Neurobehavioral sequelae of fetal cocaine exposure

Volume 120 Number 4, Part 1

somewhat contradict the data of Dietz et al. Their results represent the average of two subsequent measurements; our data are based on a single determination of the RMR. This could be a factor causing the difference between the results. However, we determined the R M R twice in 21 children and found no difference between the results of the two measurements (first: 1517 _+ 78.1; second: 1524 + 82.2 kcal/day), with a mean variation of 3.6% (range: 1.3% to 7.7%). The subjects included in our study were younger (age range: 10.1 to 17.2 years) than those investigated by Dietz et al. (age range: 12 to 18 years). Because of the quick changes during puberty (e.g., in body composition, hormone levels, and growth rate), even small age differences may cause changes in metabolic rate. Nevertheless, we believe that there is an urgent need of new age- and gender-specific standards for estimation of the RMR. Dbnes Molnhr, MD Department o f Pediatrics University Medical School o f Pecs Yozsef A.U. 7 H-7623 Pecs, Hungary

E d i t o r i a l correspondence

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ologic or environmental factors that may be directly or indirectly related to drug exposure. Adequate clinical services and social resources for families--including drug treatment--may prevent adverse behavioral and developmental consequences in these children. In addition, we wish to correct the authors on their reporting of our study results. 2 In our research on the effects of cocaine exposure on infant behavior, we did not exclude women with no prenatal care. Singer et al, reported that we found group differences on the Neonatal Behavioral Assessment Scale in motor functioning at the 11- to 30-day follow-up. They neglectedto state that these were crude differences; after control for confounding effects, there was no remaining effect of cocaine exposure on these scores. Daniel R. Neuspiel, MD, M P H Associate Professor o f Pediatrics Sara C. Hamel, MD Assistant Professor o f Pediatrics Albert Einstein College o f Medicine Bronx, N Y 10467 REFERENCES

REFERENCES

1. Daly JM, Heymsfield SB, Head CA, et al. Human energy requirements: overestimation by widely used prediction equation. Am J Clin Nutr 1985;42:1170-4. 2. Owen OE, Kavle E, Owen RS, et al. A reappraisal of caloric requirements in healthy women. Am J Clin Nutr 1986;44:1-19. 3. Owen OE, Holup JL, D'Alessio DA, et al. A reappraisal of the caloric requirements of men. Am J Clin Nutr 1987;46:875-85.

Neurobehavioral sequelae of fetal cocaine exposure To the Editor: We read with interest the article by Singer et al., entitled "'Neurobehavioral Sequelae of Fetal Cocaine Exposure" (J PEDIATR 1991; 119:667-72). This review is appropriately critical of current research in this complex area of study. However, we disagree with the authors' concluding statement that gestational cocaine exposure is a ,marker" for early behavioral impairments with long-term developmental implications. Extant research in this area does not justify this position. Neonatal behavioral findings are equivocal and of limited predictive value, and no studies of the postneonatal behavioral effects of prenatal cocaine exposure have yet been published. Most studies support the behavioral heterogeneity of this population. The belief that cocaine exposure is a "marker" for developmental impairment may be dangerous; this type of one-dimensional model ignores the complexities of the problems of these children and their families, including the multiple social issues accompanying substance use and addiction. The stereotyping of these infants and children may result in a self-fulfilling prophecy of adverse behavior and development. We support an alternative model I that assumes no underlying deficit in cocaine-exposed infants but, instead, maintains that they are at greater risk for developmental compromise by virtue of bi-

1. Weston DR, Ivins B, Zuckerman B, et al. Drug-exposed babies: research and clinical issues. Zero to Three 1989;9:1-7. 2. Neuspiel DR, Hamel SC, Hochberg E, et al. Maternal cocaine use and infant behavior. Neurotoxicol Teratot 1991;13:22933.

Reply To the Editor." We appreciate the thoughtful comments of Drs. Neuspiel and Hamel and are in agreement with them on many points, In fact, our article emphasized "the complexities of the problems of these children and their families, including the multiple social issues aceompanyingsubstance abuse and addiction." We believe that we have amply summarized these issues in our brief report. The use of the term marker variable in no way implies a one-dimensional model but serves the function of allowing and directing clinical and research attention to the many associated biologic and social risks associated with fetal cocaine exposure. We based our conclusions On the combined findings of the animal studies, which allow control for multiple drug use, social and environmental factors, and the compelling data on growth retardation in both animal and human studies, as welt as on the neonatal neurobehavioral studies. Of the three extant controlled studies reviewed in the article that used the Neonatal Behavioral Assessment Scale, there were findings of abnormalities despite many exclusionary factors that may have biased the samples to the least affected infants. Neuspiel et aL 1 found significant differences in motor behavior at follow-up in cocaine-exposed infants in comparison with control subjects. Their statistical control for factors of low birth weight and multiple drug use, which are risk factors markedly increased in cocaine-exposed samples, does not diminish the clinical risk to the infant or change the actual behavior of the infant: In addition to these studies, another recently published study 2 with a large sample size also found neurobehavioral effects of fetal cocaine exposure in the neonatal period, using a different outcome measure (i.e., infant cry behaviors). We hope that long-term, pop-