LETTERS TO THE EDITOR Vitiello, R., Ricciuti, A. J. & Behar, D. (1987), P.R.N . medications in child state hospital inpatients. J. Clin. Psychiatry , 48:351-354.
A Tantrum Test? To the Editor : This letter describes a tool for assessing whether an aggressive outburst in a child, age 4 to 12 years, is manipulative or whether it is beyond his or her control. Research into aggressive behavior in children has focused on environmental and biological factors . Procedures, predictions, and outcomes of seclusion and restraints resulting in explosive behavior in children is a source of growing interest. The importance of training staff, who deal with these children, in behavior management and graded consequences for aggressive behavior has been emphasized (Trieschman et aI., 1969; Gair, 1984). Joshi et al. (1988) have demonstrated the value of having a timeout room on a children's inpatient ward to help patients reconstitute themselves when they are angry . Millstein and Cotton (1990) have further shown that the patients on a children's psychiatric unit who are most vulnerable to being secluded show poor coping skills, a history of abuse, and neurological impairments. A divergent line of investigations has demonstrated the way that aggressive behaviors are learned in ineffective parent/child interactions (Patterson, 1982). It has been shown that once coerciveness becomes an effective manner for a child to "get his way," it tends to become stable and entrenched. Work with children in residential treatment centers has brought to our attention the importance of locating aggressive behavior in time/ place and with whom these episodes occur (Trieschman et aI., 1969). All this information is consistent with the view that sometimes aggressive behavior is manipulative and, at other times, it is or becomes out of control. It would be helpful to know whether the former or latter is going on in any particular aggressive episode. The volume of the screams, as Anna Freud has sagely observed, is not a measure of the degree of the internal distress (Freud, 1965). Indeed, I am probably not alone in having witnessed a screaming child abruptly terminate his/her tantrum, when 30 to 60 seconds before he/she was being restrained by three or four staff members. The Donut Test may be a useful method of distinguishing manipulative aggressive episodes from out-of-control episodes with children age 4 to 12. The test is administered in the context of a child inpatient program that emphasizes from admission day the child's need to identify and take responsibility for his/her temper. (The child identifies a behavioral reinforcer - a "donut" which can help control his/her temper outbursts. During the temper outbursts, the child is offered the " donut" if he/she can stop the temper outburst and sit on a carpet square in a time-out/seclusion room.) If the child sits down and stops the tantrum, it is a positive Donut Test and, hence, probably manipulative in part . If the child doesn't stop, it is a negative Donut Test suggesting that the child does not wish to or cannot control his/her behavior. For the past year, the staff and I have experimented with this test on an inpatient basis and found it useful in several ways: 1. Children with a positive Donut Test-suggesting manipulationwere able to work on identifying noncoercive ways to deal with their needs. 2. Children with negative tests were evaluated for additional measures of controlling their outbursts; for example, more time-outs, a change of reinforcer for the Donut Test, an evaluation of organic factors, and an ongoing medication assessment. 3. The test helps improve the working alliance between staff and children so that the staff does not overreact to a patient's aggressive behavior, and it emphasizes to the child that his/her temper outbursts J. Am. Acad. Child Adolesc. Psychiatry, 29:6, November 1990
are his/her problem with which he/she must struggle . There are theoretical objections to the Donut Test: (a) It would increase aggressive behavior in children, and the child would act out to gain a reinforcer , and (b) It reinforces negative behavior (Donut then becomes a bribe). Anecdotally , children on our unit have not shown any increase in aggressive behavior, nor seen the test as a bribe. These negative effects may have been avoided because the test is imbedded in a working personal relationship between staff members and the child . More data would clearly be needed, however, to establish any value in this stratagem. A protocol for the test is available, and I would welcome sharing it with anyone who is interested in trying it out. Kim J. Masters, M .D. Appalachian Hall, P.O. Box 5534 Asheville, NC 28813
REFERENCES
Freud, A. (1965), Assessment of Pathology , Part I. In: The Writings of Anna Freud, Vol . VI. New York: International UMV Press . pp. 108-146. Gair, D. S . (1984), Guidelines for Children and Adolescents. In: Psychiatric Uses of Seclusion and Restraint, ed. K. Tariff. Washington, DC: American Psychiatric Press, pp. 69-85 . Joshi, P., Capozzoli, J. & Coyle, J. (1988), Use of quiet room on an inpatient unit. J. Am . Acad. Child Adolesc. Psychiatry , 27:642644. Millstein, K. & Cotton, N. (1990), Predictors of the use of seclusion on an inpatient child psychiatric unit. J. Am. Acad. Child Adolesc. Psychiatry , 29:256-264. Patterson, G. R. (1982) , A Social Learning Approach . In: Coersive Family Process , Vol. 3, Eugene , OR: Castilia Publishing Co . Trieschman, A., Whittaker, J. & Bendtro, L. (1969), The Other 23 Hours . Chicago: Aldine Publishing Company.
