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PSYCHOPATHOLOGY IN THE PARENTS OF BOYS WITH GENDER IDENTITY DISORDER
LETTERS TO THE EDITOR
In conclusion, we were unable to confirm that any pharmacokinetic interaction exists between risperidone and valproate. Moreover, given the known pharmacokinetic properties of these drugs, we are unable to identify a theoretical rationale for such an interaction. Janne Kutschera Sund, M.Sc.Pharm. Trond Aamo, M.D. Olav Spigset, M.D. Department of Clinical Pharmacology St. Olav’s University Hospital Trondheim, Norway Andersen BB, Mikkelsen M, Vesterager A et al. (1991), No influence of the antidepressant paroxetine on carbamazepine, valproate and phenytoin. Epilepsy Rev 10:201–204 Rowland M, Tozer TN (1995), Clinical Pharmacokinetics: Concepts and Applications, 3rd ed. Philadelphia: Lippincott Williams & Wilkins, pp 270–276 van Wattum PJ (2001), Valproic acid and risperidone. J Am Acad Child Adolesc Psychiatry 40:866–867 Vitiello B (2001), Valproic acid and risperidone (commentary). J Am Acad Child Adolesc Psychiatry 40:867 DOI: 10.1097/01.CHI.0000024907.60748.E1
chart review of 45 child and adolescent psychiatry inpatients who were started on divalproex sodium for mood lability and explosive temper outbursts. The goal of the study was to examine variables that may acutely alter dosage requirements for divalproex, such as drug combinations. For example, 29 of 45 patients received concurrent treatment with atypical antipsychotics. Coadministration of other psychotropic medications, including atypical antipsychotics, did not significantly alter trough serum valproate levels. Although the sample size limited the power of some analyses, there did not appear to be a significant difference in drug levels among those receiving divalproex + risperidone versus divalproex + olanzapine versus divalproex alone. Sedation was more common in children receiving combination therapy than in children receiving divalproex alone. In summary, combining neuroleptic medication with divalproex sodium does not appear to alter divalproex levels at clinically effective doses. These observations, in light of previous reports of potential drug interactions between risperidone and valproic acid, emphasize the need to proceed with caution in children requiring combination therapy to adequately control mood lability and aggression. Candace R. Good, M.D. Christopher A. Petersen, M.D. Valentins F. Krecko, M.D. Department of Psychiatry Penn State College of Medicine Hershey, PA
VALPROIC ACID AND RISPERIDONE To the Editor: Within the past year, the Journal has published two letters and a commentary that outline a potential drug interaction between valproic acid and risperidone. The nature and etiology of the interaction remain controversial. The first case report (van Wattum, 2001) was that of a 10-year-old boy whose valproic acid level rose into the toxic range after the initiation of risperidone. It was proposed that competition for protein binding sites ultimately resulted in the displacement of valproic acid into serum, resulting in increased serum concentrations of the drug. The addition of risperidone was also reported to cause a drop in valproic acid levels in a 15-year-old girl with psychosis and a seizure disorder (Bertoldo, 2002). The latter report noted that risperidone likely reduces serum valproate levels by 30% through cytochrome P-450 2D6 interactions as previously proposed by Dr. Vitiello (2001). This would be true if risperidone were in fact an inducer of cyt 2D6, like carbamazepine. However, as Dr. Vitiello outlines, risperidone is instead metabolized by and mildly inhibits the cyt 2D6 system, which would result in increased levels of unmetabolized valproic acid in plasma during combination therapy (i.e., potentially toxic levels). We propose that the longer-acting forms of valproic acid, specifically divalproex sodium, might be less likely to cause such interactions. This claim is supported by data presented by our group at the American Psychiatric Association 2002 Annual Meeting in Philadelphia. Our poster described a retrospective 2
Bertoldo M (2002), Valproic acid and risperidone (letter). J Am Acad Child Adolesc Psychiatry 41:632 van Wattum PJ (2001), Valproic acid and risperidone (letter). J Am Acad Child Adolesc Psychiatry 40:866–867 Vitiello B (2001), Valproic acid and risperidone (commentary). J Am Acad Child Adolesc Psychiatry 40:867 DOI: 10.1097/01.CHI.0000024908.60748.05
PSYCHOPATHOLOGY IN THE PARENTS OF BOYS WITH GENDER IDENTITY DISORDER To the Editor: In an essay in the Clinical Perspectives section of the Journal, titled “Children With Gender Identity Issues and Their Parents in Individual and Group Treatment,” Rosenberg (2002) made a cursory remark regarding the psychiatric status of the parents of the 12 child and adolescent patients in her current program: “All of the parents in my sample have had a clinical psychiatric examination…. Unlike Zucker and Bradley (1995), I did not find parental psychopathology at a rate exceeding the norm” (p. 620). Rosenberg then noted that one parent was “an alcoholic in recovery for 15 years; one had been in treatment for nonpsychotic depressive disorder, another for anxiety disorder” (p. 620).
