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Developmental outcome for preschoolers prenatally exposed to crack cocaine

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Developmental outcome for preschoolers prenatally exposed to crack cocaine behavioral and adaptive sequelae
Alternate title:
Developmental outcome for toddlers prenatally exposed to crack cocaine behavioral and adaptive sequelae
Alternate title:
Behavioral and adaptive sequelae
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Holler, Karen Anne
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ix, 142 leaves : ; 29 cm.

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Subjects / Keywords:
Alcohols ( jstor )
Child psychology ( jstor )
Cocaine ( jstor )
Fetal cocaine exposure ( jstor )
Hyperactivity ( jstor )
Infants ( jstor )
Mathematical dependent variables ( jstor )
Normativity ( jstor )
Parents ( jstor )
Socialization ( jstor )
Child Behavior ( mesh )
Child Behavior Disorders -- chemically induced ( mesh )
Child Development ( mesh )
Crack Cocaine -- adverse effects ( mesh )
Department of Clinical and Health Psychology thesis Ph.D ( mesh )
Dissertations, Academic -- College of Health Related Professions -- Department of Clinical and Health Psychology -- UF ( mesh )
Prenatal Exposure Delayed Effects -- Child ( mesh )
Prenatal Exposure Delayed Effects -- Infant ( mesh )
Research ( mesh )
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bibliography ( marcgt )
non-fiction ( marcgt )

Notes

Thesis:
Thesis (Ph.D.)--University of Florida, 1996.
Bibliography:
Bibliography: leaves 131-141.
General Note:
Typescript.
General Note:
Vita.
Statement of Responsibility:
by Karen Anne Holler.

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Copyright [name of dissertation author]. Permission granted to the University of Florida to digitize, archive and distribute this item for non-profit research and educational purposes. Any reuse of this item in excess of fair use or other copyright exemptions requires permission of the copyright holder.
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AMA7840 ( NOTIS )

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DEVELOPMENTAL OUTCOME FOR PRESCHOOLERS PRENATALLY EXPOSED TO
CRACK COCAINE: BEHAVIORAL AND ADAPTIVE SEQUELAE






By

KAREN ANNE HOLLER



















A DISSERTATION PRESENTED TO THE GRADUATE SCHOOL
OF THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT
OF THE REQUIREMENTS FOR THE DEGREE OF
DOCTOR OF PHILOSOPHY

UNIVERSITY OF FLORIDA

1996











ACKNOWLEDGMENTS


I would like to thank my cochairs, Eileen B. Fennell,

Ph.D., ABPP, and Fonda D. Eyler, Ph.D., for their support and

guidance throughout this project. The breadth of their

combined expertise in the world of child psychology and

development is substantial. I would also like to thank my

committee members, Marylou Behnke, M.D., Michael Conlon,

Ph.D., Steven Boggs, Ph.D., and Sheila Eyberg, Ph.D., for

their advice and practicality in the management of the

research.

I would particularly like to thank Drs. Eyler, Behnke, and

Conlon for making this project possible by generously allowing

me to in participate on their research grant. My association

with their group was among the best of my graduate school

experiences. I would also like to thank Kathie Wobie, M.A.

and Lisa Maag for the all the help and friendship they have

offered before and during the course of this project. My

thanks are also extended to Annie, Kristen, Lorraine, Bruce,

Bridget, Jack and others who, at various times over the past

five years, have been the mainstay of the grant's success.









Last but not least, I would like to thank my parents for

their constant encouragement and support, and Tiffany,

Samantha, and Ben, who make the rest of my life better.

This research was supported in part by NIDA grant

R01DA05854 and GCRC grant M01RR00082.













TABLE OF CONTENTS

page

ACKNOWLEDGMENTS............. ...... .................... ii

LIST OF TABLES...................................... vi

ABSTRACT ................. .................. .......... viii

INTRODUCTION ......................................... 1

LITERATURE REVIEW................ .... .............. 8

Physiological and Behavioral Effects............. 8
Summary of Literature Review.................... 32

PURPOSE OF RESEARCH .................................. 35

MATERIALS AND METHODS.................................... 37

Subjects .......................................... 37
Parent Report Measures........................... 43
Behavioral Observation Measures................. 45
Procedures..................................... 47

ANALYSES .............................................. 49

Descriptive Analyses.................. ....... 49
Hypothesis 1..................................... 49
Hypothesis 2..................................... 51
Hypothesis 3..................................... 51
Hypothesis 4..................................... 51
Hypothesis 5.................................... 52

RESULTS.............................................. 53

Descriptive Analyses............................. 53
Initial Between Groups Analyses.................. 57
Initial Correlations............................ 61
Hypothesis 1..................................... 65








Hypothesis 2.................................... 70
Hypothesis 3..................................... 72
Hypothesis 4.................................... 74
Hypothesis 5..................................... 76

DISCUSSION........................................... 108

Background..................................... 108
Comparison to Norms............................. 110
Between Groups Comparisons...................... 116
Covariate Findings.............................. 122
Strengths and Weaknesses....................... 126
Suggestions for Further Study................... 129
Conclusion....................................... 130

REFERENCES......... .................... ........... 131

BIOGRAPHICAL SKETCH.................................. 142













LIST OF TABLES


Table page

1 Demographic Characteristics of the Total
Sample............................. ........... 79

2 Covariate Characteristics of the Total
Sample.......................................... 80

3 Reliability of Video Coding of Selected
DPICS-II Categories in the Child-Directed
Interaction................................... 81

4 Reliability of Video Coding of Selected
DPICS-II Categories in the Parent-
Directed Interaction ........................... 82

5 Between Group Differences Defined by
Maternal Depression............................ 83

6 Between Group Differences Defined by Home
Inventory..................................... 85

7 Between Group Differences Defined by
Foster Care Status............................ 87

8 Between Group Differences Defined by
Gender......................................... 89

9 Between Group Differences Defined by
Alcohol Use.................................... 91

10 Correlations between Covariates and
Behavioral and Adaptive Variables.............. 93

11 Correlations between Covariates................ 95

12 Correlations between Dependent Subscales........ 96








13 Means and Standard Deviations of Tested
Sample with Age-Based Norms Parent
Report.......................................... 98

14 Means and Standard Deviations of Tested
Sample with Normative Sample DPICS-II
Child Directed Interaction..................... 99

15 Means and Standard Deviations of Tested
Sample with Normative Sample DPICS-II
Parent Directed Interaction.................... 100

16 Dependent Variables Means and Standard
Deviations for Exposed and Nonexposed
Children for the Total Sample.................. 101

17 MANCOVA with Covariates Child Gender and
Maternal Depression and Dependent
Variables from the Connors..................... 104

18 MANOVA with Dependent Variables from the
ECBI............................................ 105

19 MANOVA with Dependent Variables from the
Vineland........................................ 106

20 MANOVA with Dependent Variables from the
DPICS-II Derived Variables.................. 107










Abstract of the Dissertation Presented to the Graduate
School of the University of Florida in Partial Fulfillment
of the Requirements for the Degree of Doctor of Philosophy

DEVELOPMENTAL OUTCOME FOR TODDLERS PRENATALLY EXPOSED TO
CRACK COCAINE: BEHAVIORAL AND ADAPTIVE SEQUELAE

By

Karen Anne Holler

August, 1996

Chairpersons: Eileen B. Fennell, Ph.D., ABPP
Fonda D. Eyler, Ph.D.
Major Department: Clinical and Health Psychology

Early studies indicated that infants exposed prenatally

to cocaine and cocaine derivatives may be at risk for

increased spontaneous abortions, fetal death, preterm labor,

abruptio placentae, decreased length, weight, and head

circumference, congenital malformations, and deviant

neurobehavior. However, very little long-term followup has

been done to assess the functioning of these children as they

mature. The present study compared two groups of three-year

old preschoolers who were a) exposed in utero to crack, or b)

not exposed in utero to crack. Information about child

behavior and adaptive functioning was collected by primary

caregiver report using the Vineland Adaptive Behavior Scales

Survey Form, the Connors Parent Rating Scale, and the Eyberg








Child Behavior Inventory. Child behavior was also assessed by

direct objective observation using the Dyadic Parent-Child

Interaction Coding System-II. Administered instruments

intended to determine whether a) scores for the total sample

conformed to norms provided by psychological measures, and b)

whether behavioral or adaptive deficits were present in the

crack-exposed preschoolers when compared to same-aged

nonexposed peers. Results showed significant differences

between the total study cohort which included exposed and

nonexposed children and normative groups on which many

standardized psychological measures are based. For example,

the total sample was more likely to display elevations in

conduct problems, learning problems, hyperactivity, and

impulsivity compared to normative groups. Second, at three

years of age, no differences were found between a prenatally

crack-exposed cohort on parent and objective measures of

behavior and adaptive functioning when compared with

nonexposed matched peers. Thus elevations on disordered

behavior compared to normative groups cannot be attributed to

exposure status. Implications of findings and possible

explanation for nonsignificant between groups findings are

discussed.













INTRODUCTION

Cocaine is one of the most popular illicit drugs used in

the United States. Approximately 30 million Americans have

tried cocaine at least once and as many as five million use

cocaine on a regular basis (Abelson & Miller, 1985). The two

common forms of illicit cocaine are cocaine hydrocholoride

(HC1) in a powder form, and 'crack,' a highly purified

alkaloidal base also known as 'freebase.'

Cocaine (methylbenzoylecgonine) is a central nervous

system (CNS) stimulant that works in part by increasing the

activation of the neurotransmitter dopamine in the mesolimbic

and/or mesocortical pathways. Increased activation results in

a stimulant induced reward or the 'euphoria' commonly

experienced by cocaine users (Goeders & Smith, 1983; Wise,

1984). Neurotransmitter reuptake is simultaneously reduced in

the cerebral cortex, hypothalamus, and cerebellum resulting in

the hyperaroused state also typical of cocaine intoxication

(Ryan, Ehrlich, & Finnegan, 1987). Cocaine taken intranasally

(or 'snorted') causes vasoconstriction of the nasal mucous

membranes which reduces its own absorption. Subsequently, the

plasma drug concentration rises relatively slowly for











insufflatted cocaine. Cocaine in powder form is also

frequently diluted or cut before sale further limiting plasma

drug concentrations in the body.

Crack on the other hand is almost 70% pure cocaine, made

by precipitating alkaloidal cocaine from an aqueous solution

of cocaine HC1. Unlike the powder form of cocaine, crack is

not destroyed by moderate heating and vaporizes at

temperatures over 98 degrees celcius (Medical Letter, 1986).

Crack, named for the popping sound it makes when heating, may

be smoked via freebasing with a base pipe or rolled with

tobacco in a cigarette. Crack may also be injected. Smoking

crack delivers large quantities of cocaine directly to the

vascular bed of the lungs. The plasma drug concentration in

this instance is substantially higher than for insufflatted

cocaine and rises almost instantaneously producing an effect

more intense than that experienced with intravenous injection

(Medical Letter, 1986).

Crack when smoked reaches the brain in approximately

eight seconds producing an intense, immediate euphoria

(Howard, Mofenson, & Caraccio, 1987). These euphoric effects

are short lived, lasting approximately 45 minutes followed by

a severe crash (dysphoria) during which the user becomes

depressed and agitated (Howard, 1989). This cycle is








3

reportedly shorter and more intense when smoking crack than

for either intranasally or intravenously administered cocaine.

Users may feel a greater compulsion to repeat the experience

when smoking crack both for its magnified euphoric effects as

well to avoid the subsequent crash (Howard et al., 1987).

Binges, characterized by frequent readministration of the

drug, reportedly may last 12 hours but may go on for several

days (Gawin & Kleber, 1985). In addition, the price of crack

continues to decrease, making it accessible to people of all

socioeconomic levels. A 'rock' may cost as little as five to

ten dollars (Howard, 1989). Combined, these factors

precipitate abuse.

While it is uncertain whether cocaine is physically

addictive, it clearly has powerful psychological effects. It

is estimated that five times as many people are addicted to

cocaine than to heroin (Grinspoon & Balkalar, 1980). Indeed,

treatment for cocaine use, and crack use in particular, is

escalating while age of first use appears to be dropping

(Adams, Gfroerer, Rouse, & Kosel, 1986). In reaction to

epidemic use, researchers are beginning to describe not only

the immediate effects of cocaine intoxication but also to

contemplate the long-term implications of using what had










initially been considered a 'safe' stimulant (Schnoll,

Karrigan, Kitchen, Daghestani, & Hansen, 1985; Siegel, 1985).

Associated with the use of cocaine are a number of

behavioral changes as well as substantial physical risk.

Behavioral effects that have been described in adult users

include impulsivity, disinhibition, repetitive actions,

anxiety, psychomotor activation and a loss of appetite which

can result in malnutrition (Howard et al., 1987; Levine,

Washington, Jefferson, Kieran, Moen, Feit, & Welch, 1987;

Medical Letter, 1986). Severe and toxic physiological effects

have been described in the literature. Hypertension,

tachycardia, ventricular arrhythmias, seizures, loss of

consciousness, stroke, and myocardial infarctions are

increasingly attributed to cocaine use. Even deaths due to

respiratory and cardiac arrest have been reported (Howard et

al., 1987; Levine et al., 1987; Medical Letter, 1986).

Further, there are indications that the inhibitory

receptors of dopamine neurons become supersensitive as an

adaptation to chronic activation of the reward pathways which

occurs with stimulant use (Gawin & Kelber, 1986). Thus, there

is some evidence that long-term cocaine use may lead to

permanent neurophysiological changes in the brain that impact

on mood states and the user's experience of pleasure. Such










findings are mirrored in clinical observations of protracted

anhedonia and anergia in some cocaine users (Gawin & Kleber,

1986). Generally, these symptoms resolve over time. However,

there are sporadic reports of high dose users with chronic

anhedonia, anergia and a craving for stimulants that does not

remit (Ellinwood, 1974; Schuster & Fischman, 1985).

Pregnant women are not immune to either the pleasurable

effects of crack or to the physiological consequences of use.

Over the last several years researchers have turned their

attention to the possible impact of in utero exposure to

cocaine and cocaine derivatives on the neonate. This interest

has accelerated due partially to shifting attitudes towards

drug use in general as well as justified alarm at the recent

explosion in crack use (Grinspoon & Balkalar, 1980). Still,

the toxic effects of cocaine use are only beginning to be

understood, and focus has been almost entirely on adult users.

Early reports concerning infant outcomes of in utero exposure

to cocaine has been limited, often anecdotal, contradictory

and predominantly focused on medical outcomes (Ryan et al.,

1987) Thus, while reports in the popular media of antisocial

or hyperactive toddlers created by in utero exposure to

cocaine make sensational copy, they are distinctly premature.











Research, medical or otherwise, on preschoolers exposed to

cocaine in utero is very limited.

The absence of literature notwithstanding, concern for a

generation of children exposed to cocaine is certainly

warranted. One survey suggested that 10% of women may use

cocaine at least once during pregnancy, and 50% of these use

other drugs in addition to cocaine (Howard et al., 1987).

Cocaine is highly water and lipid soluble and passes through

the placentae by simple diffusion. Cocaine may concentrate in

the fetus because fetal blood has a lower pH. In addition,

plasma cholinesterase, which is necessary to metabolize

cocaine, is less active in the fetus and in pregnant women

(Bingol, Fuchs, Diaz, Stone, & Gromisch, 1987). Conceivably,

even small doses of cocaine could have negative consequences

on a developmentally vulnerable embryo and fetus. Although

results in the literature are equivocal, cocaine has been

implicated in a number of negative outcomes including

spontaneous abortions, fetal death, preterm labor, precipitous

labor, abruptio placentae, fetal distress, fetal meconium

staining and other conditions which qualify the newborn for

high risk status (Chasnoff, Burns, Schnoll, & Burns, 1985; Oro

& Dixon, 1987; Ryan et al., 1987).








7

Exposed infants have also been shown to exhibit decreased

length, weight and head circumference, higher rates of

congenital malformations, deviant neurobehavior, rapid shifts

between irritability and lethargy, and be at increased risk

for Sudden Infant Death Syndrome (SIDS) although many of these

outcomes remain controversial (Bingol et al., 1987; Chasnoff,

1989; Chasnoff, Burns, & Burns, 1987; Oro & Dixon, 1987).

However, negative findings are not consistently found in well

controlled studies. Reports of investigations into the

behavioral and long-term developmental outcome of cocaine-

exposed infants remain unclear.













LITERATURE REVIEW


Physiological and Behavioral Effects

The physiological impact of in utero cocaine exposure has

been extensively modelled in animal investigations. The

underlying assumption in such studies is that cocaine may

affect development in two principle ways: 1) by disturbing

dopaminergic functioning in the developing fetus, and/or 2)

via hypoxic effects.

The dopamine system is implicated in the modulation of

reward systems, reinforcement, sensorimotor integration, and

environmental responding. Cocaine acts as an inhibitor of

dopamine reuptake presynaptically, serving to increase the

amount of amines in the synaptic cleft. There is evidence

that repeated cocaine administration decreases the amount of

dopamine synthesis presynaptically and increases the number of

dopamine receptors postsynaptically (Fung, Reed, & Lau, 1989).