The Genetic Latent Structure Model To the Editor: We read with interest the recent section on genetics, especially the article by Deutsch et al. (1990) which addressed a possible genetic model for attention deficit disorder (ADD) and dysmorphology. We have a number of questions about the study and its conclusions . First, the authors did not address the situation that minor physical anomalies (MPA) are also found in other psychiatric populations (Steg and Rapoport , 1975). High MPAs have been found in heterogeneous groups. High anomaly scores have been reported for retarded, learning disabled, hyperactive, atypical , psychotic, and autistic children. Since dysmorphology is also found with other disorders, we would appreciate a discussion of how that factor might affect the genetic analysis of these children . The article seems to imply that dysmorphology is only associated with ADD. Minor physical anomalies appear to be linked to paternal hyperactivity or perinatal difficulties (Quinn and Rapoport, 1974). Did the authors notice if there was a gender difference in first-degree relatives of ADD probands? The above study showed a gender difference in that fathers had a higher incidence of ADD symptoms , alcoholism, and sociopathy . In this study, MPAs were reported to be formed in the first 4 months of pregnancy. This is a critical period of CNS development when control systems for impulsivity and aggressive behavior are developing. How would this congenital factor be accounted for in your genetic model? The sample study included 48 boys with ADD with "no other medical diagnosis other than ADD." By "medical," do the authors mean to say that the ADD group had no other comorbid psychiatric
983
LEITERS TO THE EDITOR
or developmental disorders? This would be an unusually pure population, despite the ever evolving data on comorbidity of ADD with learning disabilities, anxiety, or depression. If other disorders coexisted, it would be helpful for the authors to address their effect on the study's genetic conclusions. Lastly, the MPA scores (Waldrop and Halverson , 1971) were used in your study for children and adults . Presumably there is a standardization for MPA in an adult population . As Waldrop and Halverson used standardized scores for correlation with MPAs, it would be useful for the authors to refer to the adult standardization. Were racial differences taken into account? If the genetic conclusions are based on adult MPA standardized scores, this might affect the authors' conclusions. John P. Steg, M.D. William L. Licamele, M.D. Georgetown University Medical Center Washington, D.C. REFERENCES
Deutsch, C. K. et al. (1990), Genetic latent structure analysis of dysmorphology in attention deficit disorder. J . Am . Acad. Child Adolesc. Psychiatry, 29:189-194 . Quinn, P. & Rapoport, J. (1974), Minor physical anomalies and neurologic status in hyperactive boys. Pediatrics, 53:742-747. Steg, J. P. & Rapoport, J. (1975), " Minor physical anomalies in normal, neurotic, learning disabled, and severely disturbed children. Journal of Autism and Childhood Schizophrenia, 5:299-307. Waldrop, M. & Halverson, C. E. (1971) , Minor physical anomalies and hyperactive behavior in young children. In: The Exceptional Infant, Vol. 2, ed. J. Hellmuth, New York: Brunner/Mazel, pp. 343-381.
