Theoretical Foundations of ACT

ACT is grounded in Relational Frame Theory (RFT), a behavioral theory of language and cognition that posits human suffering often stems from the ways in which language and thought processes contribute to experiential avoidance and cognitive fusion. Rather than attempting to eliminate distressing thoughts and emotions, ACT encourages individuals to accept them, defuse their impact, and commit to actions aligned with personal values. Psychological flexibility—the capacity to remain in contact with the present moment and act in service of chosen values despite difficult internal experiences—is the overarching aim of ACT.

This shift from symptom reduction to functional improvement is especially relevant for adolescents, whose cognitive and emotional capacities are still developing. ACT provides a developmentally appropriate framework that helps teens navigate emotional distress while fostering autonomy, identity formation, and purpose.

Core Processes in ACT and Their Application in Adolescents

ACT comprises six interrelated core processes:

1. Cognitive Defusion: Adolescents are taught to observe their thoughts without automatically accepting them as truth. Techniques like labeling thoughts (“I’m having the thought that…”) or using metaphors (e.g., leaves on a stream) help reduce the literal impact of self-critical or anxious thinking.
2. Acceptance: Rather than avoiding painful feelings—common in adolescent presentations such as self-harm or substance use—ACT promotes openness to emotion. Through mindfulness practices and experiential exercises, teens learn that distress is a normal part of human experience, not a signal to disengage.
3. Contact with the Present Moment: Adolescents are often preoccupied with past events or future worries. Grounding exercises and present-focused attention aim to build awareness and reduce rumination, improving emotional regulation.
4. Self-as-Context: Adolescents frequently struggle with self-identity and negative self-concepts. ACT fosters a perspective shift from rigid self-definitions (“I am depressed”) to a more flexible sense of self (“I notice I’m experiencing depression”), allowing for greater resilience and adaptability.
5. Values Clarification: Through guided reflection, adolescents explore what truly matters to them—relationships, creativity, justice, learning—thus anchoring their behaviors in intrinsic motivation rather than external approval or peer pressure.
6. Committed Action: ACT culminates in behavior change rooted in values. Teens are supported in setting realistic goals and taking concrete steps, even when faced with emotional discomfort.

Evidence Base for ACT in Adolescent Populations

A growing body of research supports the efficacy of ACT for adolescents across a spectrum of conditions, including anxiety disorders, depression, chronic pain, and behavioral issues. Systematic reviews and randomized controlled trials (e.g., Swain et al., 2015; Hayes et al., 2021) indicate that ACT can lead to significant improvements in psychological flexibility, mood symptoms, and overall functioning.

Notably, ACT has shown promise in school-based interventions and brief formats, making it accessible for primary care settings. Given the limited availability of specialized mental health services for youth, ACT’s adaptability enhances its utility in integrated care models.

Practical Integration into Clinical Practice

Primary care and mental health providers can incorporate ACT in both brief encounters and ongoing therapy. For example:

• During a routine visit, a provider might use a quick mindfulness exercise to help an anxious teen ground themselves.
• A pediatrician discussing adherence to medical treatment could frame the conversation around the teen’s values (e.g., staying healthy to continue playing sports).
• Mental health clinicians can use ACT metaphors and exercises to shift the focus from symptom elimination to living a meaningful life despite discomfort.

Furthermore, ACT’s emphasis on experiential learning aligns well with adolescents’ concrete thinking styles. Visual aids, metaphors, and experiential exercises (e.g., tug-of-war with a monster) make ACT both engaging and developmentally appropriate.

Challenges and Considerations

While ACT offers many benefits, providers should be aware of potential limitations. Adolescents with severe cognitive impairments or limited verbal skills may require modifications. Additionally, cultural and familial contexts should be considered when exploring values and promoting individual autonomy. Training and supervision in ACT are essential for effective delivery, especially in navigating complex cases.

Conclusion

ACT provides a flexible, evidence-based approach for addressing adolescent mental health concerns, emphasizing acceptance, mindfulness, and values-driven action over symptom suppression. For primary care and mental health providers, integrating ACT into practice can enhance therapeutic rapport, empower adolescents, and support long-term psychological resilience. As mental health challenges among youth continue to rise, ACT represents a timely and transformative tool in the clinician’s repertoire.

