Conjuring a New Category of Disability
from Prenatal Cocaine Exposure:
Are the Infants Unique Biological
or Caretaking Casualties?
Linda S. Schutter and Richard P. Brinker, University of Illinois at Chicago
The paper reviews the available literature on the biological mechanisms
and effects of cocaine exposure impacting pregnant women, the fetus, the
neonate, and the infant. The potential causal mechanisms for neural
damage to the fetus are quite robust; however, the empirical literature does
not support an inevitable developmental consequence for infants exposed
in utero to cocaine. The most impaired of the cocaine-exposed infants
do not seem to differ, behavior ally, from other groups of neurologically
impaired infants. However, the infant exposed to cocaine in utero may
have the added disadvantage of a dysfunctional caregiving environment
focused more on drug habit maintenance than on caretaking. This combination of biological vulnerability and caretaking inadequacy increases
the odds that a child will be a "caretaking casualty." Classifications of
children are useful only if they organize and name individuals with the
same biological or behavioral characteristics. The classification of infants
and young children as prenatally cocaine-exposed does not constitute a
coherent cluster of either biological or behavioral characteristics. Hence,
the construct of "cocaine babies" that has received considerable attention
in the popular and professional press is neither descriptive nor predictive
of behavior. Recommendations are offered for classification of behavior
rather than labeling of the child. In addition, an overview of types of early
intervention appropriate for various kinds of behavior exhibited by some
children exposed to cocaine is presented. Finally, the development of
empowerment strategies and professional partnerships with families of
infants exposed to cocaine in utero is discussed.
The focus of national attention on the crack cocaine epidemic
has been on the criminal aspects of illegal drug distribution and use.
TECSE 11(4), 84-111 (1992)
© PRO-ED Inc.
84
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PRENATAL COCAINE EXPOSURE, 85
The effects of cocaine on its users have been less prominent as a focus
for public policy. A unique feature of the present epidemic of cocaine
use is that women apparently constitute a higher proportion of the
user population than is true for other illegal drugs. It is etimated that
approximately 15% of users are females of childbearing age (Rosenak,
Diamant, Yaffe, & Hornstein, 1990), making cocaine currently one
of the most increasingly abused illicit drugs ingested by women during
pregnancy. However, its effect on offspring exposed in utero has only
recently been explored. Nevertheless, because of the increase in usage
of cocaine, especially by women, we are tempted to conclude that a
new category of child with developmental disabilities will emerge. News
coverage has already begun to shape public opinion, leading society
to conclude that the public schools will be swamped by such children
who will require special education if they are to benefit at all from
schooling (Daley, 1991; Viadero, 1989).
The purpose of the present paper is to review the empirical foundation for the existence of a "new category" of special education students who were exposed to cocaine in utero. What are the biological
mechanisms by which such a population would be created, what specific disabilities might be expected, and does the field of early intervention need to develop intervention techniques different from those
used for other children with biological and/or environmental vulnerabilities at birth? How might such children and their families be accommodated by the provisions of P.L. 94-142 and P.L. 99-457? The belief
that a sole biological mechanism could create a category of children
who share a style of human adaptation requires discussion of issues
of cocaine use in the context of other maternal life-style issues such
as nutritional habits, health care utilization, general health, and
multiple drug use. Because this epidemic of cocaine use is relatively
new, dated from the widespread introduction of crack cocaine in the
mid-1980s, long-term evaluation of the developmental and behavioral
outcomes for children exposed in utero is not yet available. Recent
research, though, has begun to evaluate the consequences of cocaine
use among childbearing women, and preliminary descriptions of such
impact during infancy and early childhood are reviewed. The nature
and purpose of classification systems, and issues of intervention for
the child and for the family with reference to the parent-professional
partnership envisaged in P.L. 99-457, are also reviewed.
Prevalence of Use by Pregnant Women. Although patterns of
abuse of alcohol, heroin, marijuana, and other substances have not
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86, TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION 11:4
changed much in the last 10 years, cocaine abuse has been rapidly
rising and has increased across all socioeconomic classes, ethnicities,
races, ages, and sexes (Chasnoff, 1989b; Gold, 1987). Cocaine is
reported to be the number one illicit drug used by women of childbearing age, with between 10% and 30% of mothers using during
their pregnancy (Bandstra et aL, 1989; Chasnoff, 1989a; Clayton,
1986; Frank et al., 1988; Greer, 1990; Little, Snell, Palmore, &C Gilstrap, 1988; Pollin, 1985). Hospitals that performed routine toxicologies reported a higher number of substance abusers than hospitals
that relied on verbal report (Chasnoff, 1989a). The lack of legal mandate for systematic laboratory testing for various drugs as part of
routine obstetric care or upon delivery (Moore, 1990) confounds
identification of these infants and makes it difficult to establish cocaine's
effects on development. A major obstacle to presently obtaining accurate incidence figures is that pregnant women are unwilling to report
their use of cocaine during pregnancy. Data collection to determine
prevalence and identifying symptomatology may become even more
difficult to obtain as drug prosecution and child abuse laws become
more stringent, causing drug-abusing mothers to opt for nonhospital
deliveries. Already, fears that the authorities, on whom disadvantaged
women are dependent for health care, will refer the women to child
protective services with a charge of abuse or neglect likely leads to
underreporting, which may be differential in low income areas. In
contrast, a woman whose physician is paid from third-party health
insurance and her own resources may have greater confidence in the
confidentiality of the doctor-patient relationship.
Thus, data based on self-report are likely to underestimate the
true incidence of cocaine usage, especially among disadvantaged
women. Routine screening through urine analysis or blood analysis
would provide the strongest foundation for estimating incidence of
various substance abuse. Clearly, the task of producing accurate
research to determine risks from prenatal cocaine usage is complex
and undermines the possibility of effective prevention and intervention strategies. By the time an early interventionist or schoolteacher
discovers a child's problems, the causal source has become lost in a
plethora of other biological and environmental factors.