We agree that tests of the model would ideally include refined ADD phenotypes, but these analyses must await a larger sample size (p. 193). We, too, are intrigued by the sex differences in the psychiatric symptomatology in ADD probands' parents (i.e ., prevalent alcoholism and sociopathy in fathers but not mothers) and would like to include this information in our model. Yet, we cannot assume that these psychiatric diagnoses are adult manifestations of childhood ADD . Drs. Steg and Licamele asked whether sex and generational differences were taken into account in our study. Caucasian ethnicity was a selection criterion (p. 190), since our normative data were limited to this group. We have collected data on MPAs in normal children and adults, and these figures are in good agreement with others' (Pomeroy et al., 1988). Our findings confirm that the Waldrop and Halverson full-scale MPA score is developmentally stable (Krouse and Kauffman, 1982). Finally, we would like to emphasize that genetic latent structure analysis, like factor analysis, is an interpretation of data and not a test of the model's validity. Yet the critical test for a genetic latent trait was met in our study-namely, that ADD probands who are not dysmorphic have nonADD relatives who are dysmorphic . This observation strongly suggests that a latent trait exists . Curtis K. Deutsch , Ph.D . Eunice Kennedy Shriver Center Harvard Medical School Steven Matthysse , Ph.D . McLean Hospital Harvard Medical School James M. Swanson, Ph.D. University of California, Irvine Leslie G. Farkas, M.D ., D.Sc. Hospital for Sick Children University of Toronto
The authors reply: We thank Drs. Steg and Licamele for their interesting letter. In answering their questions, we would like to take the opportunity to elaborate on aspects of our genetic latent structure model. In this model, attention deficit disorder (ADD) and dysmorphology, in the form of minor physical anomalies (MPAs), are independent expressions of a single underlying trait which is transmissible. This formulation is plausible because the CNS and craniofacial morphology arise from common primordia and are sculpted by shared forces. Thus, a single pathological process could disrupt the formation of both the brain and the delicate features of the head and face. Our correspondents correctly point out that MPAs are present in individuals without ADD. We agree, and our model explicitly states that dysmorphology often appears in the absence of the latent trait for ADD (Deutsch et al., 1990; Fig. I and Table 2, p. 192). Individuals with diagnoses other than ADD may well be overrepresented in this dysmorphic group, since a miscellany of psychiatric populations reportedly have excessive MPAs (Pomeroy et al., 1988). Drs. Steg and Licamele claim that the MPAs assessed in the Waldrop and Halverson scale arise in the first 4 months of pregnancy. Our appraisal of the data, on the other hand, suggests that some of these anomalies might arise early in fetal development , but others could arise later in gestation (Cummings et al., 1982). We suggested chronological origin as an example of examining combinations of individual MPAs chosen to reflect embryological factors (Deutsch et al., 1990, p. 193). This type of natural biological subdivision may help to delineate critical periods of brain maldevelopment and to clarify the mechanism of pleiotropy. Our correspondents suggested including psychiatric diagnoses other than ADD in our genetic model. For instance, ADD probands might be subgrouped by comorbid psychiatric diagnoses, which were prevalent in our patients (e.g., conduct disorder; Bowden et al., 1988).
984
REFERENCES
Bowden, C. L., Deutsch , C. K. & Swanson, J. M. (1988), Plasma dopamine-beta-hydroxylase and platelet monoamine oxidase in attention deficit disorder and conduct disorder. J. Am. Acad. Child
Adolesc. Psychiatry, 27:171-174 . Cummings, C., Flynn, D. & Preus, M. (1982), Increased morphological variants in children with learning disabilities. J. Autism Dev , Disord., 12:373-383. Deutsch, C. K., Matthysse , S., Swanson, J. M. & Farkas, L. G. (1990), Genetic latent structure analysis of dysmorphology in attention deficit disorder. J . Am . Acad . Child Adolesc . Psychiatry , 29:189-194. Krouse, J. P. & Kauffman, J. M. (1982), Minor physical anomalies in exceptional children: a review and critique of research. J. Abnorm. Child Psychol., 10:247-264 . Pomeroy, J. c., Sprafkin, J. & Gadow, K. D. (1988), Minor physical anomalies as a biologic marker for behavior disorders . J . Am. Acad . Child Adolesc. Psychiatry, 27:466-473.