J . A M . A C A D . C H I L D A D O L E S C . P S YC H I AT RY, 4 2 : 1 , J A N U A RY 2 0 0 3
LETTERS TO THE EDITOR
Several aspects of Rosenberg’s brief reference to psychopathology in the parents of children and adolescents with gender identity disorder (GID) concern us. First, Rosenberg provided no information regarding what constituted her “clinical psychiatric examination.” What does this actually mean? How long did the examination take? Was it carried out individually? In the presence of a spouse? In the presence of the child? What domains of psychiatric functioning were covered? What criteria were used in establishing the presence or absence of disorder? What evidence is there for such an examination’s validity? Second, Rosenberg made no effort to reconcile her data with the data that we reported in our volume (Zucker and Bradley, 1995), nor did she try to reconcile it with regard to other reports of parental psychopathology, including data by Marantz and Coates (1991) in this Journal and by Wolfe (1990). Third, Rosenberg tells the reader little in the way of how parental psychopathology might be understood in a clinical formulation regarding its relation, or nonrelation, to the genesis and/or perpetuation of GID or other psychopathology in her child and adolescent patients. From a clinical practice perspective, all of these limitations are not of particular help for the nonspecialist reader of the Journal who is curious to learn more about the families of children with GID.
Over the past 12 years, we have conducted a systematic ascertainment of parental psychopathology in our child patients who are referred for gender identity concerns. Our measures include the Symptom Checklist 90-Revised and the Diagnostic Interview Schedule, Version IIIA (DIS). The latter is a well-known, reliable, and valid assessment method of a number of DSM disorders. In this letter, we would like to illustrate how Rosenberg’s rather dismissive remarks about parental psychopathology are discrepant in relation to our own DIS data. Table 1 shows DIS diagnoses for mothers and fathers of the last 10 boys with GID (mean age, 7.8 years; range, 4.4–12.5; mean Full Scale IQ, 108.9; range, 75–140) assessed in our clinic. The mean age of the mothers was 37.8 years (range, 31–42) and the mean age of the fathers was 39.1 years (range, 34–46). On Hollingshead’s Four Factor Index of Social Status (absolute range, 8–66), the mean social class background of the parents was 47.8 (range, 24–63.5). Following a more open-ended life history interview, the DIS was administered individually to each parent. It can be seen in Table 1 that 8 of the 10 mothers met DIS criteria for at least one disorder. The mean number of diagnoses was 2.7 (range, 0–6), and the mode and median were both 2. Of the seven fathers who were living with their sons and were thus part of the assessment, three met DIS criteria
TABLE 1 Diagnostic Interview Schedule (DIS) Diagnoses in the Parents of 10 Boys With Gender Identity Disorder Case ID
Age of Parent (yr)
Marital Status DAS Scorea
01-M
37
1st marriage
89
01-F 02-M
38 34
1st marriage 2nd marriage
99 112
02-F 03-M 03-F 04-M 04-F 05-M 05-F 06-M
35 31 34 40 46 41 42 39
2nd marriage Divorced Remarried 1st marriage 2nd marriage 1st marriage 1st marriage 1st marriage
118 68 — 118 119 94 99 100
06-F 07-M
41 42
1st marriage 3rd marriage
109 23
07-F 08-M 08-F 09-M 09-F 10-M 10-F
35 36 37 41 41 37 42
Unknown 3rd marriage 1st marriage 2nd marriage 1st marriage 2nd marriage 2nd marriage
— 125 NA 80 81 62 —
DIS Diagnosis(es) Major depression (single episode); obsessive-compulsive disorder; agoraphobia None Major depression (recurrent); obsessive-compulsive disorder; agoraphobia; agoraphobia with panic; simple phobia; generalized anxiety disorder Alcohol abuse; alcohol dependence Dysthymic disorder; grief reaction; generalized anxiety disorder Not seen Social phobia; panic disorder None None Major depression (recurrent); dysthymic disorder Major depression (recurrent); alcohol abuse; obsessive-compulsive disorder; social phobia; panic disorder None Major depressive episode (single); alcohol abuse; generalized anxiety disorder Not seen None Alcohol abuse Major depressive episode (single) None Major depression (recurrent); obsessive-compulsive disorder Not seen
Note: M = mother; F = father; NA = not available. For case 8, the parents of the proband divorced when he was an infant. The father listed in the table had lived with the proband since the age of 2. He declined to complete questionnaires, including the DAS. a DAS = Dyadic Adjustment Scale (absolute range, 0–151).
