Outcome Groups
(Intermediate or Good
Outcome by Weight >
85% IBW)

Supportive therapy=18% p<.02

EOIT=65% p<.05

CBT = 22%

TAU = 31%

NS

CBT =42%

NS

SIT = 19%

P = .049

Table 2

Treatment Type

Eating Disorder

Studies

Level of Evidence

Recommendation

Family-Based Treatments

AN

5 RCTs( Eisler et al., 2000; Le Grange et al., 1992; Lock et al., 2005; Lock et al., in press-b; Robin et al., 1999; Russell et al., 1987)

+++

A good first line treatment

Other Family Therapies( Minuchin et al., 1978)

AN

Case series data

+

A possible treatment option

Adolescent Focused Therapy(Lock et al., submitted-b; Robin et al., 1999)

AN

2 RCTs

++

A reasonable treatment option

Cognitive Behavioral Therapy( Gowers et al., 2007; Lock, 2005; Schapman and Lock, 2006; Schmidt et al., 2007)

AN

1 RCT

+

A possible treatment option

Antidepressants( Kotler et al., 2003)

AN

No RCT

0

Unknown usefulness

Atypical Antipsychotics( Broachie et al., 2003; Hagman et al., 2009)

AN

1 RCT; case series

++

Evidence suggests no benefit

Nutritional Advice/Counseling( Hall and Crisp, 1987; Pike et al., 2004)

AN

2 RCTs in adults, none in adolescents

+

Limited evidence suggests little specific benefit

References

Fitzpatrick K, Moye A, Hostee R, Le Grange D, Lock J. Adolescent Focused Therapy for Adolescent Anorexia Nervosa. Journal of Contemporary Psychotherapy. (in press) [Google Scholar]

Hagman J, Gralla J, Dodge M, Eller S, Gardner R, Wamboldt M. American Academy of Child and Adolescent Psychiatry. Honolulu, HI: 2009. A double-blind placebo controlled study of risperidone for anorexia nervosa. [[PMC free article] [PubMed] Google Scholar]

# data[].attributes.attachment_link.title
Treatment of Adolescent Eating Disorders: Progress and Challenges

# data[].attributes.attachment_link.description
Although eating disorders are common psychiatric disorders that usually onset during adolescence, few evidence-based treatments for this age group have been identified. A critical review of treatments used for Anorexia Nervosa (AN) and Bulimia Nervosa (BN) and related conditions (EDNOS) is provided that summarizes the rationale for the treatments, evidence of effectiveness available, and outcomes.

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Treating Teens with Social Anxiety Disorder in Schools

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Treating Teens with Social Anxiety Disorder in Schools

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Clinical Points

■ Hallucinatory experiences and delusions are more common in our patients than we may realize and occur frequently in the pediatric population. While not a benign occurrence, psychotic symptoms do not necessarily portend the future development of schizophrenia.

■ Psychotic symptoms in children and adolescents can occur in the context of a bevy of psychiatric disorders other than schizophrenia (eg, depression, anxiety, attention-deficit/hyperactivity disorder, posttraumatic states, and autism spectrum disorders) or can be secondary to a wide variety of medical conditions.

■ The onset of psychosis is usually preceded by a period of nonpsychotic symptoms known as prodromal symptoms. In recent years, there has been substantial research in early intervention efforts (eg, with psychotherapy or antipsychotic medicines) focused on the early stages of schizophrenia and on young people with prodromal symptoms. At present, outcome data are insufficient to draw definitive conclusions.

■ The pharmacologic treatment of psychotic symptoms in a pediatric population is similar in many ways to the treatment of infection with antibiotics-the clinician needs to choose the proper medication at a sufficient dose and then await therapeutic results while monitoring for potential side effects.

Over the past decade, psychiatric illnesses and, in particular, psychotic disorders in children and adolescents have been recognized more frequently. This increase in recognition, combined with changing trends in the provision of mental health care, has led primary care physicians and pediatricians to increasingly serve as the principal treaters of psychiatrically ill youth and their families. Primary care providers and behavioral health services (eg, in colocated care, embedded care practices, patient-centered homes, and consultation) form the backbone of contemporary psychosis evaluation and management. It is unclear whether psychotic disorders in younger individuals are actually becoming more prevalent, or whether educational efforts directed at enhanced screening and treatment have improved case detection. Efficacious and safe interventions should be employed to maximize beneficial effects and to minimize medication-related complications, such as weight gain, diabetes, and heart disease.

The question for today's health care providers is not whether psychotic symptoms will be encountered in daily practice, but how to confidently and effectively diagnose and treat the conditions in which they manifest. In order to frame this discussion, several areas of inquiry will be explored: "Have you ever been unsure about whether a young person in your practice was psychotic or simply imaginative? Have you wondered how to evaluate such a patient (eg, with laboratory testing or with neuropsychological testing) and what resources to recommend? Have you been concerned about using antipsychotics in young people? Does the potential for adverse side effects of antipsychotics in the short-term or long-term concern you?" For practitioners faced with these concerns, the following discussion should prove useful.

WHAT IS PSYCHOSIS AND HOW COMMON IS IT IN YOUNG PEOPLE?

Narrowly defined, psychosis denotes the presence of either delusions (false implausible beliefs) or hallucinations (false perceptions involving any sensory modality). Broader definitions of psychosis include manifestations of thought disorders, behavioral disorganization, or catatonia. Family members, particularly parents, are often concerned that children who manifest delusions or hallucinations might have schizophrenia. Fortunately, most forms of psychosis in children and adolescents are not a result of schizophrenia.

Population-based surveys show that the prevalence of psychotic symptoms may be far greater than had been previously considered, with a meta-analysis suggesting a prevalence rate of 5%-8% in the general population (which is nearly 10 times higher than the prevalence of diagnosed psychotic disorders). Prevalence rates of such symptoms may be even higher among young people. In 2000, Poulton and colleagues reported that 14% of 11-year-old children endorsed psychotic symptoms upon interview and showed that these symptoms were associated with a 5-fold to 16-fold increased rate of psychotic illness in early adulthood (depending on the strength of the initial symptoms). Since then, large, population-based studies surveying psychotic symptoms among adolescents have found rates of 9%-14% in interview-based studies, and rates greater than 25% in some studies using self-report questionnaires. ⁻ Positive answers on self-report questionnaires have been validated on clinical interview. This emerging body of research suggests that a sizable minority of young people experience psychotic symptoms.

DOES THE PRESENCE OF PSYCHOTIC SYMPTOMS NECESSARILY PORTEND A DIAGNOSIS OF SCHIZOPHRENIA?

However, rather than being a harbinger of schizophrenia, psychotic symptoms in childhood and adolescence more likely accompany other psychiatric conditions (eg, major depression, bipolar disorder, or dissociative states). lists psychiatric disorders that can be accompanied by psychosis. Differentiating early-onset schizophrenia or childhood-onset schizophrenia from other psychiatric disorders has important treatment implications. For example, a pediatric patient with bipolar disorder often experiences hallucinations and delusions but also has the clinical characteristics of mania, depression, or both. In children with psychological trauma-related hallucinations (typically associated with nightmares and trance-like states), psychotic symptoms may quickly abate with psychotherapeutic and/or social interventions. Compared to traumatized children, children with schizophrenia are more apt to display a formal thought disorder, negative symptomatology (eg, apathy, social isolation), and impulsive aggression. Like children and adolescents with schizophrenia, those with autism spectrum disorders may also have odd beliefs (eg, believing that they are able to communicate with valued inanimate toys). Children with milder forms of autism (eg, Asperger's syndrome) may be misdiagnosed with psychosis due to their idiosyncratic beliefs, social awkwardness, and concrete thought process. Taking a comprehensive clinical history helps to disentangle diagnostic uncertainties.

Table 1

Psychotic symptoms have been associated with, or are secondary to, a wide variety of medical disorders as well. Psychosis may develop in response to central nervous system lesions, as a consequence of medical illness, or after traumatic injury or drug use. Recently, reports have linked a particularly severe form of new-onset psychosis-often associated with insomnia, catatonia, and autonomic instability-to antibodies against the glycine-binding NR ₁ subunits of the anti- N-methyl-d-aspartate (NMDA) receptor. Overall, studies from the adult literature show that about 3% of new-onset presentations of psychosis can be attributed to a medical condition., Therefore, before making a diagnosis of a primary psychotic disorder, secondary causes should be ruled out by a thorough-but not indiscriminate-medical workup.