Biological Mechanisms for Effects of Cocaine
on Mothers and Infants
Pharmacological Effects. The direct effects of cocaine are achieved
by two simultaneous mechanisms, peripheral and central, occurring
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PRENATAL COCAINE EXPOSURE, 87
in both the mother and fetus. The peripheral mechanism is the anesthetic effect of cocaine, achieved by its capacity to block the return
of neural cells to a resting electrical potential after the cell has fired.
This effect is achieved along with a vasoconstriction of the blood vessels, in which blood vessel diameter is reduced, increasing circulation
to the brain and reducing blood flow volume at the site of the constriction. The direct vasoconstrictive effect is the basis for direct damage
to the heart and other damage of circulatory origin to the brain, such
as rupture of an aneurysm or rupture of underdeveloped vascular systems in the developing fetus (Caplan, Hier, &C Banks, 1982; Schwartz
& Cohen, 1984).
The central mechanism mimics the effect of a response from the
adrenal gland. The cocaine blocks reabsorption of dopamine,
norepinephrine, and other catecholamines, which leads to an excessive
accumulation of these neurotransmitters at the postsynaptic sites and
in the bloodstream. The net result is activation of the "pleasure pathways" of the brain through the excess circulating dopamine (Gawin
& Ellinwood, 1988). Moreover, the excessive neurotransmitters
increase the responsivity of neural cells to activation by stimuli that
normally would produce a less general neural response. It is because
of these mechanisms that cocaine is such a highly addictive central
nervous system stimulant.
The properties of cocaine facilitate its crossing from maternal circulation to fetal circulation (Chasnoff, Bussey, Savitch, &c Stack, 1986).
This exchange occurs by diffusion through the placenta, and an
equilibrium of mother-fetal blood occurs rapidly (Chasnoff, 1988b).
In the mother, cocaine use induces euphoria, acceleration of both heart
rate (tachycardia) and respiration (tachypnea), and increased blood
pressure (Chasnoff, 1989b). The maternal circulatory response to
norepinephrine increases blood flow to her brain while reducing it to
her uterus. Hence, the supply on which the fetus draws is less well
oxygenated, resulting in anoxia (absence of oxygen carried in blood)
and ischemia (tissue anemia) in the developing fetus (Dixon &c Bejar,
1988, 1989). Thus, the infant circulates cocaine-saturated blood more
quickly because of increased fetal blood pressure.
Teratogenic Effects. The amount and duration of drug use by
the pregnant woman is related to the effect on the fetus (Finnegan,
1976). For example, ingesting a drug during the first trimester may
directly affect differentiation of organ systems such as the heart, which
is extremely vulnerable 20 to 40 days postconception (Yaffe, 1978).
The central nervous system, though, continues to mature throughout
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88, TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION 11:4
gestation and actually increases its vulnerability to teratogens throughout pregnancy (Grimm, 1987). The most likely vulnerabilities are
destruction of neural areas through disruption of the circulatory system normally supplying those areas with richly oxygenated blood.
Although few controlled studies exist relating cocaine exposure of the
human fetus to embryonic differentiation, animal models have demonstrated, experimentally, the impact on limb, heart, eye, urologic, and
intestinal differentiation (Bingol, Fuchs, Diaz, Stone, &; Gromisch,
1987; Bingol et al., 1986; Chasnoff, Burns, & Burns, 1987; Chasnoff &C Chisum, 1987; Chasnoff, Chisum, & Kaplan, 1988; Isenberg,
Spierer, & Inkelis, 1987; Telsey, Merrit, & Dixon, 1988).
Confounding of Environmental Effects w i t h Maternal
Cocaine Use
Specific maternal life-style issues impacting the developing fetus
confound the issues of newborns' health and development and make
it difficult to separate the direct effects of cocaine from indirect effects
such as poor nutrition and poor prenatal care. Physical conditions of
cocaine-abusing women contribute to the deteriorating health of the
cocaine-exposed fetus. Pregnant women who abuse substances experience a higher rate of infectious diseases (e.g., hepatitis, venereal disease) than non-substance-abusing women (Chasnoff, 1987; Chasnoff
et al., 1987; Frank et al., 1988). Vitamin deficiencies (especially B 6 ,
B 1 , and C) common in substance abusers are especially prevalent in
cocaine users due to cocaine's anorexic action (Ryan, Ehrlich, &C Finnegan, 1987). In addition, cocaine-abusing women often have irregular
menstrual cycles, delaying awareness of pregnancy and increasing fetal
risk due to excessive or strenuous activity (Chasnoff, 1987). Users also
generally have a decreased interest in bodily needs, and evidence of
poor prenatal care appears prevalent in this population. Sixty percent
to 70% of cocaine-abusing pregnant women in several studies received
no prenatal care (Cherukuri, Minkoff, Feldman, Parekh, & Glass,
1988; Dixon & Bejar, 1989; Oro & Dixon, 1987). Clearly, these lifestyle issues contribute to reduced maternal and fetal health and can
complicate labor and delivery. The pregnant, cocaine-using woman
who suffers the increased risk of infectious diseases, vitamin deficiencies, and poor prenatal care very possibly increases the teratogenic
effects on her fetus because available biological buffers against such
effects are reduced or absent (Cherukuri et al., 1988).
