- Email: [email protected]
POSTTRAUMATIC FEEDING DISORDERS
LETTERS TO THE EDITOR
normal brain tissue. Further research using combinations of CNS imaging techniques will be the only way to resolve these issues. Samuel Kuperman, M.D. University of Iowa, Iowa City Mann CA. Lubar JF, Zimmerman AW, Miller CA. Muenchen RA (1992), Quantitative analysis ofEEG in boys with mention-deficit-hyperactiviry disorder: controlled study with clinical implicarions. P,diatr N,urol 8:30-36 Pivik RT, BroughlOn RJ, Coppola R. Davidson RJ, Fox N, Nuwer MR (1993), Guidelines for the recording and quantitative analysis of electroencephalographic activiry in research contexrs (review). Psycho-
physiology 30:547-558 Smerfield JH, Schell AM, Backs RW, Hidaka KC (1984). A cross-sectional and longitudinal srudy of age effeers of electrophysiological measures in hyperactive and normal children. BioI Psychiatry 19:973-990 Zametkin AJ, Liebenauer LL. Fitzgerald GA, er al. (1993), Brain metabolism in teenagers wirh atrention-deficir hyperacriviry disorder. Arch Gm
Psychiatry 50:333-340
DRUG THERAPY IN AUTISM
To the Editor: I am reporting the amelioration of psychotic symptoms with marked agitation and aggressive outbursts in a 12 1/zyear-old boy, B.Z., with autism. I first evaluated B.Z. when he was 2 Yz years old because ofgrossly delayed language, social, and play skills. I diagnosed autism and referred the family to a therapeutic nursery program. I lost contact with the parents, who could not accept the diagnosis at that time. I then saw B.Z. again when he was 12Yz years old for pharmacological management of severe aggressive outbursts interspersed by hours of sleeping, after having stripped himself naked and shut himself in the bathroom, both at home and at school. He also had communicated to his mother that he wished to die because "I have autism and there is not hope for me." Since I had last seem them, B.Z.'s parents had accepted his diagnosis and were doing everything possible to maximize his high cognitive skills via the use of a communicating board, partial mainstreaming in a small, private elementary school, and ancillaty psychotherapy. B.Z. had become a 6-fooHall, heavy, fully developed young man. Because of auditory command hallucinations to act up and strike at people, chlorpromazine had been prescribed by another psychiatrist for the preceding 3 years, after thioridazine was no longer effective. His chlorpromazine dose had been successfully tapered from 125 mg to 40 mg when I was asked to see him. Several EEGs were done to rule out seizures; SMA 27 and complete blood cell counts were all within normal limits.
J.
AM. ACAD. CHILD ADOLESC. PSYCHIATRY. 36:5. MAY \'197
On examination B.Z. was sedated and without tardive dyskinesia. He would become aroused, begin to hum, flap his hands, tap his feet, and say only a few isolated words with poor intonation. His affect was generally blunted and his mood labile, but he "facilitated" to his mother that he was severely depressed and that the hallucinations were not active. I tapered and discontinued the chlorpromazine to initiate therapy with haloperidol, eventually titrated up to 0.5 mg bj.d. B.Z. became more verbal, less depressed, with occasional fleeting auditory hallucinations, and reported feeling "supercharged" for about an hour and a half after taking the haloperidol. I added buspirone to manage the hyperarousal, with success at 15 mg/day (Cook and Leventhal, 1995). By week 5 of haloperidol, marked akathisia and extrapyramidal symptoms developed, so I discontinued haloperidol to initiate a trial of risperidone (Simeon et al., 1995). Within a few weeks, a remarkable and steady improvement began on the combined regimen of eventually 1.5 mg of risperidone and 20 mg bj.d. of buspirone. B.Z. spoke more words, was focused, and had only occasional episodes of attempting to strike out or throw things. His depression remitted completely. Autism is a complex disorder, and B.Z. retains many of the distressing and debilitating features, despite improvement on the combined regimen. Elisabeth Frischauf, M.D. Columbia University, New York Cook EH Jr. Leventhal BL (1995), Auristic disorder and other pervasive developmental disorders. Child Adol,sc Psychiatr Clin North Am 4:381-401 Simeon JG. Carrey NJ, Wiggins OM. Milin RP. Hosenbocus SN (1995). Risperidone effects in rrearment resistanr adolescents: preliminary case «pores. J Child Adaksc Psychopharmaco/ 5:69-79
POSTTRAUMATIC FEEDING DISORDERS