AUTHOR:

Shawn Singh Sidhu, MD, DFAPA, DFAACAP

Co-Medical Director, Vista Hill Foundation

Diagnostic Overview
SSRDs include several distinct disorders:

1. Somatic Symptom Disorder (SSD)
   Characterized by one or more distressing somatic symptoms that are accompanied by excessive thoughts, feelings, or behaviors related to those symptoms. Importantly, the symptoms may or may not be medically explained. The focus is on the psychological response to the symptoms rather than the presence or absence of a medical explanation.
2. Illness Anxiety Disorder (IAD)
   Previously known as hypochondriasis, IAD involves preoccupation with having or acquiring a serious illness despite minimal or no somatic symptoms. Patients frequently misinterpret normal bodily sensations and engage in repeated health checks or avoidant behaviors.
3. Conversion Disorder (Functional Neurological Symptom Disorder)
   This condition involves neurological symptoms (e.g., paralysis, seizures, blindness) that are inconsistent with recognized medical conditions. Symptoms often emerge in the context of psychological stress or trauma.
4. Psychological Factors Affecting Other Medical Conditions
   This diagnosis applies when psychological or behavioral factors significantly affect the course, treatment, or outcome of a medical illness.
5. Factitious Disorder
   Involves intentional falsification of physical or psychological symptoms without obvious external incentives, distinguishing it from malingering.

Epidemiology and Clinical Features
SSRDs are common across healthcare settings. SSD affects approximately 5-7% of the general population, with a higher prevalence in women. IAD affects 1.3-10% of the population, with equal gender distribution. Conversion disorder is more frequently diagnosed in females and typically presents in adolescence or early adulthood.

Patients with SSRDs often have co-occurring psychiatric disorders such as depression or anxiety. Adverse childhood experiences, trauma, and chronic stress are significant risk factors. Additionally, these patients often have complex relationships with the healthcare system—frequent visits, diagnostic procedures, and a feeling of being misunderstood or invalidated are possible.

Challenges in Diagnosis
Diagnosing SSRDs requires careful differentiation from medical conditions, malingering, and other psychiatric disorders. The DSM-5-TR emphasizes the need to avoid over pathologizing patients with medically unexplained symptoms and instead focus on the degree of psychological distress and functional impairment.

Clinicians are best served to conduct comprehensive assessments that include medical, psychiatric, and psychosocial components. Collateral information from family and medical records is often helpful. Importantly, SSRDs are not diagnoses of exclusion but require positive identification of specific clinical features.

Best Practices in Treatment

1. Psychoeducation and Therapeutic Alliance
   Establishing a strong therapeutic alliance is foundational. Patients often feel invalidated by previous medical encounters, so clinicians must acknowledge their suffering without reinforcing somatic preoccupation. Psychoeducation should reframe the illness using a biopsychosocial model, emphasizing the truly felt nature of the symptoms while introducing the role of stress and emotional factors.
2. Cognitive Behavioral Therapy (CBT)
   CBT is the most evidence-based treatment for SSRDs. It targets beliefs and thoughts about illness and health, and avoidant or excessive health behaviors. CBT helps patients develop more accurate appraisals of bodily sensations and encourages gradual re-engagement in activities.
3. Mindfulness and Acceptance-Based Therapies
   Interventions such as mindfulness-based stress reduction (MBSR) and acceptance and commitment therapy (ACT) show promise by helping patients observe their symptoms non-judgmentally and reduce experiential avoidance. These approaches may be particularly helpful in patients with chronic pain or functional neurological symptoms.
4. Pharmacotherapy
   While no medications are FDA-approved specifically for SSRDs, selective serotonin reuptake inhibitors (SSRIs) may be helpful when comorbid depression or anxiety is present. SNRIs and tricyclic antidepressants have also shown utility in somatoform pain syndromes. For example, the SNRI Duloxetine has an FDA approval for chronic pain. However, polypharmacy and iatrogenic harm should be avoided.
5. Interdisciplinary Care and Coordination
   Patients benefit from collaborative care models involving primary care providers, psychiatrists, psychologists, physical therapists, and sometimes neurologists or pain specialists. Coordinated care prevents redundant testing and provides consistent messaging. Regular case conferences and shared treatment plans are key to success.
6. Limit Medical Investigations and Set Boundaries
   While it is essential to rule out medical conditions, repeated investigations reinforce illness behavior. Providers should adopt a “diagnostic closure” strategy, providing reassurance based on appropriate evaluation, and shift focus to functional recovery. Structured visits, time-limited appointments, and continuity with a single provider help reduce fragmentation.
7. Address Trauma and Comorbidities
   Because many patients have histories of trauma, integrating trauma-informed care is essential. Screening for PTSD, dissociation, and borderline personality disorder is often appropriate. Psychotherapy targeting trauma (e.g., EMDR, trauma-focused CBT) can reduce somatic symptom intensity.