The dopaminergic system is developing in the third trimester

of human fetal development and is functional and capable of

mediating behaviors in rat fetuses towards the end of their

gestational period. Moody, Robison, Spear, and Smotherman,











(1993) found that administration of cocaine to rat dams

resulted in increases in fetal activity which they

subsequently considered a reflection of altered CNS

development.

Subsequent investigations found that prenatal exposure to

cocaine in late gestation results in a decrease in the number

of spontaneously active midbrain dopaminergic cells in adult

rats, whereas rats exposed to cocaine only in adulthood showed

an increase in the number of spontaneously active dopaminergic

cells (Minabe, Ashby, Heyser, Spear, & Wang, 1992). The

decrease of midbrain dopamine activity in adult rats exposed

prenatally to cocaine has been used to explain early findings

of irritability and decreased interactive behaviors in human

infants. These reports suggest, not surprisingly, that

prenatal cocaine exposure may be toxic to the fetus or impact

negatively on the developing neuronal system in a manner that

does not necessarily parallel consequences of adult exposure.

Studying cell development in brain regions, Seidler and

Slotkin (1993) compared rat pups exposed in utero to cocaine

during late gestation to a nonexposed comparison group. They

found retarded maternal weight gain but no effect on pup body

or brain region weights. DNA content was also largely

unaffected. Although postnatal cell growth was reduced in the










forebrain, the magnitude of the reduction was small when

compared to the impact of other drugs such as the hypoxic or

ischemic effects of nicotine. Seidler and Slotkin (1992)

concluded that functional deficits attributable to fetal

cocaine exposure probably result from actions directed toward

specific cell or synaptic populations as opposed to global

effects on cell development.

In another investigation, Seidler and Slotkin (1992)

found somewhat conflicting results when studying the effect of

fetal cocaine exposure on rats given 30 mg/kg daily from

gestational days 2 to 20. As a toxic referent, a dose of

approximately 80 to 100 mg/kg of cocaine is generally fatal in

adult rats. The exposed group showed minor differences from

controls in body and brain region weights and in levels of

norepinephrine. However, investigators found marked

noradrenergic hyperactivity as assessed by noradrenergic

turnover, which they attributed to the effects of

glucocorticoids and hypoxia on noradrenergic cell

differentiation. These results suggest that hypoxia rather

than dopaminergic disruption may be the more critical result

of cocaine exposure in utero.

Animals prenatally exposed to cocaine generally show

differential physiologic responses to hypoxia compared to










controls. Weese-Mayer and Barkov (1993) studied the responses

of rabbit pups to hypoxia following exposure to 30 mg/kg of

cocaine from days seven to 15 gestation. They found the

cocaine-exposed pups had more significant oxyhemoglobin

desaturation and pulse deceleration during exposure to severe

hypoxia than controls, suggesting that cocaine exposure in

utero may reduce the normal defense mechanisms for metabolic

adjustment to low oxygen.

These results supported findings from an earlier study by

Weese-Mayer, Klemka-Walden, Barkov, and Gingras (1992) who

also found that, while baseline ventilation did not differ

significantly among study groups, cocaine-exposed pups had a

deficient ventilatory response during an hypoxic challenge.

Weese-Mayer et al. (1992) argued that these findings may

represent perturbed maturation of respiratory control. Other

researchers have found similar results which suggest that

infants exposed to cocaine have an impaired repertoire of

protective responses to hypoxia and hypercapnia during sleep

which may play a role in increased risk for SIDS (Ward,

Bautista, Woo, Chang, Schuetx, Wachsman, Sehgal, & Bean,

1992).

Similarly, Woods, Plessinger, and Clark (1987) found that

pregnant ewes exposed to cocaine produced increases in










maternal blood pressure and decreases in uterine blood flow

accompanied by fetal hypoxemia, hypertension, and tachycardia.

Cocaine administration to the fetus directly resulted in

relatively smaller increases in fetal heart rate and blood

pressure than those observed following maternal

administration, and no changes in fetal arterial blood gas

values. These results were interpreted to indicate that

maternal administration of cocaine alters fetal oxygenation by

reducing uterine blood flow and impairing oxygen transfer to

the fetus and that resulting fetal cardiovascular changes may

reflect fetal hypoxemia, increased fetal levels of cocaine, or

a combination of these events.

Birth outcome studies with animals demonstrate a range of

postnatal results following cocaine exposure in utero.

Henderson and McMillen (1990) studied postnatal development in

rats exposed to cocaine daily in utero. The cocaine-exposed

group weighed less, had more stillbirths, and more birth

defects when compared to a nonexposed group. In addition,

cocaine-exposed pups had delayed righting reflexes although no

delay was noted in opening their eyes, both indices of

developmental integrity. Their findings led Henderson and

McMillen (1990) to conclude that cocaine exposure in utero










impacted neonatal outcome and long term development in the

rats due to disruption of the dopamine system.

In a study designed to mimic moderate cocaine use by

humans during pregnancy, Fung et al. (1989) examined the

neurobehavioral responses and striatal dopaminergic system in

cocaine-exposed newborn rats. No change in length of

gestation, litter size, birth weight and length of pups, and

the ratio of male to female pups was noted. At 14 days old,

exposed and nonexposed pups showed similar locomotor

performance in righting reflex, position reflex and negative

geotaxic tests. Results demonstrated that prenatal exposure

to cocaine did not alter the development of motor coordination

suggesting no significant impact on the developing

dopaminergic and striatal systems with moderate exposure.

Spear, Kirstein, Bell, Yoottanasumpun, Greenbaum, O'Shea,

Hoffmann, and Spear (1989) also studied the early development

of cocaine-exposed rats. They found that when pups were

exposed a relatively large dose of cocaine daily (40 mg/kg)

late in gestation, there were no differences in maternal

weight gain, duration of pregnancy, or number of live

male/female pups per litter were found. Like Fung et al.

(1989), they found no differences in offspring body weights at

birth and weaning, physical maturation and reflex development.










However, cocaine-exposed pups were deficient in learning and

odor/milk association and showed enhanced locomotion. The

researchers concluded that prenatal cocaine exposure impacts

behavioral and cognitive function during the early postnatal

period even in the absence of overt physiological changes.

A review of studies of postnatal integrity of animals

exposed to moderate amounts of maternal cocaine administration

reveals some consistencies. Generally studies have found no

differences in dam weight gain, litter size or weight, or

early postnatal behavioral tests (Smith, Mattran, Kurkjian,

and Kurtz, 1989; Hutchings, Fico, & Dow-Edwards, 1989; Spear,

Kirstein, & Frambes, 1989). However, drug effects have been

noted on the level of locomotion, exploratory behavior, tail

flick, footshock sensitivity and some learning and/or

retention tasks. Arguments explaining significant results are

generally dependent on altered neurodevelopment during

critical prenatal periods, poor maternal nutrition, and

hypoxia.

While animal models for cocaine exposure in utero may be

useful, there are several difficulties in extrapolating the

effects found in animals to humans. In addition to the

obvious problem of equating human and rat, sheep, or rabbit

neurodevelopment, results of animal studies also tend to vary










by species or strain. Furthermore, they appear to be heavily

dose-dependent including some studies using extremely high

doses of cocaine, and demonstrate that impact appears

contingent upon the gestational period of drug administration.

Clearly fetal exposure to cocaine is not a benign perinatal

event. But the deficiencies noted in the animal literature

such as locomotor changes or alterations in learning and

"cognition" are frequently difficult to demonstrate in

parallel forms in human infants. In addition, it is unclear

whether such alterations in functioning found in the animal

literature are transient or long-term.

Preliminary attempts have been made to study human

infants in terms of the physiological impact of cocaine

exposure in utero. For example, Link, Weese-Mayer, and Byrd

(1991) performed magnetic resonance imagery (MRIs) on infants

exposed to cocaine prenatally to determine the presence of

hypoxic injuries. In all 21 infants studied, at a mean age of

3.6 years, they found myelination was appropriate compared to

age-matched norms; brain and brainstem anatomy were also

normal with no evidence of infarct or hemorrhage. Link et al.

(1991) concluded that negative findings could be due to the

small sample size, limited maternal use, or the possibility

that cocaine use without concomitant use of other illicit










substances may not be as significant as some studies have

suggested.

Doberczak, Shanzer, Senie, and Kandall (1988) likewise

examined 39 infants with in utero exposure to cocaine for

neurologic and electroencephalographic (EEG) abnormalities.

During the first week of life, 17 of the infants had abnormal

EEGs and abnormal behavior characterized by irritability. By

the second week of life, nine of the 17 EEGs remained

abnormal. By three to 12 months of age, however, findings had

normalized, suggesting effects attributed to cocaine may be

transient. There was no control group utilized in this study

and it is unclear whether examiners were blinded to drug

status. Despite these methodological flaws, it may be

significant that EEG findings could not be predicted by

neurologic dysfunction or perinatal variables, and ultimately,

findings normalized for all infants.

Preliminary study of human infants indicates that cocaine

exposure results in worse outcomes than nonexposed infants in

terms of birth weight, length and head circumference,

spontaneous abortion, fetal death, and sudden infant death

syndrome (SID) (Ryan et al., 1987). In an early study, Oro

and Dixon (1987) examined neonatal growth, behavior and

physiologic organization in 104 mother/infant pairs including










a cocaine and methamphetamine group, a narcotic group and a

drug free group. Findings in this study were plentiful and

dramatic. The researchers found significantly lower birth

weight, length, occipitofrontal head circumference (OFC), and

gestational ages in both the cocaine/methamphetamine and

narcotics groups compared to the illicit drug free group.

They also found significantly higher incidence of prematurity,

intrauterine growth retardation, fetal distress, and

complications during the neonatal period in both the

cocaine/methamphetamine and narcotics groups compared to the

illicit drug free group.

Significant increases in neurologic and physiologic

problems in the cocaine/methamphetamine group were also

reported including (in order of decreasing significance)

abnormal sleep patterns, tremors, poor feeding, hypertonia,

vomiting, sneezing, high pitched crying, frantic fist sucking,

tachypnea, loose stools, fever, yawning, hyperreflexia, and

excoriation. Physician and nurse descriptions of the behavior

of these exposed infants included disorganization, poor visual

processing of faces and objects, random sucking and long dull-

alert periods with eyes open. Decreased spontaneous activity

and fixed catatonic postures were seen in four of the

cocaine/methamphetamine group. Even accounting for various








18

maternal factors, cocaine/ methamphetamine and narcotic use

still made significant independent and negative contributions

to gestational age, birth weight, length and OFC (Oro & Dixon,

1987).

The results of this study and of many early studies like

it appeared to confirm the clinicians' worse fears regarding

cocaine exposure in utero. However, a critical evaluation of

the methodology mitigates the findings to a degree. For

example, in the above study, the combined effects of certain

drugs (in this case methamphetamine and cocaine) may have had

some unique or synergistic properties not found when the same

drugs are taken separately. Further, it is unclear whether

evaluators in this study were blinded to the drug group

affiliation of the babies being studied. Confounds and

researcher bias have been frequently apparent in this body of

literature on prenatal cocaine exposure, especially in earlier

reports.

In another study concerned with the teratogenic effects

of cocaine, Bingol et al. (1987) compared a polydrug, a

cocaine only, and a no illicit drug control group. The

cocaine group was comprised of 60% intranasal, 30% free base

inhalation, and 10% intravenous users. While no statistical

differences were reported in the spontaneous abortion rates










among the three groups, stillbirth rates were significantly

higher in the cocaine only group compared to the no drug

group. Also, there were significantly more congenital

malformations in the cocaine only group compared to both

contrast groups. Five of fifty infants in the cocaine only

group had major congenital malformations including

exencephaly, intraparietal encephalocele, and parietal bone

defects. Although complications occurred in women after all

three routes of cocaine administration, the sequelae were more

frequent in those who smoked crack regularly or injected it

intravenously. These findings are dramatic and suggest that

cocaine is a powerful teratogen to the developing fetus.

However, this study was conducted in a large inner city

hospital where the confound of polydrug use was common among

the cocaine-using group, and it is unclear whether examiners

were blinded as to the drug status of the infants.

Little, Snell, Klein, and Gilstrap (1989) also examined

perinatal outcome following maternal cocaine use during

pregnancy in 53 exposed infants compared to a 100 infant

control group. Cocaine use in their study was associated with

preterm labor; birth complications including meconium

staining, tachycardia, and lower birth weight; and an excess

of congenital cardiac anomalies. There were several








20

methodological shortcomings in this study which may impact the

reliability of the authors' conclusions. Mothers were self

reported drug users whose neonates were automatically referred

to a high risk nursery for observation of withdrawal symptoms

compromising blind evaluations. Furthermore, the cocaine-

using mothers were generally older, more likely to be black,

and use tobacco and other illicit drugs when compared to

controls. Controls were not matched to drug using mothers,

and it is unclear whether other risk variables were controlled

adequately in the analysis.

In a subsequent study, Little and Snell (1991) studied

the pattern of brain growth in cocaine-exposed newborn infants

where brain growth was defined as head circumference in

addition to other growth variables including birth weight,

length, and gestational age. Groups were cocaine-exposed

infants without alcohol exposure, alcohol but no cocaine

exposure, and neither cocaine nor alcohol exposure. Results

showed significant differences in head size between unexposed

and cocaine-exposed infants. Head circumference was reduced

proportionately more than birth weight in cocaine-exposed

infants. Cocaine and alcohol exposed groups were not

statistically different in terms of head size. Little and

Snell (1991) concluded that cocaine exposure results in a








21

pattern of growth retardation similar to alcohol exposure and

that this retardation may be asymmetrical with head size more

involved. However, mothers in the cocaine group tended to be

polydrug users, control groups were not matched, nor were

statistical controls used for possible confounding maternal

variables.

Chiriboga, Bateman, Brust, and Hauser (1992) reported

that, compared to a no illicit drug exposure control group (n

= 16), cocaine-exposed infants (n = 14) had significantly

lower birth weights, lengths and head circumferences.

Neurologic abnormalities were also associated with exposure

and included hypertonia, plantar extension, tremors and gaze

abnormalities. These findings led researchers to conclude

that prenatal cocaine exposure results in tone and movement

abnormalities in newborn infants. Strengths of this research

were the blinded status of the neurologic examiners and the

fact that toxicology screens were used in addition to

histories to determine cocaine use. However, this study also

was conducted in an inner city hospital serving primarily low

socioeconomic status (SES) women and information on

confounding polydrug use by mothers was considered either

somewhat unreliable or was unavailable to the researchers.








22

Alternately, Hadeed, and Siegel (1989), when studying

neonates of 56 mothers who used cocaine prenatally, found no

differences in the frequency of maternal preeclampsia or

caesarian section (C/S) rate, teratogenicity, narcotic

withdrawal symptoms, or illnesses compared to a no illicit

drug control group. Alternately, weight, length and head

circumference growth curves of infants born to cocaine-using

mothers shifted below the 25th percentile, although this

finding was not thought to be clinically significant. In

addition, cocaine use did seem to precipitate more spontaneous

abortions, abruptio placentae, and meconium stained amniotic

fluid. Advantages of this study included the use of a cocaine

only group and blinded evaluations. In addition, maternal

factors were controlled for differences in age, parity,

socioeconomic status (SES), ethnicity, and smoking, making

findings apparently more reliable.

One of the most prolific researchers in this area, Ira

Chasnoff, consistently reported a number of negative outcomes

for infants exposed to cocaine in utero in his early

investigations. In addition to the effects described by both

Oro and Dixon (1987) and Ryan et al. (1987), Chasnoff (1989)

reported a higher incidence of significant genitourinary tract

malformations. In one study of a pool of 70 infants with










cocaine-using mothers, Chasnoff (1989) found two infants with

prune belly syndrome, (a congenital nephrotic disorder) one

with female pseudohermaphroditism, two with hypospadias and

undescended testes, and three with hydroureter/hydronephrosis.

Further, two infants in this study suffered perinatal cerebral

infarctions that he attributed to maternal cocaine use in the

48 to 72 hours preceding delivery.

In a similar study, Chasnoff, Chisum, and Kaplan (1988)

found nine of 50 infants born to prenatal cocaine users had

some form of physical anomaly compared to only one of 30

infants born to polydrug noncocaine-using women. These

anomalies included two with ileal atresia and seven with

malformations of the genitourinary tract. While the

researchers attributed these effects to cocaine exposure, all

women in the study were known substance users specifically

enrolled for treatment possibly confounding outcome, and

polydrug use was common.

Researchers who have considered the outcome of cocaine-

exposed children in the context of other factors have found

more moderate results. For example, Bauchner, Zuckerman,

McClain, Frank, Fried, and Kayne (1988) assessed the risk of

SID among cocaine-exposed infants and found one of 175

prenatally cocaine-exposed infants died of SID and four of 821








24

unexposed children died of SID. These results suggested to

Bauchner et al. (1988) no increased risk of SID among infants

exposed in utero to cocaine. They observed that cocaine-using

mothers tended to use other drugs and alcohol, and tended to

have low birth weight babies. They further noted that SID

usually accounts for one to two deaths in a thousand; in poor

black groups, the rate may be as high as five to six per

thousand.

MacGregor, Keith, Chasnoff, Rosner, Chisum, Shaw and

Minogue (1987) again examined the perinatal outcome data of 70

women receiving care at a large urban drug treatment center.

