Psychopharmacology of the Rage Attack Phenomenon in a Child with Obsessive Compulsive Disorder

Chief Complaint and Presenting Problem

M. was a 13-year-old boy with recently diagnosed obsessive compulsive disorder (OCD) and attention-deficit/hyperactivity disorder (ADHD) referred for increasing frequency and intensity of rage attacks and homicidal ideation directed toward his mother.

History of Present Illness

M. was brought to the hospital by his mother and voluntarily admitted after a “rage attack” during which he vocalized homicidal ideation toward her. According to mother, onset of these symptoms occurred 6 months before admission, and they had been increasing dramatically in frequency, intensity, and duration during the past month. Typically, during the attacks M. yelled, pounded on the floor with his fist at times, or threw objects to the ground. Occasionally, he became physically violent with mother, grabbing and pushing her during an attack. During the most recent attack before admission, mother reports that he picked up a knife in a threatening gesture, although he did not physically injure anyone with it.

M. reported that the rage attacks occurred when feeling that he was invalidated by his mother, and that she had “consistently wronged and manipulated” him throughout his life. He believed that mother's provocation had led to intense, anxiety-inducing intrusive thoughts to harm/kill her. The thoughts were both overwhelming and distressing to him, and when calm, he would state that although he did not wish to hurt or kill her, he was afraid that he might. M. was able to distinguish these intrusive thoughts from voices, stating that they came “from my own head.”

He reportedly once grabbed his mother during a rage attack, and once had an angry outburst at school when frustrated by the noises a classmate was making, and slammed his fist repeatedly on his desk while yelling, “stop.”

In addition to intrusive thoughts about killing mother and rage attacks, M. endorsed contamination obsessions. He stated that he was extremely fearful of becoming “sick and infected” when he went to the bathroom, and washed his hands for 1 minute or more each time he went. He also endorsed harm obsessions about his cat being in danger every time he left the house. He compulsively checked that the door was locked thrice before he was willing to leave. Mother reported he would continuously ask if she thought the cat would be okay when they were away, and at times became extremely anxious because of these worries. He denied panic attacks or a fear of public spaces.

Mother reported that 2 months before admission, M. developed a bacterial streptococcal pharyngitis, raising a question of Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcus (PANDAS). He was treated with a 7- to 10-day course of amoxicillin. However, the majority of M.'s OCD symptoms (ruminations, harm/contamination obsessions) began 6 months before the pharyngitis, and the rage attacks began 2 months before the diagnosis. There was no explosive or abrupt increase of OCD symptoms at the time of or following infection, as well as no increase in food restriction behaviors.

Notably M. endorsed new-onset suicidal ideation during the past 6 months, with thoughts of cutting his throat with a knife or dying in bed. He reported that these urges were precipitated by intrusive thoughts, and were extremely anxiety-inducing; when calm, he stated that he did not actually want to die. He had not attempted to harm himself since onset of these intrusive thoughts or in the past. In the month before admission, M. also endorsed intermittent depressed mood. He reported decreased sleep (6 hours instead of 8 per night), feelings of guilt regarding urges to harm his mother, difficulty concentrating in school, and lower energy level. He denied anhedonia as well as psychomotor changes.

After evaluation by an outpatient child and adolescent psychiatrist 1 month before admission, a diagnosis of OCD was made. M. was subsequently started on fluoxetine 10 mg daily, 10 days before admission. After starting fluoxetine, the child and adolescent psychiatrist questioned the possibility of selective serotonin reuptake inhibitor (SSRI)-induced mania, given increased aggression and decreased sleep. However, increased fatigue and decreased energy were inconsistent with mania, and there was no evidence of increased goal-directed activity, racing thoughts, distractibility, grandiosity, or impulsivity outside of his rage attacks.

Past Psychiatric History

M. had no previous medication treatment or hospitalization, and had no history of prior suicide attempts or self-injurious behavior.

Developmental History

Mother, a single mother by choice, became pregnant at age 36 through sperm donor insemination. M. was the product of a full-term, uncomplicated pregnancy with full prenatal care, and no maternal drug or alcohol use. M. was delivered by normal spontaneous vaginal delivery. Mother had a fever during delivery, but labor was otherwise noneventful. Birth weight was 7.9 lbs.