WHAT ARE PRESENTING CHARACTERISTICS OF PSYCHOSIS IN CHILDREN AND ADOLESCENTS?

The most common manifestations in young people with psychosis are hallucinations, impaired functioning, flattened affect, and social withdrawal., Caregivers are more likely than the child patients themselves to report these problems to the clinician, as children often minimize, misinterpret, or avoid mentioning their symptoms. Hence, a comprehensive psychiatric assessment should include interviews with the child and his or her family members, review of records, information gathered from other involved adults (including a detailed description of the presentation and course of the psychotic symptoms), attention to developmental delays, a family psychiatric history, a history of abuse and/or neglect, and a mental status examination.,

Unlike adults, children with psychosis rarely demonstrate waxy flexibility or become catatonic. On the other hand, they can be emotionally reactive or agitated. The majority of children with childhood-onset schizophrenia often exhibit "soft" neurologic signs, including primitive reflexes, abnormal stereognosis, 2-point discrimination, and dysdiadochokinesia (impaired rapid alternating movements). Affected youth may manifest either a decreased or increased rate of eye blinking, as well as paroxysmal saccadic eye movements (inability to follow an object with smooth eye movements).

HOW ARE CHILDREN AND ADOLESCENTS DIAGNOSED WITH SCHIZOPHRENIA?

The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders ( DSM-5) made several changes to the category of schizophrenia, including raising the symptom threshold. A diagnosis of schizophrenia now requires 2 of the following conditions: delusions, hallucinations, disorganized speech, grossly disorganized or catatonic behavior, or negative symptoms such as affective flattening or paucity of thought or speech (in the manual's previous editions, the threshold was 1). To meet diagnostic criteria, symptoms must be present for at least 6 months (including at least 1 month of active symptoms); must result in deterioration in social, school-related, and self-care functioning; and should not be accounted for by a diagnosis of schizoaffective disorder, a mood disorder, a substance use disorder, or general medical conditions.

Additionally, an "attenuated psychosis syndrome" was included in the research section as a category for persons who do not meet criteria for a full-blown psychotic disorder but exhibit minor variations of relevant symptoms. This category seeks to identify individuals with an increased risk for developing a psychotic disorder, which may be significant for the implementation of effective early interventions.

Personality tests and projective tests should not be used to diagnose schizophrenia in youth; research indicates that tests, such as the Rorschach, do not increase the diagnostic accuracy in early-onset schizophrenia.

WHAT CAUSES SCHIZOPHRENIA IN CHILDHOOD AND ADOLESCENCE?

While there is no single confirmed etiology of childhood-onset or early-onset schizophrenia, it is likely that genetic, behavioral, and environmental factors all contribute to the development of this disease.

Genetic risk has been well-studied. First-degree relatives of patients with childhood-onset schizophrenia have a higher prevalence rate of schizophrenia and schizophrenia spectrum disorders, as well as impairment in smooth pursuit eye movements similar to those observed in patients with adult-onset schizophrenia. One study found that healthy siblings of patients with childhood-onset schizophrenia had decreased cerebral gray matter in the same pattern as was seen in the probands. In an investigation of youth identified as being at "high risk," the young relatives of patients with schizophrenia demonstrated an increased rate of Axis I psychopathology (eg, attention-deficit/hyperactivity disorder [ADHD], conduct disorder), soft neurologic signs, and a high level of outwardly expressed emotion. On neuropsychological examination, these "high-risk" nonprobands also demonstrated impairment in attention, spatial working memory, and executive function, as well as a volume reduction in the amygdala, hippocampus, and superior temporal gyrus.

WHICH NEURODEVELOPMENTAL AND NEUROBIOLOGICAL ABNORMALITIES ARE ASSOCIATED WITH YOUTH WHO DEVELOP SCHIZOPHRENIA?

Structural brain abnormalities are an established feature of schizophrenia, and recent evidence suggests a progressive nature of this pathology. Like adults with schizophrenia, youth with childhood-onset schizophrenia show bilateral enlargement of the lateral ventricles on neuroimaging. However, unlike adults, the abnormalities in brain morphology in patients with childhood-onset schizophrenia evolve during adolescence. Rapoport and associates, reported that adolescents with schizophrenia have significantly reduced frontal and temporal gray matter volumes compared with those observed in healthy age-matched controls. Moreover, youth with childhood-onset schizophrenia appear to lose more cortical gray matter compared to children who suffer from transient psychosis. Subsequent studies from this group have shown that the healthy siblings of afflicted patients also have reductions in cerebral volume and gray matter. Similar to patients with adult-onset schizophrenia, over the course of development, youth with childhood-onset schizophrenia appear to lose cortical thickness in prefrontal and temporal regions, regardless of their treatment with medications. In a systematic review of 66 articles comparing brain volume in patients with a first psychotic episode with the volume seen in healthy controls, a meta-analysis demonstrated that whole-brain and hippocampal volumes are reduced and that ventricular volumes are increased in affected patients compared to healthy controls. Future improvements in neuroimaging technology hold the potential to reveal more about neurobiological disturbances and their correlates in schizophrenia. Yet, at present, results of neuroimaging studies have not made the leap from bench to bedside.

WHICH NEUROTRANSMITTERS ARE THOUGHT TO BE INVOLVED IN SCHIZOPHRENIA?

The neurotransmitter most commonly implicated in the pathophysiology of schizophrenia is dopamine. Drugs that increase dopaminergic receptor activity (eg, cocaine, amphetamines) may induce an acute psychotic episode, whereas drugs that block postsynaptic D ₂ receptors help to alleviate psychotic symptoms. Furthermore, persons with schizophrenia also have fewer D ₁ receptors in the prefrontal cortex. Disturbances in a variety of other neurotransmitters such as glutamate, serotonin, and γ-aminobutyric acid (GABA) have been implicated in the pathophysiology of schizophrenia. Researchers are also interested in glutamate because phencyclidine (PCP or angel dust) is an NMDA/glutamine antagonist; NMDA receptor dysfunction can also cause psychotic symptoms. As mentioned earlier, anti-NMDA receptor antibodies, sometimes secondary to teratomas or autoimmune dysfunction, can cause psychosis in children, often in conjunction with autonomic instability and seizures. Serotonin may also be important; most second-generation antipsychotics share relatively potent antagonism of serotonin 5-HT 2A receptors coupled with relatively weaker antagonism of dopamine D ₂ receptors. Preliminary studies suggest that GABA may also play a role in the development of chronic psychotic syndromes. Overall, disrupted neurotransmission and cognitive functions are key components in the pathophysiology of schizophrenia; however, no single neurotransmitter is clearly responsible for the onset and progression of schizophrenia.

ARE THERE ENVIRONMENTAL RISKS FOR THE DEVELOPMENT OF SCHIZOPHRENIA?

It is clear now that "the grass is not greener," as data from 6 longitudinal studies in 5 countries have shown that regular cannabis use predicts an increased risk for schizophrenia and symptoms of psychosis. Cannabis use during early adolescence coupled with a specific genetic vulnerability and changes in brain development are correlated with risk for the development of schizophrenia and overall cognitive decline. However, the direction of the effect has been called into question. Some suggest that individuals with psychosis use cannabis to alleviate their psychotic symptoms or to improve their mood. Others, however, suggest that cannabis causes or exacerbates psychotic symptoms. A pooled analysis of 35 studies showed a dose-response effect, with greater risk of psychosis in people who used cannabis most frequently. Moreover, individuals with schizophrenia who are moderate to heavy cannabis users show a greater brain volume reduction over a 5-year follow-up compared with nonusers.

Despite the fact that fewer adolescents believe that regular cannabis use is harmful to their health and increasingly permissive state laws governing the use of medical marijuana, the medical literature presents clear evidence for a neurotoxic effect of cannabis on the adolescent brain. These findings highlight the importance of efforts targeting adolescent cannabis use, including policy measures and psychoeducation in the doctor's office.

HOW CAN ONE DISTINGUISH PRIMARY PSYCHOSIS FROM SECONDARY PSYCHOSIS?