J . A M . A C A D . C H I L D A D O L E S C . P S YC H I AT RY, 4 2 : 1 , J A N U A RY 2 0 0 3
3
LETTERS TO THE EDITOR
for at least one disorder. The mean was 0.71 (range, 0–2). Here it should be noted that the DIS focuses primarily on Axis I disorders, not Axis II disorders, so our data, if anything, underestimate the potential range of parental psychopathology. The data on mothers are quite consistent with the general patterns reported in Zucker and Bradley (1995). The rate of maternal psychopathology is high by any standard and, as noted in Zucker and Bradley (1995), a composite measure of maternal psychopathology correlated quite strongly with Child Behavior Checklist indices of behavior problems in boys with GID. Quantitative data, although important, can fail to capture the complexity of a patient’s life history. Thus we provide some additional qualitative data on the parents of our 10 child patients. Of the 10 mothers, 8 had been or were currently receiving some form of psychotherapy. Six of the mothers had been or were currently receiving pharmacotherapy. Four of the mothers reported a severe history of sexual abuse (e.g., incest or rape). Of the two mothers who had no DIS diagnosis, one was in long-term psychotherapy to deal with complex interpersonal issues related to her own family background and the other was often disabled by severe migraine headaches. In contrast, only one of the fathers had been in psychotherapy; this same father had been treated with pharmacotherapy and reported a history of intrafamilial sibling incest. Father 7, who was not seen during our assessment, had a severe and chronic substance abuse disorder, prostituted himself for money (for drugs), and was dying of acquired immunodeficiency syndrome. Of the 10 families, there was a parental separation/divorce (in relation to the child proband) in four (cases 3, 7, 8, 10). Using ratings by the mother on the Dyadic Adjustment Scale (Spanier, 1976), 6 of the 10 families met criteria for a discordant marital relationship, as defined by a score of ≤97 (i.e., 1 SD below the mean of married couples in the standardization sample) (Table 1). Of the six families in which the parents of the proband were still married (cases 1, 2, 4, 5, 6, 9), three had been or were currently in marital therapy. There are, of course, several ways in which the discrepancy between our data and Rosenberg’s may be understood. We relied on a highly structured, reliable, and valid assessment instrument. Rosenberg used a clinical psychiatric examination of unknown psychometric properties. Our sample consisted of consecutive referrals of patients to a specialized clinic, housed within a child and adolescent psychiatry program. Because Rosenberg tells the parents that her treatment “will not attempt to change gender identity” (p. 619) in their child, she acknowledges that her sample might be skewed because “families intent on changing their child’s gender identity may be avoiding my practice” (p. 619). It is not clear, however, whether this factor would be related to rates of parental psychopathology. It is conceivable that demographic factors contribute to the rather different patterns of psychopathology that we have observed compared with Rosenberg. For example, although she provides no information in this regard, it is quite likely that her sample is skewed in the direction of 4
upper-middle-class families whereas in our sample we see parents who cover the entire spectrum of social class backgrounds. However, in Zucker and Bradley (1995, p. 238), we reported only a very weak correlation between social class and a composite measure of maternal psychopathology (r = –0.21). Thus we are inclined to reject this hypothesis and instead attribute the difference between our data and Rosenberg’s to method variance, i.e., we have used measures of well-established psychometric properties whereas Rosenberg did no such thing. Understanding the role of parental psychopathology in the genesis and/or perpetuation of any child psychiatric disorder is complex and its impact on the child likely operates at multiple levels of influence (biological, intrapsychic, relational, systemic). We would