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PRENATAL COCAINE EXPOSURE, 89
Perinatal and Neonatal Outcomes
Some evidence has been found that cocaine can precipitate onset
of labor and increase fetal activity (Acker, Sachs, Tracey, & Wise,
1983; Chasnoff et al., 1987; Chasnoff, Burns, Schnoll, & Burns, 1985;
Keith et al., 1989; MacGregor et al., 1987). Nevertheless, it has not
been firmly established that cocaine use is associated with higher rates
of premature births (Chasnoff et al., 1985; Chasnoff et al., 1988;
Chasnoff, Lewis, Griffith, & Willey, 1989; Dixon &c Bejar, 1989;
Kaye, Elkind, Goldberg, & Tytun, 1989). Significantly higher fetal
death rates through spontaneous abortions have been reported for
cocaine-using mothers in comparison to other drug-dependent women
and drug-free women (Chasnoff et al., 1985; Oro &C Dixon, 1987).
Ryan et al. (1987) reported a fetal death rate of cocaine-exposed infants
2 times higher than other drug-exposed infants, and 4 times higher
than infants not exposed to drugs. Other studies have found that a
significantly greater proportion of cocaine-using, pregnant women
experienced abruptio placentae in comparison to other drug-using and
drug-free women (Acker et al., 1983; Bingol, Fuchs, Diaz, Stone, &
Gromisch, 1987; Chasnoff et al., 1985; Oro &c Dixon, 1987).
Although abruptio placentae often complicates delivery (Keith et al.,
1989), it appears this condition is also responsible for a significantly
higher stillbirth rate in cocaine-exposed infants than in drug-free infants
(Bingol et al., 1987).
Low birth weight appears to be a more predictable characteristic
of cocaine-exposed infants. Both full-term and premature infants
exposed to cocaine exhibit significantly decreased birth weights compared to drug-free infants of the same gestational age (Bingol et al.,
1987; Chasnoff, 1989b; Kaye et al., 1989; Keith et al., 1989; MacGregor et al., 1987; Oro & Dixon, 1987; Woods, Eyler, Behnke, &
Conlon, 1990; Zuckerman et al., 1989). Along with low birth weight,
cocaine-exposed infants on average have a smaller head circumference
and shorter body length than drug-free infants. Researchers have been
associating intrauterine growth retardation and microcephaly with
cocaine use during pregnancy (Bingol et al., 1987; Chasnoff, 1989b;
Cherukuri et al., 1988; Hadeed & Siegel, 1989; Oro & Dixon, 1987;
Ryan et al., 1987; Zuckerman et al., 1989), and believe the lack of
rich blood flow to the fetus to be responsible for these reduced fetal
growth conditions. Cherukuri et al. (1988) found that crack-exposed
infants experienced growth retardation 3.5 times more often than drugfree infants, but contended that many of the adverse outcomes may
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90, TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION 11:4
be related to the mother's life-style (lack of prenatal care and poor
nutrition), rather than cocaine's pharmacologic effects. It appears, then,
that the combination of maternal cocaine use with poor self-care is
currently the strongest indicator of reduced neonatal size.
Cerebral insults observed in cocaine-exposed infants include
cranial abnormalities and cerebral infarctions, most commonly hemorrhages (Dixon & Bejar, 1989). These types of cerebral injury are consistent with those seen in adult cocaine abusers and are probably due
to the vasoconstrictive and hypertensive properties of the drug. Some
of these infarctions are found to be "old," indicating that brain injury
probably occurred before birth. Other findings have reported cerebral
infarctions and associated seizures occurring in babies of mothers who
used cocaine 48 to 72 hours before labor (Chasnoff et al., 1987; Chasnoff et al., 1986). Spires, Gordon, Choudhuri, Maldonado, &c Chan
(1989) detected an intracranial hemorrhage in a cocaine-exposed infant
at 96 hours which then resolved by 16 days. Overlooking such an event
can easily complicate the understanding of later developmental problems, should they appear. In addition, Dixon and Bejar (1989) stated
that the type, location, and distribution of cranial lesions indicate that
they may not be clinically evident in infancy or early childhood.
Damage in frontal lobes and the basal ganglion may become evident
only after the first year, when more complex visual, motor, and social
cognition tasks develop. Thus, early detection could help predict possible abnormal neurological, cognitive, and behavioral development,
but this will be achieved only with routine, repeated ultrasound
examinations (Bozynski et al., 1990).
Sudden Infant Death Syndrome (SIDS) has been found to have
incidence rates ranging from 8% to 15% in cocaine-exposed infants
compared to a rate of only 5% among infants delivered to narcoticaddicted women (Chasnoff et al., 1987; Chasnoff et al., 1985; Chasnoff, Hunt, Kletter, &c Kaplan, 1989). The incidence of SIDS in the
general population of the United States is 0.5% (Chasnoff et al., 1987).
In general, infants of substance-abusing mothers, including cocaineabusing mothers, have abnormal sleeping respiratory patterns, characterized by an increased frequency of apnea episodes, which may be
related to an increased SIDS risk of 5 to 10 times that of the general
population (Riley & Porat, 1987; Ward et al., 1989; Ward et al.,
1986). Mothers who use only cocaine deliver infants who exhibit a
higher incidence of cardiorespiratory abnormalities than infants with
methadone or no prenatal drug exposure (Chasnoff, 1989a). Thus,
although the exact mechanism of SIDS is not yet understood, the risk
appears increased in infants exposed to cocaine in utero.
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PRENATAL COCAINE EXPOSURE, 91
Neonatal Behavioral Differences
Although most legal and illegal drugs used prenatally do not
produce congenital malformations, they may have definite, negative
behavioral and neurological effects on the infant, toddler, and child
(Chasnoff, 1989b). It is unclear whether the temporary withdrawal
symptoms exhibited by detoxifying newborns, and persisting for as
long as 14 days after birth (Chasnoff, 1989b), are the extent of cocaineinduced damage, or whether these symptoms are also the result of permanent neurological damage, resulting in future neurobehavioral
deficits (Lewis, Bennett, & Schmeder, 1989). Abundant literature
describes neonatal behavior exhibited by cocaine-exposed newborns:
irritability, poor feeding patterns, frequent crying, tremulousness, frequent startles, irregular sleep patterns, hypertonia, increased respiratory
and heart rates, vomiting, frantic sucking, and poor consolability
(Chasnoff et al., 1985; Chasnoff, Griffith, MacGregor, Dirkes, &
Burns, 1989; Eisen, 1990; Geggel, Mclnerny, & Estes, 1989; LeBlanc,
Parekh, Naso, & Glass, 1987; Oro &c Dixon, 1987; Shannon, Lacouture, Roa, & Woolf, 1989).