In this study, the use of cocaine during pregnancy was

associated with younger gestational age at delivery, increase

in preterm labor and delivery, lower birth weight and delivery

of smaller for gestational age infants. However, no cocaine

related differences were found in the incidence of abruptio

placentae and congenital anomalies. Further, no differences

were noted on the basis of patterns of substance use. Again,

problems in this study included the possible biases of

unblinded investigators and confounding of polydrug use.

Schneider and Chasnoff (1992) also investigated the motor

development of cocaine/polydrug infants at four months of age.

Assessing 50 nonillicit drug exposed infants and 74 cocaine-










exposed infants, Schneider and Chasnoff (1992) found

significant differences between groups in muscle tone,

primitive reflexes and volitional movement with cocaine-

exposed infants performing more poorly. Results demonstrated

that motor differences were evident in cocaine-exposed infants

at a postnatal period beyond the first month of life. As in

other studies from the Chasnoff group, mother/infant

involvement in a drug treatment program was known by

investigators, and subjects in the cocaine group included

polydrug users.

In a two year followup, Chasnoff, Griffith, Freier and

Murray (1992) investigated the growth and developmental

outcome of cocaine-exposed infants. Comparing a cocaine-

exposed group (with marijuana and alcohol exposure), a

marijuana/alcohol exposed group, and a nonexposed control

group, they found that cocaine-exposed children no longer

lagged behind nonexposed children in terms of length and

weight although the cocaine group and marijuana/alcohol group

both lagged in head growth. No differences in performance on

the Bayley Scales of Infant Development (BSID) were noted

between the three groups. Again, these children were all

known to the researchers through a drug treatment program, and

polydrug use was a confound. Further, the study sample had a








26

high rate of attrition. The conclusion that head growth after

birth may be a biological marker for drug exposure may be

correct; however, this cannot be attributed solely to cocaine

exposure in utero, particularly since the marijuana/alcohol

but no cocaine group also lagged in head growth.

In the context of longer term development, Azuma and

Chasnoff (1993) subsequently assessed the three year outcome

of cocaine-exposed children using cognitive and behavioral

measures. They found that children prenatally exposed to

cocaine were no different from controls in terms of

intelligence measured on the Stanford Binet (SBIT). However,

statistical modelling using path analysis suggested that drug

exposure, home environment and level of perseverance

(attention) had direct effects on cognitive function, while

head growth and parent report of behavioral functioning did

not have a direct effect on test scores. The authors

considered this a "best case" outcome study because all women

were involved in a treatment program. However, as in the two

year followup of the same population, possible biases and

confounds existed particularly with regard to subject

attrition.

From the same research team, Griffith, Azuma, and

Chasnoff (1994) also evaluated the three-year behavioral and








27

developmental outcome of children prenatally exposed to

maternal substances of abuse. Their subjects included 93

children exposed prenatally to cocaine and other drugs, 24

children exposed to polydrugs without cocaine and 25 children

who were nonexposed. Drug exposed children had smaller head

circumferences than nonexposed children; the

polydrug/noncocaine group performed worse than nonexposed

children on tasks of abstraction and visual reasoning; the

cocaine/polydrug group performed worse on a task of verbal

reasoning; and a marijuana group performed more poorly on a

task of abstract/visual reasoning. Caregivers also rated drug

exposed children as more aggressive than nonexposed children.

The authors concluded that not all substance exposed

children suffer the same poor prognosis, and that

generalizations about outcome for drug-exposed children need

to be qualified pending more thorough investigations of the

roles of maternal and environmental factors such as SES

levels. Recognizing that cocaine may not account for all

negative findings and that bias on the part of researchers and

even parents could convolute findings was an important pivot

point, not only for this group of researchers but for other

investigators in the field as well.








28

Studies focusing on the behavioral outcome of cocaine-

exposed infants present a range of findings and methodology.

In a study of fetal behavioral state as a predictor of

neonatal outcome, Hume, O'Donnell, Stanger, Killam, and

Gingras (1989) performed fetal assessments which included

ultrasonographic examination, videotaping and scoring of a

behavioral protocol developed by the authors. Abnormal or

delayed state behavior was identified in 13 of 20 fetuses

exposed to cocaine. State organization was also suspect or

abnormal for 16 of 20 exposed newborns, and the disorganized

behavioral states in fetuses successfully predicted abnormal

newborn behaviors. The authors concluded that cocaine

disrupts (CNS) development. Again, problems in this early

study included lack of a control group, small sample size,

unblinded examiners, and the use of unnormed scales which,

because they were developed by the authors for this study, may

have led to biased observations.

Davis, Fennoy, Laraque, Kanem, Brown and Mitchell (1992),

who were also interested in behavioral outcome, studied 70

children with cocaine exposure in utero who had been targeted

by positive urine screen, maternal report, or by doctor/agency

notation. All children in the study had been referred to a

large inner city hospital for developmental evaluation. Davis










et al. (1992) found significant neurodevelopmental

abnormalities including language delay and a high frequency of

autism (11.4%) in the cocaine-exposed group. Since autistic

disorders have not been linked to alcohol or opiate exposure

alone, Davis et al. (1992) attributed their findings to

cocaine use. There are obvious deficiencies in this study

including the nonblinded status of clinical evaluators, the

skewed sampling of clinically referred children, the polydrug

use status of the mothers, and the conclusion that results

must be narrowly attributed to cocaine exposure in utero.

In a study of 51 cocaine-exposed infants and 60

nonexposed infants targeted by maternal report or positive

infant urine screening, Neuspiel, Hochberg, Greene, and

Campbell (1991) found no differences on the Brazelton Neonatal

Behavioral Assessment Scale (BNBAS) administered between one

and three days of age. A second examination at 11 to 30 days

of age showed a significant difference in motor functioning in

the cocaine-exposed group. However, this difference

disappeared when researchers controlled for confounding

variables such as perinatal and social factors. No

differences were detected in observed maternal or infant

behaviors indicating that prenatal cocaine use had no

significant impact on maternal/infant interactions.








30

In a study with variable outcomes, Eisen, Field,

Bandstra, Roberts, Morrow, Larson, and Steele (1991) studied

26 target and 26 control infants for the effects of maternal

cocaine use on the Brazelton Neonatal Behavior Assessment

Scale (BNBAS). Infants were excluded if their mothers used

opiates; and mothers were matched for maternal age, ethnicity,

gravida, previous abortions, and hepatitis. Cocaine-using

mothers were more likely to be tobacco and marijuana smokers

and alcohol drinkers.

Results showed no differences between controls and

cocaine-exposed infants in sex distribution, gestational age,

chronological age, birth weight, birth length or postnatal

complications. However, cocaine-exposed infants had smaller

head circumferences and more obstetric complications than the

nonexposed infants. In addition, cocaine-exposed infants

showed more stress behaviors defined as abnormal reflex

behavior and autonomic instability on the Neonatal Stress

Scale. However, regression analysis showed obstetric

complications and maternal alcohol use were the only

significant variables that contributed to the variance on the

Neonatal Stress Scale. Finally, the cocaine group

demonstrated impaired ability to habituate responses to

repeated stimuli; regression analysis showed cocaine exposure










to account for a significant amount of the variance in

habituation scores. Maternal polydrug use may confound

findings somewhat in this study.

In an attempt to improve upon the methodology in the

prenatal cocaine exposure literature, Woods, Eyler, Behnke,

and Conlon (1993) longitudinally assessed infant behavior

using the BNBAS at birth and again at one month. Mothers

enrolled in this study were from a rural, low income

population with little or no drug treatment. All examinations

were performed blindly. Woods et al. (1993) found cocaine-

exposed infants had lower birth weights and shorter gestations

than controls, a finding typical of many investigations.

However, there were no differences in neonatal performance on

the BNBAS at birth or at one month of age. These results

indicate that not all cocaine-exposed infants show

neurobehavioral deficits in the neonatal period.

Again, studies of infant neurobehavior report varying

results. For example, Mayes, Granger, Frank, Schottenefeld,

and Bornstein (1993) reported that exposed infants had poorer

orientation than nonexposed infants, while Richardson and Day

(1991) reported no differences on any Brazelton scale. In

general, studies documenting birth outcome using repeated

BNBAS assessments report a pattern of developmental recovery








32

over the first few weeks of life for the cocaine-exposed

infant (Black, Schuler, & Nair, 1993; Coles, Platzman, Smith,

James, & Felix, 1992).



Summary of Literature Review

A review of the literature concerning cocaine effects on

fetal development indicates several serious methodological

problems in human clinical studies, including probable

underreporting of cocaine use and the increased likelihood

that cocaine users also use more alcohol and other drugs.

There is also the likelihood of confounding of other maternal

risk factors that are more common in cocaine-using groups than

nonusers such as sexually transmitted diseases (including

HIV); previous spontaneous and elective abortions, and less

prenatal care; low birth weight infants; polydrug use; poor

health and nutrition; and poverty (Dow-Edwards, 1991). Other

methodological problems endemic to the literature include a

preponderance of unblinded evaluations. Further, most

research has concentrated on urban populations and

inappropriate control groups and analyses which frequently

ignore important environmental and maternal factors.

In terms of specific animal research findings, cocaine

generally has no effect on gestational length in the rat, a








33

few studies report an increase in stillbirth rate, and cocaine

appears to reduce litter size but only at the most toxic doses

which may not be relevant to human studies. In animals, odor-

associated learning appears to be impaired in some studies.

Altered neuronal circuits, including nigrostriatal pathway

(fine motor tuning) and mesolimbic dopaminergic system

(reinforcement), have been also demonstrated. Head size in

animals does not appear to be associated with prenatal cocaine

use.

While some reports in the human clinical literature

suggest that cocaine use during pregnancy is associated with

smaller babies, others do not find statistically significant

effects on fetal growth. Evidence of decreased length in

human fetal growth has been found, but it is unclear whether

these results can be attributed to cocaine or to other factors

such as maternal malnutrition and hypoxia. Further, no

specific constellation of fetal malformations is found with

prenatal cocaine use although case reports of craniofacial

defects, missing digits, and genitourinary malformations exist

(Dow-Edwards, 1991).

Transient neurological deficits have been noted in

neonates exposed to cocaine in utero which have included

tremors, rigidity, hyperactivity, abnormal EEG, seizures,











abnormal orientation, sensory and motor functions. Most of

these problems appear to resolve by six months of age. Some

studies have found exposed infants at risk for SID whereas

others have not found a significant association with cocaine.

Additionally, neonates exposed in utero to cocaine do not

appear to suffer from addiction to cocaine which is unlike

infants exposed to opiates in utero.

At the present time, reduced length and head

circumference appear to be the most consistent findings

reported for neonates exposed prenatally to cocaine, and

again, these deficiencies are usually resolved by one year of

age. There does not appear to be a clinical syndrome which

adequately captures the impact of cocaine exposure in utero on

the developing human. Individual variation in outcome appears

to be the most consistent finding. The methodological

difficulties of working with a drug-using population,

exaggerated media portrayals of 'crack babies,' and the need

to control for investigator bias in studies have added to the

confusion evident in the cocaine literature. Thus, while

cocaine exposure in utero may reasonably be expected to have

deleterious effects on some children, it is not possible at

this time to define a syndrome in any, even globally,

meaningful way.













PURPOSE OF RESEARCH

While the particular results of studies vary somewhat,

reports consistently portray cocaine as an agent strongly

implicated in a host of negative outcomes. Further, crack has

been singled out as the most potent form of cocaine both in

terms of abuse potential and morbid impact (Kaye, Elkind,

Goldberg, & Tytun, 1989). Clearly research on the

implications of in utero exposure to cocaine, and especially

crack, needs to be ongoing and continually refined from a

methodological, medical and psychosocial perspective.

At present, long-term followup on the effects of prenatal

exposure to cocaine and cocaine derivatives is extremely

limited. Because of the variability in outcome cited in the

neonatal literature, it remains unclear what long-term impact

in utero cocaine exposure may have on the developing child.

In the past, the media have portrayed cocaine-exposed infants

and toddlers as behaviorally disordered, impulsive,

nonempathetic, and autistic, generally without benefit of

sound empirical evidence. These prejudices have frequently

been supported by biased investigations making hasty

unwarranted projections as to future status while ignoring the








36

very significant presses of poverty, malnutrition and a

caregiving environment compromised by addiction. While the

potential toxicity of cocaine exposure should be in no way

minimized, it has been the recent onus of researchers in this

area to produce methodologically sound and conservatively

interpreted accounts of the impact of cocaine on the

developing infant and toddler. Only recently has sound

research on the infant and toddler been possible as

prospectively enrolled cohorts mature to preschool age and

older. Thus, there are a number of interesting questions to

be investigated. Whether the effects linked to cocaine

exposure in utero are stable over time, and how they translate

behaviorally and developmentally will require increasing

attention as these infants mature.

The present study is intended as an initial exploration

of some of these developmental issues within improved

methodological design. Addressed here is whether toddlers

exposed in utero to crack differ from same aged unexposed

peers in their level of behavioral and adaptive development.













MATERIALS AND METHODS


Subjects

Subjects were 30 children exposed to crack in utero and

30 nonexposed control children who were part of a large,

ongoing, prospective longitudinal research project conducted

at Shands Teaching Hospital through the Department of

Pediatrics, Division of Neonatology. Subjects were the

children of women who were originally recruited predominantly

from public health department (PHD) prenatal clinics in two

counties in an understudied rural area of north central

Florida. Recruitment began in the Fall of 1991. These women

represented a range of low to moderate reproductive risk and

all were scheduled to deliver at the referral hospital. There

was a wide range of drug use with most smoking crack cocaine

and few having access to drug treatment.

Criteria for inclusion in the original study were: 1)

women over 18 years of age to reduce the confounding influence

of perinatal risk known to be associated with pregnancy in the

young teenager and to eliminate problems with obtaining

informed consent from minors, 2) women with no major illnesses










diagnosed prior to pregnancy that are known to affect

pregnancy or developmental outcome or maternal interaction or

caregiving, such as diabetes, chronic hypertension, immune

complex disease, seizure disorders, mental illness or

retardation, etc., 3) women with no history of illegal drug

use other than marijuana and cocaine, 4) English speaking, and

5) women who did not use any of the following drugs without a

prescription or chronically with prescription: amphetamines,

benzodiazepines, barbiturates, opiates, methadone, and

methaqualone.

Target subjects were selected during a screening

interview from those who admitted any prenatal use of cocaine

or had a full toxicology screen positive for metabolites of

cocaine; maternal urine specimens were taken at two

unanticipated times, study enrollment and delivery. Any

patient who during the screening interview denied the use of

cocaine, the illicit substances and drugs listed above, and

had a negative cocaine toxicology screen were retained in the

subject pool as a potential match for a cocaine-using subject.

Matching was done within each county health department to

equate level of prenatal risk and included the following

subject conditions: 1) maternal race: black vs. nonblack; 2)

parity: primiparity vs. multiparity; and 3) socioeconomic










status: level of Hollingshead Index. These are factors which

have been shown to mediate caregiving and affect outcome of

high risk infants.

All subject mothers were interviewed once or twice

prenatally and/or at the time of birth, and their surviving

infants were evaluated at each followup time. Detailed drug-

use histories and psychosocial interviews were done by

helpful, nonjudgmental, experienced interviewers. Calendars

were used to help women identify timing of use, and probing

for drug use details was done about past but not present use

in an effort to be less threatening. Infants were assessed

one to three times in their first week of life and six more

times over three years. Three followup assessments were made

in the homes and three in the clinics. All infant assessments

were performed by trained, reliable examiners blinded to drug

exposure history. Subjects in the present study were seen at

three years of age plus or minus eight weeks, and measures

included parent report instruments and behavioral observation.

Several variables were chosen for use as covariates

during statistical analysis in order to strengthen results

including maternal alcohol use, maternal depression, child

gender, and home environment. Covariates were chosen a'priori

based on literature that indicated such variables correlate










significantly with infant/toddler development. Placement in

foster care was chosen post hoc to be included as a covariate

in the analysis due to the difference in frequency between the

two groups and due to the potential impact of foster placement

on child outcome at three years of age. Foster care was

defined as a child being placed in a home away from, or with

a relative other than, their biological mother. Thus, five

variables (alcohol use, maternal depression, child gender,

home environment, and foster placement) were included as

covariates in the initial analyses between groups.

In order to further strengthen the analyses, subjects

were excluded from the study based on several birth

characteristics which could significantly skew results. These

included any child born with a birth weight below 2,500 grams

and/or a congenital malformation. Children exposed to cocaine

in any form other than crack were also excluded from the

study. It was decided a'priori to exclude children from the

study who suffered any accident or illness (such as sickle

cell anemia) that might seriously affect their performance on

developmental measures independent of crack exposure in utero.

Altogether, 90 children from the longitudinal study were

evaluated between July 1, 1995 and January 30, 1996. Subjects

were assessed in the order that they came in for their three










year followup as part of the ongoing study. Thirteen children

(14.4%) were dropped from the study. Of the thirteen excluded

children, 9 were low birth weight (69.3%; 5 targets and 4

controls), 3 were exposed to forms of cocaine other than crack

(23.1%), and one had sickle cell anemia (7.7%). At the close

of enrollment for this study, the matches for 17 (18.9%) of

the original 90 had not been tested. Thus, the 17 unmatched

subjects had to be dropped from the study.

