- Email: [email protected]
OF NORMS AND CUTOFFS
LETTERS TO THE EDITOR
accurately reflect the population's demographic vananons with respect to characteristics such as socioeconomic status (SES) and ethnicity. Norms can be used to judge how scores obtained by individuals compare with scores in a population. However, if individuals score below or above the middle of a normative sample, we would be wrong to conclude that, ipso facto, these individuals are pathologically deviant. We would be equally wrong to conclude that norms are invalid just because a local sample obtains a mean score below or above the middle of the normative sample. A5 an example, IQs in normative samples range from about 40 to 160, with relatively few falling precisely at the standardization mean of 100. IQs of 95 are no more pathologically deviant than IQs of 105. Furthermore, if impoverished Seattle children obtain a mean IQ of 95, this does not cast doubt on the test's norms nor on its standardization mean of 100. If local scores differ from nationally representative scores for demographically similarsubjects, this may warrant further exploration. For example, suppose that impoverished Seattle children obtain lower IQs than impoverished children elsewhere. This finding may warrant a search for local factors that reduce IQ, such as mercury in seafood. The same applies to other types of scores obtained by impoverished children in Seattle versus elsewhere. However, to test hypothesized etiological factors, we must compare subjects who are as similar as possible except for the presence versus absence of the hypothesized etiological factor. A5 Sandberg et al. (1991, p. 134) correctly concluded, study-specific control groups are required to support precise conclusions about etiological factors. Norms alone cannot provide strong tests of etiological hypotheses. Furthermore, if the mean score in a local sample differs from the mean score in a national normative sample, this says nothing about the validity of the norms. The generalizability of local scores is especially limited when the local sample embodies many selective factors, such as the following in Raadal and colleagues' study: restriction to low SES children participating in a dental screening program in a subset of Seattle public schools; selection of children according to their dental condition; telephone screening to accumulate the desired N; use of Cantonese and Vietnamese translations with some respondents; inclusion of children receiving mental health services or special education services, when such children were excluded from the CBCL national normative sample. The need for better understanding of norms is also revealed by Raadal and colleagues' statement that "low-income children were underrepresented and middle-class children were overrepresented in the CBCL normative sample (36% upper, 45% middle, 20% lower. ..)" (p, 1022). By "underrepresented," Raadal et al. evidently meant that only 20% of
J.
AM. ACAD. CHILD ADOLESC. PSYCHIATRY, 34:5, MAY 1995
parents had occupations that were scored less than 4 on Hollingshead's 9-point scale, which was the criterion for lower SES. However, if 20% of American parents indeed have such occupations, then 20% is representative of the target population. The 20% says nothing about whether low SES children are" Underrepresented." On the contrary, the question of underrepresentation concerns the accuracy with which a sample reflects each group's proportion in the population from which the sample was drawn. I hope that this clarifies the meaning of norms. Thomas M. Achenbach, Ph.D. University of Vermont Achenbach TM (1991), Manual for the Child Behavior Checklistl4-18 and 1991 Profile. Burlington: University of Vermont Department of Psychiatty Raadal M, Milgrom P, Cauce AM, Mancl L (1994), Behavior problems in 5- to l l-year-old children from low-income families. JAm Acad ChildAdolesc Psychiatry 33:1017-1025 Sandberg DE, Meyer-Bahlburg HFL, Yager TJ (1991), The Child Behavior Checklist nonclinical standardization samples: should they be utilized as norms? JAm Acad ChildAdolesc Psychiatry 30:124-134
Dr. Cauce responds: Achenbach is, of course, correct in his lucid clarification of the meaning of norms. He accurately notes that a finding of higher mean scores for poor Seattle children is not sufficient to cast doubts on the CBCL's norms. He is also correct in pointing out that the findings of Raadal et al. (1994) do not provide a strong test of the hypothesis that poverty is a risk factor for behavioral problems. It simply posits that poverty is the most likely explanation for the differences found between their sample and the CBCL normative sample. From his letter, I gather that Achenbach agrees with this as a likely explanation. He further notes that the findings of Raadal et al. may even have some crosscultural consistency. Given the apparent robustness of these findings, I was doubly surprised that the Manual for the Child Behavior Checklistl4-18 (Achenbach, 1991), which is almost 300 pages long, devotes only one paragraph to demographic differences among CBCL scores. Both the content of this paragraph and its brevity lead one to conclude that while some variation in scores by SES exists within the normative sample, it is "small" and trivial. In contrast, there was nothing small or trivial about the differences we found between the scores obtained by the CBCL sample and ours. Ofparticular concern was the rather large disparity (e.g., 18% versus 31 %) between the percentage of children classified as "clinical/borderline" in our respective samples. These "clinical" norms/cutoffs are not only meant for epidemiological use, but are intended for use in making referral decisions
537
LETTERS TO THE EDITOR
in local settings about individual children. If use of such norms leads to such high referral (and labeling) rates for poor children, I would like to see more empirical evidence for the validity of such norms for low SES children specifically. Do poor children really manifest such high levels of behavioral problems or does the CBCL "overdiagnose" poor children as "clinical/borderline"? The Raadal et al. (1994) paper simply raises this question. Becauseof the methodological limitations that Achenbach aptly notes, it does not answer it, nor was it intended to.