The behavioral symptomatology of withdrawal in a newborn is
very similar to the behavior associated with central nervous system
damage (Als, 1986; Fajardo, Browning, Fisher, & Paton, 1990;
Holditch-Davis, 1990), yet the confirmation of cocaine-induced central nervous system damage remains unanswered. Newborns excrete
unchanged cocaine 12 to 24 hours after delivery if their mothers used
cocaine 1 to 2 days prior to delivery (Chasnoff, 1989b) and continue
to excrete benzoylecgonine, the primary cocaine metabolite, for up
to 5 days (Chasnoff et al., 1986). It is the prolonged demonstration
of the withdrawal-like symptoms, beyond 5 days, that concerns
reseachers and professionals.
One study did attempt to differentiate between withdrawal and
neurological damage. Chasnoff, Griffith, MacGregor, Dirkes, and
Burns (1989) compared behavioral symptomatology of infants whose
mothers used cocaine only in the first trimester of pregnancy, to infants
whose mothers used cocaine throughout pregnancy. They reported
significant neurobehavioral response deficiencies in orientation, motor
ability, state regulation, and abnormal reflexes in both cocaine-exposed
infant groups as compared to a drug-free control group. This appears
to support the contention that central nervous system damage does
occur, and early in gestation, as the first-trimester-exposed infants could
not be exhibiting withdrawal due to detoxification.
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92, TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION 11:4
Further support of cocaine's neurological harm in utero may be
the abnormal and labile electroencephalograms (EEGs) that have been
detected in cocaine-exposed infants (Chasnoff et al., 1986; Dixon &c
Bejar, 1989; Dixon, Coen, & Crutchfield, 1987; Doberczak, Shanzer,
Senie, & Kandall, 1988; Telsey et al., 1988), although follow-up
documentation of later central nervous system functioning has not been
performed. Dixon et al. (1987) reported visual disturbances still present
at 4 to 6 months in newborn cocaine-exposed infants, long after cocaine
and its metabolites are excreted. Very poor, if any, visual attention
and tracking, and abnormal flash-evoked visual potentials were
observed in all infants studied, indicating possible brain or neurological damage.
Thus, research to date indicates that infants exposed to cocaine
in utero have a higher risk of both neonatal withdrawal symptoms
due to detoxification and neurological abnormalities. Additional studies
are needed, though, to thoroughly assess the relationship of intrauterine
cocaine exposure to initial development and longer term neurodevelopmental outcome. Knowledge of developmental outcome will assist in
determining the extent of nervous system damage.
Developmental Differences in Infancy
and Early Childhood
Research on the developmental outcome of cocaine-exposed
infants is commencing, and the few studies reported are reviewed
below. It should be noted that because of the difficulty in establishing
the frequency, duration, and method of cocaine exposure, it is difficult
to conduct an adequate prospective study of the developmental impact
of prenatal cocaine exposure.
Motor development of cocaine-exposed infants has been found
to differ in much the same way as motor development of other infants
born with low birth weight differs. More infants exposed to cocaine
in utero retain primitive reflexes relative to non-drug-exposed infants
(Chasnoff, 1988a). This is of concern because primitive reflexes are
generally replaced by more mature movement patterns as development
proceeds in non-drug-exposed infants. Stiff extension of the legs and
weight-bearing on the toes when held in a supported upright position
have been observed. Volitional movement patterns have been noted
to be deficient (Chasnoff, 1988a), and excessive extensor tone limits
infant pelvic mobility in supine, necessary for lifting legs and buttocks
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PRENATAL COCAINE EXPOSURE, 93
off a supporting surface to explore the lower body (Schneider, Griffith,
& Chasnoff, 1989). Excessive extensor tone and the persistence of
primitive reflexes can limit reaching for and manipulating objects, and
reductions in manual exploration can delay sensorimotor development.
The long-term ramifications of these early motor problems are unclear,
although van Baar (1990) reported no differences between drug-exposed
infants (including cocaine) and a control group on the Psychomotor
Developmental Index (PDI) of the Bayley Scales of Infant Development
(Bayley, 1969) when infants were in their first and second years of
life. This study excluded premature children and children in foster care
to control for those alternative explanations. Thus, more studies like
this are necessary to determine the long-range effects on motor ability.
Language and Behavioral Response to Stimulation. Delayed language acquisition and attentional deficits in both the first and second
years of life have been reported for full-term children exposed to cocaine
in utero (Griffith, Chasnoff, &c Freier, 1990; van Baar, 1990). These
children displayed low thresholds for stimulation, and when presented
with a task of choice-making, the cocaine-exposed infant was less able
to self-organize and process multiple stimulation than a cocaine-free
infant.
Play, Organization, and Affect. Howard, Beckwith, Rodning,
and Kropenske (1989) are currently performing one of the first studies
observing the social and cognitive consequences in older children of
drug-using mothers. Deficits were noted in the emotional expression,
intellectual functioning, quality of play, and organization of attachment
behavior in 18-month drug-exposed children as compared to a drugfree group. However, no higher proportion of insecurely attached
infants was found in the cocaine-exposed group in comparison to comparable socioeconomic status control infants. The children in this study
were exposed to multiple drugs, including cocaine, so the findings must
not be generalized as an effect of cocaine per se, despite the reality
that few pregnant cocaine-using women use only cocaine.