The remaining 30 pairs of matched children (66.7%)

constituted the study sample. Forty of the children (66.7%)

were from Alachua County, and 20 children (33.3%) were from

neighboring Marion County. Two of the mothers were

primiparous (3.3%) and 58 were multiparous (96.7%). Fifty of

the mothers were African American (83.3%) and ten were of

other ethnic origin (16.7%). Sixteen of the women earned a

Hollingshead Index of four (26.7%) while 44 of the women

earned a Hollingshead of five (73.3%). The Hollingshead Index

is a measure of socioeconomic status based on level of

education and employment. Scores range from one to five with

scores of four and five representing the lowest levels of

employment and education. Thirty of the children (50.0%) were

exposed to crack cocaine in utero and 30 were not exposed

(50.0%). Tables 1 and 2 outline basic demographic and








42

covariate characteristics for the sample. For the remainder

of this document, 'sample' will refer to the 60 children in

this study which was completed in the context of the larger

longitudinal study as previously described.

The children in the sample (n = 60) included 34 girls

(56.7%) and 26 boys (43.3%). Sixteen children were placed in

a home other than that of their biological mother (26.7%).

Average birth weight was 3326 grams (SD = 413 grams), and mean

age at time of testing was 36.8 months (SD = 1.9 months). The

nonexposed group of children was comprised of 18 girls (60.0%)

and 12 boys (40.0%). Only two children were in foster care

(6.7%). Average birth weight in nonexposed children was 3355

grams (SD = 401.469 grams), and mean age at time of testing

was 37.3 months (SD = 1.446 months). The exposed group was

comprised of 16 girls (53.3%) and 14 boys (46.7%). Fourteen

of the children were in foster placement (46.7%). Average

birth weight in exposed children was 3297 grams (SD = 431

grams), and mean age at time of testing was 36 months (SD =

2.3 months).

In the sample, maternal depression scores ranged from one

to 43 (M = 19.7, SD = 9.8) with 16 being the clinical cutoff

score. Home Environment total scores ranged from 18 to 52 (M

= 37.0, SD = 8.4) with a normative sample M = 37.54, SD =








43

10.41. Alcohol use, calculated as average number of 4-ounce

drinks per day over three trimesters, ranged from zero to 3.66

(H = .253, SD = .649). In the nonexposed group, average

maternal depression score was 20.9 (SD = 9.5), and average

home inventory score was 36.5 (SD = 8.1). Alcohol use in the

nonexposed groups averaged .2667 drinks per day (SD = .450).

In the exposed group, average maternal depression score was

18.4 (SD = 10.1), and average home inventory score was 37.6

(SD = 8.7). Mean drinks per day in the exposed group was

.9333 (SD = .640). For purposes of further analyses, alcohol

was coded as a dichotomous variable, either present or absent

in the prenatal period.



Parent Report Measures

Vineland Adaptive Behavior Scales

The Vineland (Sparrow, Balla, & Cicchetti, 1984) is a

nationally normed measure of adaptive behavior for children

birth to adulthood and assesses competency in four skill

areas: Socialization, Communication, Motor Skills, and Daily

Living. The Survey Form used in this study consists of 297

questions administered to the primary caregiver. Items to be

answered on a range from 'yes, usually' to 'don't know'

include such examples as "Uses sentences of four or more











words" or "Feeds self with spoon without spilling."

Administration time is approximately 15 minutes. Split-half

coefficients and test-retest reliabilities for the Adaptive

Behavior Composite are .94 and .95 respectively and factors

reportedly load in appropriate subdomains of each of the four

areas. Scores are percentile ranks, means, and standard

deviations.



Connors Parent Rating Scale

The Connors (1990) is a parent rating report of

hyperactive and attentional problems in children aged three to

17. It was normed on 383 children and consists of 48

questions which load into six factors including Conduct

Problem, Learning Problem, Psychosomatic, Hyperactivity Index,

Impulsive-Hyperactive, and Anxiety. Higher scores indicate

increased problems in the tested area. Administration time is

approximately 15 minutes. Factors loadings of the CPRS-48

range form .41 to .82 and appear stable over time. Scores are

percentile ranks, means and standard deviations.



Evbera Child Behavior Inventory (ECBII

The ECBI (Eyberg, 1992) is a parent report screening

measure for disruptive behaviors in children ages two through










16. It includes an Intensity Scale, which indicates how often

the behaviors presently occur, and a Problem Scale, which

identifies the specific behaviors that are currently problems

for the caregiver. There are a total of 36 items.

Clinically, a Problem Scale score of 11 or greater and an

Intensity Scale score of 127 or greater are used as cutoffs

for disordered conduct. The normative sample was 798 parents

of children drawn from six pediatric health care settings

sampled so as to approximate the demographic composition of

the Southeast. Split-half correlations for both scales were

.93. Administration time is approximately 5 minutes.



Behavioral Observation Measure

Dyadic Parent-Child Interaction Coding System-II (DPICS-II1

The DPICS-II (Eyberg, Bessmer, Newcomb, Edwards, &

Robinson, 1994) is a direct, objective observation measure to

discriminate normal from conduct-disordered child/parent

interactions. The system provides a measure of both child and

parent behaviors and was originally normed on 20 families

referred for treatment of a conduct-problem child and 22

families without such a conduct-problem child. Problem

behaviors include disobedience, aggression, destructiveness,

or hyperactivity. Reliability for DPICS-II by behavior ranged










from 38% to 99% (Bessmer, 1993). The DPICS-II includes three

situations that may be coded. For this study, we selected

five minutes of child directed play between caregiver and

child (CDI) and five minutes of parent-directed play (PDI).

Administration and scoring criteria for the standardized

protocol were not altered. The DPICS-II code categories

selected for observation were child behaviors that others have

suggested might differentiate between cocaine-exposed children

and nonexposed children. Exposed children may demonstrate

conduct disordered behaviors. Alternately, the exposed child

may be withdrawn in interactive situations. To capture a

potential range of child behaviors, both positive and

negative, included here were: 1) yell and whine, 2) laugh, 3)

destructive, 4) physical negative, and 5) physical positive.

These variables were measured by frequency over two, five

minute periods. Compliance data were drawn from several

variables as follows: 1) compliance or 2) noncompliance to a

3) direct or 4) indirect command, or 5) no opportunity for

compliance. Total frequency of commands were calculated for

each child. The five compliance variables were also combined

to derive a percentage representing the rate of compliance,

noncompliance, and no opportunity for compliance for each

child. These behaviors are defined in detail in the DPICS-II










manual (Eyberg et al., 1994). Toys used in the play situation

were standard and included: 1) large primary-color blocks, 2)

a farm, and 3) and a gender-neutral stuffed animal.



Procedures

Parents and children were seen during their scheduled

visits as part of the ongoing, longitudinal project. Informed

consent was obtained from parents at the intake of the

original project approximately three years previously.

Maternal demographic and perinatal medical information was

obtained from interviews conducted prenatally and/or at the

time of birth. Parent report measures for the present study

were incorporated into the existing project interview

scheduled as part of a home visit when the children were three

years old. The play observation for this study was scheduled

separately from the parent interview as part of the three-year

clinic visit. The observation period was situated in the test

period before procedures considered aversive (e.g., physical

examination) and after generally nonaversive testing (e.g.,

Bayley II). Administration of materials was standard for each

caregiver/child dyad.

Observation periods were videotaped in a room at either

the Public Health Department or delivery hospital. The video








48

camera was concealed behind a three sided screen to limit

distractions and to maximize play opportunity. The three toys

were placed in the center of the floor before each video

session began. Verbal instructions to the parent for the free

play or child-directed play, and for the parent-directed

portion of taping were standardized and followed the format

provided with the DPICS-II manual.

Tapes were scored by two advanced graduate students

trained to reliability on pilot tapes using the DPICS-II

(Eyberg et al., 1994) scoring criterion. Examiners were

blinded to cocaine status to reduce possible bias.









ANALYSES


Descriptive Analyses

Means and standard deviations were calculated for the

total sample for dependent variables including: 1) the

Connors' (Connors, 1990) subscales Conduct Problem, Learning

Problem, Psychosomatic, Impulsive-Hyperactive, Anxiety, and

Hyperactivity Index, 2) ECBI (Eyberg & Colvin, 1994) Problem

and Intensity scales, 3) the Vineland (Sparrow et al., 1984)

subscales Socialization, Communication, Daily Living, and

Motor Skills, and 4) DPICS-II (Eyberg et al., 1994) variables.

For the DPICS-II, ten behaviors were chosen for basic

frequency observation. For purposes of higher level analyses,

four summary variables were derived from DPICS-II compliance

data. Normality assumptions for dependent variables were

tested by graphing and computing skewness scores. Covariates

were included in the initial analyses between groups only for

derived summary scores.



Hypothesis 1

To test whether the performance of the entire sample is

depressed compared to age-based norms, scores on well normed

measures were compared to age-based norms using Welch's V for










unequal n and Studentized Maximum Modulus (SMM) tables for

familywise error rates to control for multiple comparisons at

the .05 significance level. Dependent variables were grouped

conceptually for comparison to norms as follows: 1) the six

subscales of the Connors (Connors, 1990) including Conduct

Problem, Learning Problem, Psychosomatic, Impulsive-

Hyperactive, Anxiety, and Hyperactivity Index, 2) the ECBI

(Eyberg & Colvin, 1994) Problem and Intensity scales, and 3)

the four subscales of the Vineland (Sparrow et al, 1984)

including Socialization, Communication, Daily Living, and

Motor Skills.

The ten DPICS-II basic observation frequency variables

were broken into two groups for analysis. The first group

included compliance information including frequency of direct

and indirect commands, compliance, noncompliance, and no

opportunity for compliance. The second group consisted of

child behaviors including frequency of laugh, yell-whine,

physical positive, physical negative, and destructive. Scores

were compared to normative data using Welch's V for unequal n

and Studentized Maximum Modulus (SMM) tables for familywise

error rates. Comparisons to normative groups were not

performed for DPICS-II derived summary scores as norms are not

available.











Hypothesis 2

It was hypothesized that the performance of the cocaine-

exposed group would be impaired compared to the nonexposed

group in terms of behavior as measured by parent report on the

six subscales of the Connors (Connors, 1990). After graphing

to inspect relationships between scales, MANCOVA with

Hotelling's T2 was used to analyze between group differences.



Hypothesis 3

It was hypothesized that the performance of the cocaine-

exposed group would be impaired compared to the nonexposed

group in terms of behavior as measured by parent report on the

two subscales of the ECBI (Eyberg & Colvin, 1994). After

graphing to inspect relationships between scales, MANCOVA with

Hotellings T2 was used to analyze between group differences.



Hypothesis 4

It was hypothesized that the performance of the cocaine-

exposed group would be depressed compared to the nonexposed

groups in terms of adaptive behaviors as measured by the four

subscales of the Vineland (Sparrow et al., 1984) by parent

report. After graphing to inspect relationships between








52

scales, MANCOVA with Hotellings T2 was used to analyze between

group differences.



Hypothesis 5

It was hypothesized that the performance of the cocaine-

exposed group would be depressed compared to the nonexposed

groups in terms of observed disordered behaviors as measured

on the DPICS-II (Eyberg et al., 1994). Because data for

individual behaviors are observed at very low frequencies, the

basic ten observed behaviors were compared for between group

differences using t-tests. The four derived summary scores

including Total Commands, Percent Compliance, Percent

Noncompliance and Percent No Opportunity for Compliance, were

treated like parent report variables. After graphing to

inspect relationships between scales, MANCOVA with Hotellings

T2 was used to analyze between group differences.









RESULTS


Descriptive Analysis

First, means and standard deviations were calculated for

the total sample for parent report dependent variables

including: 1) the Vineland (Sparrow et al., 1984) subscales

Communication, Daily Living, Motor Skills, and Socialization,

2) the Connors' (Connors, 1990) subscales Conduct Problem,

Learning Problem, Psychosomatic, Impulsive-Hyperactive,

Anxiety, and Hyperactivity Index, and 3) the ECBI (Eyberg &

Colvin, 1994) Intensity and Problem scales.



Parent Report Measures

Normality assumptions for parent report dependent

variables were then tested by graphing and computing skewness

scores. One subscale of the Connors' scale (Psychosomatic)

and one subscale of the Vineland (Daily Living) were found to

be skewed. These were corrected for further analyses using

log transformations. All other dependent variables on

standardized parent report measures were found to approximate

normality. Data were missing for two children on all Connors

subscales, and for one child on all Vineland subscales. Data

were missing for four children on the ECBI subscales. Missing











data were substituted with group means to allow analysis of

these variables to be performed with equal sample size.



Observational Measures

Second, means and standard deviations were calculated for

the total sample for the ten basic frequency observational

variables including: 1) DPICS-II (Eyberg et al., 1994) five

compliance scores including direct and indirect commands,

compliance, noncompliance and no opportunity to comply, and

child behaviors including yell and whine, laugh, destructive,

physical negative, physical positive, and 2) DPICS-II derived

variables as described previously including commands,

compliance, noncompliance, and no opportunity to comply.

It was determined a'priori' that the ten DPICS-II

observational variables would be consolidated to derive

various scores because the frequencies of target behaviors

tended to be low. Thus, for the present analysis we were not

concerned with testing normality assumptions for the ten

individual observational scales. However, normality

assumptions for consolidated observational dependent variables

including Total Commands, Percent Compliance, Percent

Noncompliance, and Percent No Opportunity to comply were

tested by graphing and computing skewness scores.











The Total Commands score was derived by adding together

total direct command comply, total direct command noncomply,

total direct command no opportunity to comply, total indirect

command comply, total indirect command noncomply, and total

indirect command no opportunity to comply. Percent Compliance

was the sum of total direct command comply and total indirect

command comply divided by the sum of total direct command

comply, total indirect command comply, total direct command

noncomply, total indirect command noncomply, total direct no

opportunity to comply, and total indirect no opportunity to

comply. Percent Noncompliance was the sum of total direct

command noncomply and total indirect command noncomply divided

by the sum of total direct command noncomply, total indirect

command noncomply, total direct command comply, total indirect

command comply, total direct command no opportunity to comply,

and total indirect command no opportunity to comply. Finally,

Percent No Opportunity to Comply was the sum of total direct

command no opportunity and total indirect command no

opportunity divided by total direct command no opportunity,

total indirect command no opportunity, total direct command

comply, total indirect command comply, total direct command

noncomply, and total indirect command noncomply.











Of the four derived DPICS-II observational scales, only

no opportunity to comply was found to be moderately skewed.

This scale was corrected for subsequent analyses using a log

transformation. The remaining three scales, command, comply,

and noncomply, were found to approximate normality. Data were

missing for six of the children from the nonexposed group.

Because data frequency was low on observational scales, it was

considered inappropriate to substitute missing data with group

means, and analysis of these variables was performed with

unequal sample size.



Reliability of Observational Measures

Interrater reliability calculations were performed for

two raters on DPICS-II behavioral variables for both child

directed interactions and parent directed interactions (Tables

3 and 4). In general, interrater reliability was very strong

using Pearson's Product Moment values ranged from r = .84 to

1.00 across the ten basic frequency observation variables in

two situations (parent and child directed play interactions).

Pearson's correlations can be inflated or deflated based on

the frequency of occurrence. Thus, it was decided to

determine interrater reliabilities using agreement of

occurrence, agreement of nonoccurrence, and finally the mean










of agree occur and agree nonoccur for low frequency data

measured in discrete time intervals (Page & Iwata, 1986).

Percent agreement for occurrence was based on summing the

agreement of occurrence across subjects and dividing by the

agreement of occurrence plus disagreements across subjects.

Percent agreement for nonoccurrence was based on summing the

agreement of nonoccurrence divided by the agreement of

nonoccurrence plus disagreements across subjects. In the

child directed interactions, agreement of a given behavior

ranged from 89.10% to 100.00%. Similarly, agreement of

occurrence of a given behavior in the parent directed

interaction ranged from 85.74% to 100.00%. In summary,

interrater reliabilities were strong across all behaviors.



Initial Between-Groups Analyses

Demographic Between Groups Differences

Basic demographic match criteria variables measured on a

nominal or ordinal scale were analyzed for significant

differences between the exposed and nonexposed groups using

Fisher's Chi-Square with the Yates Correction for small sample

sizes. Demographic variables included parity, race, county,

and Hollingshead Index. Due to matching upon entry to the

study and limited variability, it is not surprising that no








58

significant differences were found between groups on these

variables. Similarly, no significant differences on interval

scale data using t-tests were found on basic child

characteristics including birth weight and age at testing

(Table 1).



Covariate Between Groups Differences

Covariates measured on a nominal or ordinal scale were

also analyzed for significant differences between the exposed

and nonexposed groups using Fisher's Chi-Square with the Yates

Correction for small sample sizes. Covariates included child

gender, foster care, and alcohol use where alcohol use was

converted to an ordinal variable to control for outliers. No

differences were found between groups in terms of gender.

However, children exposed to crack were significantly more

likely to be in foster care than children in the nonexposed

group with X2(1) = 10.31, R = .0013. Similarly, children who

were exposed to crack in utero were more likely to be exposed

to alcohol than nonexposed children with X2(1) = 13.08, p =

.0003.