Conclusion
Somatic Symptom and Related Disorders are complex conditions that straddle the boundary between psychiatry and medicine. When properly diagnosed and treated using evidence-based, multidisciplinary approaches, many patients experience significant improvements in functioning and quality of life. Mental health providers play a critical role in destigmatizing these conditions, guiding collaborative care, and helping patients shift from symptom preoccupation to adaptive functioning.

AUTHOR:

Shawn Singh Sidhu, MD, DFAPA, DFAACAP

Co-Medical Director, Vista Hill Foundation

Vista Hill Native American SmartCare Program

Attention-Deficit/Hyperactivity Disorder (ADHD)

Caffeine has stimulant-like properties that may improve attention and executive functioning in individuals with ADHD. A study in rodent models showed that caffeine improved memory and attention through enhanced dopaminergic signaling in the prefrontal cortex, paralleling the effects of prescription stimulants (Pandolfo et al., 2013). Human trials are limited, but a double-blind study in children with ADHD found that caffeine modestly improved behavior and attention, although not as effectively as methylphenidate (Lara et al., 2010). Nevertheless, caffeine may disrupt sleep—a significant concern for individuals with ADHD, as sleep impairment exacerbates core symptoms.

Depression

Caffeine’s psychostimulant properties and dopaminergic activation suggest potential antidepressant effects. A large prospective cohort study found that women who consumed ≥4 cups of caffeinated coffee daily had a 20% reduced risk of depression compared to those consuming little or none (Lucas et al., 2011). This protective effect is attributed to caffeine’s anti-inflammatory properties and its modulation of brain-derived neurotrophic factor (BDNF) (Kaster et al., 2015). However, excessive use may mask depressive symptoms or contribute to mood instability, especially when withdrawal effects are misinterpreted as depressive episodes.

Anxiety Disorders

Caffeine is a known anxiogenic agent, particularly in susceptible individuals. At high doses (e.g., >400 mg/day), caffeine can induce symptoms consistent with generalized anxiety or panic disorder, including restlessness, insomnia, palpitations, and irritability (Boulenger et al., 1984). A randomized trial demonstrated that patients with panic disorder were significantly more sensitive to caffeine’s stimulatory effects, exhibiting heightened cardiovascular and subjective anxiety responses (Charney et al., 1985). Clinical guidelines generally recommend limiting or avoiding caffeine in individuals with anxiety disorders.

Bipolar Disorder

Caffeine’s effects on mood stability in bipolar disorder are complex. While it may transiently alleviate depressive symptoms, its stimulant properties can disrupt sleep and potentially trigger manic or hypomanic episodes. Disrupted circadian rhythms are central to bipolar pathophysiology, and caffeine—especially when consumed late in the day—can exacerbate this vulnerability (Wehr et al., 1987). A study by Leibenluft and colleagues found that individuals with bipolar disorder frequently use caffeine during depressive phases but reported increased agitation during manic episodes (Leibenluft et al., 1996). Clinical prudence suggests moderating caffeine intake, especially during manic or mixed states.

Psychosis and Schizophrenia

Individuals with schizophrenia often consume caffeine at rates exceeding those of the general population. This may reflect attempts to counteract sedation from antipsychotic medications or cognitive dulling (Gurpegui et al., 2004). However, caffeine’s dopaminergic effects pose theoretical risks of exacerbating psychotic symptoms. Lucas et al. (1990) found that high caffeine intake was associated with increased positive symptoms, particularly in patients taking clozapine. Furthermore, caffeine is metabolized by cytochrome P450 1A2, the same enzyme responsible for metabolizing several antipsychotics, including olanzapine and clozapine, potentially leading to drug interactions (Carrillo et al., 2000).

Substance Use Disorders

Caffeine interacts with reward pathways implicated in substance use. While moderate caffeine use may not pose harm, energy drink consumption (often containing high caffeine doses) has been associated with increased risk of alcohol and stimulant misuse among adolescents and young adults (Arria et al., 2011). Caffeine also carries its own dependence potential, with recognized withdrawal symptoms such as headache, fatigue, and irritability (Juliano & Griffiths, 2004). Screening for problematic use patterns is warranted, particularly in individuals with comorbid SUDs.

