Emotional Dysregulation in a Child with Attention-Deficit/Hyperactivity Disorder and Anxiety: Psychopharmacological Stategies

Chief Complaint and Presenting Problem

D. is an 11-year-old boy in a fifth grade special education program with an individualized education plan (IEP). He lives with his mother and older sister. D. was referred to Child and Adolescent Psychiatry Family Services for declining academic performance, impulsive and oppositional behavior, anxiety, and poor sleep.

History of Present Illness

Mother reports that D. has had problems with his behavior, specifically trouble managing frustration and anger, since the age of two. Mother reported that D. had no history of developmental delays, and had not received early intervention. He received speech therapy in school until age seven.

D. was initially evaluated at the age of seven for concerns regarding his poor academic performance, lack of response to limit setting, impulsive and aggressive behavior, anxiety, and trouble sleeping. D. was subsequently diagnosed with impulse control disorder-not otherwise specified (NOS), anxiety disorder-NOS, and learning disorder-NOS.

D. received individual and family therapy, tutoring services, and pharmacotherapy. D. was treated with several medications including aripiprazole, clonidine, ziprasidone, olanzapine, diphenhydramine, and OROS methylphenidate. D. remained on OROS methylphenidate for his impulsive behavior, olanzapine for his aggression, and diphenhydramine for sleep initiation. D.'s behavior and impulsivity was reported to improve on the OROS methylphenidate and olanzapine, but his sleep remained problematic on diphenhydramine.

Unfortunately, D.'s mother experienced an exacerbation of her own mental health problems this past year when D. was age 10, and for three months was unable to bring him to his appointments. D. attended a few appointments independently, but was not consistent with his therapy or tutoring services, or adherent with his medications. As a result, D.'s services were terminated at the clinic last year, and D. was without consistent psychiatric care for a prolonged period.

About six months later, D. was referred to an academic center for child and adolescent psychiatry services. At that time, mother reported that he had “ low frustration tolerance, anger, aggressive behavior, poor academic performance characterized by declining grades, anxiety, and trouble sleeping.” Mother complained that when he does “not get what he wants,” he becomes “aggressive, self-injurious and displays oppositional behavior at home.” For example, if he does not get the “right kind of snack” he “bangs his head, punches walls” and “raises his fists” as if he was “about to punch someone.” D. was also having trouble with his peers and teachers at school. Mother noted that he appeared to be anxious “all the time” and had trouble initiating sleep at night. As a result of going to bed late, he had difficulty waking up in the morning. Because mother reported difficulty with sleep initiation herself as well, D. missed school at times.

D. was diagnosed with attention-deficit/hyperactivity disorder (ADHD) combined presentation, oppositional defiant disorder, and learning disorder. The recommendation was for a multimodal treatment plan to target his disruptive behavior, anxiety, and sleep initiation difficulties. D. began individual weekly therapy, and monthly or bimonthly medication management, but declined to participate in group therapy. Parent-child relational therapy was recommended, but mother was not able to consistently attend appointments, so this treatment was discontinued.

Past Psychiatric History

D. had no past psychiatric history.

Developmental History

Mother was reported to be taking olanzapine during her pregnancy with D. D. was the product of a 36-week gestation and uncomplicated delivery. D. had no complications in the well baby nursery and did not require respiratory or feeding support.

There was no history of developmental delays, and motor, language, and adaptive milestones were achieved on time.

Educational History

D. had been receiving special educational services since kindergarten. He had an IEP for documented difficulty in math, reading, and spelling. He had to repeat both second and third grades.

Social History

D. lived with his mother and 16-year-old sister. Father and mother separated when D. was four years old. D. saw his father, who lived in the area, sporadically. Mother remarried when D was four years old, and recently divorced D.'s stepfather.

Mother had a history of physical abuse by D.'s biological father and stepfather. D. witnessed the domestic violence between his mother and stepfather, but had reportedly not been physically or sexually abused himself.

D. was reported to get along “okay” with his sister, and had not had any difficulties with peers since the start of this school year.

Family History

Mother reported that she suffers from “anxiety, and major depressive disorder.” She also reported severe insomnia. She was receiving outpatient psychiatric care and was on trazadone for sleep and venlafaxine for mood and anxiety symptoms. Mother had received other psychiatric medications in the past; the only one she could recall was olanzapine, which she took during her pregnancy with D.