To the Editor: Feeding problems affect 6% to 25% of normally developing infants and up to 35% of young children with developmental disabilities (Lindberg et aI., 1991). Posttraumatic feeding disorders (PTFD) are feeding problems that occur primarily in infants who have experienced distressing or painful events involving the nose, throat, or esophagus (Chatoor et al., 1988; DiScipio et al., 1978). Such experiences may include insertion of nasogastric feeding tubes, endotrachael suctioning, and intubation. Pain and discomfort during feedings because of underlying anatomical or physiological problems (e.g., esophagitis secondary to gastroesophageal
S77
LETTERS TO THE EDITOR
reflux), aversive feeding techniques, or choking are other types of experiences that may result in PTFD. Symptoms of PTFO in infants may include crying, gagging. or choking at the site of a boltle or food. refusal to chew or swallow. lack of awareness of feelings of hunger. and acceptance of the bottle only when falling asleep (Chatoor and Benoit. 1996). The prevalence of PTFO is unknown, although OiScipio and his colleagues (978) estimate that about 40% of infants who are traumatized by medical, surgical, or intrusive diagnostic procedures involving the esophagus may develop continued dysphagia. Because a growing number of premature or very ill infants undergo intrusive medical procedures (e.g.• intubation. repeated suctioning). PTFO is believed to be increasingly common (Chatoor and Benoit. 1996). To date. no reports have been published to document the treatment of PTFD. However. a three-phase intervention was recently developed to treat infants with food refusal. including PTFO. The three-phase. stepwise treatment approach incorporates (I) various physiological and environmental factors to restore or enhance healthy eating habits in infants who already have feeding skills; (2) various behavior modification techniques to eliminate problem feeding behaviors and to teach new feeding skills; and (3) ongoing nutritional monitoring and parent support. To examine the effectiveness of the three-phase intervention. we reviewed the clinical records of 24 children (12 male and 12 female). aged 7 weeks to 34 months (mean = 19.13 months, SO = 7.45). who had symptoms consistent with PTFO and completed the three-phase intervention. Thirteen infants (54%) were firstborn. 12 (50%) had failure to thrive. 6 (25%) had cerebral palsy, and 15 (63%) received gastrostomy or nasogastric tube feedings. Mothers' mean age was 31.83 years (SO = 5.52) and most had some college education (mean years of schooling = 14.48. SO = 1.93). Nineteen (79%) subjects were Caucasian and five (21 %) were Asian. Most subjects (n = 23; 96%) were married or lived common-law. one (4%) was single. and most were from middle-class backgrounds. All subjects completed a structured clinical assessment that include questionnaires. clinical interviews. and observation of mealtime behaviors before starting the intervention. Three definitions of success were used. First. when success was defined by clinical judgment. the three-phase program was succesful in 17 (71 %) of 24 cases. Clinical judgment was defind as follows: 0) increased total intake of solids and liquids by mouth from pre- to posttreatment periods; (2) improved cooperation at mealtimes; (3) steady weight gain (or catch-up rates of growth if the infant was also failing to thrive); (4) initiation of oral feedings (if the child had total food refusal); (5) acceptance of a greater variety of flavors and textures (if the child had partial food refusal
or refusal to progress £0 new textures); or (6) less dependence on tube feedings (if the child was tube-fed). Second, when success was defined as the reduction in the number of problem behaviors at mealtimes (using the total score on the Infant Feeding Behaviors-Rater [IFB-R] checklist), treatment was successful in 19 (79%) of 24 cases. The IFB-R (Benoit and Green. 1995) is a checklist used £0 identify and quantify infants' maladaptive behaviots at meal times. The mean score on the IFB-R checklist for the 24 infants was 37.67 (SO = 15.20) before and 26.19 (SO = 10.21) after treatment (t = 3.07; df = 46; P < .01). Third. when treatment success was defined as the elimination of the need for tube feedings, the treatment program was successful in 6 (40%) of 15 cases. These success rates were achieved in an average of 10 sessions (range 2 £0 21; SO = 6.24). Treatment outcome was not influenced by multiple feeders, child's age, cerebral palsy, supplemental tube feeding, or failure to thrive. These encouraging preliminary results suggest that the three-phase intervention is helpful in treating food refusal, including PTFO. Factors contributing £0 treatment success and failure require additional empirical study.