Conclusions About Biological and Early Behavioral
Effects of Cocaine
Though research appears to be progressing in terms of identifying
markers of neonatal cocaine intoxication, Farrar and Kearns (1989)
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94, TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION 11:4
asserted that the total number of infants with cocaine-associated malformations is too small to merit a diagnosis of "fetal cocaine syndrome"
at this time. The above-reviewed literature supports this contention.
However, several conclusions can be drawn. First, the biological
mechanisms through which cocaine exerts its effects on the immature
central nervous system are similar to other, relatively high-incidence
influences such as prematurity and low birth weight (Freeman, 1985).
Second, as a group, infants exposed to cocaine in utero will subsequently contain more individual infants with disorganized neonatal
behavior (including irritability, state disorganization, and motor
difficulties) and more individual infants with slower development than
a group of healthy babies not exposed to drugs. However, most of
the infants exposed to cocaine will not exhibit such neonatal and behavioral differences.
The methodological complexity in performing studies on this
group of mothers and infants is so riddled with confounds that determining specific outcomes, both neonatally and in later development,
may be impossible. Conclusions have been made from studies of infants
exposed in utero to cocaine, in spite of an absence of systematic data
on measured degree and duration of exposure to the drug, and polysubstance use variations. Selective screening of urine for cocaine traces
or reliance on the mother's recall do not constitute adequate measures
of the independent variable in a prospective study. No simple solution
can assist in determining what substances a mother used throughout
her pregnancy. Research on developmental outcomes must consider
the impact of environmental factors as well as the biological impact
of the drug exposure. Furthermore, because of the social and, in some
places, criminal stigma associated with cocaine usage, the available
reports must be regarded cautiously in terms of the exposure of the
fetus. Thus, these barriers to determining who was exposed to what
and when should prevent us from creating a new category of disability,
and should lead us to intervention focused on needs conceptualized
broadly in terms of the individual's ecology.
Interventions
Sameroff and Fiese (1990) presented a perspective for early intervention derived from a complex transactional model. In reviewing
efforts to prevent or intervene in children's psychosocial disorders, they
noted that, "The two greatest myths [were] the belief that there are
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PRENATAL COCAINE EXPOSURE, 95
single causes for disorders and the belief that these causes can be eliminated by treating the child as an individual" (p. 119). Although they
arrived at their conclusion from a very different literature, we believe
the same two myths exist in attempts within education to tailor different
treatments to categories of individuals (Brinker, 1990). Thus, we
believe it is inappropriate to offer an approach to intervention that
is specifically designed for infants exposed to cocaine, because that
would merely continue a deception that has too long provided a foundation for special education.
In the early 1970s, a national panel of experts was commissioned
to evaluate systems of classification of children in the United States.
The outcome of that effort was three volumes (Hobbs, 1975a, 1975b,
1975c) summarizing the conceptual coherence and practical utility of
the current classifications of children. The problems addressed in those
volumes continue to be current, with very little change in systems for
classifying children or using such classifications in the ensuing 20 years.
Three critical points from those discussions are particularly relevant
to the classification of children based on prenatal exposure to cocaine.
First, classification systems should be based on descriptions of
actual behavior of children that typifies their response to specific
situations and contexts. The classification, therefore, is about behavioral probabilities observed for a given child (rather than a population of children) and is clearly constrained by stated contextual features.
The classification is not and should not be applied to the child as a
whole nor extended beyond the documented behavioral differences
observed for that child within certain contexts. By attaching labels
to what the child does rather than more generally to who the child
is, the conceptual coherence of a classification can be maintained. The
alternative reviewed by Hobbs (1975a, 1975b, 1975c) is a system in
which there is as much behavioral variance within a category as
between categories. Labeling the child adds considerable excess baggage to our expectations about that child's probable behavior, baggage acquired from experience with other children who had the same
label. With regard to the conceptual coherence of a category of cocaineexposed children, this approach would lead us to separately characterize individuals, for example, in terms of their ability to regulate
state, focus attention on specific tasks, display affect, and respond to
and produce symbolic communication. The fact that they had been
exposed to cocaine in utero would be treated as separate demographic
information, along with their sex, age, or their mother's educational
background.
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96, TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION 11:4
Second, the goal for classifying the child's behavior observed in
specific contexts is to provide intervention shown to improve the behavior in those contexts. The linkage of treatment to classification should
be in terms of the particular behavior and its context. There should
be no expectation on logical grounds that the treatment would have
impact on other behavior or other contexts unless they are clearly
related to the class of behavior being treated and the class of treatment contexts targeted. For example, if mothers are taught to reduce
stimulation and slow the pace of their interactions to calm their infants
in distress, then we should evaluate such intervention in terms of the
infant's distress during interaction with the mother. It would be desirable if such techniques generalized such that the infant had better state
control in other situations (e.g., during peer interaction or assessment
sessions), but such generalization is not logically necessary. The range
of effects for an intervention targeted to a specific class of behavior
should be monitored empirically. However, programs should not
expect that mothers who improve their modulation of their infant's
state will improve their employment opportunities or that mothers who
have learned new job skills will improve their interactions with their
infants. To the extent that programs work simultaneously at several
levels of the ecology, they may have more success than they would
have working successively at each level.
Third, the recommendations to classify types of behavior contextually should lead to changes in administrative classification of services. The resulting classification of interventions will be more in terms
of what they do for what kinds of behavior rather than in terms of
what one calls the children within such programs. A heterogeneity of
causes and range of other performance abilities will therefore be
clustered within an intervention. The only common feature among
children or families within a specific intervention would be the similarity of behavior in response to a type of context. Such a recommendation
would result in a true individualization of interventions rather than
assignment of types of individuals to a standard cluster of treatment.
