Childhood Sleep Terror and Mirtazapine

To the Editors:

Sleep terror (ST) is defined as a partial arousal disorder, which usually occurs during the first third of the sleep. It is characterized by intense fear, motor agitation, screaming, and prominent autonomic activity (e.g., mydriasis, tachycardia, and tachypnea). The child is typically unresponsive to the external stimulus during the attack and does not recall the episode in the morning. ST is reported to have a higher prevalence in childhood than in adulthood, affecting 3% of children. Although its etiology is mostly unknown, several factors such as sleep deprivation, fever, stress, and drugs (e.g., lithium) were described as triggers in susceptible individuals. Its management includes parental reassurance, psychoeducation, and behavioral interventions (e.g., scheduled awaking). However, pharmacotherapy may be necessary in some cases (e.g., when the child has high risk of injury or frequent night terror) (Howell 2012).

In this report, we present a pediatric case with ST successfully treated with mirtazapine.

Case

A 7-year-old boy was admitted to the child and adolescent psychiatry out-patient clinic with complaints of vomiting and night-time awakenings. According to his parents, 1–2 hours after falling asleep, he was screaming, crying agitatedly, vomiting, and sweating profusely. He appeared frightened and unresponsive to his parents' attempts to communicate. All these were continuing for nearly 5 minutes and then he fell asleep. In the morning he had no memory of this experience. Parents reported that these episodes had started 5 months ago and were evident nearly every night.

His other complaint was vomiting during daytime that was generally induced by a stressor (e.g., going to school) and occurred usually in the morning for nearly every day. His vomiting episodes started when he was 4 years old and affected his daily functioning negatively.

Neurology and gastroenterology consultations were requested to rule out organic causes for his night-time awakenings and vomiting. His neurological examination and extensive work-up were normal. He was diagnosed as having ST and functional vomiting, and we decided to initiate mirtazapine 15 mg/day treatment. On his second visit 1 month later, his complaints of ST and vomiting improved completely. During a 6-month follow-up, he had only two episodes of ST and no episode of vomiting. No adverse effect of mirtazapine was reported during this period.

Discussion

We presented a case with severe ST responsive to mirtazapine. To our knowledge, this is the first reported case of ST improved significantly with mirtazapine. Mirtazapine is a noradrenergic and specific serotonergic antidepressant with antagonist effects on adrenergic alpha-2, serotonin 2A, 2C, and 3 and histamine 1 receptors. It is effective in stimulating appetite as well as regulating sleep disturbances.

ST is seen during the slow-wave sleep (SWS) and enhanced deep sleep promotes ST (Howell 2012). Pharmacological agents, including benzodiazepines and tricyclic antidepressants, which suppress SWS, are commonly used for treatment. In the literature, there are a limited number of reports on management of ST with selective serotonin reuptake inhibitors, including fluoxetine (Guzman and Wang 2008) and paroxetine (Frölich and Gerd 2001), and atypical antidepressants such as trazodone (Balon 1994). Because serotonin has a modulator effect in regulation of SWS intensity, it was hypothesized that depletion of central serotonin may have a role in ST (Jouvet 1999). Alpha-2 adrenergic antagonism of mirtazapine increases serotonin, which may be the mechanism for improvement in ST in the reported case.

In conclusion, considering limitations of prolonged use of benzodiazepines and possible serious side effects of imipramine, mirtazapine may be an alternative agent in treatment of ST.