Fluoxetine and Anorexia To the Editor: The successful use of the bicyclic antidepressant , fluoxetine, has been reported in open label trials of adult patients suffering from bulimia (Freeman and Hampson, 1987; Mitchell et al., 1989). The only published report in the treatment of anorexia is of an adult female with a long history of both anorexia and bulimia who responded to high doses of fluoxetine (Ferguson, 1987). The following case report describes the successful use of fluoxetine in the treatment of an adolescent with both anorexia and bulimia. Ms. A, a 16-year-old white female, was referred by both her pe-
J .Am.Acad. Chi/dAdolesc . Psychiatry, Z9:6, November 1990
A Tantrum Test? To the Editor : This letter describes a tool for assessing whether an aggressive outburst in a child, age 4 to 12 years, is manipulative or whether it is beyond his or her control. Research into aggressive behavior in children has focused on environmental and biological factors . Procedures, predictions, and outcomes of seclusion and restraints resulting in explosive behavior in children is a source of growing interest. The importance of training staff, who deal with these children, in behavior management and graded consequences for aggressive behavior has been emphasized (Trieschman et aI., 1969; Gair, 1984). Joshi et al. (1988) have demonstrated the value of having a timeout room on a children's inpatient ward to help patients reconstitute themselves when they are angry . Millstein and Cotton (1990) have further shown that the patients on a children's psychiatric unit who are most vulnerable to being secluded show poor coping skills, a history of abuse, and neurological impairments. A divergent line of investigations has demonstrated the way that aggressive behaviors are learned in ineffective parent/child interactions (Patterson, 1982). It has been shown that once coerciveness becomes an effective manner for a child to "get his way," it tends to become stable and entrenched. Work with children in residential treatment centers has brought to our attention the importance of locating aggressive behavior in time/ place and with whom these episodes occur (Trieschman et aI., 1969). All this information is consistent with the view that sometimes aggressive behavior is manipulative and, at other times, it is or becomes out of control. It would be helpful to know whether the former or latter is going on in any particular aggressive episode. The volume of the screams, as Anna Freud has sagely observed, is not a measure of the degree of the internal distress (Freud, 1965). Indeed, I am probably not alone in having witnessed a screaming child abruptly terminate his/her tantrum, when 30 to 60 seconds before he/she was being restrained by three or four staff members. The Donut Test may be a useful method of distinguishing manipulative aggressive episodes from out-of-control episodes with children age 4 to 12. The test is administered in the context of a child inpatient program that emphasizes from admission day the child's need to identify and take responsibility for his/her temper. (The child identifies a behavioral reinforcer - a "donut" which can help control his/her temper outbursts. During the temper outbursts, the child is offered the " donut" if he/she can stop the temper outburst and sit on a carpet square in a time-out/seclusion room.) If the child sits down and stops the tantrum, it is a positive Donut Test and, hence, probably manipulative in part . If the child doesn't stop, it is a negative Donut Test suggesting that the child does not wish to or cannot control his/her behavior. For the past year, the staff and I have experimented with this test on an inpatient basis and found it useful in several ways: 1. Children with a positive Donut Test-suggesting manipulationwere able to work on identifying noncoercive ways to deal with their needs. 2. Children with negative tests were evaluated for additional measures of controlling their outbursts; for example, more time-outs, a change of reinforcer for the Donut Test, an evaluation of organic factors, and an ongoing medication assessment. 3. The test helps improve the working alliance between staff and children so that the staff does not overreact to a patient's aggressive behavior, and it emphasizes to the child that his/her temper outbursts J. Am. Acad. Child Adolesc. Psychiatry, 29:6, November 1990
are his/her problem with which he/she must struggle . There are theoretical objections to the Donut Test: (a) It would increase aggressive behavior in children, and the child would act out to gain a reinforcer , and (b) It reinforces negative behavior (Donut then becomes a bribe). Anecdotally , children on our unit have not shown any increase in aggressive behavior, nor seen the test as a bribe. These negative effects may have been avoided because the test is imbedded in a working personal relationship between staff members and the child . More data would clearly be needed, however, to establish any value in this stratagem. A protocol for the test is available, and I would welcome sharing it with anyone who is interested in trying it out. Kim J. Masters, M .D. Appalachian Hall, P.O. Box 5534 Asheville, NC 28813
REFERENCES
Freud, A. (1965), Assessment of Pathology , Part I. In: The Writings of Anna Freud, Vol . VI. New York: International UMV Press . pp. 108-146. Gair, D. S . (1984), Guidelines for Children and Adolescents. In: Psychiatric Uses of Seclusion and Restraint, ed. K. Tariff. Washington, DC: American Psychiatric Press, pp. 69-85 . Joshi, P., Capozzoli, J. & Coyle, J. (1988), Use of quiet room on an inpatient unit. J. Am . Acad. Child Adolesc. Psychiatry , 27:642644. Millstein, K. & Cotton, N. (1990), Predictors of the use of seclusion on an inpatient child psychiatric unit. J. Am. Acad. Child Adolesc. Psychiatry , 29:256-264. Patterson, G. R. (1982) , A Social Learning Approach . In: Coersive Family Process , Vol. 3, Eugene , OR: Castilia Publishing Co . Trieschman, A., Whittaker, J. & Bendtro, L. (1969), The Other 23 Hours . Chicago: Aldine Publishing Company.