Transactional and Ecological Interventions. The notion of individual competence, which derives from the above perspective on classification, is that competence is relative to a context. Although
competence is typically used to denote something that inheres in the
individual, it more appropriately should denote both the abilities of
an individual and the situational demands placed on the individual
(Bricker, 1967;Hobbs, 1966,1975a; Hobbs et al., 1984). The notion
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PRENATAL COCAINE EXPOSURE, 97
that competence is a relational concept, requiring specification both
of the context and the entering characteristics of the individual, can
now be linked to a rapidly expanding framework known as living systems or dynamical systems theory (Barker, 1968; Bronfenbrenner,
1979; Gunnar & Thelen, 1989; Miller, 1978; Plas, 1986; Sameroff,
1983; Senge, 1990). Although the emerging systems theories have roots
in a variety of both the biological and social sciences, one common
feature is the necessity to analyze multiple components in dynamic
relation to each other. A working synthesis for early intervention from
the systems perspective is the three Rs proposed by Sameroff and Fiese
(1990). They propose grouping intervention strategies into three broad
categories: remediation, redefinition, and reeducation.
Remediation refers to direct efforts to change the child through
medical, therapeutic, or educational interventions. Most of the literature on early intervention and the evaluations of early intervention
have examined the nature and effectiveness of remediations. Whether
re is an appropriate prefix to mediation probably depends on how
early the intervention occurs in a child's life. Nevertheless, the concept clearly places the child as the focus of the intervention. Most traditional therapies, medical management through drugs, and educational
interventions designed to accomplish specific developmental objectives
would fall into the category of remediation. One of the shortcomings
of past early intervention efforts has been this child-only focus. Certainly, P.L. 99-457 formally acknowledges the need to extend interventions to include family participation and family needs in addition
to child needs. Discussion of such extensions to the family system will
be discussed in the context of redefinition and reeducation.
Remediations might be conceptualized developmentally in terms
of behavior elaboration regardless of whether an infant's developmental
delay is related to direct neurological effects of substances, environmental effects related to rearing by an addicted primary caretaker, or
a combination of environmental and other biological influences. Initially, interventions for the infant who is biologically unstable focus
on a limited number of developmental systems and the coordination
among them. The earliest coordinations require integration among
autonomic, motor, state regulative, and attentional interactive systems
(Als, 1986; Schneider et al., 1989). Later interventions focus on the
relations between sensory input and motor output ultimately leading
to a sensorimotor intelligence (Brinker, 1985; Brinker &C Lewis, 1982;
Dunst, 1981; Robinson & Robinson, 1978). Finally, in infancy, interventions must focus on elaboration of the information to which the
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98, TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION 11:4
infant is attending and development of a conventional symbolic code
to preserve acquired knowledge and to achieve social transactions with
an expanding social network (Bricker &c Carlson, 1980; Brinker &:
Bricker, 1980; Cole, Dale, & Mills, 1991; Kaiser & Warren, 1988;
McLean & Snyder-McLean, 1988).
Redefinition. The distinction between redefinition and reeducation corresponds to the distinction between altering the parents' perception of the child or behavior of the child and altering the parents'
response to a particular behavior. Actually, many reeducation efforts
will involve redefinition when, for example, parents are taught to interpret behavior in a different way and respond to it systematically. Hence,
our use of the term redefinition will focus on efforts to change perception of the child as a whole. For example, a child with a tracheotomy may be seen primarily as a technical challenge requiring medical
management and expertise that overshadows the parents' perception
of other aspects of the child and his behavior. Sameroff and Fiese (1990)
reviewed studies in which parents of failure-to-thrive infants regarded
the infants' crying as "bad" behavior rather than as communication
of hunger. If the infant prenatally exposed to cocaine is extremely
irritable, difficult to soothe, and reactive to contact with hypertonicity
and limb extension, the mother may interpret this as avoidance or
rejection. Similarly, if the infant exhibits very little affective response
to the mother's overtures, redefinition of these behaviors in terms of
biological or temperamental differences may reduce the mother's
feelings of rejection.
Reeducation. The empirical data on behavioral differences in the
neonatal and infancy period suggest that for children prenatally exposed
to cocaine, a minority may exhibit developmental differences similar to
those observed in other neurologically compromised infants. Many of
these behavioral differences require specific redefinition of the meaning
of behavior (e.g., crying) at different points in the child's development.
Similarly, parents may also require specific strategies of interaction
such as reducing their rate of social bids so that the child has time
to emit behaviors to which the parents can respond (Seifer, Clark, &
Sameroff, in press). Specific methods of teaching parents to enhance
language production have been demonstrated to remediate children's
expressive language delays (Whitehurst, Finchel, Caulfield, DeBaryshe,
& Valdez-Menchaca, 1989). Other specific efforts to teach parents
different methods to interact with a child with disabilities have been
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PRENATAL COCAINE EXPOSURE, 9 9
reported (Baker, 1989; Booth, Barnard, Mitchell, &C Spieker, 1987;
Filler & Bricker, 1976; Jeffree &c McConkey, 1976; Jeffree, McConkey, & Hewson, 1977; Newson & Hipgrave, 1982; Sparling et al.,
1991). Since these interventions have been successful at reducing behavioral differences in other developmentally delayed populations, they
may be effective if they can be accomplished within the ecology of
an infant prenatally exposed to cocaine.
Although many of the techniques to assist parents to change patterns of interaction with their infants may be applicable to mothers
addicted to cocaine, the consideration of different levels of the child's
ecology will expand the range of interventions beyond reeducation that
focuses primarily on the microsystem of parent and child (Bronfenbrenner, 1979). Specifically, Bronfenbrenner defines the mesosystem
as "a set of interrelations between two or more settings in which the
developing person becomes an active participant" (p. 209), and the
exosystem as "consisting of one or more settings that do not involve
the developing infant as an active participant but in which events occur
that affect or are affected by what happens in that setting" (p. 237).