Capgras' syndrome is characterized by an affected individual's experience of a delusional belief that a person, usually a close relative, has been replaced by an imposter. The majority of patients are diagnosed schizophrenic. Cases of adolescent onset have been described and reports of childhood onset are rare (Berson, 1983). Tourette's syndrome (TS) is a common hereditary neuropsychiatric spectrum disorder (Comings et al., 1993; Sverd et aI., 1993). In addition to obsessive-compulsive disorder (OCD), evidence exists to suggest that a broad array of psychiatric disorders including schizophrenia-like psychosis, schizotypal thinking, and paranoid ideation are additional expressions of the TS gene or genes (Comings and Comings, 1987; Sverd et aI., 1993). The following is a report of an adolescent male who showed childhood-onset Capgras' syndrome co-occurring with TS, OCD, and schizophrenia. It is suggested that the genetic defecrts) underlying TS contributes to the cooccurrence of the disorders. F. was a 15-year-old Latino boy who was hospitalized because of aggression toward his mother and peers, sexual touching of others, threats to rape a female peer, paranoid thinking, and claims that others could read his mind. He talked to himself, showed thought blocking, selective mutism, posturing, and pacing. He resided in a group home and attended a day treatment program for psychiatrically ill adolescents. Upon admission, F. reported that he believed that his mother was not his mother, that she was the devil, and that
his real mother was in heaven. He claimed that although the face was that of his mother, the person was not she, but rather someone who had taken over her mind and body. Because he believed that the imposter poisoned his food, he refused to eat and lost 10 lb. Later he stated that the imposter was doing something to his food in order to get him to like her. He noted that from the age of 9 years he had intermittently experienced these beliefs, which resulted in violence directed toward his mother and the need for multiple hospitalizations. F. first showed behavior disturbance at age 8 years. He lost all interest in school, refused to do school work, was aggressive toward schoolmates and teachers, and evidenced social withdrawal and isolation. He evidenced devil worship, play with matches, and fecal smearing. Scores on the WISCIII were Full Scale IQ99, Verbal IQ98, and Performance IQ 100. Psychiatric staff at one hospital felt that he experienced auditory and visual hallucinations because he "talked to himself, God and the devil." However, F. denied that he had ever hallucinated. F. had long-standing OCD that consisted of counting rituals and the need to perform a variety of behaviors to ward off anxiety that harm would befall loved ones. For example, he needed to retrace his steps, change his sleeping position, or breathe in and out a specified number of times. He had to think certain thoughts while standing at his bed before he would be able to go to sleep. He described these thoughts as intrusive, disturbing, and unwanted. F. also reported the onset of a tic disorder at age 7 years before the use of neuroleptic medication. Tics consisted of head nodding, eye blinking and rolling, body jerks, jumping tics, compulsive touching, finger smelling, lip biting, mouth tics, picking at sores, knuckle cracking, and need to shake a book before turning the page, coprolalia, throat clearing, and the need to say "sh." Despite lengthy hospitalization and combined use of neuroleptics and selective serotonin reuptake inhibitors followed by a course of clozapine treatment, F. continued to believe that his mother had been replaced by an imposter. He reported that the severity of tics and compulsions ameliorated. Regarding the possible etiology of such an association, it has been hypothesized that TS and its associated cornorbidities are the result of a primary genetic defect in serotonin metabolism and common genetic defects in dopamine metabolism that aetas modifying genes (Comings et al., 1993). This hypothesis may account for the observation that seemingly distinct psychiatric disorders such as TS and schizophrenia may coexist in families at a greater than expected frequency (Comings et aI., 1993; Sverd et al., 1993). In support of the hypothesis is the observation of others that schizophrenia and OCD may share a genetic relationship and that dopaminergic and serotonergic abnormalities may contribute to the
538
]. AM. ACAD. CHILD ADOLESC. PSYCHIATRY, 34:5, MAY 1995
Ana Mari Cauce, Ph.D. University of Washington Achenbach TM (1991), Manual for the Child Behavior Checklistl4-18 and 1991 Profile. Burlington: University of Vermont Department of Psychiatry Raadal M, Milgrom P, Cauce AM, Mancl L (1994), Behavior problems in 5- to l l-year-old children from low-income families. JAm Acad ChildAdolesc Psychiatry 33:1017-1025
COMORBID CAPGRAS' SYNDROME To the Editor:
accurately reflect the population's demographic vananons with respect to characteristics such as socioeconomic status (SES) and ethnicity. Norms can be used to judge how scores obtained by individuals compare with scores in a population. However, if individuals score below or above the middle of a normative sample, we would be wrong to conclude that, ipso facto, these individuals are pathologically deviant. We would be equally wrong to conclude that norms are invalid just because a local sample obtains a mean score below or above the middle of the normative sample. A5 an example, IQs in normative samples range from about 40 to 160, with relatively few falling precisely at the standardization mean of 100. IQs of 95 are no more pathologically deviant than IQs of 105. Furthermore, if impoverished Seattle children obtain a mean IQ of 95, this does not cast doubt on the test's norms nor on its standardization mean of 100. If local scores differ from nationally representative scores for demographically similarsubjects, this may warrant further exploration. For example, suppose that impoverished Seattle children obtain lower IQs than impoverished children elsewhere. This finding may warrant a search for local factors that reduce IQ, such as mercury in seafood. The same applies to other types of scores obtained by impoverished children in Seattle versus elsewhere. However, to test hypothesized etiological factors, we must compare subjects who are as similar as possible except for the presence versus absence of the hypothesized etiological factor. A5 Sandberg et al. (1991, p. 134) correctly concluded, study-specific control groups are required to support precise conclusions about etiological factors. Norms alone cannot provide strong tests of etiological hypotheses. Furthermore, if the mean score in a local sample differs from the mean score in a national normative sample, this says nothing about the validity of the norms. The generalizability of local scores is especially limited when the local sample embodies many selective factors, such as the following in Raadal and colleagues' study: restriction to low SES children participating in a dental screening program in a subset of Seattle public schools; selection of children according to their dental condition; telephone screening to accumulate the desired N; use of Cantonese and Vietnamese translations with some respondents; inclusion of children receiving mental health services or special education services, when such children were excluded from the CBCL national normative sample. The need for better understanding of norms is also revealed by Raadal and colleagues' statement that "low-income children were underrepresented and middle-class children were overrepresented in the CBCL normative sample (36% upper, 45% middle, 20% lower. ..)" (p, 1022). By "underrepresented," Raadal et al. evidently meant that only 20% of
J.
AM. ACAD. CHILD ADOLESC. PSYCHIATRY, 34:5, MAY 1995
parents had occupations that were scored less than 4 on Hollingshead's 9-point scale, which was the criterion for lower SES. However, if 20% of American parents indeed have such occupations, then 20% is representative of the target population. The 20% says nothing about whether low SES children are" Underrepresented." On the contrary, the question of underrepresentation concerns the accuracy with which a sample reflects each group's proportion in the population from which the sample was drawn. I hope that this clarifies the meaning of norms. Thomas M. Achenbach, Ph.D. University of Vermont Achenbach TM (1991), Manual for the Child Behavior Checklistl4-18 and 1991 Profile. Burlington: University of Vermont Department of Psychiatty Raadal M, Milgrom P, Cauce AM, Mancl L (1994), Behavior problems in 5- to l l-year-old children from low-income families. JAm Acad ChildAdolesc Psychiatry 33:1017-1025 Sandberg DE, Meyer-Bahlburg HFL, Yager TJ (1991), The Child Behavior Checklist nonclinical standardization samples: should they be utilized as norms? JAm Acad ChildAdolesc Psychiatry 30:124-134
Dr. Cauce responds: Achenbach is, of course, correct in his lucid clarification of the meaning of norms. He accurately notes that a finding of higher mean scores for poor Seattle children is not sufficient to cast doubts on the CBCL's norms. He is also correct in pointing out that the findings of Raadal et al. (1994) do not provide a strong test of the hypothesis that poverty is a risk factor for behavioral problems. It simply posits that poverty is the most likely explanation for the differences found between their sample and the CBCL normative sample. From his letter, I gather that Achenbach agrees with this as a likely explanation. He further notes that the findings of Raadal et al. may even have some crosscultural consistency. Given the apparent robustness of these findings, I was doubly surprised that the Manual for the Child Behavior Checklistl4-18 (Achenbach, 1991), which is almost 300 pages long, devotes only one paragraph to demographic differences among CBCL scores. Both the content of this paragraph and its brevity lead one to conclude that while some variation in scores by SES exists within the normative sample, it is "small" and trivial. In contrast, there was nothing small or trivial about the differences we found between the scores obtained by the CBCL sample and ours. Ofparticular concern was the rather large disparity (e.g., 18% versus 31 %) between the percentage of children classified as "clinical/borderline" in our respective samples. These "clinical" norms/cutoffs are not only meant for epidemiological use, but are intended for use in making referral decisions
537
LETTERS TO THE EDITOR
in local settings about individual children. If use of such norms leads to such high referral (and labeling) rates for poor children, I would like to see more empirical evidence for the validity of such norms for low SES children specifically. Do poor children really manifest such high levels of behavioral problems or does the CBCL "overdiagnose" poor children as "clinical/borderline"? The Raadal et al. (1994) paper simply raises this question. Becauseof the methodological limitations that Achenbach aptly notes, it does not answer it, nor was it intended to.