Remaining covariates measured on an interval scale were

analyzed for significant differences between exposed and

nonexposed groups using t-tests. These covariates included










maternal depression at the three year visit and HOME (Caldwell

& Bradley, 1984) inventory total score at the time of the

three year visit. No differences were found in terms of

maternal depression or HOME inventory total scores at three

years of age using exposure status as the independent variable

(Table 2).



Group Differences using Covariates as Independent Variables

Notably, significant differences were found on parent

report measures when the groups were defined by covariates.

For example, groups were defined by maternal depression based

on provided clinical cutoffs (Radloff, 1977), the low group

with scores of 16 or less (n = 21) and a the high group with

scores over 16 (n = 39) representing elevated depression. The

elevated maternal depression group demonstrated more conduct

problems t = -2.57, p < .013, learning problems t = -3.16, R

< .003, hyperactivity L = -2.55, p < .014, and increased

intensity of problem behaviors f = -2.42, p < .019 (Table 5).

Similarly, HOME inventory scores were divided based on a

provided normative mean of 37 (Caldwell & Bradley, 1984). The

first group (low) was comprised of scores of 37 or less (n =

29) and a second group (high) was comprised of scores of

greater than 37 (n = 31) representing more enriched











environments. Findings indicated that the group representing

children from less enriched environments had more conduct

problems f = 2.57, p < .013, learning problems t = 2.25, R <

.028, worse socialization t = -2.75, g < .008, and reduced

communication skills t = -2.07, p < .043 compared to children

from relatively more enriched environments (Table 6).

When groups were defined by foster care status, children

who were with their biological mothers (n = 44) tended to have

significantly more conduct problems t = 2.25, R < .028 than

children living away from their biological mothers (n = 16)

(Table 7). Further, when groups were defined by child gender,

boys (n = 26) were significantly more likely to display

learning problems t = -2.38, R < .021, and have poorer

communication skills than girls = 2.05, g < .045. Girls (n

= 34) were significantly more likely to feel anxious t = 2.17,

p < .034 than boys (Table 8). Interestingly, although alcohol

use was significantly different between exposed and nonexposed

groups, no significant differences were found on any parent

report measure using alcohol as the independent variable

(Table 9).

In terms of observational measures and covariates, no

between groups differences were found on the four derived

DPICS-II scores when groups were defined by either maternal











depression (exposed n = 36, nonexposed n = 18) or HOME

inventory (exposed n = 29, nonexposed = 25). Further, no

differences were found on derived DPICS-II observational

scales when groups were defined by foster care status (exposed

n = 15, nonexposed n = 39), gender (exposed n = 24, nonexposed

n = 30), or alcohol use (exposed n = 31, nonexposed n = 29)

(Table 9). Together, these results suggest that chosen

covariates may have complex relationships with outcome on

behavioral measures, and that their selection for inclusion as

covariates was warranted.



Initial Correlations

Several additional analyses were done to clarify the

nature of relationships between covariates and dependent

variables, between pairs of covariates, and between pairs of

dependent variables. It should be noted that correlations

with nominal, ordinal, and interval data were done with

Pearson's Product Moment rather than point biserial

correlations as the outcome is identical (Weinberg & Goldberg,

1979).








62

Covariates and Dependent Variables

The relationships between covariates and dependent

variables are presented in Table 10. Notably, elevated

maternal depression was significantly related to increased

conduct disorder r = .3358, p < .01, learning problems r =

.3977, p < .01, and hyperactivity r = .3534, p < .01 on the

Connors. Maternal depression was also related to the problem

scale of the ECBI r = .3387, p < .01, again suggesting that

problem behaviors are more strongly associated with higher

levels of maternal depression. Similarly, a more enriched

home environment as measured by HOME inventory was

significantly related to better communication i = .3488, p <

.01. Interestingly, no significant relationships were noted

between the ten basic and four derived DPICS-II variables and

five measured covariates. It should be noted that a more

conservative significance level of .01 was chosen in order to

partially control spurious relationships that may results from

multiple corrrelations.



Covariates

In general, relationships between pairs of covariates

were insignificant using a two-tailed analysis. However,

caregivers who were raising foster children reported










significantly less depression r = -.3363, p < .01 than mothers

raising their biological children (Table 11).



Dependent Variables

Not surprisingly, when assessing relationships between

pairs of dependent variables across the three parent report

instruments (Connors, ECBI, and Vineland), behavioral

subscales tended to vary together and adaptive functioning

subscales tended to vary together. The ECBI problem scale was

significantly related to the Connors conduct problem r =

.5569, p < .001, learning problem r = .5586, p < .001,

impulsivity E = .4915, p < .001, and hyperactivity scales r =

.6089, p < .001. The ECBI Intensity score was also

significantly related to these four Connors subscales with

increased intensity associated with conduct problems r =

.6635, p < .001, learning problems r = .5827, p < .001,

impulsivity r = .6014, p < .001, and hyperactivity r = .6331,

p < .001. Interestingly, the Connors subscale learning

problem was negatively correlated to socialization r = -.4672,

p < .001 and communication r = -.3768, p < .001. In other

words, higher levels of learning problems were associated with

relatively poor socialization and communication. Higher rates

of hyperactivity from the Connors were similarly related to








64

reduced socialization r = -.3343, R < .001. Neither ECBI

score was related to any measured domain of adaptive

functioning (Table 12).



Parent Report and Derived Observational Variables

Of particular interest were relationships between parent

report dependent measures and derived observational measures.

When examining derived DPICS-II scores, results indicate that

noncompliance measured objectively was related to caregiver

reports of higher learning problems r = .3578, p < .01, and

reduced daily living skills I = -.4229, p < .01. Similarly,

higher levels of caregiver perceived socialization were

positively related to compliance r = .4384, p < .01 (Table

12).

In terms of child behaviors, yell was positively related

to conduct problems and psychosomatic behavior with r = .4186,

p < .01 and r = .4399, p < .001 respectively. Finally, child

destructive behavior was significantly associated with conduct

problems with r = .3846, p < .01. It should be noted that a

more conservative significance level of .01 was chosen in

order to partially control spurious relationships that may

result from multiple correlations. Again, preliminary between











group and correlational findings suggest complex relationships

between measured scales (Table 12).



Hypothesis 1

It was hypothesized that the performance of both groups

would be depressed on all measures compared to age-based

norms. Analyses were performed with sample scores and

population norms. To test this, Welch's V for unequal sample

size was calculated comparing total sample scores on dependent

variables to standardized norms. Dependent variables were

grouped conceptually a'priori' and Studentized Maximum Modulus

(SMM) tables for familywise error rate were used to control

for multiple comparisons at the .05 significance level.

Tables 13, 14, and 15 summarize these results.



Connors Parent Rating Scale

The first group was comprised of the six subscales of the

Connors including: Conduct Problem, Learning Problem,

Psychosomatic, Impulsive, Anxiety, and Hyperactivity Indices.

Using the SMM familywise rate for six comparisons, Conduct

Problem was significantly different from the population norm

y = 5.03, R < .01 where the mean for the sample was higher

than the population mean. According to parent report,










learning problems were also more frequent in the sample than

the normative group with y = 2.98, R < .05. Children in the

sample tended to be more impulsive than the normative group

where y = 6.76, R < .01. Similarly, parent report indicated

increased hyperactivity in the total sample than in the

normative population where y = 5.30, p < .05 (Table 13).



Eybera Child Behavior Inventory

The second conceptual grouping was comprised of the two

ECBI scores including: Problem and Intensity. Using the SMM

familywise rate for two comparisons, the total sample was

significantly more likely to display a high intensity of

problem behaviors than the normative group where y = 2.637, p

< .05. Despite the high intensity of problem behaviors,

caregivers did not endorse items indicating that the behavior

posed a significant problem in the home (Table 13).



Vineland Adaptive Behavior Scales

The third group was comprised of the four subscales of

the Vineland related to adaptive functioning: Socialization,

Communication, Daily Living, and Motor Skills. Using the SMM

familywise rate for four comparisons, none of the sample










scores on any of these measured domains were significantly

different from provided norms (Table 13).



Observational Ratinas

The final two conceptual groupings were comprised of

basic objective observational data including: 1) direct

commands, indirect commands, compliance, noncompliance and no

opportunity to comply, and 2) laugh, yell, physical positive,

physical negative, and destructive behavior over the total ten

minute play period in two situations including both child-

directed and parent-directed play. These results are

summarized on Tables 14 and 15.

Using the SMM familywise rate for five comparisons,

significant differences were noted in sample scores in the

child-directed interaction when compared to normative data.

Specifically, the caregivers in the present sample tended to

have a higher rate of direct commands than either the clinic

referred or nonreferred normative group where y = 8.61, p <

.01 and v = 9.35, p < .01 respectively. The rate of indirect

commands was similarly elevated in the sample compared to

clinic referred and nonreferred normative groups where y =

4.01, p < .01 and y = 3.37, p < .01 respectively. Not

surprisingly given the higher rates of commands, the rate of








68

compliance was also significantly higher in the sample

compared to both the clinic referred and nonreferred reference

groups with y = 5.47, p <.01 and y = 6.61, p < .01

respectively. Noncompliance was likewise elevated in the

sample group compared to referred and nonreferred group with

M = 3.24, p < .01 and y = 3.93, p < .01 respectively.

Finally, no opportunity for compliance occurred at

significantly higher rates in the study sample compared to

normative groups including clinic referred where y = 7.96, p

< .01 and nonreferred where y = 8.12, E < .01.

No significant differences between the study sample, and

referred and nonreferred normative groups were noted on child

behaviors including yell, physical negative or destructive

using the SMM familywise rate for three comparisons. It was

not possible to test differences in the rate of laugh and

physical positive as normative data were not available for

these two variables. Results suggest that overall rates of

both indirect and direct commands were elevated in the present

study sample which in turn results in higher rates of

compliance, noncompliance, and no opportunity to comply (Table

14).

Using the SMM familywise rate for five comparisons,

significant differences were found between the study sample










and referred and nonreferred normative groups in the parent-

directed interactions (Table 15). Specifically, caregivers in

the sample group displayed significantly more direct commands

than either the referred or nonreferred normative groups with

Y = 4.91, p < .01 and y = 7.64, p < .01 respectively.

Interestingly, no differences were noted in the rate of

indirect commands in the parent-directed interaction. As in

the child-directed interactions, the rate of compliance was

significantly higher in the sample group during the parent-

directed interactions than in either the referred or

nonreferred normative groups with y = 6.13, R < .01 and v =

5.28, p < .01 respectively. Similarly, the study sample

tended to have a significantly higher rate of no opportunity

to comply than either the referred or nonreferred comparative

group with v = 3.76, p < .01 and y = 5.55, 2 < .01

respectively.

Alternately, no significant differences were noted in the

rate of noncompliance between the study sample and normative

groups. It was not possible to test between groups

differences for child behaviors for laugh, yell, physical

positive, physical negative or destructive due to either the

absence of normative data or variance in the normative group

(Table 15). Finally, it should be noted that the significance










for certain comparisons may have been diminished by the use of

familywise comparisons which tends to reduce power.



Hypothesis 2

It was hypothesized that behavioral difficulties would be

more pronounced in the exposed group. Descriptive data for

the exposed and nonexposed children are summarized on Table

16. To test this hypothesis, a multivariate analysis of

covariance was performed on the six dependent variables that

comprise the Connors: Conduct Problem, Learning Problem,

Psychosomatic, Impulsive-Hyperactive, Anxiety and

Hyperactivity. In the initial analysis, adjustment was made

for five covariates including alcohol, maternal depression,

foster care, HOME inventory, and child gender. The

independent variable was exposure status (exposed to crack

versus not exposed). SPSS' (Norusis, 1987) MANCOVA was used

for the analyses with the sequential adjustment for

nonorthogonality.

With the use of Hotelling's criterion, the dependent

variables were significantly related to the combined

covariates, with E(30,232) = 1.70, p < .05. To investigate

more specifically the power of the covariates to adjust the

dependent variables, multiple regressions were run with








71

covariates acting as multiple predictors. None of the

covariates provided adjustment to the Conduct Problem or

Anxiety subscales of the Connors. However, two of the five

covariates, child gender and maternal depression, provided

significant adjustment to Learning Problems with beta values

of .34 t(53) = 2.75, p < .05 and .41 t(53) = 3.27, i < .05

respectively. Maternal depression also provided adjustment to

Psychosomatic with a beta value of .30 significantly different

from zero where t(53) = 2.13, p < .05. Similarly maternal

depression provided significant adjustment to Impulsivity and

Hyperactivity with beta values at .36 t(53) = 2.60, p < .05,

and .36 t(53) = 2.67, p < .05 respectively. For none of the

dependent variables did alcohol, foster care, or HOME

inventory provide significant adjustment. These covariates

were dropped from further analyses.

The effects of exposure status on the dependent variables

after adjustment for significant covariates were investigated

in univariate and stepdown analysis. Dependent variables were

entered in the following order: Conduct Problems, Learning

Problems, Psychosomatic, Impulsivity, Anxiety, and

Hyperactivity Indices. In the stepdown analysis, each

dependent variable was analyzed in turn with higher priority

dependent variables treated as covariates and with the highest










priority dependent variables tested in a univariate ANOVA.

Conduct Problem was chosen as the highest priority dependent

variable since the literature suggests that this may be a

marker of prenatal cocaine exposure.

The results of this analysis are shown in Table 17. The

Hotelling's criterion for the combination of dependent

variables was not significant with E(6,51) = 1.26, p > .05.

Findings indicate that there are no differences between

exposed children and nonexposed children on this combination

of variables by parent report. Even in a univariate context

at the E < .05 level, there are no significant differences

between exposed and nonexposed children on these variables.

Specifically, no significant differences were found between

groups for conduct problem F((1,56) = 1.06, p > .05, learning

problem (1,55) = 1.22, R > .05, psychosomatic E(1,54) = .74,

p > .05, impulsivity (1,53) = .55, E > .05, anxiety (1,52)

= 3.25, p > .05, or hyperactivity (1,51) = .71, p > .05.



Hypothesis 3

As before, it was hypothesized that behavioral

difficulties would be more pronounced in the exposed group.

Descriptive data for the exposed and nonexposed children are

summarized on Table 16. To test this, a multivariate analysis











of covariance was performed on the two dependent variables

that comprise the ECBI: Problem and Intensity Scales. In the

initial analysis, adjustment was made for five covariates

including alcohol, maternal depression, foster care, HOME

inventory, and child gender. The independent variable was

exposure status (exposed to crack versus not exposed to crack

in utero). SPSS' MANCOVA was used for the analyses with the

sequential adjustment for nonorthogonality.

With the use of Hotelling's criterion, the dependent

variables were not significantly related to the combined

covariates with (10,102) = .921, p > .05. Thus, all five

covariates were dropped from further analyses. The effects of

exposure status on the dependent variables without inclusion

of covariates were investigated in univariate and stepdown

analysis using SPSS' MANOVA. Dependent variables were entered

in the following order: Problem Scale and Intensity Scale.

In the stepdown analysis, each dependent variable was analyzed

in turn with higher priority dependent variables treated as

covariates and with the highest priority dependent variables

tested in a univariate ANOVA. The Problem Scale was chosen as

the highest priority dependent variable as the literature

suggests that behavioral problems may result from prenatal

cocaine exposure.










The results of this analysis are shown in Table 18. The

Hotelling's criterion for the combination of dependent

variables was not significant with E(2,57) = 1.32, R > .05.

Findings indicate that there are no differences between

exposed and nonexposed children on this combination of

variables by parent report. Inspection of univariate and

stepdown results at the a < .05 level reveal no significant

differences between exposed and nonexposed children on these

variables. Specifically, groups were not significantly

different on either the ECBI problem scale (1,58) = 2.63, Q

> .05, or intensity scale (1,57) = .05, R > .05.



Hypothesis 4

It was also hypothesized that adaptive difficulties would

be more pronounced in the exposed group. Descriptive data for

the exposed and nonexposed children are summarized on Table

16. To test this, a multivariate analysis of covariance was

performed on the four dependent variables that comprise the

Vineland: Socialization, Communication, Daily Living, and

Motor Skills. In the initial analysis, adjustment was made

for five covariates including alcohol, maternal depression,

foster care, HOME inventory, and child gender. The

independent variable was exposure status (exposed to crack










versus not exposed to crack in utero). SPSS' MANCOVA was used

for the initial analyses with the sequential adjustment for

nonorthogonality.

With the use of Hotelling's criterion, the dependent

variables were not significantly related to the combined

covariates, with (20,194) = 1.55, R > .05. Thus, all five

covariates were dropped from further analyses. The effects of

exposure status on the dependent variables without inclusion

of covariates were investigated in univariate and stepdown

analysis using SPSS" MANOVA. Dependent variables were entered

in the following order: Socialization, Communication, Daily

Living, and Motor Skills. In the stepdown analysis, each

dependent variable was analyzed in turn with higher priority

dependent variables treated as covariates and with the highest

priority dependent variables tested in a univariate ANOVA.

Socialization was chosen as the highest priority dependent

variable as the literature suggests that social relatedness

may be disturbed by prenatal cocaine exposure.