argue that parental psychopathology among the parents of children with GID is a topic that deserves thoughtful consideration. Rosenberg’s rather minimalist report on it in her Clinical Perspectives essay does little to advance our understanding of its role (or even presence) in childhood GID. Kenneth J. Zucker, Ph.D. Susan J. Bradley, M.D. Dahlia N. Ben-Dat, M.A. Caroline Ho, M.A. Laurel Johnson, M.A. Allison Owen, M.A. Child and Adolescent Gender Identity Clinic Child Psychiatry Program Centre for Addiction and Mental Health-Clarke Division Toronto Marantz S, Coates S (1991), Mothers of boys with gender identity disorder: a comparison of matched controls. J Am Acad Child Adolesc Psychiatry 30:310–315 Rosenberg M (2002), Children with gender identity issues and their parents in individual and group treatment. J Am Acad Child Adolesc Psychiatry 41:619–621 Spanier GB (1976), Measuring dyadic adjustment: new scales for assessing the quality of marriage and similar dyads. J Marriage Fam 38:15–28 Wolfe SM (1990), Psychopathology and psychodynamics of parents of boys with a gender identity disorder of childhood. Doctoral dissertation, City University of New York Zucker KJ, Bradley SJ (1995), Gender Identity Disorder and Psychosexual Problems in Children and Adolescents. New York: Guilford DOI: 10.1097/01.CHI.0000024909.60748.4C
ZIPRASIDONE-ASSOCIATED GALACTORRHEA IN A FEMALE TEENAGER To the Editor: We describe the case of a 17-year-old white female in whom galactorrhea developed within a few weeks of treatment with ziprasidone. The patient had a history of sexual assaults. She experienced nightmares, flashbacks, depressed mood, and decreased sleep.
J . A M . A C A D . C H I L D A D O L E S C . P S YC H I AT RY, 4 2 : 1 , J A N U A RY 2 0 0 3
In conclusion, we were unable to confirm that any pharmacokinetic interaction exists between risperidone and valproate. Moreover, given the known pharmacokinetic properties of these drugs, we are unable to identify a theoretical rationale for such an interaction. Janne Kutschera Sund, M.Sc.Pharm. Trond Aamo, M.D. Olav Spigset, M.D. Department of Clinical Pharmacology St. Olav’s University Hospital Trondheim, Norway Andersen BB, Mikkelsen M, Vesterager A et al. (1991), No influence of the antidepressant paroxetine on carbamazepine, valproate and phenytoin. Epilepsy Rev 10:201–204 Rowland M, Tozer TN (1995), Clinical Pharmacokinetics: Concepts and Applications, 3rd ed. Philadelphia: Lippincott Williams & Wilkins, pp 270–276 van Wattum PJ (2001), Valproic acid and risperidone. J Am Acad Child Adolesc Psychiatry 40:866–867 Vitiello B (2001), Valproic acid and risperidone (commentary). J Am Acad Child Adolesc Psychiatry 40:867 DOI: 10.1097/01.CHI.0000024907.60748.E1
chart review of 45 child and adolescent psychiatry inpatients who were started on divalproex sodium for mood lability and explosive temper outbursts. The goal of the study was to examine variables that may acutely alter dosage requirements for divalproex, such as drug combinations. For example, 29 of 45 patients received concurrent treatment with atypical antipsychotics. Coadministration of other psychotropic medications, including atypical antipsychotics, did not significantly alter trough serum valproate levels. Although the sample size limited the power of some analyses, there did not appear to be a significant difference in drug levels among those receiving divalproex + risperidone versus divalproex + olanzapine versus divalproex alone. Sedation was more common in children receiving combination therapy than in children receiving divalproex alone. In summary, combining neuroleptic medication with divalproex sodium does not appear to alter divalproex levels at clinically effective doses. These observations, in light of previous reports of potential drug interactions between risperidone and valproic acid, emphasize the need to proceed with caution in children requiring combination therapy to adequately control mood lability and aggression. Candace R. Good, M.D. Christopher A. Petersen, M.D. Valentins F. Krecko, M.D. Department of Psychiatry Penn State College of Medicine Hershey, PA