A thorough medical workup is essential for distinguishing between primary and secondary psychotic disorders. lists medical disorders that have been associated with psychosis. Although there is no generally agreed-upon medical evaluation that every patient with psychosis should undergo,, screening tests should be ordered on the basis of a patient's personal and family history, as well as on the basis of one's clinical suspicion of conditions. Blanket testing for rare disorders may increase the risk of false-positive or false-negative results. On the other hand, the search for medical etiologies of psychosis may be expanded in the face of atypical presentations or when cases are refractory to standard treatments.

Table 2

Infections

Creutzfeldt-Jakob disease

Herpes encephalitis

Human immunodeficiency virus infection

Lyme disease

Subacute bacterial endocarditis

Sydenham's chorea

Metabolic disturbances

Adrenocortical insufficiency

Cushing's disease

Hypercalcemia or hypocalcemia

Hypermagnesemia or hypomagnesemia

Hypernatremia or hyponatremia

Hyperthyroidism

Hypoglycemia

Hypokalemia

Hypophosphatemia

Lactic acidosis

Panhypopituitarism

Parathyroid disease

Thyroid storm

Neurologic

Cerebral neoplasms

Cerebrovascular disease

Cerebral lipidoses

Complex partial auras or seizures

Creutzfeldt-Jakob disease

Encephalitis (including anti- N-methyl-d-aspartate receptor encephalitis)

Focal lesions of temporal and parietal lobe

Generalized seizures

Hepatic encephalopathy

Herpes encephalitis

Multiple sclerosis

Normal pressure hydrocephalus

Temporal arteritis

Postnoxic encephalopathy

Posttraumatic encephalopathy

Fragile X syndrome

Klinfelter's syndrome

Metachromic leukodystrophy

Prader-Willi syndrome

Velocardiofacial syndrome

Wilson's disease

Vitamin deficiencies

Folate deficiency

Niacin deficiency

Vitamin B ₁₂ deficiency

Vitamin D insufficiency

Medications

Drug classes that can cause hallucinations or delusions

Amphetamine-like drugs

Anabolic steroids

Angiotensin-converting enzyme inhibitors

Anticholinergics

Antidepressants (both tricyclic antidepressants and selective serotonin reuptake inhibitors)

Antiepileptics

Barbiturates

Benzodiazepines

β-adrenergic blockers

Calcium channel blockers

Cephalosporins

Corticosteroids (prednisone, cortisone, adrenocorticotropic hormone, others)

Dopamine receptor agonists

Fluoroquinolone antibiotics

Nonsteroidal antiinflammatory drugs

Procaine derivatives (procainamide, procaine, penicillin G)

Salicylates

Sulfonamides

Alcohol toxicity/withdrawal

Illicit use of drugs (including prescribed medications)

Amphetamines

Glue sniffing/ingestion

Lysergic acid diethylamide

Methamphetamine (crystal meth)

Phencyclidine hydrochloride (PCP)

Psilocybin (mushrooms)

Toxicologic causes

Carbon monoxide poisoning

Heavy metal poisoning (eg, mercury, lead)

Key tests in the pediatric population () may include drug screens (to rule out medication or substance-related psychosis), laboratory studies (to rule out infections, metabolic disturbances, certain genetic conditions, or vitamin deficiencies), an electroencephalogram (EEG), and structural neuroimaging (eg, magnetic resonance imaging [MRI] or computed axial tomography [CT] scanning). The clinical relevance of a given EEG tracing can be difficult to discern, as almost half of the patients with new-onset psychosis will have EEG abnormalities of unclear significance. Furthermore, EEGs read as "normal" may not capture an interictal psychosis. Likewise, incidental and non-clinically meaningful MRI findings are found in approximately 20% of the non-psychiatrically ill population. Recent guidelines suggest that structural neuroimaging should not be obtained routinely during an evaluation for a first episode of psychosis. Despite the low yield of neuroimaging, counter arguments supporting its judicious use emphasize that patients and families feel reassured by negative scans. Conversely, neuroimaging can rule out rare etiologies for psychosis (eg, brain tumors) and help patients and families understand and accept the psychotic symptoms as manifestations of a psychiatric disorder.

Table 3

Electroencephalogram

Imaging studies (eg, magnetic resonance imaging or computed tomography of the brain) in select patients based on clinical suspicion

Laboratory studies

Antinuclear antibodies

Blood urea nitrogen/creatinine

Calcium and phosphorus

Ceruloplasmin (for Wilson's disease)

Complete blood count

Electrolytes

Erythrocyte sedimentation rate

FTA-Abs (for syphilis)-preferred over rapid plasma reagin

Human immunodeficiency virus screening

Liver function tests

Thyroid-stimulating hormone

Urinalysis

Urine (and/or serum) drug screen

HOW SHOULD PSYCHOSIS DUE TO AN UNDERLYING MEDICAL CONDITION BE TREATED?

The optimal treatment for secondary psychosis is treatment of the underlying medical or neurologic condition. Concomitant treatment of the secondary psychosis (usually with an antipsychotic agent) can protect both the patient and the treatment team while medical treatment is administered. Notably, most guidelines for dosing antipsychotics are based on the treatment of patients with schizophrenia and bipolar disorder. Patients treated for psychosis related to medical causes are often antipsychotic naive and sensitive to the sedating properties of lower-potency antipsychotics and to the extrapyramidal effects of higher-potency antipsychotics.

WHAT DOES THE FIRST EPISODE OF PSYCHOSIS INVOLVE?

Once functionally impairing psychotic symptoms develop-defined in terms of symptom severity and duration-a patient is no longer considered to be in the prodromal phase of illness, but instead diagnosed with an episode of psychosis. Clinically, the demarcation between prodromal (or "attenuated") symptoms and frank psychosis is rarely clear-cut, particularly in a patient with brief or intermittent bouts of mild psychotic symptoms. Moreover, few patients receive emergency treatment for psychosis. The median duration of untreated psychosis refers to the lag between the development of symptoms and the initiation of treatment. This lag time can range from 4 to 50 weeks in first episodes, and can extend longer when mood symptoms or illicit drug use cloud the diagnostic picture. The availability of mental health resources, socioeconomic factors, and cultural attitudes toward mental illness can also affect the time to treatment. Most studies show that a longer duration of untreated psychosis is associated with worse clinical outcomes. This observation has spurred increased research interest into interventions that target the period prior to, or immediately after, the development of a psychotic disorder. The hope is that these targeted interventions might forestall the onset of psychosis or improve long-term outcomes.

WHAT PSYCHOSOCIAL TREATMENTS ARE AVAILABLE FOR YOUTH WITH PSYCHOSIS OR SCHIZOPHRENIA?

Cognitive-behavioral techniques that evaluate evidence for beliefs or thinking through explanations surrounding a patient's perceptions can help to alter dysfunctional behaviors. A consistent framework with similar words/techniques used at home, at school, and with friends may allow the patient to employ a standardized approach to events across settings and to diminish misperceptions of daily events and interactions.

Research data supporting psychosocial treatments in pediatric psychotic disorders are scant. There is a controlled study comparing cognitive-behavioral therapy (CBT) with no antipsychotic to a monitoring program in prodromal patients. CBT was associated with less progression to psychosis; however, the results of this study were limited by methodological flaws. The PACE (Personal Assessment and Crisis Evaluation) trial randomly assigned prodromal patients (aged 14-28 years) to risperidone plus CBT versus a needs-based intervention of supportive therapy and psychotropics other than antipsychotics. At 6 months, 3 of 31 patients in the risperidone plus CBT group converted to psychosis, whereas 10 of 28 patients in the supportive therapy and nonneuroleptic pharmacotherapy group converted to psychosis. Since the average risperidone dose used in this study was relatively low (1.3 mg/d), there is a suggestion that CBT was a vital ingredient to the protective effects seen in this study.

WHAT DOES THE PHARMACOTHERAPY OF SCHIZOPHRENIA IN YOUTH INVOLVE?

Pharmacologic treatment for schizophrenia in youth remains an area of active research, with several large multisite trials completed within the past few years. Six, 6-week, randomized, placebo-controlled studies of second-generation antipsychotics for early onset schizophrenia have been completed thus far. They showed that aripiprazole, olanzapine, paliperidone, quetiapine, and risperidone-but not ziprasidone-were superior to placebo. In these controlled studies, aripiprazole, olanzapine, paliperidone, quetiapine, and risperidone, were superior to placebo with regard to improvement in the Positive and Negative Syndrome Scale (PANSS) total score.