Conclusion

Caffeine is a psychoactive substance with condition-specific effects on mental health. While it may offer mild symptomatic relief in ADHD and depression, it can also exacerbate symptoms in anxiety, bipolar disorder, and psychosis, or complicate treatment in substance use disorders. Mental health and primary care providers should assess individual caffeine consumption patterns, explore patient motivations for use, and provide tailored guidance based on psychiatric diagnosis, comorbidities, and medication interactions.

References

1. Vázquez JC, et al. Effects of Caffeine Consumption on Attention Deficit Hyperactivity Disorder (ADHD) Treatment: A Systematic Review of Animal Studies. Nutrients. 2022;14(4):739. https://doi.org/10.3390/nu14040739News-Medical
2. Grosso G, et al. Coffee, tea, caffeine and risk of depression: A systematic review and dose-response meta-analysis of observational studies. Mol Nutr Food Res. 2016;60(1):223-234. https://doi.org/10.1002/mnfr.201500620
3. Lara DR. Caffeine, mental health, and psychiatric disorders. J Alzheimers Dis. 2010;20 Suppl 1:S239-48. doi: 10.3233/JAD-2010-1378. PMID: 20164571. https://journals.sagepub.com/doi/abs/10.3233/JAD-2010-1378
4. Juliano LM, Griffiths RR. A critical review of caffeine withdrawal: empirical validation of symptoms and signs, incidence, severity, and associated features. Psychopharmacology (Berl). 2004;176(1):1-29. https://doi.org/10.1007/s00213-004-2000-x
5. Charney DS, Heninger GR, Jatlow PI. Increased anxiogenic effects of caffeine in panic disorders. Arch Gen Psychiatry. 1985 Mar;42(3):233-43. doi: 10.1001/archpsyc.1985.01790260027003. PMID: 2983630. https://jamanetwork.com/journals/jamapsychiatry/article-abstract/493529
6. Lucas PB, Pickar D, Kelsoe J, Rapaport M, Pato C, Hommer D. Effects of the acute administration of caffeine in patients with schizophrenia. Biol Psychiatry. 1990 Jul 1;28(1):35-40. doi: 10.1016/0006-3223(90)90429-6. PMID: 2375945. https://linkinghub.elsevier.com/retrieve/pii/0006322390904296
7. Carrillo JA, Benitez J. Clinically significant pharmacokinetic interactions between dietary caffeine and medications. Clin Pharmacokinet. 2000 Aug;39(2):127-53. doi: 10.2165/00003088-200039020-00004. PMID: 10976659. Gurpegui M, et al. Caffeine consumption in schizophrenia: associations with clinical and sociodemographic features. Prog Neuropsychopharmacol Biol Psychiatry. 2004;28(5):945-951. https://link.springer.com/article/10.2165/00003088-200039020-00004
8. Meredith SE, et al. Caffeine Use Disorder: A Comprehensive Review and Research Agenda. J Caffeine Res. 2013;3(3):114-130. https://doi.org/10.1089/jcr.2013.0016
9. Fredholm BB, et al. Actions of caffeine in the brain with special reference to factors that contribute to its widespread use. Pharmacol Rev. 1999;51(1):83-133. https://pubmed.ncbi.nlm.nih.gov/10049999/

AUTHOR:

Shawn Singh Sidhu, MD, DFAPA, DFAACAP

Co-Medical Director, Vista Hill Foundation

Vista Hill Native American SmartCare Program

A child who appears to be oppositional or aggressive may be reacting to internal anxiety—anxiety he may, depending on his age, not be able to articulate effectively, or not even fully recognize that he’s feeling. Anxiety is based on the body’s physiological response to a threat in the environment, as a response to maximize the body’s ability to either face danger or escape danger. Some children show their anxiety by becoming quiet, shrinking away from situations that make them anxious, and having trouble separating from their parents. These symptoms of anxiety are easy to detect for most providers.

However, the above symptoms are not the only way that anxiety manifests itself. Other children react with an overwhelming need to break out of an uncomfortable situation, which can be misinterpreted as anger or opposition. What people on the outside see is intense anger that is out of proportion to the situation, property destruction, elopement and aggression. In this way, anxiety can be a great masquerader.

Anxiety can present in the school setting as disruptive behavior. A child might find the academic work hard or become frustrated if he can’t do it perfectly. A child might have a hard time taking feedback or criticism from the teacher or peers. A child might be overwhelmed with the noise level in the classroom or a crowded lunch area

When a child presents with disruptive behavior, it is important to ask screening questions in other mental health areas as well, including depression, anxiety, obsessive compulsive disorder and autism. Examples of screening questions for anxiety include: Does your child worry excessively about everyday activities? Does your child have exaggerated or irrational fears?  If any of these screening questions are positive, consider asking more detailed questions or obtaining screening questionnaires (for example the GAD7 or SCARED) to elicit more details. Referral for a more thorough diagnostic evaluation with a psychologist could be helpful as well in cases that are diagnostically confusing.