Mother reported that D.'s father likely had an anxiety disorder, and previously was addicted to heroin. D.'s sister, age 16, had learning difficulties in school.

Medical History

D. had no serious medical problems, hospitalizations, or surgery. He had no history of any major childhood illnesses, and had received all his appropriate vaccinations to date.

Mental Status Exam

Mental status exam revealed a fairly cooperative child who was well groomed and appeared age appropriate; he was thin, with no dysmorphic features. His gait and muscle strength were age appropriate, and there were no tics or abnormal movements.

D. was able to sustain attention, displayed no hyperactive or impulsive behavior, and had fair eye contact. His responses to questions about his daily life were brief, but for the most part accurate. His speech was regular in rhythm, rate, tone, and volume and was mostly non-spontaneous. He was oriented to time, day, place, and situation. He described his mood as “fine” and his affect was calm with some irritability and reactivity. His thought process was linear and goal directed, and his thought content was related to school and his family life at home. There were no deficits observed in his memory or cognition, and there was no evidence of psychotic symptoms. He denied suicidal and homicidal ideation, as well as auditory and visual hallucinations. Insight was limited and judgment was poor.

Medication Treatment Course

D. was started on OROS methylphenidate 18 mg daily to target his inattention and hyperactivity, and the dose was eventually titrated to 54 mg daily. D. tolerated this without adverse effects. Methylphenidate improved D.'s inattention and hyperactivity, but rebound symptoms were noted in the afternoon., As a result, methylphenidate 5 mg IR was prescribed for the afternoon, but mother was unable to administer it on a consistent basis, so he did not receive the full potential benefit of medication. The afternoon dose was eventually discontinued. As an alternative, guanfacine 0.5 mg orally at bedtime was prescribed with good effect and better adherence. The dose was eventually titrated to 0.5 mg orally twice a day.

On OROS methylphenidate 54 mg daily and guanfacine 0.5 mg orally twice a day, D. showed an improvement in his inattention and impulsive behavior at school, but continued to act impulsively at home. In addition, he continued to have difficulty falling asleep. As a result of the persistent initial insomnia, D. continued to experience fatigue in the morning. To reduce daytime fatigue and impulsive behavior at home, the dosing schedule of the guanfacine was changed from 0.5 mg orally in the morning and at bedtime to 0.5 mg orally in the afternoon and at bedtime. Mother reported that D.'s impulsivity at home persisted on this dosing schedule; while he was reported to be more “tired” in the evenings, he continued to have difficulty “winding down” at bedtime and initiating sleep. To target initial insomnia and anxiety at night, the guanfacine dosing schedule was changed to 1.0 mg orally at bedtime, thus both simplifying the regimen and more closely targeting his night time symptoms.

Mother and teachers reported a significant improvement in D.'s ability to focus in school and at home, and complete his classwork during the day. His grades improved and he was getting along better with peers. Mother had not received any reports of disruptive behavior or poor academic performance from school since the new treatment regimen began. In addition, both D. and mother denied ongoing mood or anxiety symptoms for the past several months.

Brief Formulation

In summary, D. is an 11-year-old boy referred for declining academic performance, impulsive and oppositional behavior, anxiety, and initial insomnia. D. met diagnostic criteria for ADHD, combined presentation, oppositional defiant disorder, unspecified anxiety disorder, and specific learning disorder. Adherence to treatment had been challenging and difficult both in the past and currently.

From a biopsychosocial perspective, given a family history of major mood and anxiety disorders, substance use disorder, and learning disorders, D. had a genetic predisposition to mood, anxiety, and disruptive behavior as well as learning disorders. From a psychosocial perspective, D. was challenged by domestic violence, conflicts with his mother, a single parent, and the absence of a father figure to help him manage aggressive impulses and anxiety. D.'s academic challenges at school only further served to increase his anxiety. His coping skills were limited.