The results of this analysis are shown in Table 19. The

Hotelling's criterion for the combination of dependent

variables was not significant with E(4,50) = 1.17, a > .05.

These findings suggest that there are no differences between

exposed and nonexposed children on this combination of











variables by parent report. Inspection of univariate and

stepdown results at the p < .05 level likewise reveal no

significant differences between exposed and nonexposed

children on these variables. Specifically, no significant

between groups differences were noted for socialization

E(1,58) = .40, p > .05, communication (1,57) = .51, p > .05,

daily living (1,56) = 1.12, R > .05, or motor skills E(1,55)

= 1.67, R > .05.



Hypothesis 5

Finally, it was hypothesized that disordered behaviors by

objective observation would be more pronounced in the exposed

group. Descriptive data for the exposed and nonexposed

children are summarized on Table 16 collapsed across parent-

and child-directed interactions. To test this, a multivariate

analysis of covariance was performed on the four dependent

variables derived from compliance data on the DPICS-II: Total

Commands (frequency data), and Percent Comply, Percent

Noncomply, and Percent No Opportunity to comply (percentages).

The ten basic DPICS-II frequency observation variables were

not tested as they were not normally distributed. In the

initial analysis, adjustment was made for five covariates

including alcohol, maternal depression, foster care, home










inventory, and child gender. The independent variable was

exposure status (exposed to crack versus not exposed to crack

in utero). SPSS" MANCOVA was used for the initial analyses

with the sequential adjustment for nonorthogonality.

With the use of Hotelling's criterion, the dependent

variables were not significantly related to the combined

covariates, with E(20,142) =.229, 1 > .05. Thus, all five

covariates were dropped from further analyses. The effects of

exposure status on the dependent variables without inclusion

of covariates were investigated in univariate and stepdown

analysis using SPSS' MANOVA. Dependent variables were entered

in the following order: comply, noncomply, no opportunity to

comply, and commands. In the stepdown analysis, each

dependent variable was analyzed in turn with higher priority

dependent variables treated as covariates and with the highest

priority dependent variables tested in a univariate ANOVA.

Comply was chosen as the highest priority dependent variable

as the literature suggests that child compliance may be

disturbed by prenatal cocaine exposure.

The results of this analysis are shown in Table 20. The

Hotelling's criterion for the combination of dependent

variables was not significant with E(4,42) = .876, p > .05.

These findings suggest that there are no differences between








78

exposed and nonexposed children on this combination of

variables by parent report. Inspection of univariate and

stepdown results at the R < .05 level likewise reveal no

significant differences between exposed and nonexposed

children on these variables. Specifically, significant

differences were not found between groups for commands E(1,45)

= .26, R > .05, comply (1,44) = .86, p > .05, noncomply

(1,43) = .11, R > .05, or no opportunity (1,42) = .02, R >

.05.










Table 1


Demographic Characteristics of the Total Sample


Non-
MATERNAL Exposed Exposed % df p-value


County"
Alachua 20 20 66.7
Marion 10 10 33.3 1 1.0000

Hollingshead"
Four 8 8 26.7
Five 22 22 73.3 1 1.0000

Race"
Black 25 25 83.3
Non-Black 5 5 16.7 1 1.0000

Parity'
Prima 1 1 3.3
Multi 29 29 96.7 1 1.0000


Non-
CHILDREN Exposed Exposed df p-value

Birthweight (gm)b 3355 3297 56 .600


Test Age (months)' 37.3 36 56 .056

* Using Fisher's Chi-Square with the Yates correction for small sample sizes
bUsing Student's t-test
* = < .05










Table 2


Covariate Characteristics of the Total Sample


NOMINAL/ Non-
ORDINAL Exposed Exposed % df p-value


Child Gender
Female 18 16 56.7
Male 12 14 43.3 1 .7945


Fostercare
Yes 2 14 26.7
No 28 16 73.3 1 .0013*


Alcohol
Yes 8 23 51.7
No 22 7 48.3 1 .0003*


Non-
INTERVAL Exposed Exposed t p-value


Maternal 18.4 20.9 .99 .326
Depression


HOME 37.6 36.5 -.52 .605
Inventory


* Using Fisher's Chi-Square with the Yates correction for small sample sizes
b Using Student's t-test
*= p < .05










Table 3
Reliability of Video Coding of Selected DPICS-II Categories in the Child-Directed
Interaction

%Agree %Agree
r Occur Nonoccur Disagree Mean



Direct Command .99 95.03 96.16 .26 95.59

Indirect Command .98 90.18 95.03 .29 92.60

Compliance .97 93.56 97.44 .12 95.50

Noncompliance .84 94.19 97.00 .09 95.59

No Opportunity for Compliance .99 89.32 95.14 .29 92.23

Laugh 1.00 100.00 99.68 .02 99.84

Yell 1.00 100.00 100.00 .00 100.00

Physical Positive .89 89.10 98.90 .04 94.00

Physical Negative 1.00 100.00 100.00 .00 100.00

Destructive .98 100.00 100.00 .00 100.00


Percent agreement for occurrence is based on summing the agreements across subjects
and dividing by the agreements plus disagreements across subjects. Similarly, percent
agreement for nonoccurrence is based on summing agreements across subjects and
dividing by the agreements plus disagreements across subjects.










Table 4

Reliability of Video Coding of Selected DPICS-II Categories in the Parent-Directed
Interaction

%Agree %Agree
I Occur Nonoccur Disagree Mean


Direct Command .99 90.63 96.16 .24 93.39

Indirect Command .95 85.74 96.35 .38 91.04

Compliance .97 91.88 96.68 .18 94.14

Noncompliance .98 90.20 98.40 .11 94.34

No Opportunity for Compliance .98 86.85 93.12 .35 89.98

Laugh .99 100.00 99.62 .02 99.81

Yell .98 100.00 100.00 .00 100.00

Physical Positive .99 96.15 100.00 .00 98.07

Physical Negative 1.00 100.00 100.00 .00 100.00

Destructive .97 91.66 100.00 .00 95.83

Percent agreement for occurrence is based on summing the agreements across subjects
and dividing by the agreements plus disagreements across subjects. Similarly, percent
agreement for nonoccurrence is based on summing agreements across subjects and
dividing by the agreements plus disagreements across subjects.










Table 5
Between Group Differences Defined by Maternal Depression

Low High
MATERNAL M M P
DEPRESSION (n = 21) (n = 39)


CONNORS

Conduct 53.4286 63.2564 .013*

Learning 48.3810 58.9744 .003*

Psychosomatic 49.2381 54.4103 .217

Impulsive 55.9524 58.9487 .193

Anxiety 49.9048 51.5128 .502

Hyperactivity 53.5714 62.0769 .014*

ECBI

Problem 7.3810 11.5385 .069

Intensity 107.5238 126.9231 .019*

VINELAND

Socialization 102.6190 96.8462 .108

Communication 102.6190 102.1026 .882

Daily Living 105.4286 104.1026 .775

Motor Skills 97.0952 96.3333 .856

(Continued)










Table 5 Continued


Low High
MATERNAL M M B
DEPRESSION (n = 18) (n = 36)


DPICS-II (Derived Scores)

Total Commands' 46.0256 46.1333 .989

Percent Comply" .3460 .3514 .908

Percent Noncomplyb .0996 .0896 .696

Percent No Opportunityb .5544 .5591 .915

*= p < .05
Frequency data
percentages










Table 6
Between Group Differences Defined by HOME Inventory


Low High
HOME M M 1
INVENTORY (n = 29) (n = 31)


CONNORS

Conduct 64.6552 55.2903 .013*

Learning 59.1379 51.6452 .028*

Psychosomatic 55.2759 50.0968 .195

Impulsive 58.6552 57.1935 .508

Anxiety 52.6897 49.3226 .138

Hyperactivity 62.0690 56.3226 .085

ECBI

Problem 11.7586 8.5161 .140

Intensity 127.0000 113.7097 .095

VINELAND

Socialization 94.2414 103.1935 .008*

Communication 98.8621 105.4839 .043*

Daily Living 104.0000 105.0968 .804

Motor Skills 92.8621 100.0968 .067


(Continued)










Table 6 Continued


Low High
HOME M Mp
INVENTORY (n = 25) (n = 29)


DPICS-II (Derived Scores)

Total Commands' 45.8000 46.2759 .945

Percent Complyb .3316 .3651 .445

Percent Noncomplyb .0947 .0914 .892

Percent No Opportunityb .5738 .5435 .458

*= p < .05
* frequency data
b percentages










Table 7
Between Group Differences Defined by Foster Care Status


No Yes
M M a
FOSTER CARE (n = 44) (n = 16)


CONNORS

Conduct 62.3182 52.9375 .028*

Learning 55.6818 54.1250 .692

Psychosomatic 54.1364 48.3750 .202

Impulsive 58.3864 56.5625 .464

Anxiety 51.6818 48.9375 .287

Hyperactivity 59.8409 57.0625 .465

ECBI

Problem 11.1136 7.2500 .119

Intensity 123.3636 111.2500 .180

VINELAND

Socialization 99.7727 96.3750 .385

Communication 102.8182 100.8125 .593

Daily Living 105.9545 100.7500 .295

Motor Skills 95.6136 99.3125 .413


(Continued)










Table 7 Continued


No Yes
M M p
FOSTER CARE (n = 39) (n = 29)


DPICS-II (Derived Scores)

Total Commands' 46.0256 46.1333 .989

Percent Complyb .3592 .3247 .481

Percent Noncomplyb .0836 .1170 .212

Percent No Opportunityb .5572 .5583 .981

*=p < .05
* frequency data
percentages










Table 8
Between Group Differences Defined by Gender


Girls Boys
M M P
GENDER (n = 34) (n = 26)


CONNORS

Conduct 61.0882 58.1538 .451

Learning 51.8235 59.7692 .021*

Psychosomatic 54.0588 50.6923 .406

Impulsive 57.0294 59.0385 .366

Anxiety 53.0294 48.2308 .034*

Hyperactivity 56.7941 62.1154 .114

ECBI

Problem 10.2059 9.9231 .899

Intensity 121.3824 118.5000 .732

VINELAND

Socialization 100.3235 96.9615 .335

Communication 105.1471 98.5385 .045*

Daily Living 105.7647 103.0000 .535

Motor Skills 95.4118 98.1538 .496

(Continued)










Table 8 Continued


Low High
M M P
GENDER (n = 30) (n = 24)


DPICS-II (Derived Scores)

Total Commands' 44.1333 48.4583 .532

Percent Complyb .3746 .3183 .198

Percent Noncomplyb .0801 .1089 .233

Percent No Opportunityb .5453 .5728 .500

* =p < .05
' frequency data
b percentages










Table 9
Between Group Differences Defined by Alcohol Use


No Use Use
M M P
ALCOHOL (n = 29) (n = 31)


CONNORS

Conduct 63.0000 56.8387 .107

Learning 57.1724 53.4839 .287

Psychosomatic 56.5172 48.9355 .056

Impulsive 59.0000 56.8710 .334

Anxiety 50.7931 51.0968 .895

Hyperactivity 61.8966 56.4839 .105

ECBI

Problem 11.7931 8.4839 .132

Intensity 127.4438 113.2903 .075

VINELAND

Socialization 99.1724 98.5806 .865

Communication 100.4483 104.0000 .284

Daily Living 102.6897 106.3226 .410

Motor Skills 96.0690 97.0968 .797


(Continued)




Full Text
128
spurious significance in the assigned variable and reduce the
power of other comparisons. Multiple correlations based on a
small sample can also result in inflated significance. A more
conservative significance level (,01) was used to offset this.
Use of marijuana and cigarette smoking, which were not
controlled in this study, may have affected outcome. Despite
extensive interviewing and toxicology screens, it is possible
that the control group may have been contaminated by cocaine
either by direct maternal use or via secondhand smoke.
Further, it was not possible to determine the effect of
varying amounts or timing of cocaine exposure on outcome. At
three years of age, any behavioral or adaptive impact due to
cocaine exposure may be too subtle to capture on the chosen
psychological instruments. Alternately, systematic bias may
have been present in the responses of biological vs.
nonbiological mothers in the study obscuring potentially real
differences. Although for this reason it was critical to
include an objective measure of behavior, the infrequency of
certain behaviors such as 'cry' may have minimized their
usefulness as markers of cocaine exposure.


15
by species or strain. Furthermore, they appear to be heavily
dose-dependent including some studies using extremely high
doses of cocaine, and demonstrate that impact appears
contingent upon the gestational period of drug administration.
Clearly fetal exposure to cocaine is not a benign perinatal
event. But the deficiencies noted in the animal literature
such as locomotor changes or alterations in learning and
"cognition" are frequently difficult to demonstrate in
parallel forms in human infants. In addition, it is unclear
whether such alterations in functioning found in the animal
literature are transient or long-term.
Preliminary attempts have been made to study human
infants in terms of the physiological impact of cocaine
exposure in tero. For example, Link, Weese-Mayer, and Byrd
(1991) performed magnetic resonance imagery (MRIs) on infants
exposed to cocaine prenatally to determine the presence of
hypoxic injuries. In all 21 infants studied, at a mean age of
3,6 years, they found myelination was appropriate compared to
age-matched norms; brain and brainstem anatomy were also
normal with no evidence of infarct or hemorrhage. Link et al.
(1991) concluded that negative findings could be due to the
small sample size, limited maternal use, or the possibility
that cocaine use without concomitant use of other illicit


133
Chiriboga, C.A., Bateman, D.A., Brust, J.C.M., & Hauser, W.A.
(1993). Neurologic findings in neonates with
intrauterine cocaine exposure. Pediatric Neurology. 9,
115-119.
Coles, C.D., Platzman, K.A., Smith, I., James, M.E., & Falek,
A. (1992). Effects of cocaine and alcohol use in
pregnancy on neonatal growth and neurobehavioral status.
Neurotoxicology and Teratology. 14, 23-33.
Connors, C.K. (1994). Conners Rating Scales. Hillsdale, NJ:
Lawrence Erlbaum.
Davis, E., Fennoy, I., Laraque, D., Kanem, N., Brown, G., &
Mitchell, J. (1992). Autism and developmental
abnormalities in children with perinatal cocaine
exposure. Journal, of the National Medical Assoqi^tion,
M, 315-319.
Doberczak, T.M., Shanzer, S., Senie, R.T., & Kandall, S.R.
(1988). Neonatal neurologic and electroencephalographic
effects of intrauterine cocaine exposure. Journal of
Pediatrics. 113. 354-358.
Dow-Edwards, D.L. (1989). Long-term neurochemical and
neurobehavioral consequences of cocaine use during
pregnancy. Annals New York Academy of Sciences. 362,
280-289.
Dow-Edwards, D.L. (1991). Cocaine effects on fetal
development: a comparison of clinical and animal
research findings. Neurotoxicology and Teratology, 13,
347-352.