Interventions with other microsystems such as the father-child,
grandmother-child, or aunt-child may be more promising than strategies focusing on the mother-child microsystem. Mesosystem interventions for children exposed to cocaine would include coordinating
redefinition and reeducation with critical individuals within the child's
ecology.
Exosystem interventions would focus on strengthening aspects
of the child's ecology that do not directly include the child but, rather,
influence the context in which the child is embedded. Clearly, treatment
of the mother's addiction simultaneously with or prior to reeducation
in terms of interactions with her infant would create a context in which
the mother would be better able to process the information provided.
In addition, it is quite likely that the priorities for the mother would
be primarily to maintain her addiction and survival if she had not
received treatment for addiction. Other relevant exosystem interventions that may be appropriate to some mothers of cocaine-exposed
infants would include training to establish or improve job skills, and
basic literacy training. Although these interventions may be regarded
by some as outside the scope of early intervention, for the infant
exposed to cocaine, the effect of interventions focused on the motherinfant dyad would undoubtedly be mediated by the mother's state and
overall priorities. An assumption implicit in the reeducation strategy
is that the recognition exists of a need for such education and a motiDownloaded from tec.sagepub.com at PENNSYLVANIA STATE UNIV on May 10, 2016
100, TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION 11:4
vation to learn. Although is is unwise to assume that any parents conceptualize their role as teacher, it is particularly foolish to assume such
an understanding for mothers addicted to cocaine (Vincent, Salisbury,
Strain, McCormick, &c Tessier, 1990).
The Concept of "Coke Babies" and Aspirations of Partnerships
with Parents. Review of the available literature on prenatal cocaine
exposure demonstrates that the causal mechanisms for neural damage
to the fetus are quite robust. However, the empirical literature does
not support an inevitable developmental consequence for infants
exposed in utero to cocaine. At best, developmental status of cocaineexposed infants considered as a group is in the low-normal range. Thus,
most infants so exposed appear to be developmentally normal, whereas
some show clear signs of neurological damage. The most impaired
of the cocaine-exposed infants do not seem to differ, behaviorally, from
other groups of neurologically impaired infants whose impairment
occurred during the neural growth spurt beginning at 28 weeks gestation. However, the infant exposed to cocaine in utero may have the
added disadvantage of a dysfunctional caregiving environment focused
more on the maintenance of the drug habit than on the infant. This
combination of biological vulnerability and caretaking inadequacy
increases the odds that a child will be a "caretaking casualty" (Sameroff
&C Chandler, 1975).
Nevertheless, the implication of the media coverage of "cocaine
baby" problems conveys a category of individuals rather than a
probabilistic statement about behavior. For example, Rist (1990)
stated:
The first wave of crack babies—born after crack cocaine
hit the streets in 1985—could be enrolling in your kindergarten classes next fall. . . . They're kids wired for 110 volts,
living in a 220-volt world. And according to available evidence, many of these children will not be easy to talk to—
let alone teach, (p. 19)
The underlying premise is that we as educators will be the victims of
these children who reach us in a biologically altered state, which
together with the environment provided by their addicted caretakers
will have created intractable problems. This is a different reality than
portrayed in the typical study of children exposed to cocaine in utero
where developmental or intelligence quotients average in the 90- to
100-point range (Beckwith & Howard, 1991) with behavior depressed
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PRENATAL COCAINE EXPOSURE, 101
in some and excited in others (Lester, 1991). Unfortunately, the article
by Rist (1990) was selected by the Illinois Council for Exceptional
Children for publication in their quarterly newsletter (Rist, 1991).
Hence, the exaggerations and insufficient qualification of statements
become the knowledge base regarding the "cocaine child" category.
Although exposure to cocaine in utero has increased over the last
decade, this risk, at least in the inner city, is embedded in such a large
network of other risks that it is scientifically unlikely that we will ever
understand its impact on the development of infants exposed. For some
time the status of families and their children in inner-city areas of the
United States has been deteriorating. This deterioration is not simply
liberal rhetoric, but is reflected in rates of crime, unemployment,
teenage pregnancy, infant mortality, rates of premature births, proportions of children born with low birth weights, proportions of children
with no homes, numbers of infants infected with the HIV virus, and
rates of child neglect and abuse (Baumeister, Dokecki, &: Kupstas,
1988; Baumeister, Kupstas, &c Klindworth, 1990; Furstenberg,
Brooks-Gunn, &: Morgan, 1987; Garbarino, 1990; Testa & Lawlor,
1980, 1985; Thompson, 1990; Wilson, 1987). In terms of infants,
many of the adversities of the inner city create a context in which the
probability is high that both biological vulnerabilities and caretaking
inadequacies will occur.
If the category of cocaine-exposed individuals is so poorly defined
that a small percentage demonstrate developmental differences or some
specific behavioral or learning problems, then it would behoove us
to follow Hobbs's (1975a) advice about classifying the problem rather
than the individual. The appropriate interventions will be designed
to address problems at various levels of the child's ecology. Each of
these interventions need not be qualified as "for cocaine babies" but
rather for the infant's and family's problems. Hence, the search for
a new kind of intervention presumes a greater generality and similarity
of behavior across situations and across development than has been
demonstrated for children exposed to cocaine in utero.
The long-term developmental problems of children who are raised
in disadvantaged environments can be prevented (Garber, 1988; Wasik,
Ramey, Bryant, & Sparling, 1990). The impact of low birth weight
on development can be ameliorated or prevented through early intervention (Infant Health and Development Program, 1990; Leviton,
Leviton, &c Leviton, 1990). So, too, we hope, the negative impact
of intrauterine cocaine exposure on the development of children can
be prevented or ameliorated. However, if we view the locus of the
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102, TOPICS I N EARLY C H I L D H O O D SPECIAL E D U C A T I O N 11:4
problem to be in the altered child, or in the dynamics of the family
that produced the child, then we may abdicate both personal and collective responsibility for the problem. At the very least, our approach
as partners and collaborators with parents will be seriously
compromised.