This distinction is important to make sure a child has the right diagnosis, because it impacts treatment. The therapy approach for anxiety is different than the therapy approach for disruptive behavior disorders. Psychotropic medication, if being considered, would be different as well for these diagnoses. The SSRIs would be first line medication treatment for anxiety which the stimulants or non-stimulants like the alpha agonists (guanfacine and clonidine) or atomoxetine would be first line medication treatment for ADHD and other disruptive behavior disorders. If one is considering medication treatment for behavioral dysregulation that can be seen with anxiety, the alpha agonists can be helpful specifically for that. The stimulants can actually make the anxiety worse in these clinical situations.

In summary, it is important to ask what might be underlying the externalizing behavioral problems, because you might uncover anxiety masquerading as a disruptive behavior disorder. As always, SmartCare BHCS Parent Line 858-956-5900 is available to help families find appropriate resources and SmartCare Provider Line 858-880-6405 is available to providers to help with diagnostic clarification and medication treatment questions.

References:

https://childmind.org/article/how-anxiety-leads-to-disruptive-behavior/

Beyond Behaviors by Mona Delahooke PhD: https://monadelahooke.com/beyond-behaviors/

AUTHOR:

Charmi Patel Rao MD, DFAACAP

Co-Medical Director, Vista Hill Foundation

Health Science Clinical Professor, UCSD Department of Psychiatry

President, San Diego Academy of Child and Adolescent Psychiatry

Your 11 year old male patient with Autism level 2 without intellectual or verbal impairment and Generalized Anxiety Disorder is not tolerating sertraline well (resulting in weight gain and akathisia) with minimal positive effect. Primary concerning symptoms include: agitation, quick to anger, and difficulty with changes in routine. He previously did not tolerate trials of fluoxetine, guanfacine or aripiprazole but another physician. His mother is asking about propranolol which she read about on an autism blog she follows.

Beta-blockers:

There are medications that were developed for physical problems that have subsequently been found to be helpful for mental health problems. Several mood stabilizers, which were originally developed to be helpful for epilepsy, fall into this bucket, as do the alpha-agonists and beta blockers, which were developed for hypertension but have found to be useful for behavioral health concerns as well. This newsletter will focus on the many uses, mostly as an adjunctive treatment, of beta-blockers.

SSRIs are the first line medication treatment for anxiety disorders and are quite effective for the underlying feelings and thoughts linked to anxiety, but often aren’t as helpful for the outward behavioral and physical symptoms of anxiety. Behavioral symptoms of anxiety include: dysregulation, fight or flight response, and agitation. Physical symptoms of anxiety include: elevated heart rate, sweatiness, shaking, tremor, headache and stomachache/nausea. When these don’t respond to the combination of therapy and SSRI, it is helpful to consider alternative treatments, which can include alpha agonists and beta blockers, specifically propranolol.

Propranolol:

Propranolol is a non-selective beta-adrenergic receptor blocker that crosses the blood-brain barrier so can have effects in the central nervous system in addition to its peripheral activity, unlike most other beta-blockers. It has been around since the 1960s as an antihypertensive medication, although there are newer medications for hypertension now. When people feel anxious, their body makes more of the neurotransmitters norepinephrine and epinephrine, which historically served a survival purpose for the “fight or flight” response but can be impairing for someone with excessive anxiety. Propranolol can specifically help with the physical symptoms of anxiety including sweating and shaking but doesn’t directly treat the feeling of anxiety. It can be useful for performance anxiety and panic disorder.

There are some important guidelines to keep in mind when prescribing propranolol. Typically start with 10-20mg daily in children and 20mg in adults with a target dose of 20-40mg (40-60mg for adults) divided into two doses. There is a long acting formulation of propranolol but the minimum dose is 60mg. Someone might feel sleepy when first starting propranolol but this should resolve after a few days and is one of the reasons to start at a lower than therapeutic dose and to give the starting dose in the evening. Common side effects include: dizziness, lightheadedness, cold hands and feet and stomachache. It is important to monitor blood pressure regularly if prescribing propranolol. Use caution when prescribing with other medications that can reduce blood pressure. For example, it is not recommended to use propranolol with an alpha agonist, particularly at high doses. Its use is contraindicated in people with sinus bradycardia, heart failure, and sick sinus syndrome and should be cautioned in people with diabetes, hyperthyroidism, and asthma. It should used with caution in someone with depression because it can worsen depressive symptoms. When stopping propranolol, the medication should be tapered off to avoid discontinuation hypertension.