The Genetic Latent Structure Model To the Editor: We read with interest the recent section on genetics, especially the article by Deutsch et al. (1990) which addressed a possible genetic model for attention deficit disorder (ADD) and dysmorphology. We have a number of questions about the study and its conclusions . First, the authors did not address the situation that minor physical anomalies (MPA) are also found in other psychiatric populations (Steg and Rapoport , 1975). High MPAs have been found in heterogeneous groups. High anomaly scores have been reported for retarded, learning disabled, hyperactive, atypical , psychotic, and autistic children. Since dysmorphology is also found with other disorders, we would appreciate a discussion of how that factor might affect the genetic analysis of these children . The article seems to imply that dysmorphology is only associated with ADD. Minor physical anomalies appear to be linked to paternal hyperactivity or perinatal difficulties (Quinn and Rapoport, 1974). Did the authors notice if there was a gender difference in first-degree relatives of ADD probands? The above study showed a gender difference in that fathers had a higher incidence of ADD symptoms , alcoholism, and sociopathy . In this study, MPAs were reported to be formed in the first 4 months of pregnancy. This is a critical period of CNS development when control systems for impulsivity and aggressive behavior are developing. How would this congenital factor be accounted for in your genetic model? The sample study included 48 boys with ADD with "no other medical diagnosis other than ADD." By "medical," do the authors mean to say that the ADD group had no other comorbid psychiatric
983
LEITERS TO THE EDITOR
or developmental disorders? This would be an unusually pure population, despite the ever evolving data on comorbidity of ADD with learning disabilities, anxiety, or depression. If other disorders coexisted, it would be helpful for the authors to address their effect on the study's genetic conclusions. Lastly, the MPA scores (Waldrop and Halverson , 1971) were used in your study for children and adults . Presumably there is a standardization for MPA in an adult population . As Waldrop and Halverson used standardized scores for correlation with MPAs, it would be useful for the authors to refer to the adult standardization. Were racial differences taken into account? If the genetic conclusions are based on adult MPA standardized scores, this might affect the authors' conclusions. John P. Steg, M.D. William L. Licamele, M.D. Georgetown University Medical Center Washington, D.C. REFERENCES
Deutsch, C. K. et al. (1990), Genetic latent structure analysis of dysmorphology in attention deficit disorder. J . Am . Acad. Child Adolesc. Psychiatry, 29:189-194 . Quinn, P. & Rapoport, J. (1974), Minor physical anomalies and neurologic status in hyperactive boys. Pediatrics, 53:742-747. Steg, J. P. & Rapoport, J. (1975), " Minor physical anomalies in normal, neurotic, learning disabled, and severely disturbed children. Journal of Autism and Childhood Schizophrenia, 5:299-307. Waldrop, M. & Halverson, C. E. (1971) , Minor physical anomalies and hyperactive behavior in young children. In: The Exceptional Infant, Vol. 2, ed. J. Hellmuth, New York: Brunner/Mazel, pp. 343-381.