578
]. AM
Diane Benoit, M.D. University of Toronto Debra Green, B.A. Pepperdine University, Los Angeles Debby Arts-Rodas, R.D. Hospital for Sick Children. Toronto Benoi, D. Green 0 (1995), The Infant Feeding Behaviors-Ra,er checklist: preliminary data. Poster presented at the 42nd Annual Meeting of the American Academy of Child and Adolescent Psychiatry. New Orleans Chatoor I. Benoit D (1996). Diagnostic assessment and treatment of feeding disorders characterized by food refusal. Workshop presented at the World Association for Infant Mental Health. Sixth World Congress. Tampere. Finland. July Chatoor I. Conley C. Dickson L (1988). Food refusal after incident of choking: a posttraumatic eating disorder. J Am Acad Child Adousc Psychiatry 27:105-110 DiScipio WJ. Kaslon K. Ruben RJ (1978). Ttaumatically acquired conditioned dysphagia in children. Ann OroI87:509-514 Lindberg I. Bohlin G. Hagekull B (1991). Early feeding problems in a normal population. Int J Eating Disord 10:395-405
MUNCHAUSEN BY PROXY
To the Editor: Cassar et al. (1996) recently reported on a case of "malingering by proxy." They reported this as a variant on the more commonly known Munchausen syndrome by proxy, itself a subtype of factitious disorder. I wish £0 report a similar case in which a mother and child collaborate in the reporting of psychological disturbance for the purpose of financial gain.
ACAD. CHILD ADOl.ESC. PSYCHIATRY, 36:5. MAY 1997
normal brain tissue. Further research using combinations of CNS imaging techniques will be the only way to resolve these issues. Samuel Kuperman, M.D. University of Iowa, Iowa City Mann CA. Lubar JF, Zimmerman AW, Miller CA. Muenchen RA (1992), Quantitative analysis ofEEG in boys with mention-deficit-hyperactiviry disorder: controlled study with clinical implicarions. P,diatr N,urol 8:30-36 Pivik RT, BroughlOn RJ, Coppola R. Davidson RJ, Fox N, Nuwer MR (1993), Guidelines for the recording and quantitative analysis of electroencephalographic activiry in research contexrs (review). Psycho-
physiology 30:547-558 Smerfield JH, Schell AM, Backs RW, Hidaka KC (1984). A cross-sectional and longitudinal srudy of age effeers of electrophysiological measures in hyperactive and normal children. BioI Psychiatry 19:973-990 Zametkin AJ, Liebenauer LL. Fitzgerald GA, er al. (1993), Brain metabolism in teenagers wirh atrention-deficir hyperacriviry disorder. Arch Gm
Psychiatry 50:333-340
DRUG THERAPY IN AUTISM
To the Editor: I am reporting the amelioration of psychotic symptoms with marked agitation and aggressive outbursts in a 12 1/zyear-old boy, B.Z., with autism. I first evaluated B.Z. when he was 2 Yz years old because ofgrossly delayed language, social, and play skills. I diagnosed autism and referred the family to a therapeutic nursery program. I lost contact with the parents, who could not accept the diagnosis at that time. I then saw B.Z. again when he was 12Yz years old for pharmacological management of severe aggressive outbursts interspersed by hours of sleeping, after having stripped himself naked and shut himself in the bathroom, both at home and at school. He also had communicated to his mother that he wished to die because "I have autism and there is not hope for me." Since I had last seem them, B.Z.'s parents had accepted his diagnosis and were doing everything possible to maximize his high cognitive skills via the use of a communicating board, partial mainstreaming in a small, private elementary school, and ancillaty psychotherapy. B.Z. had become a 6-fooHall, heavy, fully developed young man. Because of auditory command hallucinations to act up and strike at people, chlorpromazine had been prescribed by another psychiatrist for the preceding 3 years, after thioridazine was no longer effective. His chlorpromazine dose had been successfully tapered from 125 mg to 40 mg when I was asked to see him. Several EEGs were done to rule out seizures; SMA 27 and complete blood cell counts were all within normal limits.