Studies have not found propranolol to be particularly helpful for PTSD, social anxiety and generalized anxiety. It is a medication to consider when patients have impairing physical and behavioral symptoms with their anxiety presentation. This includes panic disorder and performance anxiety. Propranolol has been studied in children with co-occurring anxiety and autism. It has been found to be helpful for behavioral dysregulation while being relatively well tolerated. It can be a tool in the medication toolbox when first line options do not work well or are not well-tolerated.

Back to the Case Presentation

You plan a trial of propranolol 10mg qday to start and increase to 10mg twice per day after one week. Parents and school report he is tolerating it well (blood pressure remains stable) and mother reports he is “not so quick to react and get upset”. The dose is titrated to 20mg twice per day with a 10mg as needed dose available. He continues with his school-based supports and autism intervention.

References:

https://www.ncbi.nlm.nih.gov/books/NBK557801/

https://pmc.ncbi.nlm.nih.gov/articles/PMC4724794/

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5803020/

https://www.news-medical.net/news/20240123/Blood-pressure-drug-could-help-lower-anxiety-for-kids-and-young-adults-with-ASD.aspx

AUTHOR:

Charmi Patel Rao MD, DFAACAP

Co-Medical Director, Vista Hill Foundation

Health Science Clinical Professor, UCSD Department of Psychiatry

President, San Diego Academy of Child and Adolescent Psychiatry

There has been a recent shift in the approach to patients with ID, with greater focus on adaptive functioning across domains, including cognitive, social and practical capacities, rather than based purely on an IQ score. Since ID can be caused by a variety of factors, including genetic, perinatal, environmental and other issues, it is thus important to assess the underlying etiology of the ID, because it can inform the assessment of problems symptoms and guide treatment efforts.

For a patient with Intellectual Disability exhibiting behavioral and emotional symptoms, it is important to conduct a focused medical review of systems as sometimes a patient “acts out” as a way to communicate physical discomfort (for example: from an infection or headache or abdominal issue). Other precipitants may include a behavioral profile to avoid non-preferred activities or as a protest to a change in routine—this particularly with persons who are non-verbal or verbally limited. Individuals with ID are at greater risk of trauma exposure and abuse, so assessment of these potential concerns should also be part of the evaluation protocol.

External considerations aside, co-occurring psychiatric conditions are not uncommon in the population and the most common psychiatric disorders that co-occur are Autism Spectrum Disorders (ASD), Mood Disorders (Anxiety and Depression) and Attention Deficit Hyperactivity Disorder (ADHD). Less frequently, ID patients may also present with co-occurring disorders including psychotic disorders and bipolar conditions which need therapeutic interventions comparable to that given to non-ID individuals.

It is important to ask the patient (if possible) and caregivers about current behavioral and emotional concerns, with attention to how appropriate the symptoms are given the patient’s developmental and functional capacities, and also, how the presenting symptoms are different from their baseline presentation. In this process, it is important to avoid misattributing symptoms to the patient’s ID when they may be a result of a co-morbid psychiatric condition. It can be helpful to use screening tools and use diagnostic criteria adapted for patients with ID conditions.

With respect to patients with co-occurring ID and ADHD, symptoms of hyperactivity tend to occur earlier in the patient’s life and symptoms of inattention tend to last longer into adolescence and young adulthood.   It is of note that stimulant medications, which are the mainstay of treatment for ADHD in youth, are generally less effective in children with co-morbid ID and ADHD. This said, a stimulant trial in patients with co-morbid ADHD symptoms would generally be appropriate along with careful monitoring of side effects and efficacy. Non-stimulants such as the alpha agonists and atypical antipsychotics may be helpful for the young patients with ID and co-morbid disruptive behavioral disorders (including ADHD).

With respect to anxiety and depressive disorders in the ID patient, these individuals may struggle in identifying their feelings, and it can be challenging to assess whether a non-verbal or speech-limited individual’s behaviors is related to underlying anxiety or depression. Input from caregivers across multiple settings can help with this determination. The SSRIs can be useful in patients with ID and clinical depression and/or anxiety, again with close monitoring for side effects.