We agree that tests of the model would ideally include refined ADD phenotypes, but these analyses must await a larger sample size (p. 193). We, too, are intrigued by the sex differences in the psychiatric symptomatology in ADD probands' parents (i.e ., prevalent alcoholism and sociopathy in fathers but not mothers) and would like to include this information in our model. Yet, we cannot assume that these psychiatric diagnoses are adult manifestations of childhood ADD . Drs. Steg and Licamele asked whether sex and generational differences were taken into account in our study. Caucasian ethnicity was a selection criterion (p. 190), since our normative data were limited to this group. We have collected data on MPAs in normal children and adults, and these figures are in good agreement with others' (Pomeroy et al., 1988). Our findings confirm that the Waldrop and Halverson full-scale MPA score is developmentally stable (Krouse and Kauffman, 1982). Finally, we would like to emphasize that genetic latent structure analysis, like factor analysis, is an interpretation of data and not a test of the model's validity. Yet the critical test for a genetic latent trait was met in our study-namely, that ADD probands who are not dysmorphic have nonADD relatives who are dysmorphic . This observation strongly suggests that a latent trait exists . Curtis K. Deutsch , Ph.D . Eunice Kennedy Shriver Center Harvard Medical School Steven Matthysse , Ph.D . McLean Hospital Harvard Medical School James M. Swanson, Ph.D. University of California, Irvine Leslie G. Farkas, M.D ., D.Sc. Hospital for Sick Children University of Toronto
The authors reply: We thank Drs. Steg and Licamele for their interesting letter. In answering their questions, we would like to take the opportunity to elaborate on aspects of our genetic latent structure model. In this model, attention deficit disorder (ADD) and dysmorphology, in the form of minor physical anomalies (MPAs), are independent expressions of a single underlying trait which is transmissible. This formulation is plausible because the CNS and craniofacial morphology arise from common primordia and are sculpted by shared forces. Thus, a single pathological process could disrupt the formation of both the brain and the delicate features of the head and face. Our correspondents correctly point out that MPAs are present in individuals without ADD. We agree, and our model explicitly states that dysmorphology often appears in the absence of the latent trait for ADD (Deutsch et al., 1990; Fig. I and Table 2, p. 192). Individuals with diagnoses other than ADD may well be overrepresented in this dysmorphic group, since a miscellany of psychiatric populations reportedly have excessive MPAs (Pomeroy et al., 1988). Drs. Steg and Licamele claim that the MPAs assessed in the Waldrop and Halverson scale arise in the first 4 months of pregnancy. Our appraisal of the data, on the other hand, suggests that some of these anomalies might arise early in fetal development , but others could arise later in gestation (Cummings et al., 1982). We suggested chronological origin as an example of examining combinations of individual MPAs chosen to reflect embryological factors (Deutsch et al., 1990, p. 193). This type of natural biological subdivision may help to delineate critical periods of brain maldevelopment and to clarify the mechanism of pleiotropy. Our correspondents suggested including psychiatric diagnoses other than ADD in our genetic model. For instance, ADD probands might be subgrouped by comorbid psychiatric diagnoses, which were prevalent in our patients (e.g., conduct disorder; Bowden et al., 1988).
984
REFERENCES
Bowden, C. L., Deutsch , C. K. & Swanson, J. M. (1988), Plasma dopamine-beta-hydroxylase and platelet monoamine oxidase in attention deficit disorder and conduct disorder. J. Am. Acad. Child
Adolesc. Psychiatry, 27:171-174 . Cummings, C., Flynn, D. & Preus, M. (1982), Increased morphological variants in children with learning disabilities. J. Autism Dev , Disord., 12:373-383. Deutsch, C. K., Matthysse , S., Swanson, J. M. & Farkas, L. G. (1990), Genetic latent structure analysis of dysmorphology in attention deficit disorder. J . Am . Acad . Child Adolesc . Psychiatry , 29:189-194. Krouse, J. P. & Kauffman, J. M. (1982), Minor physical anomalies in exceptional children: a review and critique of research. J. Abnorm. Child Psychol., 10:247-264 . Pomeroy, J. c., Sprafkin, J. & Gadow, K. D. (1988), Minor physical anomalies as a biologic marker for behavior disorders . J . Am. Acad . Child Adolesc. Psychiatry, 27:466-473.
Fluoxetine and Anorexia To the Editor: The successful use of the bicyclic antidepressant , fluoxetine, has been reported in open label trials of adult patients suffering from bulimia (Freeman and Hampson, 1987; Mitchell et al., 1989). The only published report in the treatment of anorexia is of an adult female with a long history of both anorexia and bulimia who responded to high doses of fluoxetine (Ferguson, 1987). The following case report describes the successful use of fluoxetine in the treatment of an adolescent with both anorexia and bulimia. Ms. A, a 16-year-old white female, was referred by both her pe-
J .Am.Acad. Chi/dAdolesc . Psychiatry, Z9:6, November 1990