56
Of the four derived DPICS-II observational scales, only
no opportunity to comply was found to be moderately skewed.
This scale was corrected for subsequent analyses using a log
transformation. The remaining three scales, command, comply,
and noncomply, were found to approximate normality. Data were
missing for six of the children from the nonexposed group.
Because data frequency was low on observational scales, it was
considered inappropriate to substitute missing data with group
means, and analysis of these variables was performed with
unequal sample size.
Reliability of Observational Measures
Interrater reliability calculations were performed for
two raters on DPICS-II behavioral variables for both child
directed interactions and parent directed interactions (Tables
3 and 4). In general, interrater reliability was very strong
using Pearson's Product Moment values ranged from r = .84 to
1.00 across the ten basic frequency observation variables in
two situations (parent and child directed play interactions).
Pearson's correlations can be inflated or deflated based on
the frequency of occurrence. Thus, it was decided to
determine interrater reliabilities using agreement of
occurrence, agreement of nonoccurrence, and finally the mean


58
significant differences were found between groups on these
variables. Similarly, no significant differences on interval
scale data using t-tests were found on basic child
characteristics including birth weight and age at testing
(Table 1).
Covariate Between Groups Differences
Covariates measured on a nominal or ordinal scale were
also analyzed for significant differences between the exposed
and nonexposed groups using Fisher's Chi-Square with the Yates
Correction for small sample sizes. Covariates included child
gender, foster care, and alcohol use where alcohol use was
converted to an ordinal variable to control for outliers. No
differences were found between groups in terms of gender.
However, children exposed to crack were significantly more
likely to be in foster care than children in the nonexposed
group with X2(l) = 10.31, p = .0013. Similarly, children who
were exposed to crack in tero were more likely to be exposed
to alcohol than nonexposed children with X2(l) 13.08, p =
.0003.
Remaining covariates measured on an interval scale were
analyzed for significant differences between exposed and
nonexposed groups using t-tests. These covariates included


REFERENCES
Abelson, H. & Miller, J. (1985). A decade of trends in
cocaine use in the household population. National
Institute of Drug Abuse Research Monograph Series, 16, 35-
49.
Adams, E.H., Gfroerer, J.C., Rouse, B.A., & Kosel, N.J.
(1986). Trends in prevalence and consequences of cocaine
use. Advances in Alcohol Substance Abuse. 6, 49-71.
Azuma, S., & Chasnoff, I.J. (1993). Outcome of children
prenatally exposed to cocaine and other drugs: a path
analysis of three-year data. Pediatrics. 92, 396-402.
Bauchner, H., Zuckerman, B., McClain, M., Frank, D., Fried,
L.E., & Kayne, H. (1988). Risk of sudden infant death
syndrome among infants with in tero exposure to cocaine.
Journal of Pediatrics. 113. 831-834.
Bee, H.L., Barnard, K.E., Eyres, S.J., Gray, C.A., Hammond,
M.A., Spietz, A.L., Snyder, C., & Clark, B. (1982).
Prediction of IQ and language skill from perinatal status,
child performance, family characteristics, and mother-
infant interaction. Child Development. 53, 1134-1156.
Bingol, N., Fuchs, M. Diaz, V. Stone, R.K., & Gromisch, D.S.
(1987) Teratogenicity of cocaine in humans. The Journal
of Pediatrics, 110, 93-96.
131


126
between parenting, the environment, and drug exposure status
on child outcome.
Strengths and Weaknesses
The study has several important strengths. First, a
variety of possible confounding variables were controlled for
between groups including alcohol exposure, foster care status,
gender, home environment, and maternal depression. Groups
were matched on a number of important variables including
race, maternal parity, county (which reflected level of
prenatal risk), and socioeconomic status in order to control
for overall variance in the sample. Children with significant
developmental difficulties, exposure to forms of cocaine other
than crack, or who were low birthweight (defined as under
2,500 grams) were excluded from the study.
Biological mothers with a significant psychiatric
history, illicit drug use (other than marijuana or crack
cocaine), or whose primary language was not English were
excluded from the study. Biological mothers were over 18
years of age to reduce neonatal risk associated with pregnancy
in the young teenager.
Appropriate statistical controls and analyses were used
to make interpretation as clear as possible. Welch's V was


87
Table 7
Between Group Differences Defined by Foster Care Status
FOSTER CARE
No
M
(n = 44)
Yes
M
(n = 16)
u
CONNORS
Conduct
62.3182
52.9375
.028*
Learning
55.6818
54.1250
.692
Psychosomatic
54.1364
48.3750
.202
Impulsive
58.3864
56.5625
.464
Anxiety
51.6818
48.9375
.287
Hyperactivity
59.8409
57.0625
.465
ECBI
Problem
11.1136
7.2500
.119
Intensity
123.3636
111.2500
.180
VINELAND
Socialization
99.7727
96.3750
.385
Communication
102.8182
100.8125
.593
Daily Living
105.9545
100.7500
.295
Motor Skills
95.6136
99.3125
.413
(Continued)


62
Covariates and Dependent Variables
The relationships between covariates and dependent
variables are presented in Table 10. Notably, elevated
maternal depression was significantly related to increased
conduct disorder r = .3358, p < .01, learning problems r =
.3977, p < .01, and hyperactivity r = .3534, p < .01 on the
Connors. Maternal depression was also related to the problem
scale of the ECBI r = .3387, p < .01, again suggesting that
problem behaviors are more strongly associated with higher
levels of maternal depression. Similarly, a more enriched
home environment as measured by HOME inventory was
significantly related to better communication r = .3488, p <
.01. Interestingly, no significant relationships were noted
between the ten basic and four derived DPICS-II variables and
five measured covariates. It should be noted that a more
conservative significance level of .01 was chosen in order to
partially control spurious relationships that may results from
multiple corrrelations.
Covariates
In general, relationships between pairs of covariates
were insignificant using a two-tailed analysis. However,
caregivers who were raising foster children reported


BIOGRAPHICAL SKETCH
Karen Holler is currently a clinical psychology intern at
the Brown University Psychology Training Consortium. She is
completing degree requirements toward her Ph.D. in clinical
psychology in the Department of Clinical and Health Psychology
at the University of Florida in Gainesville where she received
her M.S. in clinical psychology in 1993. She received her
B.S. in biology in 1983 from Bates College in Lewiston, Maine,
and has done post-baccalaureate work at San Francisco State
University. Ms. Holler has a special interest in pediatric
neuropsychology. In addition to her research interest in
developmental outcome in children who have been exposed to
teratogens perinatally, she has an ongoing interest in the
neuropsychology of hydrocephalus, spina bifida, childhood TBI,
and cerebral palsy.
142


9
(1993) found that administration of cocaine to rat dams
resulted in increases in fetal activity which they
subsequently considered a reflection of altered CNS
development.
Subsequent investigations found that prenatal exposure to
cocaine in late gestation results in a decrease in the number
of spontaneously active midbrain dopaminergic cells in adult
rats, whereas rats exposed to cocaine only in adulthood showed
an increase in the number of spontaneously active dopaminergic
cells (Minabe, Ashby, Heyser, Spear, & Wang, 1992), The
decrease of midbrain dopamine activity in adult rats exposed
prenatally to cocaine has been used to explain early findings
of irritability and decreased interactive behaviors in human
infants. These reports suggest, not surprisingly, that
prenatal cocaine exposure may be toxic to the fetus or impact
negatively on the developing neuronal system in a manner that
does not necessarily parallel consequences of adult exposure.
Studying cell development in brain regions, Seidler and
Slotkin (1993) compared rat pups exposed in tero to cocaine
during late gestation to a nonexposed comparison group. They
found retarded maternal weight gain but no effect on pup body
or brain region weights. DNA content was also largely
unaffected. Although postnatal cell growth was reduced in the


6
Research, medical or otherwise, on preschoolers exposed to
cocaine in tero is very limited.
The absence of literature notwithstanding, concern for a
generation of children exposed to cocaine is certainly
warranted. One survey suggested that 10% of women may use
cocaine at least once during pregnancy, and 50% of these use
other drugs in addition to cocaine (Howard et al., 1987).
Cocaine is highly water and lipid soluble and passes through
the placentae by simple diffusion. Cocaine may concentrate in
the fetus because fetal blood has a lower pH. In addition,
plasma cholinesterase, which is necessary to metabolize
cocaine, is less active in the fetus and in pregnant women
(Bingol, Fuchs, Diaz, Stone, & Gromisch, 1987). Conceivably,
even small doses of cocaine could have negative consequences
on a developmentally vulnerable embryo and fetus. Although
results in the literature are equivocal, cocaine has been
implicated in a number of negative outcomes including
spontaneous abortions, fetal death, preterm labor, precipitous
labor, abruptio placentae, fetal distress, fetal meconium
staining and other conditions which qualify the newborn for
high risk status (Chasnoff, Burns, Schnoll, & Burns, 1985; Oro
& Dixon, 1987; Ryan et al., 1987).


4
initially been considered a 'safe' stimulant (Schnoll,
Karrigan, Kitchen, Daghestani, & Hansen, 1985; Siegel, 1985).
Associated with the use of cocaine are a number of
behavioral changes as well as substantial physical risk.
Behavioral effects that have been described in adult users
include impulsivity, disinhibition, repetitive actions,
anxiety, psychomotor activation and a loss of appetite which
can result in malnutrition (Howard et al., 1987; Levine,
i
Washington, Jefferson, Kieran, Moen, Feit, & Welch, 1987;
Medical Letter, 1986). Severe and toxic physiological effects
have been described in the literature. Hypertension,
tachycardia, ventricular arrhythmias, seizures, loss of
consciousness, stroke, and myocardial infarctions are
increasingly attributed to cocaine use. Even deaths due to
respiratory and cardiac arrest have been reported (Howard et
al., 1987; Levine et al., 1987; Medical Letter, 1986).
Further, there are indications that the inhibitory
receptors of dopamine neurons become supersensitive as an
adaptation to chronic activation of the reward pathways which
occurs with stimulant use (Gawin & Kelber, 1986). Thus, there
is some evidence that long-term cocaine use may lead to
permanent neurophysiological changes in the brain that impact
on mood states and the user's experience of pleasure. Such


73
of covariance was performed on the two dependent variables
that comprise the ECBI: Problem and Intensity Scales, In the
initial analysis, adjustment was made for five covariates
including alcohol, maternal depression, foster care, HOME
inventory, and child gender. The independent variable was
exposure status (exposed to crack versus not exposed to crack
in tero) SPSS* MANCOVA was used for the analyses with the
sequential adjustment for nonorthogonality.
With the use of Hotelling's criterion, the dependent
variables were not significantly related to the combined
covariates with £(10,102) = .921, p > .05. Thus, all five
covariates were dropped from further analyses. The effects of
exposure status on the dependent variables without inclusion
of covariates were investigated in univariate and stepdown
analysis using SPSS* MANOVA. Dependent variables were entered
in the following order: Problem Scale and Intensity Scale.
In the stepdown analysis, each dependent variable was analyzed
in turn with higher priority dependent variables treated as
covariates and with the highest priority dependent variables
tested in a univariate ANOVA. The Problem Scale was chosen as
the highest priority dependent variable as the literature
suggests that behavioral problems may result from prenatal
cocaine exposure.


23
cocaine-using mothers, Chasnoff (1989) found two infants with
prune belly syndrome, (a congenital nephrotic disorder) one
with female pseudohermaphroditism, two with hypospadias and
undescended testes, and three with hydroureter/hydronephrosis.
Further, two infants in this study suffered perinatal cerebral
infarctions that he attributed to maternal cocaine use in the
48 to 72 hours preceding delivery.
In a similar study, Chasnoff, Chisum, and Kaplan (1988)
found nine of 50 infants born to prenatal cocaine users had
some form of physical anomaly compared to only one of 30
infants born to polydrug noncocaine-using women. These
anomalies included two with ileal atresia and seven with
malformations of the genitourinary tract. While the
researchers attributed these effects to cocaine exposure, all
women in the study were known substance users specifically
enrolled for treatment possibly confounding outcome, and
polydrug use was common.
Researchers who have considered the outcome of cocaine-
exposed children in the context of other factors have found
more moderate results. For example, Bauchner, Zuckerman,
McClain, Frank, Fried, and Kayne (1988) assessed the risk of
SID among cocaine-exposed infants and found one of 175
prenatally cocaine-exposed infants died of SID and four of 821


95
Table 11
Correlations between Covariates
Alcohol
Exposure
Foster
Care
Gender
Maternal
Depression
HOME
Inventory
Alcohol
1.0000
.3191
-.0316
-.0928
-.0541
Foster
1.0000
.3093
-.3363*
.0656
Gender
1.0000
-.0830
.0248
Depression
1.0000
-.2629
HOME
1.0000
* p < .01
** p < .001


18
maternal factors, cocaine/ methamphetamine and narcotic use
still made significant independent and negative contributions
to gestational age, birth weight, length and OFC (Oro & Dixon,
1987).
The results of this study and of many early studies like
it appeared to confirm the clinicians' worse fears regarding
cocaine exposure in tero. However, a critical evaluation of
the methodology mitigates the findings to a degree. For
example, in the above study, the combined effects of certain
drugs (in this case methamphetamine and cocaine) may have had
some unique or synergistic properties not found when the same
drugs are taken separately. Further, it is unclear whether
evaluators in this study were blinded to the drug group
affiliation of the babies being studied. Confounds and
researcher bias have been frequently apparent in this body of
literature on prenatal cocaine exposure, especially in earlier
reports.
In another study concerned with the teratogenic effects
of cocaine, Bingol et al. (1987) compared a polydrug, a
cocaine only, and a no illicit drug control group. The
cocaine group was comprised of 60% intranasal, 30% free base
inhalation, and 10% intravenous users. While no statistical
differences were reported in the spontaneous abortion rates


DEVELOPMENTAL OUTCOME FOR PRESCHOOLERS PRENATALLY EXPOSED TO
CRACK COCAINE: BEHAVIORAL AND ADAPTIVE SEQUELAE
By
KAREN ANNE HOLLER
A DISSERTATION PRESENTED TO THE GRADUATE SCHOOL
OF THE UNIVERSITY OF FLORIDA IN PARTIAL FULFILLMENT
OF THE REQUIREMENTS FOR THE DEGREE OF
DOCTOR OF PHILOSOPHY
UNIVERSITY OF FLORIDA
1996


139
presenting for treatment. National Institute on Drug
Abuse Research Monograph Series, 61, 171-181.
Schuster, C.R., & Fischman, M.W. (1985). Characteristics of
humans volunteering for a cocaine research project.
National Institute on Drug Abuse Research Monograph
Series. 61, 158-170.
Seidler, F.J., & Slotkin, T. A. (1992). Fetal cocaine
exposure causes persistent noradrenergic hyperactivity in
rat brain regions: effects on neurotransmitter turnover
and receptors. The Journal of Pharmacology and
Experimental Therapeutics. 263, 413-421.
Seidler, F.J., & Slotkin, T.A. (1993). Prenatal cocaine and
cell development in rat brain regions: effects on
ornithine decarboxylase and macromolecules. Brain
Research Bulletin. 30, 91-99.
Siegel, R.K. (1985). New patterns of cocaine use: changing
doses and routes. National Institute on Drug Research
Monograph Series. 61, 204-220.
Singer, L.T., Yamashita, T.S., Hawkins, S., Cairns, D., Baley,
J., & Kliegman, R. (1994). Increased incidence of
intraventricular hemorrhage and developmental delay in
cocaine-increased incidence of intraventricular
hemorrhage and developmental delay in cocaine-exposed,
very low birth weight infants. Journal of Pediatrics,
124, 765-771.
Smith, R.F., Mattran, K.M., Kurkjian, M.F., & Kurtz, S.L.
(1989). Alterations in offspring behavior induced by


64
reduced socialization r = -.3343, p < .001. Neither ECBI
score was related to any measured domain of adaptive
functioning (Table 12).
Parent Report and Derived Observational Variables
Of particular interest were relationships between parent
report dependent measures and derived observational measures.
When examining derived DPICS-II scores, results indicate that
noncompliance measured objectively was related to caregiver
reports of higher learning problems r .3578, p < .01, and
reduced daily living skills r = -.4229, p < .01. Similarly,
higher levels of caregiver perceived socialization were
positively related to compliance r = .4384, p < .01 (Table
12).
In terms of child behaviors, yell was positively related
to conduct problems and psychosomatic behavior with r = .4186,
p < .01 and r = .4399, p < .001 respectively. Finally, child
destructive behavior was significantly associated with conduct
problems with r = .3846, p < .01. It should be noted that a
more conservative significance level of .01 was chosen in
order to partially control spurious relationships that may
result from multiple correlations. Again, preliminary between


Hypothesis 2 70
Hypothesis 3 72
Hypothesis 4 74
Hypothesis 5 76
DISCUSSION 108
Background 108
Comparison to Norms 110
Between Groups Comparisons 116
Covariate Findings 122
Strengths and Weaknesses 126
Suggestions for Further Study 129
Conclusion..., 130
REFERENCES 131
BIOGRAPHICAL SKETCH 142
v


135
matched on maternal risk factors. Neurotoxicology and
Teratology, 16. 81-87.
Fung, Y.K., Reed, J.A., & Lau, Y.S. (1989). Prenatal cocaine
exposure fails to modify neurobehavioral responses and
the striatal dopaminergic system in newborn rats.
General Pharmacology. 20, 689-693.
Gawin, F.H., & Kleber, H.D. (1985). Cocaine use in a
treatment population: patterns and diagnostic
distinctions. National Institute on Drug Abuse Research
Monograph Series. 61, 182-192.
Gawin, F.H., & Kleber, H.D. (1986). Abstinence
symptomatology and psychiatric diagnosis in cocaine
abusers. Archives of General Psychiatry, 43., 107-113.
Goeders, N.E. & Smith, J.E. (1983). Cortical dopaminergic
involvement in cocaine reinforcement. Science. 221. 773-
775.
Griffith, D.R., Azuma, S.D., & Chasnoff, I.J. (1994). Three-
year outcome of children exposed prenatally to drugs.
Journal of the American Academy of Child_ and Adolescent
Psychiatry. 33, 20-27.
Grinspoon, L. & Balkalar, J.B. (1980). Drug dependence:
non-narcotic agents. In: H.I., Kaplan, A.M. Freedman,
B.J. Sadock (Eds.) Comprehensive textbook of psychiatry,
3rd ed. Baltimore: Williams & Wilkins, 1980.
Hadeed, A.J., & Siegel, S.R. (1989). Maternal cocaine use
during pregnancy: effect on the newborn infant.
Pediatrics. 84. 205-210.