In terms of atypical antipsychotic dosing, typically, these medications are initiated at a low dose and gradually titrated upward to achieve efficacy. Risperidone, for example, is generally started at 0.25 mg twice a day and can be increased every 1 to 2 days in association with close observation. In general, olanzapine and quetiapine are more sedating; their dosing is usually started at 2.5 to 5 mg/d and 25 to 50 mg/d, respectively. As most antipsychotic medications have a relatively long half-life, they typically do not need be administered more than twice daily. For patients maintained on antipsychotics, clinicians should monitor weight, vital signs, and relevant laboratory results (eg, triglycerides, cholesterol, fasting glucose, and prolactin levels).

Newer atypical antipsychotics (eg, asenapine, iloperidone, lurasidone) may eventually have a role in the treatment of patients with childhood-onset or early onset schizophrenia and in patients deemed at-risk of developing schizophrenia due to genetic and/or environmental factors. However, at present, there is little evidence to support the safety, tolerability, or efficacy of these agents in the pediatric population.

In sum, current pharmacologic research for early-onset and childhood-onset schizophrenia focuses on the identification of antipsychotic agents that will provide optimal efficacy without also causing undue adverse events. Many typical and atypical antipsychotics have been shown (based on open trials, randomized clinical trials, and head-to-head comparisons) to be efficacious in the treatment of early-onset and childhood-onset schizophrenia; however, they are well known to cause side effects such as weight gain, extrapyramidal symptoms, and metabolic abnormalities.

WHAT IS THE ROLE OF LONG-ACTING (INJECTABLE) ANTIPSYCHOTICS IN CHILDHOOD-ONSET SCHIZOPHRENIA?

In the near future, as many as 4 new atypical antipsychotic long-acting therapy formulations may become available. In clinical situations wherein adherence with oral preparations has proven difficult, it is reasonable-especially in older adolescents-to consider using a long-acting medication. Risperidone long-acting therapy has been shown to be efficacious and well tolerated in the treatment of schizophrenia, including those with newly diagnosed schizophrenia. Short-term and long-term studies found that risperidone long-acting therapy was associated with low rates of discontinuation related to adverse events and few reports of pain from injections. Evidence for newer long-acting injectables (eg, olanzapine, paliperidone) remains limited. The available evidence suggests that long-acting injectable antipsychotics can be used safely and effectively in early stages of the illness and that they may be associated with better outcomes than with oral medications. However, this is largely supported by evidence from naturalistic cohort studies and by a small number of controlled trials of risperidone long-acting injection. Given the paucity of data of long-acting therapy in the adolescent population, the use of these preparations in adolescents remains empiric. provides the side effect risk profiles of common second-generation antipsychotic medications used in children and adolescents.,

Table 4

Second-Generation Antipsychotics
(trade name)

Anticholinergic

Diabetes

Hyperlipidemia

Hyperprolactinemia

Hypotension

Sedation

Tardive Dyskinesia

Weight
Gain

WHAT ARE THE ADVERSE EFFECTS OF ANTIPSYCHOTICS?

In reviewing the available randomized, controlled studies and head-to-head comparisons of antipsychotics, Schimmelmann and colleagues noted, "Antipsychotics are efficacious in the treatment of early-onset schizophrenia. The lack of evidence for efficacy differences between various antipsychotics (except for clozapine for treatment-refractory early-onset schizophrenia) suggests that a primum non nocere principle should be applied when choosing and antipsychotic."(p228) Therefore, the side effect profile of the antipsychotics often dictates the choice of pharmacologic agent for young people with psychotic symptoms. Antipsychotic therapy has been linked to a bevy of metabolic changes (eg, dyslipidemia, weight gain, plasma prolactin increases), sedation, extrapyramidal symptoms, and dyskinesias (see ). With the exception of tardive dyskinesia, young people with schizophrenia seem more likely to experience these side effects from atypical neuroleptics compared with their adult counterparts. Children and adolescents may gain weight, even when treated with antipsychotics that are considered "weight-neutral" in adults. Similarly, there are reports of prolactin elevations in youth treated with prolactin-sparing agents such as quetiapine.

Other common adverse effects of antipsychotics include drowsiness and anticholinergic effects (eg, dry mouth, nasal congestion, blurred vision), particularly with the low-potency phenothiazines. Caregivers can usually manage the short-term adverse effects of antipsychotics with adjustments of dose and timing of administration. One can avoid undue sedation by using less sedating agents and by prescribing most of the daily dose at bedtime. One should not confuse drowsiness with impaired cognition; drowsiness can usually be corrected by adjusting the dose and the timing of administration. Furthermore, there is no evidence that antipsychotics adversely affect cognition when used in low doses. One can minimize anticholinergic effects by choosing a medium-potency or high-potency antipsychotic.

Extrapyramidal Side Effects

Extrapyramidal side effects such as acute dystonia, akathisia (motor restlessness), and parkinsonism (bradykinesia, tremor, and lack of facial expressions) are more commonly seen with use of high-potency agents (eg, butyrophenones, thioxanthenes) and have been reported in up to 75% of children receiving these agents. The extent to which antiparkinsonian agents (eg, anticholinergic drugs such as benztropine, trihexyphenidyl, antihistamines, and the antiviral agent amantadine) should be used prophylactically when antipsychotics are introduced is controversial, although coadministration has been shown to reduce the incidence of extrapyramidal side effects by a factor of 7.

Other Movement Disorders

Abrupt cessation of antipsychotic drugs can cause withdrawal dyskinesias (typically benign, but occasionally more pronounced) and a syndrome of deteriorating behavior. As with adults, the long-term administration of antipsychotic drugs can produce tardive dyskinesia. Although children appear generally less likely to develop tardive dyskinesia than adults, the fact that tardive dyskinesia is potentially irreversible prompts caregivers to evaluate the benefits of such medications, including documenting a clear indication and identifying target symptoms; to periodically discontinue the drug to assess continued need; and to monitor closely to ensure early detection. Current practice parameters recommend monitoring neurologic side effects with standardized scales (eg, Abnormal Involuntary Movement Scale or Simpson Angus Scale) at baseline and periodically during any treatment regimen requiring antipsychotic agents.

Akathisia

Akathisia is a movement disorder characterized by anxiety and an inability to sit still; it can be a side effect of either antipsychotics or antidepressants. Akathisia may be particularly problematic in young patients because of underrecognition or misdiagnosis as ADHD or agitation. Caregivers should consider akathisia in the differential when a child or adolescent starts an antipsychotic and becomes acutely agitated with an associated inability to sit still (and/or with aggressive outbursts).

Treatment of akathisia involves reduction of the offending agent to the lowest effective dose and then using either a benzodiazepine (eg, lorazepam, 0.5 to 1 mg 3 times per day) or a β-blocker. Although all β-blockers are likely to be effective, propranolol, initiated at 10 mg 2 or 3 times per day with an increase every few days until the desired effect is achieved, is a good choice. Alternately, betaxolol hydrochloride, a long-acting β ₁-selective adrenergic antagonist with few medication interactions, may be useful.

Neuroleptic Malignant Syndrome

Little is known about the potentially lethal neuroleptic malignant syndrome in children and adolescents; however, preliminary evidence indicates that its presentation is similar to that in adults. This syndrome may be difficult to distinguish from primary central nervous system pathology, concurrent infection, anti-NMDA receptor encephalitis, or other, more benign, side effects of antipsychotic treatment, including extrapyramidal side effects or anticholinergic toxicity. Neuroleptic syndrome is a life-threatening medical emergency; treatment is largely supportive but can include dopamine reuptake inhibitors like amantadine, similar to strategies used in adults.

WHAT STRATEGIES ARE HELPFUL FOR NONRESPONDERS?

A unique head-to-head randomized controlled trial of olanzapine and clozapine in the treatment of patients with childhood-onset schizophrenia showed that clozapine led to a statistically significant reduction in all outcome measures (particularly negative symptoms of schizophrenia) even when compared to another atypical agent.

WHAT STRATEGIES ARE AVAILABLE FOR EARLY INTERVENTION AND PREVENTION OF CHILDHOOD-ONSET SCHIZOPHRENIA?

The notion of early intervention and perhaps even prevention of schizophrenia remains at the forefront of early-onset psychosis research. Further research in this area is ongoing. However, at present, the literature does not support clear treatment guidelines for these vulnerable patients.