Discussion

This case represents the presentation of classical developmental psychopathology and very typical psychopharmacological challenges for the child and adolescent psychiatrist. Children with ADHD have a variety of other symptoms that need to be addressed in addition to inattention, hyperactivity, and impulsivity. In addition to disruptive behavior, D. appeared to struggle with anxiety and emotional dysregulation characterized by low frustration tolerance, temper outbursts, and mood lability (Biederman et al. 2012).

Deficient emotional self-regulation (DESR) in ADHD is a relatively newly investigated phenomenon. Although long described (Biederman et al. 2012; Wender 1995; Barkley 1997; Nigg and Casey 2005), it has only recently been systematically studied. DESR has been described as 1) deficits in self regulation of the physiological arousal caused by strong emotions; 2) difficulties inhibiting inappropriate behavior in response to either positive or negative emotions; 3) problems refocusing attention from strong emotions; and 4) disorganization of coordinated behavior in response to emotional activation. (Spencer et al. 2011). An operational definition reported by one research group was an aggregate cut-off score of >180 but <210 on the Anxiety/Depression, Aggression and Attention Scales of the CBCL (CBCL-DESR). In a recent study of 197 children with and 224 without ADHD, 44% of the ADHD children had a positive CBCL-DESR profile, as compared to 2% of the controls (p<0.001). The CBCL-DESR profile was found to be associated with higher rates of disruptive behavior disorders and anxiety, and greater impairments in emotional and social functioning (Spencer et al. 2011).

One recent study of emotional lability (EL) in 1186 children age 6–18 with combined type ADHD, and their 1,827 siblings demonstrated that severe emotional lability was associated with more severe ADHD core symptoms, primarily hyperactive-impulsive, and more comorbid oppositional, affective, and substance use disorders (Sobanski et al. 2010). EL was described as a frequent problem and associated with greater severity and more comorbid psychopathology.

D. appeared to have a profile of DESR. Little psychopharmacological research has been conducted to address this aspect of ADHD. DESR symptoms are often variably responsive to stimulants depending on the individual child. Other interventions and medications may be needed to target emotional dysregulation symptoms. It is interesting that D.'s hyperactivity and inattention improved on long-acting methylphenidate, but he experienced rebound later in the day. The rebound may have overlapped with or was exacerbated by his anxiety and impulsivity, which was not addressed by the stimulant alone. Addition of guanfacine in relatively low doses in the evening appeared to be helpful for several of his DESR symptoms, including impulsivity, anxiety, and initial insomnia.

Recent neurobiological studies have facilitated our understanding of the biological underpinnings of ADHD (Arnsten 2009). Increasingly, the importance of the prefrontal cortex (PFC) in ADHD has been described. The PFC is crucial for regulation of attentional functioning, as well as regulation of emotion and behavior; these regulatory functions are often described as executive functions. Animal studies provide data to suggest that catecholamine actions in the PFC are of significance for ADHD (Arnsten 2009). Medications that enhance alpha-2 receptor stimulation improve PFC function; whereas methylphenidate increase endogenous norepinephrine and dopamine and indirectly improves PFC function through alpha-2A and D1 receptor actions, guanfacine acts directly on post-synaptic alpha-2A receptors in the PFC. (Arnsten 2009).

Guanfacine has been found efficacious in treatment of core ADHD symptoms (Biederman et al. 2008) and extended release guanfacine (Intuniv) has recently been approved by the FDA for treatment of ADHD in children and adolescents (FDA 2009). It has also been found to be beneficial for anxiety in children and adolescents with traumatic stress related symptoms (Connor et al. 2013). Guanfacine may address deficient emotional self-regulation by enhancement of attentional and cognitive controls; this may have been the mechanism by which the addition of guanfacine was helpful for D.

Another important issue in this case is the difficulty with adherence to treatment, which is a common problem in treatment of youth with ADHD. A recent systematic literature review on ADHD medication discontinuation reported that adherence was generally poor among patients with ADHD. Long acting formulations and amphetamines were associated with longer treatment duration than short acting formulations and methylphenidate (Gajra et al. 2014). Although adverse effects were reported to be the most common reason for discontinuation across studies, in the original research studies, lack of symptom control and dosing inconvenience were the most common reasons. Thus, it is not surprising that it was not until D.'s mother found a long-acting and convenient dosing schedule that resulted in optimal adherence.