VALPROIC ACID AND RISPERIDONE To the Editor: Within the past year, the Journal has published two letters and a commentary that outline a potential drug interaction between valproic acid and risperidone. The nature and etiology of the interaction remain controversial. The first case report (van Wattum, 2001) was that of a 10-year-old boy whose valproic acid level rose into the toxic range after the initiation of risperidone. It was proposed that competition for protein binding sites ultimately resulted in the displacement of valproic acid into serum, resulting in increased serum concentrations of the drug. The addition of risperidone was also reported to cause a drop in valproic acid levels in a 15-year-old girl with psychosis and a seizure disorder (Bertoldo, 2002). The latter report noted that risperidone likely reduces serum valproate levels by 30% through cytochrome P-450 2D6 interactions as previously proposed by Dr. Vitiello (2001). This would be true if risperidone were in fact an inducer of cyt 2D6, like carbamazepine. However, as Dr. Vitiello outlines, risperidone is instead metabolized by and mildly inhibits the cyt 2D6 system, which would result in increased levels of unmetabolized valproic acid in plasma during combination therapy (i.e., potentially toxic levels). We propose that the longer-acting forms of valproic acid, specifically divalproex sodium, might be less likely to cause such interactions. This claim is supported by data presented by our group at the American Psychiatric Association 2002 Annual Meeting in Philadelphia. Our poster described a retrospective 2
Bertoldo M (2002), Valproic acid and risperidone (letter). J Am Acad Child Adolesc Psychiatry 41:632 van Wattum PJ (2001), Valproic acid and risperidone (letter). J Am Acad Child Adolesc Psychiatry 40:866–867 Vitiello B (2001), Valproic acid and risperidone (commentary). J Am Acad Child Adolesc Psychiatry 40:867 DOI: 10.1097/01.CHI.0000024908.60748.05
PSYCHOPATHOLOGY IN THE PARENTS OF BOYS WITH GENDER IDENTITY DISORDER To the Editor: In an essay in the Clinical Perspectives section of the Journal, titled “Children With Gender Identity Issues and Their Parents in Individual and Group Treatment,” Rosenberg (2002) made a cursory remark regarding the psychiatric status of the parents of the 12 child and adolescent patients in her current program: “All of the parents in my sample have had a clinical psychiatric examination…. Unlike Zucker and Bradley (1995), I did not find parental psychopathology at a rate exceeding the norm” (p. 620). Rosenberg then noted that one parent was “an alcoholic in recovery for 15 years; one had been in treatment for nonpsychotic depressive disorder, another for anxiety disorder” (p. 620).
J . A M . A C A D . C H I L D A D O L E S C . P S YC H I AT RY, 4 2 : 1 , J A N U A RY 2 0 0 3
LETTERS TO THE EDITOR
Several aspects of Rosenberg’s brief reference to psychopathology in the parents of children and adolescents with gender identity disorder (GID) concern us. First, Rosenberg provided no information regarding what constituted her “clinical psychiatric examination.” What does this actually mean? How long did the examination take? Was it carried out individually? In the presence of a spouse? In the presence of the child? What domains of psychiatric functioning were covered? What criteria were used in establishing the presence or absence of disorder? What evidence is there for such an examination’s validity? Second, Rosenberg made no effort to reconcile her data with the data that we reported in our volume (Zucker and Bradley, 1995), nor did she try to reconcile it with regard to other reports of parental psychopathology, including data by Marantz and Coates (1991) in this Journal and by Wolfe (1990). Third, Rosenberg tells the reader little in the way of how parental psychopathology might be understood in a clinical formulation regarding its relation, or nonrelation, to the genesis and/or perpetuation of GID or other psychopathology in her child and adolescent patients. From a clinical practice perspective, all of these limitations are not of particular help for the nonspecialist reader of the Journal who is curious to learn more about the families of children with GID.