CONCLUSION

Clinicians should be vigilant and consider psychotic illnesses when evaluating children and adolescents with emotional and behavioral disturbances. Given the high developmental, financial, and functional toll associated with chronic psychotic illness, clinicians should employ a variety of diagnostic and treatment modalities to mitigate the risks associated with this illness. These modalities may include performing careful psychiatric and physical examinations, relevant laboratory testing, neuropsychological testing, and employing relevant cognitive therapies, as well as the use of antipsychotic and other pharmacologic interventions. Advances in the understanding of childhood-onset and early-onset schizophrenia, as well as the elucidation of prodromal psychotic symptomatology, will benefit both children and adults.

Footnotes
LESSONS LEARNED AT THE INTERFACE OF MEDICINE AND PSYCHIATRY
The Psychiatric Consultation Service at Massachusetts General Hospital (MGH) sees medical and surgical inpatients with comorbid psychiatric symptoms and conditions. During their twice-weekly rounds, Dr Stern and other members of the Consultation Service discuss diagnosis and management of hospitalized patients with complex medical or surgical problems who also demonstrate psychiatric symptoms or conditions. These discussions have given rise to rounds reports that will prove useful for clinicians practicing at the interface of medicine and psychiatry.

Dr Stevens is physician-in-charge at Westpark (Dearborn), Henry Ford Health Systems, Dearborn, Michigan, and clinical assistant professor at Wayne State University, Detroit, Michigan. Dr Prince is director of child psychiatry at North Shore Medical Center in Salem, Massachusetts, and an instructor in psychiatry at Harvard Medical School, Boston, Massachusetts. Dr Prager is director of the Child Psychiatry Emergency Service at Massachusetts General Hospital, Boston, and assistant professor of psychiatry (child psychiatry) at Harvard Medical School, Boston, Massachusetts. Dr Stern is chief of the Avery D. Weisman Psychiatry Consultation Service at Massachusetts General Hospital, Boston, and the Ned H. Cassem professor of psychiatry in the field of psychosomatic medicine/consultation at Harvard Medical School, Boston, Massachusetts.

Dr Prince has received honoraria from the American Physician Institute and has provided expert legal reviews in malpractice cases. Dr Stern is an employee of the Academy of Psychosomatic Medicine, has served on the speaker's board of Reed Elsevier, is a stock shareholder in WiFiMD (Tablet PC), and has received royalties from Mosby/Elsevier and McGraw Hill. Drs Stevens and Prager report no conflicts of interest related to the subject of this article.

References

1. Freudenreich O. Psychotic Disorders: A Practical Guide. Philadelphia, PA: Lippincott Williams and Wilkens; 2008.

20. McDonell M, McClellan J. Early-onset schizophrenia. In: Mash E, Barkley R, editors. Assessment of Childhood Disorders. 4th ed. New York, NY: Guilford Press; 2007. pp. 526-550.

26. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. Fifth Edition. Washington, DC: American Psychiatric Press; 2013.

28. Kodish I, McClellan J. In: Handbook of Psychological Assessment, Case Conceptualization, and Treatment: Vol. 2, Children and Adolescents. Hersen M, Reitman D, editors. Hoboken, NJ: John Wiley & Sons; 2008. pp. 405-443.

42. Millichap JJ, Goldstein JL, Laux LC, et al. Ictal asystole and anti- N-methyl-d-aspartate receptor antibody encephalitis. Pediatrics. 2011;127(3):e781-e786.

49. Freudenreich O, Goff DC. Psychotic patients. In: Stern TA, Fricchione GH, editors. Massachusetts General Hospital Handbook of General Hospital Psychiatry. Amsterdam, The Netherlands: Elsevier Science Publishers; 2010.

52. Structural neuroimaging in first-episode psychosis. London (UK): National Institute for Health and Clinical Excellence (NICE); 2008 Feb. 24 p. (technology appraisal guidance; no. 136) http://www.guideline.gov/content.aspx?id=12284. Accessed December 4, 2013.

54. Marshall M, Rathbone J. Early intervention for psychosis. Cochrane Database Syst Rev. 2011;(6):CD004718. [ PMC free article]

60. Xia J, Merinder LB, Belgamwar MR. Psychoeducation for schizophrenia. Cochrane Database Syst Rev. 2011;(6):CD002831. [ PMC free article]

61. Jones C, Cormac I, Silveira da Mota Neto JI, et al. Cognitive behaviour therapy for schizophrenia. Cochrane Database Syst Rev. 2004;(4)(CD000524)

71. Yan J. FDA advisors back additional antipsychotics for use in teens. Psychiatr News. 2009;44(13):1-29.

80. Celano CM, Beach SR, Huffman JC, et al. Side effects profiles of psychotropic medications from cardiovascular and other side effects of psychotropic medications. In: Stern TA, Herman JB, Gorrindo T, editors. The Massachusetts General Hospital Psychiatry Update and Board Preparation. 3rd ed. Boston, MA: MGH Psychiatry Academy Publishing; 2012.

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Psychotic Disorders in Children and Adolescents: A Primer on Contemporary Evaluation and Management

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■ Hallucinatory experiences and delusions are more common in our patients than we may realize and occur frequently in the pediatric population. While not a benign occurrence, psychotic symptoms do not necessarily portend the future development of schizophrenia.

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OCD Treatment Guide: Best Evidence-Based Therapies, Medications, and New Advances

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OCD can be a chronic and sometimes debilitating disorder. Fortunately, effective treatments are available to help manage OCD symptoms, greatly reduce suffering and possibly experience full relief. While there is... Read more »

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American Foundation for Suicide Prevention

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As a parent, you can approach suicide prevention in the same way you do other safety or health issues for your children. By educating yourself, you can learn what puts kids at greatest risk for suicide - and what protects them most strongly.

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Should parents be concerned about teen suicide?

Suicide is in the news and in popular entertainment now more than ever, especially in regard to teens. You can play a role in building up your child's mental health simply by becoming aware of the risk factors and warning signs that can lead to suicide, making yourself available to your child, knowing how to practice having a caring conversation, and being aware that help is always available.

The facts

There were approximately 100,000 teen (15-19 year-olds) suicide deaths over the 40 year period between 1975 through 2015, the most recent year covered by the study.

Boys take their lives at 3-4 times the rate of girls. The suicide rate for teen boys saw a rise that peaked in the late '80s and early '90s, then lowered in the late '90s and early 2000's. This may be attributed to pediatricians increasingly taking on the role of treating depression. However, the rate has unfortunately been rising again since 2006.

The suicide rate for teen girls had a similar but less dramatic pattern. There has been an increase for girls over the last 10-12 years.

It's worth noting there are fluctuations in suicide rates of all age groups over time. Youth rates remain significantly lower compared to every older age group.

Learn more about suicide

Additional resources

Risk factors and warning signs

While there is no single cause for suicide, there are risk factors and warning signs which may increase likelihood of an attempt. Learn what to look out for to keep your child or children safe.

More Than Sad

The More Than Sad program shows you how to recognize signs of depression and other mental health problems, initiate a conversation about mental health with your child, and get help.

Find a mental health professional

Who is a mental health professional, and how can they help? Find mental health providers in your area.

LGBTQ crisis and support resources

LGBTQ crisis hotlines and support resources.

What can I do to protect my teen or tween from suicide risk?

As a parent, you can teach and model healthy habits for mental health just as you would with physical health. Taking care of your own mental health, talking about it openly, and seeking therapy when warranted is one way to model healthy practices.

If your child sees you approaching your own challenges and learning for your own mistakes in an open way, they will understand that it's okay to struggle and to learn from mistakes. They may develop flexibility and compassion for their own missteps - possibly even empathy for others, seeing how you navigate challenging times. They will also understand that life is messy and challenging for everyone at different times.

Check in with your child regularly, beyond just day-to-day tasks such as homework. You can learn how to invite deeper conversations through further guidance listed on this page.

If your child has a history of depression, anxiety, suicidal thoughts, self-harm or substance use, you should monitor them more closely, and consider involving a professional, either at key times, or for the longer term for more chronic conditions.

How can I tell if my child is behaving like a normal teenager - i.e. moody, etc. - or if there might be something wrong?

When children hit puberty, there are changes in their body and brain that can and do lead to behavioral changes. But there is a normal range which can manifest as moodiness, irritability, and pushing you away. This is a natural part of adolescent development. What should be concerning is if you notice indications of hopelessness or worthlessness, a withdrawal from friends and activities, or suicidal thinking or behavior. These are not typical manifestations for teenage angst.