M. was easy to soothe as an infant, and had no difficulty being weaned. Developmental milestones were within normal limits except for a slight delay in language acquisition, which did not occur until age 2.5. He was reported to have had no difficulty with separation or interactions with strangers or extended family.

Mother had support from her family, and lived with maternal grandmother until M. was 6 years old. Mother reported that M. became rather explosive starting at age 6, with a volatile mood (“he would snap”). At around this time, he developed a habit of hair pulling, resulting in a small bald patch at the back of his head. There was no history of any motor or phonic tics.

M. experienced nightly enuresis until age 12, which resolved at that time with enuresis alarms and desmopressin.

Educational History

M. had an Individualized Education Plan with speech therapy when he first started school, but thereafter he received regular education. At the time of his referral for admission, M. was in regular education in grade 8 at a local private school. He excelled academically, receiving grades of mostly A/A- with occasional Bs, and had been offered scholarships to multiple high schools. His favorite subjects were mathematics and English. M. endorsed having friends at school and denied any bullying.

Social History

M. was an only child and lived with his mother in a residential area of a major metropolitan region. M. had never had contact with his biological father, an anonymous sperm donor. He denied physical, sexual, and verbal abuse (although he stated that his mother was controlling and had “done so many things” to make him “like this”). He endorsed having several close friends at school, and denied any bullying. He denied current or past sexual activity and there was no history of substance use.

Pertinent Family History

There was no known paternal family history, as father was an anonymous sperm donor. Maternal grandfather was reported to have an unspecified manic disorder and alcohol use disorder, both untreated. Maternal grandmother also had untreated alcohol use disorder.

A female maternal first cousin with unspecified manic disorder and substance use disorder reportedly completed suicide as a teenager by hanging. A maternal male first cousin was reported to have schizophrenia and multiple hospitalizations, and completed matricide in his 20s during a psychotic episode. He was currently incarcerated. Another maternal male cousin without a formal psychiatric diagnosis reportedly set himself on fire in a suicide attempt.

Medical History/Medications/Recent Physical Examination

M. had a history of asthma, for which he used an Albuterol inhaler as needed (last >1 year ago).

M. had been diagnosed with bacterial streptococcal pharyngitis twice in the past, once at age eight, and then 2 months before admission. He was treated with a 7- to 10-day course of amoxicillin both times.

There was no other significant medical history. Growth and development were reported to be within normal limits and M. was postpubertal.

Mental Status Examination

M. was a well-groomed and well-appearing, slender, but not underweight (body mass index 20.8), postpubertal 13-year-old boy who appeared his stated age. He related well and was cooperative with the interview. He occasionally picked at his fingers, tapped his foot, and wrung his hands, typically when discussing emotionally charged subjects. His speech was fluent and spontaneous, expressing himself clearly. Affect fluctuated between dysphoric/anxious and euthymic, with corresponding mood. His thought process was linear and there was no evidence of paranoia or persecutory thoughts, ideas of reference, thought broadcasting, thought insertion, or auditory/visual hallucinations.

M. endorsed frequent, ego-dystonic ruminative/intrusive thoughts of harming his mother/himself/others on the unit. He showed limited insight into the source of his symptoms, placing blame solely on his mother's behaviors. Although he exhibited good judgment in cooperating with treatment, he was easily agitated at times after visits with his mother. Cognition was appropriate to age and level of education.

Hospital Course

Physical examination upon admission was unremarkable; M. was a healthy appearing, postpubertal boy. M. and mother agreed to increase the fluoxetine for his OCD symptoms, rage attacks, and depressive symptoms. In addition, the treatment team offered M. and mother the option of guanfacine or aripiprazole as adjunctive treatment. Guanfacine was presented as a more benign option for rage symptoms in the context of some observed, but previously undiagnosed symptoms of ADHD, including impulsivity and decreased frustration tolerance, while aripiprazole could potentially be more efficacious for mood stabilization, but with a less desirable adverse effect profile. After obtaining additional details regarding a past history of mild inattention and hyperactivity/impulsivity symptoms, a formal diagnosis of mild ADHD was made.

