Effects of prenatal cocaine exposure

Developmental Outcomes of Prenatal Cocaine Exposure in Infants and Young Children

Assessments in language, cognition, and motor and behavioral development is currently under study in this population. The research, therefore, is not conclusive as investigators begin to isolate confounding factors and determine the solitary effects of prenatal cocaine exposure and adverse long-term developmental outcomes.

Language

Research indicates prenatal exposure to cocaine may affect the young child's language development, although the findings are inconsistent. Hurt, Malmud, Betancourt, Brodsky, and Giannetta (1997) investigated the early language development of 76 2 1/2-year-old children prenatally exposed to cocaine to a matched control group of 81 children. After administering the Preschool Language Scale-3 (PLS-3), the authors found no documented cocaine-related differences in terms of language function (receptive, expressive, or total language). The authors did not state whether poly-drug use was a control variable. Similarly, Kilbride, Castor, Hoffman, and Fuger (2000) reported no statistically significant difference in language development of term or near term infants prenatally exposed to cocaine, up to 3 years of age, by the Receptive-Expressive Emergent Language Scale and the Sequenced Inventory for Communicative Intent. In fact, the authors noted infants exposed to cocaine who received special early case management had a higher verbal score at 3 years of age.

In contrast, several investigators have found significant language delays among infants prenatally cocaine-exposed. Koren et al. (1998) examined the language functioning of 2 1/2-year-old children prenatally cocaine-exposed (n = 23) and adopted at birth into middle to upper class families to non cocaine-exposed control group (n = 23). After administering the Reynell language test, the authors found the children exposed to cocaine prenatally had statistically significant language delays. The authors identified that their design provides exclusion of postnatal environment influences on language functioning of infants prenatally exposed to cocaine. Similarly, Morrow et al. (2003) evaluated the association between prenatal cocaine exposure and language development of 253 African American full-term infants prenatally exposed to cocaine from the Miami Prenatal Cocaine Study. Kent Scoring Adaptation for language test was administered at 4, 8, 12, 18, and 24 months and the Clinical Evaluation of Language Fundaments-Preschool (CEL-P) at 3 years of age. After controlling for confounding factors, the authors reported the young children cocaine exposed prenatally had a lower overall language scores.

Singer et al. (2001) and a recent study by Morrow et al. (2004) both found language delay in infants/young children exposed to cocaine prenatally to be associated with increasing exposure. Singer et al. (2001) performed a longitudinal investigation of speech-language skills of 1-year-old infants (134 infants prenatally exposed to cocaine, 66 heavily exposed, and 68 lightly exposed) to a matched control group of 131 infants by administering the PLS-3. The authors reported infants heavily prenatally exposed to cocaine performed poorer on total language and auditory comprehension (receptive language) than infants with light or no exposure to cocaine prenatally. Morrow et al. (2004) looked at 424 African American full-term young children at 3 years of age (226 prenatally exposed to cocaine and 196 not) and measured their language function using the CEL-P to assess the expressive and receptive language skills. They found a significant difference in expressive and receptive language function with increasing prenatal cocaine exposure.

Cognition
The results of studies to determine an association between a cognitive delay and prenatal cocaine exposure are conflicting. Several studies documented no statistically significant differences on cognitive development assessed by the Bayley Scale of Infant Development's Mental Development Index (BSID-MDI) among infants/young children exposed to cocaine prenatally when tested at 6-24 months (Frank et al., 2002; Jacobson et al., 1996; Kilbride et al., 2000; Messinger et al., 2004).

Similarly, Koren et al. (1998) investigated the intelligence quotient (IQ) of 2 1/2-year-old children prenatally cocaine-exposed (n = 23) and adopted at birth into middle to upper class families to a control group (n = 23). The authors identified that their design provides exclusion of postnatal environment influences on the cognitive functioning of infants prenatally exposed to cocaine. After administering the Bayley and McCarthy IQ tests, they found no differences in global IQ between the two groups; however, they reported a trend towards lower IQ of the children in the cocaine-exposed group.