You know your child. You know their usual patterns, their common reactions to frustration and challenges, and what their good days and bad days look like. Trust your instincts if their behavior goes beyond these usual patterns of behavior. It could be just the tip of the iceberg of possible changes in their physical or mental health. It's worth engaging them in conversation to get a fuller understanding of what they are experiencing so you can provide support, and get a better sense of how severe it is.

If your teen or tween's sleep, energy, appetite, motivation, substance use, and frustration aren't bouncing back to normal after a few days, have them see their pediatrician or a mental health practitioner.

How can I talk to my teen about mental health and suicide?

Don't be afraid to have a conversation with your child about mental health and suicide. Ask your child how they're doing, what's happening in their world these days, and what their concerns are. It can start simply by asking, "Are you okay?"

Listen intently and without judgment. Ask open-ended questions, i.e. those that cannot be answered with a simple yes or no. Resist the urge to offer quick fixes or solutions to their challenges, which tends to shut down further dialog. Validate and support their feelings.

Follow their cues, and say things like, "Tell me more about that. I'd love to understand more about what that's like for you. When he said that/did that to you, how did that make you feel?"

Should I use the same approach for different age groups, i.e. tweens (ages 8 to 12) or teens (13 to 17)?

The approach is very similar for tweens and teens, but with changes in language based on their level of sophistication and self-awareness. Use language that makes sense to your child, given their age, development, and what you know of how they think about things.

For a young child, you can ask about physical symptoms like stomach aches, and changes in feelings like getting upset or angry more lately. If it seems to you that they feel hopeless, trapped or overwhelmed - then ask if they ever think about hurting themselves or ending their life.

For older children, or kids who have demonstrated they are aware of their own thoughts and feelings, ask about their perceptions, as well as other symptoms like sleep problems, mood changes, and feelings of hopelessness, or of feeling trapped or overwhelmed.

What if they don't want to talk?

If your child isn't ready to talk, leave the invitation open for later by saying, "Whenever you want to talk, I'm here to listen and support you." You could add "I won't judge, and I'll never stop supporting you, no matter what challenges you face."

The likelihood is that your child will open up when you least expect it, sitting side-by-side rather than face-to-face, in the car or engaged in some other activity together.

When your teen starts to open up, be careful not to fall into the trap of jumping in with a solution or by saying, "You should..." or "Why didn't you..."

What if I'm concerned my child is thinking about suicide?

If your child is talking about any level of distress, do not hesitate to ask them whether they're feeling changes in their mood or level of stress, or having suicidal thoughts. Asking your child directly about suicide will not increase their risk, or plant the idea. It will create an opportunity to offer support, and let them know you care enough to have the conversation.

You can say, "It sounds like you've been dealing with a lot lately. Does it ever get so tough that you think about ending your life?"

If your child gives any indication they have been thinking about suicide (unless they are in the act of self-harming) take them seriously. Continue to listen and engage in a caring, concerned, supportive manner. You can say things like, "Can you say more about that? I'm so sorry you've been feeling this way. I want to understand more about your perspective. I'm here for you no matter what. There is no problem too big that we as a family can't get through. I'm going to keep supporting you and will also make sure you get the help you need to feel yourself again."

Talk with your child about how to seek help. If you fear they may be at risk, get professional help right away.

Let them know you'll be there for them no matter what, that your love is unconditional, and that you'll help them get the support they need to get through this challenging time.

In a crisis situation, call the National Suicide Prevention Lifeline at 1-800-273-TALK or text the Crisis Text Line by texting 'TALK' to 741741 to speak or text with a trained counselor who can provide guidance on the most appropriate next steps and resources. Calling 911 is best for situations when self-harm is occurring or is about to occur.

For help finding a Mental Health Professional, consult with your child's pediatrician, call your insurance, or use this treatment finder.

What if my child knows someone who has taken their life? How do talk with them?

It is important as a parent to be there for your child if a friend or a classmate has died by suicide. You can find specific guidance in AFSP's Children, Teens, and Suicide Loss booklet, written in partnership with the Dougy Center, The National Center for Grieving Children & Families.

The booklet can be viewed online here.

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Teens and suicide: What parents should know

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As a parent, you can approach suicide prevention in the same way you do other safety or health issues for your children. By educating yourself, you can learn what puts kids at greatest risk for suicide - and what protects them most strongly.

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Today, C. (2022, July 18). Taming impulses. Counseling Today. https://ct.counseling.org/2019/08/taming-impulses/

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Schizophrenia vs. Autism

(plus, a brief history of Autism)

Historically speaking, Autism is a relatively new diagnosis. Schizophrenia and Autism share a long, intertwining history. For much of the 20th century, Autistic children were diagnosed under the umbrella of Schizophrenia (childhood-onset Schizophrenia or COS).

The term autism first found its way into the literature in the early 1900s when it was used to describe the tendency for schizophrenic children to create and live in a world of their own ( Vortsman and Burbach, 2014). The Swiss Psychiatrist Paul Eugen Bleuler coined the term "autism" as a key feature of Schizophrenia in 1911 ( Evans, 2013).

The term was used to describe the social withdrawal and detachment from reality so often observed in children with Schizophrenia ( Zeldovich, 2018). The term began to take on its own meaning as researchers began to discern differences between a subset of children who presented slightly differently and had a different trajectory than other children with Schizophrenia. It wasn't until the research of Kolvin (1971) that Autism was distinguished from Schizophrenia, and finally, in 1980 Autism was separated from Schizophrenia in the DSM-III.

A Brief History of Autism

It's challenging to talk about the differences between schizophrenia and Autism without exploring the history of Autism. Or maybe it's not challenging, but my autistic brain likes understanding and situating this conversation within the larger, historical context :)

As early as 1924, Grunia Sukhareva-a Russian Child Psychiatrist began observing and writing about distinctive features of the children she worked with. Sukhareva argued that a subset of her patients came into the world with a condition resembling schizophrenia, but that was essentially different. Namely, she observed that while her schizophrenic patients tended to decline and become less engaged with the world (more internal), a subgroup of children improved throughout their lifespan and became less inward-focused and increased in their engagement with the external world. She observed that these children had rich inner lives, describing one young boy as "an introverted type, with an autistic proclivity into himself" ( Zeldovich, 2018). While at first Sukhareva used the term "autistic" in the same way intended by Bleuler, over time, she adapted it as she saw more and more boys who demonstrated these "Autistic tendencies." She began creating more crystalized observations about these "autism tendencies.".

In 1925 she published a paper outlining the specific traits she saw within the group of boys she was working with. She was remarkable in her insight and precision, as her early observations essentially parallel the DSM-5 current diagnosis for Autism ( Zeldovich, 2018). She described a "lack of facial expressiveness," "talking in stereotypical ways," "strong interests pursued exclusively," and "sensitivities to specific noises or smells" Zeldovich, 2018). Ironically, it took nearly a century for the DSM to arrive at the same conclusions Sukhareva arrived at in 1925.

Sukhareva herself was skeptical of the overlap between Schizophrenia and this emerging condition she was observing; she cautioned her colleagues that the term "schizoid" might lead to confusion and misinterpretation of this syndrome (Silberman, 2015).

As early as the 1950s, she was speculating as to different brain regions of the brain impacted by these different conditions; her speculations were later confirmed with the development of brain scans ( Zeldovich, 2018). Her work was legendary, unfortunately, her work didn't reach the English-speaking world til 1996. Had her work reached the English-speaking world earlier than it did, perhaps the confusion between schizophrenia and autism would have been cleared up long before 1980 ( Zeldovich, 2018).

Autism research has not always been kind to women, including Sukhareva. Despite her research coming nearly two decades before Leo Kanner and Hans Asperger first published, she is often not talked about in Autism history, and the credit for "discovering" Autism is typically given to Kanner and Asperger. Certainly, there were some linguistic and political barriers that impacted her work being reached the English-speaking world; however, there may also be more sinister reasons behind her notable absence in Autism history.

Egos get messy when it comes to scientific discovery. There is speculation that Kanner intentionally did not cite Asperger's work so as to appear original (Silberman, 2015). Now there is speculation that Hans Asperger intentionally did not cite Sukhareva ( Zeldovich, 2018) as to appear to be the founder when he published his research. Sukhareva's work was translated to German as early as 1925s; reasonably Asperger should have had access to her work. Given her wide publications and specialization on the topic, the absence of reference to her is notable ( Zeldovich, 2018).