The decision was made to start guanfacine extended release (Intuniv) at 1 mg, with the understanding that a switch to aripiprazole might be desirable at a later date if no improvement was seen. The guanfacine extended release was increased rapidly, by ∼1 mg every 5 days, while the fluoxetine was increased approximately every 5 days. By discharge, fluoxetine was titrated to 40 mg daily and guanfacine ER to 3 mg at bedtime. Although M. displayed occasional agitation early during the course of hospitalization, typically triggered by visits with mother, he maintained good behavioral control for most of his hospitalization. He reported improvement in his mood, and reduced frequency of obsessional thoughts and urges to hurt his mother or anyone else. At discharge, he denied suicidal and homicidal ideation, and adverse medication effects. He was discharged home with his mother with follow-up at a partial hospitalization program.

Brief Formulation

In summary, M. was a 13-year-old boy with recently diagnosed OCD referred for increasing frequency and intensity of rage attacks and homicidal ideation toward his mother.

From a biopsychosocial perspective, biological factors may have rendered M. vulnerable to OCD. He had experienced onset of trichotillomania, an OCD spectrum disorder, with impulse control deficits in early childhood as well as explosive outbursts with onset at age six. Other clinical phenomenology associated with the ADHD diagnosis made in the hospital included an early speech–language disorder, and enuresis. Family psychiatric history of mania and psychosis would render M. vulnerable to the development of these disorders as well.

Medical contributions included consideration of PANDAS after bacterial pharyngitis. However, given that M.'s OCD symptoms that preceded his diagnosis of pharyngitis were severe, and did not abruptly or explosively increase in association with the infection, it was unlikely that his presentation was consistent with PANDAS.

From a psychosocial perspective, psychological and developmental factors likely played a strong role, as is often the case in OCD. Separation-individuation tasks in early adolescence may have been particularly frightening for M., given the intensity and chronicity of his anger toward his mother. The absence of father may have rendered him particularly vulnerable to poor modulation of aggressive affects and contributed to his explosive outbursts. Despite the presence of a loving extended family system, the absence of a spousal support system and fears that matricide and severe violence could recur may have had a unique impact on M.'s development.

Multiaxial Diagnoses

Discussion

Explosive outbursts, or rage attacks, are a challenging clinical construct with unique interactions with OCD (Johnco et al. 2015). Traditionally understood as a phenomenon associated with Tourette's disorder (Budman et al. 2003), there is now an increasing awareness of the significance of rage attacks in childhood-onset OCD (Stewart 2012).

Rage attacks in pediatric OCD are characterized by episodes of explosive anger triggered by minor provocations (Storch et al. 2012). Conceptually, they are context specific and functionally interact with core OCD symptoms. Rage attacks may generate from a child's frustration and mounting anxiety when he or she is unable to complete the anxiety-reducing compulsions that counter anxiety-inducing obsessions. Rage attacks may also serve to avoid feared triggers before compulsions or other avoidance behaviors. Finally, when safety concerns become significant they may impact family accommodation patterns. This was certainly the case with M.

The hospital stay facilitated the opportunity to characterize M.'s OCD phenomenology by additional evaluation of potential contribution of PANDAS (Leckman et al. 2010). Additional laboratory evaluation, including throat culture, and antistreptolysin O and anti-DNase B titers, may have revealed additional information suggestive of PANDAS. However, the absence of a clear-cut clinical picture of abrupt, explosive exacerbation of OCD symptoms in the context of a favorable response to conventional treatment with an SSRI (Sigra et al. 2018) led to the decision not to pursue this opportunity. As further investigation of PANDAS takes place, clear guidelines on evaluation and management of youth with this presentation are likely to be formulated and allow for standardized application.

M. was admitted to hospital out of concern that he would kill his mother in the context of his rage episodes. The urgency and safety risk necessitated an uptick in psychopharmacological treatment, which resulted in the decision to consider treatment with a second-generation antipsychotic (SGA) before the time course that would have enabled an adequate trial of fluoxetine. Studies have supported the use of risperidone and aripiprazole in children with tic-related OCD. In addition, M.'s family history of mania and concern for possible SSRI activation was important in consideration of use of a neuroleptic. However, application of a tailored risk assessment and first-line use of an agent least likely to cause adverse effects ruled out the use of a neuroleptic in this case.

Given the identified history of impulse control deficits consistent with ADHD, it was a reasonable choice in the safety of the inpatient setting to first try an alpha-2 agonist in tandem with SSRI titration. We felt that an SGA, with potential for more significant adverse effects, particularly in children and adolescents, would have been indicated only if guanfacine failed. There was no evidence of mania in this child, as the episodes of aggression were better understood as OCD-related rage attacks (Maayan and Correll 2011).