In contrast, Singer and colleagues (2002) reported infants prenatally exposed to cocaine are twice as likely to have significant cognitive delays throughout their first 2 years of life than non-exposed infants. Alessandri, Bendersky, and Lewis (1998) and Lewis, Misra, Johnson, and Rosen (2004) reported lower MDI scores among infants/young children heavily prenatally cocaine-exposed. Alessandri and colleagues (1998) examined the cognitive functioning of infants prenatally cocaine-exposed (heavily exposed [n = 30) and lightly exposed [n = 30] to a matched control group [n = 169] at 8 and 18 months of age) using the BSID-II's MDI. They documented a decrease in MDI scores only at 18 months of age among infants prenatally cocaine-exposed overall, but the infants heavily exposed had the poorest scores. Lewis and associates (2004) examined the effects of prenatal cocaine exposure and cognitive development at 12, 18, 24, and 36 months of 147 young children who were exposed and 89 who were not. After controlling for confounding factors and using the BSID-MDI, the authors found the young children with higher meconium concentrations of cocaine metabolites had lower test scores with a decline at 18 months on mental development.

Motor
Motor performances in infants/young children prenatally exposed to cocaine assessed by motor developmental scales are also not consistent. Various researchers have reported no statistically significant findings of motor developmental delays among infants/young children exposed to cocaine prenatally (Jacobson et al., 1996; Kilbride et al., 2000; Messinger et al. 2004; Singer et al., 2002) assessed by the BSID-Psychomotor Developmental Index (PDI). Jacobson et al. (1996) examined 464 young children exposed to cocaine prenatally at 13 months of age. Kilbride et al. (2000) investigated term or near term infants prenatally exposed to cocaine (those who received early case management [n = 70] or routine follow-up [n = 48]) and infants who were not exposed (n = 41) up to 3 years. Singer and colleagues (2002) looked at 218 infants prenatally cocaine-exposed and 197 infants non-exposed at 6.5, 12, and 24 months. The authors noted only an increase in lower motor scores from 6.5 months to 2 years, and boys were more affected than girls in the infants/young children exposed to cocaine prenatally. Messinger and associates (2004) examined infants/young children exposed to cocaine (n = 474), opiates (n = 50), cocaine and opiates (n = 48), and neither substances (n = 655) at 1, 2, or 3 years of age.

Again, in contrast, Arendt, Angelopoulos, Salvator, and Singer (1999) assessed the motor development of an inner city population of primarily African American 2-year-old children, 98 prenatally cocaine exposed, to a matched group of 101 non-exposed children using the Peabody Developmental Motor Scales (PDMS). They found a statistically significant poorer performance among the young children exposed to cocaine prenatally on both gross (balance and the receipt and propulsion subscales) and fine (the hand use and the eye-hand coordination subscales) motor while controlling for covariates. Similarly, Lewis et al. (2004) investigated the effects of prenatal cocaine exposure on motor development at 12, 18, 24, and 36 months of 147 young children who were exposed and 89 who were not. After controlling for confounding factors and using the BSID-PDI, the authors found the young children with higher meconium concentrations of cocaine metabolites and males had lower performance scores with a decline at 18 months on motor sequelae.

Behavior
Currently, there are only a few studies investigating behavioral development up to the age of 3 in children prenatally exposed to cocaine. Researchers are now looking at these children in their school age years.
Beeghly, Frank, Rose-Jacobs, Cabral, and Tronick (2003) examined the infant-caregiver attachment behavior of 154 full-term 12-month-old infants (heavily prenatally cocaine-exposed [n = 29], lightly prenatally cocaine-exposed [n = 61], and not exposed [n = 64]) using Ainsworth's Strange Situation. They found no statistically significant effects between secure/insecure or disorganized attachment status and the infant's level of prenatal cocaine exposure. However, the mother-infant dyads of the infants heavily prenatally exposed to cocaine and whose mother did not receive public financial assistance were shown to exhibit a higher level of behavioral disorganization with their caregivers during the Strange Situation. Similarly, Messinger et al. (2004) documented no association between prenatal cocaine exposure and behavior development deficit in the young child at 1, 2, or 3 years of age after accounting for confounding factors. This study examined these young children exposed to cocaine (n = 474), opiates (n = 50), cocaine and opiates (n = 48), and neither substances (n=655) on the BSID-II, Behavioral Record Scales.

Pediatr Nurs. 2005;31(5):427-436.