J.
AM. ACAD. CHILD ADOLESC. PSYCHIATRY. 36:5. MAY \'197
On examination B.Z. was sedated and without tardive dyskinesia. He would become aroused, begin to hum, flap his hands, tap his feet, and say only a few isolated words with poor intonation. His affect was generally blunted and his mood labile, but he "facilitated" to his mother that he was severely depressed and that the hallucinations were not active. I tapered and discontinued the chlorpromazine to initiate therapy with haloperidol, eventually titrated up to 0.5 mg bj.d. B.Z. became more verbal, less depressed, with occasional fleeting auditory hallucinations, and reported feeling "supercharged" for about an hour and a half after taking the haloperidol. I added buspirone to manage the hyperarousal, with success at 15 mg/day (Cook and Leventhal, 1995). By week 5 of haloperidol, marked akathisia and extrapyramidal symptoms developed, so I discontinued haloperidol to initiate a trial of risperidone (Simeon et al., 1995). Within a few weeks, a remarkable and steady improvement began on the combined regimen of eventually 1.5 mg of risperidone and 20 mg bj.d. of buspirone. B.Z. spoke more words, was focused, and had only occasional episodes of attempting to strike out or throw things. His depression remitted completely. Autism is a complex disorder, and B.Z. retains many of the distressing and debilitating features, despite improvement on the combined regimen. Elisabeth Frischauf, M.D. Columbia University, New York Cook EH Jr. Leventhal BL (1995), Auristic disorder and other pervasive developmental disorders. Child Adol,sc Psychiatr Clin North Am 4:381-401 Simeon JG. Carrey NJ, Wiggins OM. Milin RP. Hosenbocus SN (1995). Risperidone effects in rrearment resistanr adolescents: preliminary case «pores. J Child Adaksc Psychopharmaco/ 5:69-79
POSTTRAUMATIC FEEDING DISORDERS
To the Editor: Feeding problems affect 6% to 25% of normally developing infants and up to 35% of young children with developmental disabilities (Lindberg et aI., 1991). Posttraumatic feeding disorders (PTFD) are feeding problems that occur primarily in infants who have experienced distressing or painful events involving the nose, throat, or esophagus (Chatoor et al., 1988; DiScipio et al., 1978). Such experiences may include insertion of nasogastric feeding tubes, endotrachael suctioning, and intubation. Pain and discomfort during feedings because of underlying anatomical or physiological problems (e.g., esophagitis secondary to gastroesophageal
S77
LETTERS TO THE EDITOR
reflux), aversive feeding techniques, or choking are other types of experiences that may result in PTFD. Symptoms of PTFO in infants may include crying, gagging. or choking at the site of a boltle or food. refusal to chew or swallow. lack of awareness of feelings of hunger. and acceptance of the bottle only when falling asleep (Chatoor and Benoit. 1996). The prevalence of PTFO is unknown, although OiScipio and his colleagues (978) estimate that about 40% of infants who are traumatized by medical, surgical, or intrusive diagnostic procedures involving the esophagus may develop continued dysphagia. Because a growing number of premature or very ill infants undergo intrusive medical procedures (e.g.• intubation. repeated suctioning). PTFO is believed to be increasingly common (Chatoor and Benoit. 1996). To date. no reports have been published to document the treatment of PTFD. However. a three-phase intervention was recently developed to treat infants with food refusal. including PTFO. The three-phase. stepwise treatment approach incorporates (I) various physiological and environmental factors to restore or enhance healthy eating habits in infants who already have feeding skills; (2) various behavior modification techniques to eliminate problem feeding behaviors and to teach new feeding skills; and (3) ongoing nutritional monitoring and parent support. To examine the effectiveness of the three-phase intervention. we reviewed the clinical records of 24 children (12 male and 12 female). aged 7 weeks to 34 months (mean = 19.13 months, SO = 7.45). who had symptoms consistent with PTFO and completed the three-phase intervention. Thirteen infants (54%) were firstborn. 