Over the past 12 years, we have conducted a systematic ascertainment of parental psychopathology in our child patients who are referred for gender identity concerns. Our measures include the Symptom Checklist 90-Revised and the Diagnostic Interview Schedule, Version IIIA (DIS). The latter is a well-known, reliable, and valid assessment method of a number of DSM disorders. In this letter, we would like to illustrate how Rosenberg’s rather dismissive remarks about parental psychopathology are discrepant in relation to our own DIS data. Table 1 shows DIS diagnoses for mothers and fathers of the last 10 boys with GID (mean age, 7.8 years; range, 4.4–12.5; mean Full Scale IQ, 108.9; range, 75–140) assessed in our clinic. The mean age of the mothers was 37.8 years (range, 31–42) and the mean age of the fathers was 39.1 years (range, 34–46). On Hollingshead’s Four Factor Index of Social Status (absolute range, 8–66), the mean social class background of the parents was 47.8 (range, 24–63.5). Following a more open-ended life history interview, the DIS was administered individually to each parent. It can be seen in Table 1 that 8 of the 10 mothers met DIS criteria for at least one disorder. The mean number of diagnoses was 2.7 (range, 0–6), and the mode and median were both 2. Of the seven fathers who were living with their sons and were thus part of the assessment, three met DIS criteria
TABLE 1 Diagnostic Interview Schedule (DIS) Diagnoses in the Parents of 10 Boys With Gender Identity Disorder Case ID
Age of Parent (yr)
Marital Status DAS Scorea
01-M
37
1st marriage
89
01-F 02-M
38 34
1st marriage 2nd marriage
99 112
02-F 03-M 03-F 04-M 04-F 05-M 05-F 06-M
35 31 34 40 46 41 42 39
2nd marriage Divorced Remarried 1st marriage 2nd marriage 1st marriage 1st marriage 1st marriage
118 68 — 118 119 94 99 100
06-F 07-M
41 42
1st marriage 3rd marriage
109 23
07-F 08-M 08-F 09-M 09-F 10-M 10-F
35 36 37 41 41 37 42
Unknown 3rd marriage 1st marriage 2nd marriage 1st marriage 2nd marriage 2nd marriage
— 125 NA 80 81 62 —
DIS Diagnosis(es) Major depression (single episode); obsessive-compulsive disorder; agoraphobia None Major depression (recurrent); obsessive-compulsive disorder; agoraphobia; agoraphobia with panic; simple phobia; generalized anxiety disorder Alcohol abuse; alcohol dependence Dysthymic disorder; grief reaction; generalized anxiety disorder Not seen Social phobia; panic disorder None None Major depression (recurrent); dysthymic disorder Major depression (recurrent); alcohol abuse; obsessive-compulsive disorder; social phobia; panic disorder None Major depressive episode (single); alcohol abuse; generalized anxiety disorder Not seen None Alcohol abuse Major depressive episode (single) None Major depression (recurrent); obsessive-compulsive disorder Not seen
Note: M = mother; F = father; NA = not available. For case 8, the parents of the proband divorced when he was an infant. The father listed in the table had lived with the proband since the age of 2. He declined to complete questionnaires, including the DAS. a DAS = Dyadic Adjustment Scale (absolute range, 0–151).