Capgras' syndrome is characterized by an affected individual's experience of a delusional belief that a person, usually a close relative, has been replaced by an imposter. The majority of patients are diagnosed schizophrenic. Cases of adolescent onset have been described and reports of childhood onset are rare (Berson, 1983). Tourette's syndrome (TS) is a common hereditary neuropsychiatric spectrum disorder (Comings et al., 1993; Sverd et aI., 1993). In addition to obsessive-compulsive disorder (OCD), evidence exists to suggest that a broad array of psychiatric disorders including schizophrenia-like psychosis, schizotypal thinking, and paranoid ideation are additional expressions of the TS gene or genes (Comings and Comings, 1987; Sverd et aI., 1993). The following is a report of an adolescent male who showed childhood-onset Capgras' syndrome co-occurring with TS, OCD, and schizophrenia. It is suggested that the genetic defecrts) underlying TS contributes to the cooccurrence of the disorders. F. was a 15-year-old Latino boy who was hospitalized because of aggression toward his mother and peers, sexual touching of others, threats to rape a female peer, paranoid thinking, and claims that others could read his mind. He talked to himself, showed thought blocking, selective mutism, posturing, and pacing. He resided in a group home and attended a day treatment program for psychiatrically ill adolescents. Upon admission, F. reported that he believed that his mother was not his mother, that she was the devil, and that
his real mother was in heaven. He claimed that although the face was that of his mother, the person was not she, but rather someone who had taken over her mind and body. Because he believed that the imposter poisoned his food, he refused to eat and lost 10 lb. Later he stated that the imposter was doing something to his food in order to get him to like her. He noted that from the age of 9 years he had intermittently experienced these beliefs, which resulted in violence directed toward his mother and the need for multiple hospitalizations. F. first showed behavior disturbance at age 8 years. He lost all interest in school, refused to do school work, was aggressive toward schoolmates and teachers, and evidenced social withdrawal and isolation. He evidenced devil worship, play with matches, and fecal smearing. Scores on the WISCIII were Full Scale IQ99, Verbal IQ98, and Performance IQ 100. Psychiatric staff at one hospital felt that he experienced auditory and visual hallucinations because he "talked to himself, God and the devil." However, F. denied that he had ever hallucinated. F. had long-standing OCD that consisted of counting rituals and the need to perform a variety of behaviors to ward off anxiety that harm would befall loved ones. For example, he needed to retrace his steps, change his sleeping position, or breathe in and out a specified number of times. He had to think certain thoughts while standing at his bed before he would be able to go to sleep. He described these thoughts as intrusive, disturbing, and unwanted. F. also reported the onset of a tic disorder at age 7 years before the use of neuroleptic medication. Tics consisted of head nodding, eye blinking and rolling, body jerks, jumping tics, compulsive touching, finger smelling, lip biting, mouth tics, picking at sores, knuckle cracking, and need to shake a book before turning the page, coprolalia, throat clearing, and the need to say "sh." Despite lengthy hospitalization and combined use of neuroleptics and selective serotonin reuptake inhibitors followed by a course of clozapine treatment, F. continued to believe that his mother had been replaced by an imposter. He reported that the severity of tics and compulsions ameliorated. Regarding the possible etiology of such an association, it has been hypothesized that TS and its associated cornorbidities are the result of a primary genetic defect in serotonin metabolism and common genetic defects in dopamine metabolism that aetas modifying genes (Comings et al., 1993). This hypothesis may account for the observation that seemingly distinct psychiatric disorders such as TS and schizophrenia may coexist in families at a greater than expected frequency (Comings et aI., 1993; Sverd et al., 1993). In support of the hypothesis is the observation of others that schizophrenia and OCD may share a genetic relationship and that dopaminergic and serotonergic abnormalities may contribute to the
538
]. AM. ACAD. CHILD ADOLESC. PSYCHIATRY, 34:5, MAY 1995
Ana Mari Cauce, Ph.D. University of Washington Achenbach TM (1991), Manual for the Child Behavior Checklistl4-18 and 1991 Profile. Burlington: University of Vermont Department of Psychiatry Raadal M, Milgrom P, Cauce AM, Mancl L (1994), Behavior problems in 5- to l l-year-old children from low-income families. JAm Acad ChildAdolesc Psychiatry 33:1017-1025
COMORBID CAPGRAS' SYNDROME To the Editor: