LEITERS TO THE EDITOR

Drs. Spencer and Biederman reply:

REFERENCES

We read the letter by Dr. Holt with great interest. She raises the intriguing possibility that changes in weight parameters observed in ADHD children treated with tricyclic antidepressants (TCAs) may be associated with changes in appetite secondary to possible comorbid mood disorders. As reviewed in our recent article, reports of the treatment of children with TCAs consistently include symptoms of anorexia or suppression of weight gain. Although in our sample of children with ADHD, the suppression of weight gain occurred primarily in the group with a relatively higher (above the median) initial weight percentile, for most desipramine-treated children the weight parameters at baseline did not strongly indicate that our sample consisted of meaningfully overweight or underweight children. Although comorbid major depressive disorder (MDD) was not systematically assessed in our study sample, we found a rate of approximately 25% MDD among ADHD pediatrically and psychiatrically referred children in our research (Biederman et aI., 1992). As Dr. Holt suggests, the common comobid disorder of MDD with its attendant appetite disturbance is an important potential confounder in the investigation of the effects of desipramine on weight in children with ADHD. Thomas J. Spencer, M.D. Joseph Biederman, M.D. Massachusetts General Hospital, Boston REFERENCE

Biederman, J., Faraone, S. V., Keenan, K. et al. (1992), Further evidence for family-genetic risk factors in attention deficit hyperactivity disorder: patterns of comorbidity in probands and relatives in psychiatrically and pediatrically referred samples. Arch. Gen. Psychiatry, 49:728-738.

Mania and Anticonvulsant Therapy To the Editor: Ethosuximide is considered to be the treatment of choice for absence seizures. Psychiatric complications such as psychotic behaviors have been reported in the past. However, the following case demonstrates a full-blown manic episode in a child with no personal or family history of a mood disorder (Fishcher et aI., 1965; Dreifus, 1989). C. L. is an 11-year-old white boy who was referred to our psychiatric inpatient unit for hyperactivity, short attention span, impulsivity, aggressive behavior toward other students at school, and. punch~n~ walls at home. There was a positive family history of attentiOn-defiCit hyperactivity disorder in his mother and two siblings. As an inpatient, he was observed to have multiple episodes of staring spells lasting from a few seconds to no more than 1 minute. He was amnestic for each episode. A sleep-deprived EEG showed frequent and recurrent bursts of 3/second second spikes and waves and polyspikes and slowwave activity every 10 to 20 seconds. A diagnosis of absence seizure was made, and the patient began receiving ethosuximide, 250 mg/day, which was increased gradually up to 250 mg t.i.d. during a 2-week period. On the third week, he gradually became more argumentative. His attention span shortened significantly, and his speech became pressured and overproductive. He demonstrated flight an~ shift of ideas. His sleep pattern decreased to almost 3 hours a mght, and he had an elated mood. On the fifth week, his ethosuximide was discontinued and the patient's behavior returned to his baseline, as seen at admission. He then was treated with a trial of valproic acid, which successfully addressed the absence seizures. Katina Matthews-Ferrari, M.D. Nabil Karroum, M.D. University of Florida

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Fischer, M., Korskjaer, G. & Pedersen, E. (1965), Psychotic episodes in Zarondan treatment. Epilepsia, 6:325-334. Dreifuss, F. E. (1989), Ethosuximide toxicity. In: Antiepileptic Drugs, Third Edition, Eds. Rene H. Levy, F. E. Dreifuss, Richard H. Mattson, Brian S. Meldrum & J. Kiffin Penry. New York: Raven Press, pp. 669-705.

Clomipramine Side Effects To the Editor: I read with interest the report by Alarcon et al. (1991) about paranoid and aggressive behavior in two obsessive compulsive adolscents treated with clomipramine. I have observed the new onset of selfabusive behavior in a child with Tourette's syndrome and obsessivecompulsive disorder .(OCD) treated with clomipramine. The patient is an Ill/2-year-old black male admitted to a psychiatric day hospital with presenting difficulties including aggressive conduct problems, distractibility, hyperactivity, rare tics of shoulder shrugging and yawning, coprolalia, and a compulsive checking ritual performed before entering rooms. There was no history of self-destructive behavior or threats. Psychosocial stressors included parental divorce. The patient had difficulty accepting his mother's boyfriend. A year and a half before admission, the patient had been treated on an outpatient basis with clonidine, 0.1 mg/day, for hyperactivity and simple motor and vocal tics. No complex tics, obsessions, or compulsions were noted at that time. The simple tics had decreased with clonidine treatment, which was discontinued after several months by the patient's mother. Twelve days after a trial of clomipramine at a dose of 25 mg/day was begun for attention-deficit hyperactivity disorder (ADHD) and obsessions, the patient developed new symptoms of self-abusive behavior that included trying to pinch his finger with a staple remover and repetitively twirling and pulling at his hair. When he was interviewed, he had obsessive fears of injury. In a counterphobic fashion, he challenged others to dare him to hurt himself. I increased the clomipramine to 25 mg b.i.d., thinking that the patient's obsessive preoccupation with self-destructive thoughts might decrease with a higher dose of clomipramine. His compulsive hair twirling and pulling persisted. The clomipramine was discontinued after a 20-day trial because of concerns that it was contributing to compulsive self-abusive behavior. Self-abusive behavior and threats and compulsive hair twirling and pulling ceased within 2 weeks after the clomipramine was discontinued. His hyperactivity and coprolalia remained persistent problems, and his depression intensified. The patient feared he would not be saved and would go to Hell. He began another treatment with clonidine at a dose of 0.05 mg/day with little effect on hyperactivity and coprolalia. Six weeks after the clomipramine was discontinued, the patient attempted to hang himself in a suicide attempt. He alleged that his mother beat him, but no bruises were found at a physical examination. He was admitted to the inpatient service for 3 weeks. Clonidine was discontinued, and he was treated with pimozide, 3 mg/day. There was a significant decrease in coprolalia and an improvement in mood with remission of suicidal ideation, which persisted for 3 weeks after the patient returned to live at home while continuing in-day hospital treatment. Three weeks after transfer to the day hospital, he threatened to again hang himself and was readmitted to the inpatient service. !Ie alleged that his mother was drinking heavily and was verbally abUSive toward him. The new onset of self-abusive behavior and compulsive hair twirling and pulling roughly 2 weeks after treatment with clomipramine was started and the remission of these symptoms 2 weeks after the J. Am. Acad. Child Adolesc. Psychiatry, 31:6, November 1992

Mania and anticonvulsant therapy.

LEITERS TO THE EDITOR Drs. Spencer and Biederman reply: REFERENCES We read the letter by Dr. Holt with great interest. She raises the intriguing po...
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