J . A M . A C A D . C H I L D A D O L E S C . P S YC H I AT RY, 4 2 : 1 , J A N U A RY 2 0 0 3
3
LETTERS TO THE EDITOR
for at least one disorder. The mean was 0.71 (range, 0–2). Here it should be noted that the DIS focuses primarily on Axis I disorders, not Axis II disorders, so our data, if anything, underestimate the potential range of parental psychopathology. The data on mothers are quite consistent with the general patterns reported in Zucker and Bradley (1995). The rate of maternal psychopathology is high by any standard and, as noted in Zucker and Bradley (1995), a composite measure of maternal psychopathology correlated quite strongly with Child Behavior Checklist indices of behavior problems in boys with GID. Quantitative data, although important, can fail to capture the complexity of a patient’s life history. Thus we provide some additional qualitative data on the parents of our 10 child patients. Of the 10 mothers, 8 had been or were currently receiving some form of psychotherapy. Six of the mothers had been or were currently receiving pharmacotherapy. Four of the mothers reported a severe history of sexual abuse (e.g., incest or rape). Of the two mothers who had no DIS diagnosis, one was in long-term psychotherapy to deal with complex interpersonal issues related to her own family background and the other was often disabled by severe migraine headaches. In contrast, only one of the fathers had been in psychotherapy; this same father had been treated with pharmacotherapy and reported a history of intrafamilial sibling incest. Father 7, who was not seen during our assessment, had a severe and chronic substance abuse disorder, prostituted himself for money (for drugs), and was dying of acquired immunodeficiency syndrome. Of the 10 families, there was a parental separation/divorce (in relation to the child proband) in four (cases 3, 7, 8, 10). Using ratings by the mother on the Dyadic Adjustment Scale (Spanier, 1976), 6 of the 10 families met criteria for a discordant marital relationship, as defined by a score of ≤97 (i.e., 1 SD below the mean of married couples in the standardization sample) (Table 1). Of the six families in which the parents of the proband were still married (cases 1, 2, 4, 5, 6, 9), three had been or were currently in marital therapy. There are, of course, several ways in which the discrepancy between our data and Rosenberg’s may be understood. We relied on a highly structured, reliable, and valid assessment instrument. Rosenberg used a clinical psychiatric examination of unknown psychometric properties. Our sample consisted of consecutive referrals of patients to a specialized clinic, housed within a child and adolescent psychiatry program. Because Rosenberg tells the parents that her treatment “will not attempt to change gender identity” (p. 619) in their child, she acknowledges that her sample might be skewed because “families intent on changing their child’s gender identity may be avoiding my practice” (p. 619). It is not clear, however, whether this factor would be related to rates of parental psychopathology. It is conceivable that demographic factors contribute to the rather different patterns of psychopathology that we have observed compared with Rosenberg. For example, although she provides no information in this regard, it is quite likely that her sample is skewed in the direction of 4
upper-middle-class families whereas in our sample we see parents who cover the entire spectrum of social class backgrounds. However, in Zucker and Bradley (1995, p. 238), we reported only a very weak correlation between social class and a composite measure of maternal psychopathology (r = –0.21). Thus we are inclined to reject this hypothesis and instead attribute the difference between our data and Rosenberg’s to method variance, i.e., we have used measures of well-established psychometric properties whereas Rosenberg did no such thing. Understanding the role of parental psychopathology in the genesis and/or perpetuation of any child psychiatric disorder is complex and its impact on the child likely operates at multiple levels of influence (biological, intrapsychic, relational, systemic). We would argue that parental psychopathology among the parents of children with GID is a topic that deserves thoughtful consideration. Rosenberg’s rather minimalist report on it in her Clinical Perspectives essay does little to advance our understanding of its role (or even presence) in childhood GID. Kenneth J. Zucker, Ph.D. Susan J. Bradley, M.D. Dahlia N. Ben-Dat, M.A. Caroline Ho, M.A. Laurel Johnson, M.A. Allison Owen, M.A. Child and Adolescent Gender Identity Clinic Child Psychiatry Program Centre for Addiction and Mental Health-Clarke Division Toronto Marantz S, Coates S (1991), Mothers of boys with gender identity disorder: a comparison of matched controls. J Am Acad Child Adolesc Psychiatry 30:310–315 Rosenberg M (2002), Children with gender identity issues and their parents in individual and group treatment. J Am Acad Child Adolesc Psychiatry 41:619–621 Spanier GB (1976), Measuring dyadic adjustment: new scales for assessing the quality of marriage and similar dyads. J Marriage Fam 38:15–28 Wolfe SM (1990), Psychopathology and psychodynamics of parents of boys with a gender identity disorder of childhood. Doctoral dissertation, City University of New York Zucker KJ, Bradley SJ (1995), Gender Identity Disorder and Psychosexual Problems in Children and Adolescents. New York: Guilford DOI: 10.1097/01.CHI.0000024909.60748.4C
ZIPRASIDONE-ASSOCIATED GALACTORRHEA IN A FEMALE TEENAGER To the Editor: We describe the case of a 17-year-old white female in whom galactorrhea developed within a few weeks of treatment with ziprasidone. The patient had a history of sexual assaults. She experienced nightmares, flashbacks, depressed mood, and decreased sleep.
J . A M . A C A D . C H I L D A D O L E S C . P S YC H I AT RY, 4 2 : 1 , J A N U A RY 2 0 0 3