12 (50%) had failure to thrive. 6 (25%) had cerebral palsy, and 15 (63%) received gastrostomy or nasogastric tube feedings. Mothers' mean age was 31.83 years (SO = 5.52) and most had some college education (mean years of schooling = 14.48. SO = 1.93). Nineteen (79%) subjects were Caucasian and five (21 %) were Asian. Most subjects (n = 23; 96%) were married or lived common-law. one (4%) was single. and most were from middle-class backgrounds. All subjects completed a structured clinical assessment that include questionnaires. clinical interviews. and observation of mealtime behaviors before starting the intervention. Three definitions of success were used. First. when success was defined by clinical judgment. the three-phase program was succesful in 17 (71 %) of 24 cases. Clinical judgment was defind as follows: 0) increased total intake of solids and liquids by mouth from pre- to posttreatment periods; (2) improved cooperation at mealtimes; (3) steady weight gain (or catch-up rates of growth if the infant was also failing to thrive); (4) initiation of oral feedings (if the child had total food refusal); (5) acceptance of a greater variety of flavors and textures (if the child had partial food refusal
or refusal to progress £0 new textures); or (6) less dependence on tube feedings (if the child was tube-fed). Second, when success was defined as the reduction in the number of problem behaviors at mealtimes (using the total score on the Infant Feeding Behaviors-Rater [IFB-R] checklist), treatment was successful in 19 (79%) of 24 cases. The IFB-R (Benoit and Green. 1995) is a checklist used £0 identify and quantify infants' maladaptive behaviots at meal times. The mean score on the IFB-R checklist for the 24 infants was 37.67 (SO = 15.20) before and 26.19 (SO = 10.21) after treatment (t = 3.07; df = 46; P < .01). Third. when treatment success was defined as the elimination of the need for tube feedings, the treatment program was successful in 6 (40%) of 15 cases. These success rates were achieved in an average of 10 sessions (range 2 £0 21; SO = 6.24). Treatment outcome was not influenced by multiple feeders, child's age, cerebral palsy, supplemental tube feeding, or failure to thrive. These encouraging preliminary results suggest that the three-phase intervention is helpful in treating food refusal, including PTFO. Factors contributing £0 treatment success and failure require additional empirical study.
578
]. AM
Diane Benoit, M.D. University of Toronto Debra Green, B.A. Pepperdine University, Los Angeles Debby Arts-Rodas, R.D. Hospital for Sick Children. Toronto Benoi, D. Green 0 (1995), The Infant Feeding Behaviors-Ra,er checklist: preliminary data. Poster presented at the 42nd Annual Meeting of the American Academy of Child and Adolescent Psychiatry. New Orleans Chatoor I. Benoit D (1996). Diagnostic assessment and treatment of feeding disorders characterized by food refusal. Workshop presented at the World Association for Infant Mental Health. Sixth World Congress. Tampere. Finland. July Chatoor I. Conley C. Dickson L (1988). Food refusal after incident of choking: a posttraumatic eating disorder. J Am Acad Child Adousc Psychiatry 27:105-110 DiScipio WJ. Kaslon K. Ruben RJ (1978). Ttaumatically acquired conditioned dysphagia in children. Ann OroI87:509-514 Lindberg I. Bohlin G. Hagekull B (1991). Early feeding problems in a normal population. Int J Eating Disord 10:395-405
MUNCHAUSEN BY PROXY
To the Editor: Cassar et al. (1996) recently reported on a case of "malingering by proxy." They reported this as a variant on the more commonly known Munchausen syndrome by proxy, itself a subtype of factitious disorder. I wish £0 report a similar case in which a mother and child collaborate in the reporting of psychological disturbance for the purpose of financial gain.
ACAD. CHILD ADOl.ESC. PSYCHIATRY, 36:5. MAY 1997