SSRIs FOR “DIFFICULT” TEMPERAMENT

LETTERS TO THE EDITOR

clinical promise with significantly lower risk of extrapyramidal symptoms, and possibly of tardive dyskinesia as well, they can induce significant weight gain, which may be a cause of medical morbidity. Little is known about the mechanism and/or the cause of the weight gain associated with risperidone. Weight gain, whether induced by risperidone or present soon before its initiation, may place that child at increased risk for hepatic dysfunction. Until studies can clarify these associations and/or their underlying mechanisms, it may be prudent to monitor LFTs in children who are taking risperidone, particularly obese children or those who are rapidly gaining weight during treatment. Jeffrey Landau, M.D. Andres Martin, M.D. Yale Child Study Center New Haven, CT Baldridge AD, Perez-Atayde AR. Graeme-Cook F. Higgins L. Lavine JE (1995), Idiopathic sreatohepatitis in childhood: a multicenter retrospective study. J Pediatr 127:700-704 Franzese A. Vajro P. Argenziano A er al. (1997), Liver involvement in obese children: ultrasonography and liver enzyme levelsat diagnosis and during follow up in an Italian population. Dig Dis Sci 42:1428-1432 Geller WK, Zuiderwijk PBM (1998), Risperidone-induced hepatotoxicity? (letter). J Am Acad Child AdolescPsychiatry37:246-247 Kumra S. Herion D, Jacobsen LK, Briguglio C, Grothe D (1997), Case study: risperidone-induced hepatotoxicity in pediatric patients. J Am Acad Child Adolesc Psychiatry 36:701-705

SSRIs FOR "DIFFICULT" TEMPERAMENT

To the Editor: I would like to draw the attention of your readers to an article recently published in the AmericanJournalofPsychiatry, which I believe has profound implications for the practice of child and adolescent psychiatry, particularly under managed care. Knutsen et al. gave paroxetine to normal adult volunteers in a double-blind study. Personality measures, administered at o and 4 weeks, showed increased affiliative behaviors and decreased negative affect and focal hostility (Knutsen et al., 1998). I would also like to remind readers of a study showing that serotonergic agents can decrease the behavioral and emotional difficulties of children with "obsessive difficult temperament" (Garland and Weiss, 1997). Two other relevant points are from the literature on temperament: "Difficult" traits may be inborn (cf. Thomas and Chess, 1984). However, in their extensive work on temperament, Chess and Thomas reiterate that "goodness of fit" between parent and child, and/or the parent's ability to appreciate and make the world manageable for the child, are the predictors of good psychological outcome (Thomas and Chess, 1984). Other studies have shown that temperament, especially difficult temperament, is partly in the eye of the beholder (Pettit and Bates, 1984), implying

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that the mother's early experience of the infant sets the stage for later relationship disturbances. I am by no means implying that Garland and Weiss' families were in any way deficient. I am observing that "difficult" traits of rigidity, sensitivity, intensity, etc., exist along a continuum of severity, from pathological to well within normal limits. Knutsen and colleagues' study indicates that the selective serotonin reuptake inhibitors (SSRIs) modulate even mild degrees of these personality variables. Putting these studies together, we are faced with a dilemma. Where do we draw the line that says that "difficult" behaviors are of sufficient severity to merit medication? What do we do in cases in which it is clear that the origins of disturbed behavior lie, in a large part, in such a failure of fit and might respond to intensive psychotherapy or family therapy? If we know that an SSRI will make a difficult child easier to manage, can we withhold it, especially when the family refuses other interventions? But is it ethical to knowingly alter the personality of the child (as demonstrated by Knutsen and colleagues'work) and tacitly remove responsibility from the parents for recognizing and working with their child's unique personality? At the same time, it is hard to resist using these medicines, whose morbidity tends to be low, and which can so rapidly improve day-to-day functioning for families under stress. Two further comments are worthy of inclusion. First, many of my patients have commented that, when taking SSRls, they are less capable of feeling appropriate sadness, including empathy for the sadness of others. This has worrisome implications for their use in children. Second, as parents become more preoccupied outside the home and less available to their children, they are less willing to encompass the full range of their children's emotional needs (Hoshchild, 1997). The philosophical and ethical question is this: Should we treat children with SSRls in order to make them more "convenient" for their parents? Can we deny the use of an effective treatment that may very well improve a child's current relationships, and therefore long-term prognosis? Currently I am treating several families where these issues have been raised, and I am finding that there is no easy solution. I hope to foster discussion of this issue among my local colleagues and, as always, appreciate hearing from you through the Journal. Mary G. Burke, M.D. San Francisco Garland E. Weiss M (1997). Case study: obsessive difficult temperament and its response to serotonergic intervention. JAm Acad Child Adolesc Psychiatry 35:916-920 Hoshchild A (1997). There's no place like work. Nno York Times Magazin« April 20:50-84 Knutsen B, Wolkowitz O. Cole S er al. (1998). Selective alteration of personality and social behavior by serotonergic intervention. Am J Psychiatry 155:.~73~379

AM. ACAD. CHILD ADOLESC. PSYCHIATRY, j7:IO, OCTOBER 1998

LETTERS T O TH E E D ITO R

Pet tit G . Bates J (1984). Co nt inu ity and individual di fferen ces in the mother-infant relationsh ip from six to thirteen months. Child Dru 55:729-739 T ho mas A. C hess S (1984) , G enesis and evoluti on of beha vioral d isorder s from infancy to early adult life. Am} Psychiatry 141 :1-9