In summary, when seeing patients with Intellectual Disability, it is important to assess for co-morbid behavioral and emotional concerns and possible psychiatric disorders with full attention to their overall medical and their psychosocial status.

Treatment of insomnia related to anxiety includes pharmacological and non-pharmacological approaches. For most patients with co-morbid anxiety and insomnia, one should consider treating the insomnia separately, as treatment for anxiety traditionally with an SSRI or other antidepressant medication can take a few weeks to be effective. Several studies have shown that treating the insomnia concurrently helps improve the response of the anxiety disorder.

Currently, the FDA has several approved drugs for the treatment of insomnia: nonbenzodiazepines including eszopiclone (Lunesta), zolpidem (Ambien), zolpidem ER (Ambien ER), and zaleplon (Sonata); benzodiazepines including estazolam (Pro Som), flurazepam (Dalmane), quazepam (Doral), temazepam (Restoril), and triazolam (Halcion); a tricylic antidepressant low-dose sinequan (Doxepin); an orexin inhibitor (Belsomra or suvorexant) and a melatonin agonist: ramelteon (Rozerem).

Both nonbenzodiazepines and benzodiazepines are associated with adverse effects that include fatigue, dizziness, ataxia, and the development of dependence and tolerance with long-term use. Belsomra also shares some of these concerns. If there is concern about alcohol or other substance abuse, consider ramelteon or low-dose sinequan to avoid potential issues of abuse and addiction.

Long-term use of nonbenzodiazepines or benzodiazepines needs to be reassessed monthly. Short-acting benzodiazepines like Xanax and Ativan are not effective medications for insomnia, particularly if sleep maintenance is an issue. Non-FDA approved options for insomnia include: Melatonin, Benadryl and Trazodone. Even though they are not FDA approved, they are good first line options because they can be used on a more long-term basis if needed.

Non-pharmacological approaches to treat insomnia related to anxiety are also well-studied. Cognitive behavioral therapy for insomnia (CBT-I) is a well studied therapy approach to treating insomnia but it is underutilized. Components of CBT-I include stimulus control, sleep hygiene, sleep restriction, relaxation techniques, and cognitive therapy. If one cannot find a therapist to help a patient with CBT-I, there are self-help books offering CBT-I that are also available, including “The Insomnia Answer” by Paul Glovinsky and Art Spielman and “Quiet Your Mind and Get to Sleep” by Colleen E. Carney and Rachel Manber.

Consider referral to a sleep specialist if treatment is not working and/or if a specific sleep disorder, like obstructive sleep apnea, periodic limb movements, narcolepsy or rapid eye movement behavior disorder, is suspected.

The goal of this article is to reiterate the importance of assessing for and potentially treating sleep disturbance that is related to anxiety. The treatment for insomnia specifically can help to see better outcomes for the treatment of the anxiety disorder as a whole.

The team at SmartCare would like to wish all of you a safe and happy Thanksgiving. There will be no e-weekly next week. Enjoy your holiday!

 First, it is important to determine what makes anxiety clinically significant. Anxiety is an expected, normal, transient response to stress and can be helpful with the warning of danger or coping with the stress. Clinically significant anxiety is an excessive response to external stress or related to an unidentifiable trigger. It is persistent rather than transient. It causes functional impairment, by exceeding the patient’s ability to cope with the stress and/or leading to avoidance behaviors.

 General symptoms of anxiety in children include many worries about things before they happen, constant worries or concerns about family, school, friends or activities, fears or embarrassment or making mistakes, low self-esteem and lack of self-confidence. There are often somatic complaints as well, like stomachaches, headaches, and sleep disturbance, as well as a desire to avoid school and friends.

 Specific symptoms of separation anxiety include constant thoughts and intense fears about the safety of parents and caregivers, refusing to go to school, frequent stomachaches and other physical complaints, extreme worries about sleeping away from home, being overly clingy, panic or tantrums at times of separation from parents, trouble sleeping or nightmares, and refusing to sleep without parents.

 Specific symptoms of a phobia include extreme fear about a specific thing or situation (ex. dogs, insects, needles) and the fears cause significant distress and interfere with usual activities (ex. child refuses to go to the park because of a fear of seeing a dog).

 Specific symptoms of social anxiety include fears of meeting or talking to people, avoidance of social situations despite a desire to attend, and few friends outside the family.