Hans Asperger working in Germany, and Leo Kanner writing in the context of the United States, pushed the literature forward as they further clarified the Autism phenotype. Hans Asperger also saw the overlap between schizophrenia and Autism, while also working to distinguish this new syndrome from schizophrenia. Asperger saw within the children he worked with the tendency toward what Bleuler referred to as "Autistic thinking" or the tendency toward "self-centered rumination and retreat into fantasy" (Silberman, 2015, 98).

Asperger observed how children pursued their goals with intensity and with little regard for the external world. He thus coined the term "Autisischen Psychopathen" to describe the condition of the children he worked with. In addition to describing pathology, he coined the term " Autismus" which referred to a more natural element, like when a scientist discovers a new life form (Silberman, 2015, para 98).

It almost seems as if Asperger was expressing an early idea of neurodiversity. He seemed to see it as a natural biological element and observed how it showed in a myriad of expressions. His research highlighted that Autism encompassed a vast spectrum of people--from the most intellectually gifted to the severely disabled. He highlighted that many different varieties of Autism occurred naturally within the population (Silberman, 2015).

Kanner, working at John Hopkins, in the context of the United States, took a slightly different approach. Where Asperger highlighted the wide range of the spectrum, Kanner was quicker to zoom in and rigidly define Autism as a monolithic group. Kanner primarily worked with younger children, heavily impacted by Autistic traits. Kanner's narrative of Autism was that it was an incredible, rare and extreme condition (Silberman, 2015). Kanner primarily worked with infants and young children.

He suggested that a subset of children diagnosed with schizophrenia had an innate inability to form relationships with people, which was a separate, and rare condition that he termed early infantile Autism (Siberman, 2015). While Kanner's work helped distinguish Autism from Schizophrenia, unfortunately, it later served to perpetuate a narrative that Autism is a rare, extreme, and monolithic condition. This was a stark difference from Asperger's research which emphasized the broad spectrum of Autism.

Following Kanner's work, there was speculation that infantile Autism could be an early manifestation of childhood schizophrenia ( Vortsman and Burbach, 2014). During the 1960s and 1970s, this was often talked about as "early-onset psychosis" (infancy) vs. late-onset psychosis" (adolescence).

It was the work of Israel Kolvin in the early 1970s that eventually helped to distinguish the different traits of "early-onset psychosis" (characterized by Ritualistic and compulsive phenomena i.e., Autism) from late-onset psychosis (characterized by more thought disorder and hallucination symptoms i.e. schizophrenia). His work was foundational for providing a basis from which to differentiate these two conditions. Finally, in 1980, Autism was given its own categorization with the DSM-III and thus the intertangling of Schizophrenia and Autism was put to rest ( Dvir, and Frazier, 2011).

Schizophrenia Overview

Like Autism, Schizophrenia is considered a spectrum condition. The schizophrenia spectrum includes schizophrenia, schizotypal personality disorder, schizophrenia-spectrum personality disorders, schizophreniform, and schizoaffective disorder. Some of the features of schizophrenia include difficulty discerning reality vs. non-reality and the presence of disorganized thought patterns, emotions, and behaviors. Schizophrenia has an element of complexity that has led to misconceptions in the media and in the culture at large.

Schizophrenia is not the same thing as having multiple personalities, and people with schizophrenia are not dangerous or violent. Many may experience hallucinations and paranoia while maintaining good insight into these experiences. Symptoms of schizophrenia can ebb and flow. So, a person may have a season of acute delusions, and hallucinations and may have seasons of "remission" where their symptoms are well-managed.

During an active episode of schizophrenia, a person struggles to distinguish between what is real vs. unreal. They may have active delusions, hallucinations, paranoid thinking, disorganized speech and thought patterns, disorganized body movement, and lack of motivation.

Use of alcohol, marijuana, stress, and loss of sleep tend to exacerbate and make symptoms worse. Additionally, underlying executive functioning difficulties may be exacerbated during a flare of symptoms (Psychiatry.org). Generally, symptoms fall into three major categories: Positive, Negative, and Disorganized ( Psychiatry.org):

Positive Symptoms

(the presence of abnormal symptoms). Positive symptoms include: delusional and paranoid thought processes, auditorily or visual hallucinations, perception distortions, paranoid beliefs, and thought processes.

Negative Symptoms

Negative symptoms refer to a decreasing or absence of typical experiences/actions. Examples include: flat affect, difficulty with expressing emotions, diminished sense of emotions, reduced pleasure, failure to initiate activity, and sudden decrease in motivation. Other negative symptoms may involve difficulty organizing and initiating plans or limited ability to speak.

Disorganized Symptoms

Difficulty with logical and linear thinking, disordered thinking processes, bizarre behavior, and abnormal body movements. The person may have disorganized speech meaning they do not say complete sentences and others often have difficulty understanding what they are saying.

Co-Occurrence of Schizophrenia

and Autism

After sharing nearly, a century of shared history, a great deal of effort was put forward to distinguish autism from schizophrenia. However, emerging genetic research is causing people to revisit the conversation about the potential relationship between schizophrenia and autism. Recent research suggests that there are both clinical and biological links between autism and schizophrenia, with a growing awareness of the number of genes/chromosomal variance being shared by schizophrenia and autism ( Rapoport et al., 2009).

Several genes have been identified that potentially play a role in autism and schizophrenia. Interestingly several of these genes (approximately 15-25%) increase the risk of both autism and schizophrenia ( Vortsman and Burbach, 2014). This discovery of this genetic overlap has led to new conversations about the shared phenotypes and shared etiological and biological pathways for both conditions ( Vortsman and Burbach, 2014). Furthermore, these conditions appear to co-occur at higher rates than in the general population.

One study of Autistic adults found that 7.8% had co-occurring schizophrenia. Stahlberg et al., 2004

Elevated rates of autism among people with childhood-onset schizophrenia have been observed.

Two large studies found that COS (childhood-onset schizophrenia) was preceded by a co-morbid autism/pervasive development disability (PDD) in 30-50% of cases ( Rapoport et al., 2009).

In the coming years, we will likely do new research that helps us understand the phenotypic and biological overlap and co-occurrence of these conditions with more precision.

Overlapping Traits

Abnormal Perceptions/Paranoid Thinking

Hallucinations, abnormal perceptions, and paranoid thinking are core features of schizophrenia. Interestingly, Autistics are three times more likely than the general population to have hallucination-like experiences( Milne, 2017; Milne et al., 2017). Psychosis/hallucinations, like Autism, is also on a spectrum. They can be intense and can lead to a blurring of reality/non-reality, or they can be fainter in nature (the knock you thought you heard, the music you hear playing in the background, the touch you thought you just experienced).

Autistic adults experience more abnormal perceptions (hearing, sight, sound, touch). It is believed neurotransmitters, and social isolation/discrimination, may all be involved. The following information comes from the research of Elizabeth Milne.

Abnormal perceptions are distinct and different from sensory sensitivities.

47% of autistic adults answered yes to the question: "Do you ever see shapes, lights, or colors even though there is nothing there?" (compared to 14% of the control).

63 percent of Autistic adults answered yes to the question: "Do you ever feel that someone is touching you, but when you look, nobody is there?" (compared to 7 percent of the control) ( Milne, 2017)

Other abnormal perceptions include strange body sensations such as experiencing a burning sensation and strange feelings in the body, hearing one's own thoughts, or fearing those near you can hear your thoughts.

Autistics were more likely to report experiencing distress associated with their abnormal perceptions.

Speculated that abnormal perceptions may be related to altered GABA levels in the autistic bran

Past research has shown that those who experience isolation and discrimination (such as in the case of migration) also have more hallucinatory and paranoid feelings than people who are not discriminated against. Bullying, discrimination, and social isolation related to Autism may thus increase the risks of hallucinatory and paranoid feelings.

In the context of autism, the auditory perceptions/hallucination-like experiences are on the milder end of the psychic spectrum. Having an experience that causes one to be unable to distinguish reality from non0reality (i.e. Psychosis) could not be attributed to autism alone.