Punishment, Empowerment, Trust, and Negotiation
of Resources
Two approaches toward family involvement in intervention for
children exposed to cocaine in utero seem likely: a punishment
approach and an empowerment approach. The former approach may
predominate to the extent that the focus of the intervention is primarily
on remediation of the child's disabilities. The latter approach may
dominate to the extent that the child's problems are analyzed from
the perspective of dynamic ecological systems. We prefer and recommend the empowerment approach, but believe that early intervention
teams will require considerable restructuring to achieve this. Unfortunately, we believe that the punishment approach is more likely to
occur, given current resources and the predominantly implemented
models of early intervenion.
The continued use by the mother of cocaine, alcohol, or other
drugs after an infant has been exposed in utero implies a continuing
parental irresponsibility. Such a mother increases the risk that early
interventionists, social workers, teachers, or physicians will report to
appropriate authorities (as they are legally mandated) what they believe
to be instances of child abuse or neglect. Failure to adhere to a recommended regimen of treatment could be construed as neglect. This legal
situation exacerbates an inequality of power that is implicit in any
helper-client relationship (Sigel, 1983; Skinner, 1978). Unfortunately,
the child welfare systems in large urban areas provide a very small
safety net for children at risk for neglect or abuse from their immediate
family. Recent litigation has characterized Illinois's child welfare system as so ineffective and frequently harmful as to be a serious risk
to the child. Thus, the positive benefits of referral must be weighed
against the probabilities of harm from the child care arrangement
provided by the system. This weighting has led to the court recommendation that children should be removed from their families only
in cases in which there is strong evidence that imminent physical harm
is likely. Often the search for successful placement can involve transiDownloaded from tec.sagepub.com at PENNSYLVANIA STATE UNIV on May 10, 2016
PRENATAL COCAINE EXPOSURE, 103
tions through many foster care arrangements in the first few years of
life. Since presence of cocaine in an infant's system can constitute
de facto evidence for abuse, children can be introduced into the child
welfare system at their birth. However, a growing number of "boarder
babies" are so referred or are abandoned such that they remain in hospitals for several of their first months of life.
The goal of empowering families leads early interventionists to
bolster resources within the child's natural ecology to enable that ecology to successfully address the child's problems. The addicted woman's
priorities may not include the child's needs, and many of the resources
supporting the mother can be undermined by her pursuit of resources
to support her addiction. In such circumstances it is unrealistic to
attempt to ameliorate or prevent the child's developmental disabilities
through improvements in the mother's interactions with and caregiving
to the child. The empowerment effort would require assistance to the
mother to overcome her addiction while seeking other caregiving
resources for the child within the healthiest aspects of the family ecology
or through an alternative ecology such as a full-time early intervention
program for the child.
Establishing trust with an addicted mother will be a critical aspect
of whether empowerment and family recovery are possible. Although
removing the child from the family ecology may seem the most feasible
short-term solution for the child, clear developmental risks are present
if the child is placed in a series of short-term temporary care arrangements in which the foster parents are unwilling to involve the child
in an early intervention/prevention program. Employment of professional and paraprofessional staff w h o share characteristics with the
family, especially race and experience of socioeconomic adversity,
broadens the avenues for establishing trust. Inner-city early intervention
programs should consider such staffing patterns as equally critical to
success as the distribution of professional expertise on the intervention
team. Regardless of the professional competence of early interventionists, occupational therapists, physical therapists, speech pathologists, social workers, child psychologists, or nurses, their effectiveness
will be constrained by their access to the infant and family. Without
family and infant participation, no level of expertise will be sufficient
either to ameliorate or prevent developmental disabilities. N e w models
of teamwork are required to integrate staff whose expertise is narrowly
focused on critical aspects of child development along with staff w h o
may possess "people skills" and are better culturally attuned, but w h o
do not possess knowledge of child development or intervention techDownloaded from tec.sagepub.com at PENNSYLVANIA STATE UNIV on May 10, 2016
104, TOPICS IN EARLY CHILDHOOD SPECIAL EDUCATION 11:4
niques. Both the goals of early intervention and the criteria for professional practice will require ongoing negotiation within such an early
intervention staff. Few of us have been prepared for or exposed to
the need for such negotiation.
In addition to building the culturally knowledgeable staff described
above, serious efforts should be made to include on the intervention
team someone with broad political connections across urban bureaucracies. Critical spheres of influence for such a person should include
public housing, transportation, and the major churches serving the
community. Without access to public policymakers, it is highly unlikely
that an early intervention program will be successful in empowering
families to obtain resources that are nonexistent or extremely scarce
in their community.
We realize these are rather unorthodox recommendations for early
intervention, but we believe such team-building efforts are necessary
to include substance abusing families whose infants are victims of their
habits. Our own serious attempts to implement such early intervention
programs have resulted in frequent failure and sporadic limited success.
It is difficult to acknowledge such realities, especially in our culture.
Yet it is foolhardy to predict unqualified success with some of the most
disenfranchised and compromised families in our country. Jobs, detoxification, addiction treatment and recovery, housing outside the sphere
of the drug culture, adequate nutrition, personal safety, literacy, and
skills that are marketable are some of the major needs facing families
in the inner cities. Early intervention, however much expanded by
P.L. 99-457, is not likely to impact on children when these family
priorities are ignored. We should all feel ashamed if the early intervention partnerships lead families into increased risks for being judged
incompetent, having their children removed into a failing child welfare system, or fix cultural expectations for the future of a new category
of failing child. The evidence does not support our absolution through
a belief in a new category: children of cocaine. They are children of
the United States.
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