 Anxiety disorders have a high rate of co-morbidity with other psychiatric disorders, primarily mood disorders, ADHD and other disruptive behavior disorders, and substance use disorders. It is therefore important to assess for these co-morbidities. To complicate things further, there can be some overlap with the specific symptoms of anxiety and other psychiatric disorders. For example, patients with Generalized Anxiety Disorder may “obsess” about daily worries, patients with Autism Spectrum Disorders have rituals, and patients with Major Depressive Disorder may ruminate or “obsess” over negative self-thoughts, but it does not mean that these patients also have Obsessive-Compulsive Disorder.

Treatment options primarily involve therapy and/or medication. For patients presenting with mild-moderate anxiety symptoms, a therapy approach first is preferred, with a plan to incorporate medication if the therapy is not effective or symptoms worsen. For patients with moderate-severe anxiety symptoms with significant impairment on daily functioning, it might be warranted to consider starting with a combination of medication and therapy. The key message is that therapy is the important component to treatment of anxiety disorders in pediatric patients, and medication can be an effective adjunctive treatment if needed. Therapy to address anxiety can easily be tailored to work with very young patients and is very effective in a dyadic format . Types of therapy used for anxiety disorders include: cognitive behavioral therapy, exposure response prevention therapy, and relaxation techniques, among others. It would be important to refer to a therapist who is well versed in treating anxiety in children and adolescents.

Now we will focus on the medications used to treat anxiety. They fall into two general categories: medications to treat the underlying anxiety and prevent future symptoms of anxiety and medications that treat acute symptoms, like a panic attack. In most cases, if a primary care provider is considering medication treatment for anxiety in a young patient, it will be from the first category. This category includes medications like the selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), mirtazipine, and buspirone. The SSRIs are the first line agents for this population. This class includes: fluoxetine, citalopram, escitalopram, sertraline, fluvoxamine, and paroxetine. Just like with treating depression, the medication can take 4-6 weeks to see the positive effective. Often a higher dose is needed to fully treat the anxiety symptoms compared to depressive symptoms. There is a motto to “start low and go slow” to limit increasing anxiety and causing activation during the titration process. So, for example if one is considering prescribing citalopram for anxiety for a 10 year-old patient, consider starting at 5 mg qday for one week then 10 mg qday for 1 week then 20 mg qday and assessing the response. Some patients experience akathisia (internal feeling of restlessness), which can feel like a worsening of their anxiety, if the dose is titrated too quickly. Other side effects include sleep disturbance, GI upset and headache but most of these symptoms resolve over time.

The treatment of anxiety disorders in pediatric patients is mostly off label. Only fluoxetine (ages 7+), sertraline (ages 6+) and fluvoxamine (ages 8+) have FDA approval for treatment of obsessive-compulsive disorder (OCD).

When prescribing any antidepressant medication to treat anxiety, it is important to review the FDA black box warning about the increased risk of spontaneous reporting of suicidal thoughts, even if the medication is not being prescribed to treat depression per se.

When deciding on medication treatment, it is standard practice to first use the SSRIs. If a patient has 2 or more adequate (in terms of dose and length of treatment) trials of SSRIs that are ineffective, one could consider an alternative, either an SNRI (venlafaxine or duloxetine) or mirtazipine. If there is some benefit from the SSRI, one could consider augmentation with mirtazipine or buspirone. The primary side effects to be concerned with mirtazipine include sedation and increased appetite. Buspirone has an onset of action of about 2 weeks. The primary side effects to be concerned with include: dizziness, fatigue and GI upset. Occasionally the atypical antipsychotics are considered as adjunctive treatment to treatment-resistant OCD.

The medications that treat acute symptoms of anxiety, like the benzodiazepines, are rarely used in this population. Pediatric patients can have a paradoxical reaction to benzodiazepines and exhibit behavioral disinhibition. Other side effects include: physiological and psychological addiction, confusion, sedation and impaired fine motor coordination. If a medication to treat acute anxiety is needed, for example for a teenager who has very occasional panic attacks, one could consider hydroxyzine 25-50 mg on a prn basis (available in 10mg tablets as well for younger patients), which is not associated with dependence. Side effects include: sleepiness, dizziness, and dry mouth.

It is important for primary care providers to be comfortable assessing anxiety symptoms and helping to establish a treatment plan for their pediatric patients. Sometimes rating scales can be helpful in the assessment process. Here is a useful screening tool with a child version and parent version:

http://www.midss.org/sites/default/files/scaredchild1.pdf

http://www.midss.org/sites/default/files/scaredparent1.pdf

Hopefully this series of articles has been a helpful tool to establish a level of comfort to assess and treat anxiety syndromes in the primary care setting.