Sensory Differences

Hyper and hypo-sensory sensitivities are well-known features of Autism. And, this is a lesser-known feature of Schizophrenia. Recent research suggests that there can also be sensory dysfunctions in the context of Schizophrenia: Javitt, 2009). Differences in the auditory system (hearing) are the most widely documented area of sensory concern among people with schizophrenia.

Executive Functioning Difficulties

Both Autistics and people with Schizophrenia tend to experience executive functioning difficulties, including difficulty with cognitive flexibility, task-switching, memory, and attention. For the person with Schizophrenia, their executive functioning tasks tend to get worse during an acute onset of systems ( Orellana and Slachevsky, 2013).

Early Symptom Overlap

Children with both may present with language delay, social withdrawal, be prone to fantasy, and a tendency to get "lost" in their internal world.

Paranoid and thought disorganization

Disorganized thinking and paranoia are well-known features of Schizophrenia. Many autistic people experience significant anxiety when under pressure which can present as disorganized thinking or paranoid thinking. This tends to worsen when they are asked to task-switch amidst pressure/anxiety ( Berney, 2000). Autistics who have experienced discrimination and bullying are also more vulnerable to paranoid feelings and thought patterns.

Social-Relational Traits

Social withdrawal, communication impairment, and poor eye contact seen in ASD are similar to the negative symptoms seen in people with Schizophrenia ( Posey et al., 2004).

Neuroimaging Studies (Gray Matter)

In a study done by Cheung et al., 2010. people with ASD and Schizophrenia had lower gray matter volumes within limbic-striato-thalamic neurocircuitry. There were slight variations, as the gray matter was reduced in the amygdala, caudate, and frontal and medial gyrus for Schizophrenia, while it was reduced in the putamen for Autism. Cheung et al. demonstrated clear overlap in terms of brain volumetrics, suggesting that Autism and Schizophrenia likely share a common etiology.

Psycho-Social Risks

In addition to overlapping phenotypes. We also share many psycho-social risks.

Self-Harm: In one study, 50% of patients with schizophrenia reported a history of Self-Harm. This was increased among females, those with depression, and those experiencing suicidality ( Mork et al., 2012). Similarly, self-harm is high among autistics with average to high IQs. One study found that parents reported self-harm behavior among autistic youth in 15% of cases ( Huang).

Suicidality: Both groups have an increased risk of suicidality and an increased risk of dying by suicide. Approximately 4.9% of people with schizophrenia die by suicide ( Palmer et al., 2005), rates are higher among men and among those who had co-occurring substance conditions ( Hor et al., 2010) Autistics with average to high IQ are three times more likely to attempt or die by suicide than the general population ( South et al.). Suicidality was particularly high among youth and young adults and was more elevated among women than men ( South et al.)

Substance Abuse: Substance abuse is high among both groups. Nearly half of people with schizophrenia will have a substance abuse disorder at one point in their life Volkow N. D. (2009). A recent study in Sweden found that folks with Autism with average to high IQs were twice as likely to struggle with addiction to alcohol or other drugs.

Victimization: Autistic adults are at an increased risk of experiencing interpersonal violence. In one study, Autistic adults were 7.3 times more likely to endorse having experienced sexual assault from a peer during adolescence ( Weiss and Fardella). Fitzgerald et al. 2005 study found an increased risk of victimization (both violent and non-violent victimization) among people with schizophrenia. And women with schizophrenia have higher rates of being sexually victimized ( Goodman and Harris, 1995).

How to Spot the Difference

Criteria A of autism may look like Negative symptoms of Schizophrenia. And so, it is critical to assess for Criteria B symptoms of Autism and Positive symptoms of Schizophrenia to get a complete clinical picture.

Focus on Criteria B for Autism

Given criteria A symptoms may overlap with Schizophrenia negative symptoms, it is essential to assess for the presence of criteria B symptoms (rigidity and repetitive behaviors, special interests, sensory issues). If a clinician is assessing for Schizophrenia but not considering ASC, they won't assess for these things, and ASC may be missed. The RAADS can be a helpful tool for assessing some of the criteria B traits.

1. Repetitive, stereotyped movements, use of objects, and/or speech (i.e., stimming, repeated vocal phrases, lining up or categorizing objects).

2. Inflexibility of behavior and thought, ritualistic behaviors, concrete thinking (i.e., echolalia, listening to songs on repeat, adherents to routine, tendency to take things literally, and being high context thinkers)

3. Intense interests and/or attachment to objects (i.e., Special interests)

4. Sensory processing symptoms (under-reactivity, over-reactivity, or fascination to sensory input.

Assess for Positive Symptoms of Schizophrenia

When assessing for Autism, if you aren't also considering Schizophrenia, you may discount negative symptoms of Schizophrenia as criteria A for Autism. If it doesn't occur to you to rule out schizophrenia, you may not consider assessing for positive symptoms of schizophrenia and thus the Schizophrenia may be missed. To assess positive symptoms, include consideration of delusional thought patterns, paranoid thoughts, and the presence of hallucinations. However, be aware that abnormal perceptions are more common among autistic adults. Overall patterns, the intensity of paranoia and hallucinatory experiences, and the level of insight into the experiences must be considered (i.e., is there good insight into reality vs. non-reality).

Consider using Routine Screeners

The AQ and RAADS are standard routine screeners for Autism (you can find a roundup of several free screeners here. For Schizophrenia, consider using the EPS9 or EPS26. While there is an online version, consider that clients with active paranoia may prefer the paper version.

Consider Incorporating a Robust Personality Assessment

The PAI has both a schizophrenia scale (SCZ), and emerging research suggests the PAI can also help capture the likelihood of Autism. Based on the research of Harrison et al (2020) an ASD-Differential calculator was created. You can input PAI results here and receive a score that provides the likelihood of an Autism diagnosis.

Citations

Cheung C, Yu K, Fung G, et al. Autistic disorders and schizophrenia: related or remote? An anatomical likelihood estimation. PLoS One. 2010;5:e12233. Link

Berney TP. Autism-an evolving concept. Br J Psychiatry. 2000;176:20-25. Link

Hor, K., & Taylor, M. (2010). Suicide and schizophrenia: a systematic review of rates and risk factors. Journal of psychopharmacology (Oxford, England), 24(4 Suppl), 81-90. https://doi.org/10.1177/1359786810385490

Kolvin. I. 1971. Infantile Autism, Concepts Characteristics and Treatment in Infantile Autism, Concepts Characteristics and Treatment, M. Rutter (ed.) "Psychoses in childhood - a comparative study", pp. 7-26. ( Link to chapter)
Kolvin, I. (1971) Studies in childhood psychoses: I. Diagnostic criteria and classification. British Journal of Psychiatry, 118, 381-384. CrossRef

Milne E, Dickinson A, Smith R (2017) Adults with autism spectrum conditions experience increased levels of anomalous perception. PLoS ONE 12(5): e0177804. https://doi.org/10.1371/journal.pone.0177804

Palmer BA, Pankratz VS, Bostwick JM (2005). The lifetime risk of suicide in schizophrenia: a reexamination. Arch Gen Psychiatry, 62(3):247-53. [ PubMed] [ Ref list]

Posey DJ, Kem DL, Swiezy NB, et al. A pilot study of D-cycloserine in subjects with autistic disorder. Am J Psychiatry. 2004;161:2115-2117.

Stahlberg O, Soderstrom H, Rastam M, Gillberg C. Bipolar disorder, schizophrenia, and other psychotic disorders in adults with childhood onset AD/HD and/or autism spectrum disorders. J Neural Transm. 2004; 111:891-902. Link

Silberman, S. (2015). Neurotribes: The legacy of autism and the future of neurodiversity. Penguin.

Vorstman J.A.S., Burbach J.P.H. (2014) Autism and Schizophrenia: Genetic and Phenotypic Relationships. In: Patel V., Preedy V., Martin C. (eds) Comprehensive Guide to Autism. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-4788-7_96

Zeldovich, L. 2018. How history forgot the woman who defined autism. Autism Spectrum Research. Retrieved October 16, 2021: https://www.spectrumnews.org/features/deep-dive/history-forgot-woman-defined-autism/

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Schizophrenia or Autism: A brief history of schizophrenia and autism and how to spot the difference - Insights of a Neurodivergent Clinician

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Schizophrenia and Autism have a long and intertwining history. This article provides a brief overview of their history, explores their overlapping phenotypes, traits and symptoms. It also provides clinician's with some ideas on how to differentiate the diagnosis between schizophrenia and autism.