VALPROATE AND POLYCYSTIC OVARIES

To the Editor:

As a pediatric endocrinologist with an interest in child psychiatry, I am familiar with the article by Isojarvi et al. (1993), in which it is reported that 80% of the women treated with valproate for epilepsy before age 20 had polycystic ovaries (PCO) or hyperandrogenism, PCO frequently are part of a synd ro me that includes hirsutism , obes ity, and menstrual disturbances (Stein and Lcvinrhal, 1935). While there are many causes of PCO, elevated androgens are usually present . Since valproate can be very helpful for the treatment of bipolar disorder in children and adol escents, this report presems a serious dilemma for psychiatrists caring for young girls with disabling bipolar disorder and prompts a close look at the data on which this statement was made. Isojarvi et al. (1993) stud ied menstrual disturbances in 238 adult epileptic women treated with antiseizure medic ations and in 51 normal controls. Twenty-nine epileptic women were treated with valproate and 120 with carbamazep ine. Forty-five percent (n = 13) of women taking valproate had abn ormal menses, while 19% (n = 23) of those taking carbamazepine did . In normal women 16% (n = 8) had abnormal menses. Twenty-three women taking valproate were studied further with ultrasound and hormone testing, as were 49 women taking carbamazepine. Forty-three percent (n = 10) of women taking valproate had PCO on ultrasound, and all these women were obese. PCO were found in 22% (n = 11) of women taking carbamazepine, but onl y 7 were obese. Four women taking carbamazepine had PCO bur were not obese. Nine (18%) normal cont rols had PCO. A second articl e by Isojarvi et al. (1996 ) reported more data on the same women . Fourteen women (64% ) taking valproate had PCO or increased testosterone levels. Thirteen of these women were obese (body mass index [BM I] > 25), 11 were very obese (BM I > 27), and 10 were severely obese (BMI 30-39). None of the normal women or women taking carbamazepine were very or severely obese. Eleven women began to take valproate before age 20 . Nine (82%) were severely obese and had PCO, elevated testosterone levels, and elevated insulin levels. Eleven women started to take valproate at or after age 20. Two (18%) were severely obese and one obese woman had PCO and an elevated testosterone level. Obesity is a well-recognized cause of insulin resistance. Insulin resistance leads to incre~sed insulin levels. High levels

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of insulin promote the ovarian production of testosterone, a potent androgen (D unaif, 1992). Elevated testost erone produce s hirsutism, anovulato ry cycles, and the ovarian pathol ogy of PCO (Sizonenko et al., 1972). Data from the two articles by Isojarvi et al. are cons istent with the conclusion that severe obesity is responsible for PCO in the studied women on valproate, not the valproate itself. All the women takin g valproate who had polycystic ovaries were severely obese and had elevated testosterone and insulin levels. There were no nonobese women taking valproare who had PCO. The 82% of women who began to take valproate before age 20 had severe obesity, leading to PCO. Carbamazepine, however, was associated with PCO in four women who were not obese. These cases of PCO would not be preventable by cont rolling weight, and the mechan ism is unknown. No other studiesof PCO in valproate- or carbamazepinetreated women have been reported. Review of data in the two articles by Isojarvi et al. suggests that since carbamazepine may be associated with PCO in nonobese women, careful monitoring of girls who are taking either valproate or carbamazepine is indicated. At this time there is no evidence that valproate directly causes PCO. Although increased appetite was reported in 6% of valproa re-rreated patients, withholding valproare from young, seriously ill girls because of possible weight gain must not be undertaken lightly.

AM . ACAD. C H ILD AOOLES C:. PSYC H IAT RY. 3 7 :1 0 . OCTO BER 1998

Andrea J. Eberle, M.D., Ph.D. Children's Ho spit al, Omaha Dunaif A (1992 ). Insulin resistance and ovarian hyperandrogen ism . Endocrinologist2:248-260 Isojarvi JIT. Laarikainen TJ, Kn ip K er al, (1996). Obesity and end ocrine disorders in women takin g valproat e for epilepsy. Ann Nruro/3 9:579-584 Isojarvi JIT. Laatikainen 1J. Pakarinen AJ er al. (1993). Polycystic ovaries and hyperandrogenism in wom en taki ng valproate for epilepsy. N Engl} Mrd 329:1383-1388 Sizonenko PC . Sch indler AM , Kohlb erg et al, (1972). G onadotr op ins. testosterone . and oestrog en levels in relat ion to ovaria n morphology in l 1Phyd roxylase deficiency. Acta Endocrinol7 1:539- 550 Stein IF, Levinrhal ML (1935) . Ame no rrhoea associated wit h bilateral po lycystic ovaries. Am} Obstet Gynrcol29: 18 1- 19 1

BIASES IN REPORTING OF ADHD

To the Editor: As a psychosoc ially orientated Professor Emeritus of Pediatrics, who had dealt with and still deals with school problems, abuse, custody, behavior, and so called attention deficit disorder, I was int erested in the internecine "warfare" in the Janu ary 1998 Letters of Biederman et al. and Ch ilcoat and Breslau. These related to "biased maternal reporting of child psychopathology." I would like to suggest that both groups are biased in their assessments and conclusions. I would say that studying, as I

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