68
compliance was also significantly higher in the sample
compared to both the clinic referred and nonreferred reference
groups with y = 5.47, p <.01 and y = 6.61, p < .01
respectively. Noncompliance was likewise elevated in the
sample group compared to referred and nonreferred group with
y = 3.24, p < .01 and y = 3.93, p < .01 respectively.
Finally, no opportunity for compliance occurred at
significantly higher rates in the study sample compared to
normative groups including clinic referred where y = 7.96, p
< .01 and nonreferred where y = 8.12, p < .01.
No significant differences between the study sample, and
referred and nonreferred normative groups were noted on child
behaviors including yell, physical negative or destructive
using the SMM familywise rate for three comparisons. It was
not possible to test differences in the rate of laugh and
physical positive as normative data were not available for
these two variables. Results suggest that overall rates of
both indirect and direct commands were elevated in the present
study sample which in turn results in higher rates of
compliance, noncompliance, and no opportunity to comply (Table
14).
Using the SMM familywise rate for five comparisons,
significant differences were found between the study sample


124
Vineland indicating that children in more enriched homes have
better communication skills at three years of age. Child
gender was not significantly related to any dependent
variable.
Relationships between covariates and dependent variables
and the lack of drug exposure findings highlight the
importance of considering parenting and environmental
variables when studying outcome for cocaine-exposed children.
There are actually few studies in the cocaine literature which
have evaluated the impact of parenting and rearing environment
on child outcome. Eyler et al. (1994) reported that cocaine
using women tended to suffer more depression, poor self
esteem, and feel less in control of their lives than nonusing
controls. Cocaine-using women also experienced significantly
more stressful life events than nonusers. Although studies
have not reported significant differences in the interactions
of depressed mothers with their children in infancy (Black et
al., 1993? Neuspiel et al., 1994), by the age of three,
chronic maternal depression and/or stressful life events may
exert a measurable impact on child outcome.
Finally, in an effort to clarify possible relationships
between covariates and dependent variables, exploratory
between-groups analyses were made using covariates as


26
high rate of attrition. The conclusion that head growth after
birth may be a biological marker for drug exposure may be
correct? however, this cannot be attributed solely to cocaine
exposure in tero, particularly since the marijuana/alcohol
but no cocaine group also lagged in head growth.
In the context of longer term development, Azuma and
Chasnoff (1993) subsequently assessed the three year outcome
of cocaine-exposed children using cognitive and behavioral
measures. They found that children prenatally exposed to
cocaine were no different from controls in terms of
intelligence measured on the Stanford Binet (SBIT). However,
statistical modelling using path analysis suggested that drug
exposure, home environment and level of perseverance
(attention) had direct effects on cognitive function, while
head growth and parent report of behavioral functioning did
not have a direct effect on test scores. The authors
considered this a "best case" outcome study because all women
were involved in a treatment program. However, as in the two
year followup of the same population, possible biases and
confounds existed particularly with regard to subject
attrition.
From the same research team, Griffith, Azuma, and
Chasnoff (1994) also evaluated the three-year behavioral and


10
forebrain, the magnitude of the reduction was small when
compared to the impact of other drugs such as the hypoxic or
ischemic effects of nicotine. Seidler and Slotkin (1992)
concluded that functional deficits attributable to fetal
cocaine exposure probably result from actions directed toward
specific cell or synaptic populations as opposed to global
effects on cell development.
In another investigation, Seidler and Slotkin (1992)
found somewhat conflicting results when studying the effect of
fetal cocaine exposure on rats given 30 mg/kg daily from
gestational days 2 to 20. As a toxic referent, a dose of
approximately 80 to 100 mg/kg of cocaine is generally fatal in
adult rats. The exposed group showed minor differences from
controls in body and brain region weights and in levels of
norepinephrine. However, investigators found marked
noradrenergic hyperactivity as assessed by noradrenergic
turnover, which they attributed to the effects of
glucocorticoids and hypoxia on noradrenergic cell
differentiation. These results suggest that hypoxia rather
than dopaminergic disruption may be the more critical result
of cocaine exposure in tero.
Animals prenatally exposed to cocaine generally show
differential physiologic responses to hypoxia compared to


81
Table 3
Keiiamnty or video coding or selected 11 categories in tne cnna-uirecteo
Interaction
I
% Agree
Occur
% Agree
Nonoccur
Disagree
Mean
Direct Command
.99
95.03
96.16
.26
95.59
Indirect Command
.98
90.18
95.03
.29
92.60
Compliance
.97
93.56
97.44
.12
95.50
Noncompliance
.84
94.19
97.00
.09
95.59
No Opportunity for Compliance
.99
89.32
95.14
.29
92.23
Laugh
1.00
100.00
99.68
.02
99.84
Yell
1.00
100.00
100.00
.00
100.00
Physical Positive
.89
89.10
98.90
.04
94.00
Physical Negative
1.00
100.00
100.00
.00
100.00
Destructive
.98
100.00
100.00
.00
100.00
Percent agreement for occurrence is based on summing the agreements across subjects
and dividing by the agreements plus disagreements across subjects. Similarly, percent
agreement for nonoccurrence is based on summing agreements across subjects and
dividing by the agreements plus disagreements across subjects.


41
year followup as part of the ongoing study. Thirteen children
(14.4%) were dropped from the study. Of the thirteen excluded
children, 9 were low birth weight (69.3%; 5 targets and 4
controls), 3 were exposed to forms of cocaine other than crack
(23.1%), and one had sickle cell anemia (7.7%). At the close
of enrollment for this study, the matches for 17 (18.9%) of
the original 90 had not been tested. Thus, the 17 unmatched
subjects had to be dropped from the study.
The remaining 30 pairs of matched children (66.7%)
constituted the study sample. Forty of the children (66.7%)
were from Alachua County, and 20 children (33.3%) were from
neighboring Marion County. Two of the mothers were
primiparous (3.3%) and 58 were multiparous (96.7%). Fifty of
the mothers were African American (83.3%) and ten were of
other ethnic origin (16.7%). Sixteen of the women earned a
Hollingshead Index of four (26.7%) while 44 of the women
earned a Hollingshead of five (73.3%). The Hollingshead Index
is a measure of socioeconomic status based on level of
education and employment. Scores range from one to five with
scores of four and five representing the lowest levels of
employment and education. Thirty of the children (50.0%) were
exposed to crack cocaine in tero and 30 were not exposed
(50.0%). Tables 1 and 2 outline basic demographic and


57
of agree occur and agree nonoccur for low frequency data
measured in discrete time intervals (Page & Iwata, 1986).
Percent agreement for occurrence was based on summing the
agreement of occurrence across subjects and dividing by the
agreement of occurrence plus disagreements across subjects.
Percent agreement for nonoccurrence was based on summing the
agreement of nonoccurrence divided by the agreement of
nonoccurrence plus disagreements across subjects. In the
child directed interactions, agreement of a given behavior
ranged from 89.10% to 100.00%. Similarly, agreement of
occurrence of a given behavior in the parent directed
interaction ranged from 85.74% to 100.00%. In summary,
interrater reliabilities were strong across all behaviors.
Initial Between-Groups Analyses
Demographic Between Groups Differenqes
Basic demographic match criteria variables measured on a
nominal or ordinal scale were analyzed for significant
differences between the exposed and nonexposed groups using
Fisher's Chi-Square with the Yates Correction for small sample
sizes. Demographic variables included parity, race, county,
and Hollingshead Index. Due to matching upon entry to the
study and limited variability, it is not surprising that no


82
Table 4
Reliability _Qf Video Coding of Selected DPICS-II Categories in the Parent-Directed
Interaction
% Agree % Agree
r Occur Nonoccur Disagree Mean
Direct Command .99
Indirect Command .95
Compliance .97
Noncompliance .98
No Opportunity for Compliance .98
Laugh .99
Yell .98
Physical Positive .99
Physical Negative 1.00
Destructive .97
90.63
96.16
.24
93.39
85.74
96.35
.38
91.04
91.88
96.68
.18
94.14
90.20
98.40
.11
94.34
86.85
93.12
.35
89.98
100.00
99.62
.02
99.81
100.00
100.00
.00
100.00
96.15
100.00
.00
98.07
100.00
100.00
.00
100.00
91.66
100.00
.00
95.83
Percent agreement for occurrence is based on summing the agreements across subjects
and dividing by the agreements plus disagreements across subjects. Similarly, percent
agreement for nonoccurrence is based on summing agreements across subjects and
dividing by the agreements plus disagreements across subjects.


Ill
Conduct problem on the Connors scale is characterized by
items such as 'sassy to grownups,' 'destructive,' and 'bullies
others.' The learning problem subscale is comprised by items
such as 'difficulty learning,' and 'fails to finish things.'
The impulsivity subscale on the Connors was also elevated in
the sample and indicates increased incidence of behaviors such
as 'excitable, impulsive,' and 'restless in the squirmy
sense.' Elevation on the hyperactivity subscale of the
Connors in the sample group is consistent with 'restless,
always up and on the go,' and 'distractibility or attention
span problem.' Again, all but one of these subscales were
positively related to maternal depression but were not related
to any other covariate.
Similarly, noted differences on the ECBI between the
normative group and the total sample on the Intensity scale
were represented by high scores on items such as 'acts defiant
when told to do something,' and 'has temper tantrums.'
Although the sample was not significantly different from the
normative group on the Problem scale of the ECBI, higher
ratings on this scale were associated with increased maternal
depression. The relationship between maternal depression and
problem behaviors in children is reflected in the current
findings by parent report. Interestingly, inspection of means


118
sampled behaviors that are indeed different between groups.
Addressing the first point, speculating about differences
between groups that are too subtle to be measured with current
instruments is interesting but scientifically and clinically
meaningless. Again, instruments were chosen for the present
study based on their good sensitivity to group differences and
broad sampling of behaviors. Measures were also theoretically
based on existing literature and the presumed disruptive
action of cocaine on the developing child.
It appears unlikely that gross differences in behavioral
or adaptive functioning were simply missed due to the use of
inappropriate measures. As an interesting aside, none of the
subscale means on the Connors or Vineland for either the
exposed or nonexposed groups actually fall in the clinically
impaired range. Thus, even if significant differences between
groups existed in the present study, clinical relevance might
be debated. The only scale which approaches significance in
the clinically impaired range of behavior is the nonexposed
group on the ECBI Intensity Scale by parent report.
This finding is mirrored in nonsignificant trends in the
data. Inspection of between groups means on behavioral parent
report variables indicates that the nonexposed group means
were higher on all six Connors subscales including Conduct,


79
Table 1
Demographic Characteristics of the Total Sample
MATERNAL
Non-
Exposed
Exposed
%
df
p-value
County*
Alachua
20
20
66.7
Marion
10
10
33.3
1
1.0000
Hollingshead*
Four
8
8
26.7
Five
22
22
73.3
1
1.0000
Race*
Black
25
25
83.3
Non-Black
5
5
16.7
1
1.0000
Parity*
Prima
1
1
3.3
Multi
29
29
96.7
1
1.0000
Non-
CHILDREN
Exposed
Exposed
df
p-value
Birthweight (gm)b
3355
3297
56
.600
Test Age (months)b
37.3
36
56
.056
a Using Fishers Chi-Square with the Yates correction for small sample sizes
b Using Students t-test
* = p < .05


INTRODUCTION
Cocaine is one of the most popular illicit drugs used in
the United States. Approximately 30 million Americans have
tried cocaine at least once and as many as five million use
cocaine on a regular basis (Abelson & Miller, 1985). The two
common forms of illicit cocaine are cocaine hydrocholoride
(HC1) in a powder form, and 'crack,' a highly purified
alkaloidal base also known as 'freebase.'
Cocaine (methylbenzoylecgonine) is a central nervous
system (CNS) stimulant that works in part by increasing the
activation of the neurotransmitter dopamine in the mesolimbic
and/or mesocortical pathways. Increased activation results in
a stimulant induced reward or the 'euphoria' commonly
experienced by cocaine users (Goeders & Smith, 1983? Wise,
1984). Neurotransmitter reuptake is simultaneously reduced in
the cerebral cortex, hypothalamus, and cerebellum resulting in
the hyperaroused state also typical of cocaine intoxication
(Ryan, Ehrlich, & Finnegan, 1987). Cocaine taken intranasally
(or 'snorted') causes vasoconstriction of the nasal mucous
membranes which reduces its own absorption. Subsequently, the
plasma drug concentration rises relatively slowly for
1


77
inventory, and child gender. The independent variable was
exposure status (exposed to crack versus not exposed to crack
in tero). SPSS* MANCOVA was used for the initial analyses
with the sequential adjustment for nonorthogonality.
With the use of Hotelling's criterion, the dependent
variables were not significantly related to the combined
covariates, with F(20,142) =.229, p > .05. Thus, all five
covariates were dropped from further analyses. The effects of
exposure status on the dependent variables without inclusion
of covariates were investigated in univariate and stepdown
analysis using SPSS* MANOVA. Dependent variables were entered
in the following order: comply, noncomply, no opportunity to
comply, and commands. In the stepdown analysis, each
dependent variable was analyzed in turn with higher priority
dependent variables treated as covariates and with the highest
priority dependent variables tested in a univariate ANOVA.
Comply was chosen as the highest priority dependent variable
as the literature suggests that child compliance may be
disturbed by prenatal cocaine exposure.
The results of this analysis are shown in Table 20. The
Hotelling's criterion for the combination of dependent
variables was not significant with F(4,42) = .876, p > .05.
These findings suggest that there are no differences between


42
covariate characteristics for the sample. For the remainder
of this document, 'sample' will refer to the 60 children in
this study which was completed in the context of the larger
longitudinal study as previously described.
The children in the sample (n = 60) included 34 girls
(56.7%) and 26 boys (43.3%). Sixteen children were placed in
a home other than that of their biological mother (26.7%).
Average birth weight was 3326 grams (£D = 413 grams) and mean
age at time of testing was 36.8 months (£D = 1.9 months). The
nonexposed group of children was comprised of 18 girls (60.0%)
and 12 boys (40.0%). Only two children were in foster care
(6.7%). Average birth weight in nonexposed children was 3355
grams (Sfi = 401.469 grams), and mean age at time of testing
was 37.3 months (SD = 1.446 months). The exposed group was
comprised of 16 girls (53.3%) and 14 boys (46.7%). Fourteen
of the children were in foster placement (46.7%). Average
birth weight in exposed children was 3297 grams (£D = 431
grams), and mean age at time of testing was 36 months (S¡) =
2.3 months).
In the sample, maternal depression scores ranged from one
to 43 (M = 19.7, SD = 9.8) with 16 being the clinical cutoff
score. Home Environment total scores ranged from 18 to 52 (M
= 37.0, SD 8.4) with a normative sample M = 37.54, SD =


85
Table 6
Between Group Differences Defined bv HOME Inventory
HOME
INVENTORY
Low
M
(n = 29)
High
M
(n = 31)
P
CONNORS
Conduct
64.6552
55.2903
.013*
Learning
59.1379
51.6452
.028*
Psychosomatic
55.2759
50.0968
.195
Impulsive
58.6552
57.1935
.508
Anxiety
52.6897
49.3226
.138
Hyperactivity
62.0690
56.3226
.085
ECBI
Problem
11.7586
8.5161
.140
Intensity
127.0000
113.7097
.095
VINELAND
Socialization
94.2414
103.1935
.008*
Communication
98.8621
105.4839
.043*
Daily Living
104.0000
105.0968
.804
Motor Skills
92.8621
100.0968
.067
(Continued)


63
significantly less depression r = -.3363, p < .01 than mothers
raising their biological children (Table 11).
Dependent Variables
Not surprisingly, when assessing relationships between
pairs of dependent variables across the three parent report
instruments (Connors, ECBI, and Vineland), behavioral
subscales tended to vary together and adaptive functioning
subscales tended to vary together. The ECBI problem scale was
significantly related to the Connors conduct problem £ =
.5569, p < .001, learning problem £ = .5586, p < .001,
impulsivity r = .4915, p < .001, and hyperactivity scales r =
.6089, p < .001. The ECBI Intensity score was also
significantly related to these four Connors subscales with
increased intensity associated with conduct problems £ =
.6635, p < .001, learning problems £ = .5827, p < .001,
impulsivity £ = .6014, p < .001, and hyperactivity £ = .6331,
p < .001. Interestingly, the Connors subscale learning
problem was negatively correlated to socialization £ -.4672,
P < .001 and communication £ = -.3768, p < .001. In other
words, higher levels of learning problems were associated with
relatively poor socialization and communication. Higher rates
of hyperactivity from the Connors were similarly related to


109
Most interesting were negative findings when comparing
exposed to nonexposed children. Results indicated no
significant differences between the two groups based on drug
exposure status on: 1) the Connors subscales including
Conduct, Learning, Psychosomatic, Impulsive, Anxiety, and
Hyperactivity, 2) the ECBI Problem and Intensity Scales, 3)
the Vineland subscales including Socialization, Communication,
Daily Living, and Motor Skills, and 4) on the DPICS-II
observational measures including derived scales Total
Commands, Percent Comply, Percent Noncomply and Percent No
Opportunity in addition to Laugh, Yell, Physical Positive,
Physical Negative, and Destructive.
Evidence that cocaine exposure may have at least a short
term neurological impact has been described in the literature,
including smaller head circumferences, jitteriness, poor
orienting and habituation, tone abnormalities, increased
aggression, language delays, and even autism (Bingol et al.,
1987; Chasnoff, 1989; Chasnoff et al., 1987; Davis et al.,
1989; Eisen et al., 1991; Griffith et al., 1994; Hume et al.,
1989; Oro & Dixon, 1987). Although neurological involvement
in this group has been inconsistently and often unreliably
documented, the concern that cocaine may affect
neurodevelopment and subsequent behavior is certainly


132
Black, M. Schuler, M., & Nair, P. (1993). Prenatal drug
exposure: Neurodevelopmental outcome and parenting
environment. Journal of Pediatric Psychology. 18, 605-
620.
Breitmayer, B.J., & Ramey, C.T. (1986). Biological
nonoptimality and quality of postnatal environment as
codeterminants of intellectual development. Child
Development, 57, 1151-1165.
Caldwell, B.M., & Bradley, B.H. (1984). Home Observation for
Measurement of the Environment. Little Rock, AR:
University of Arkansas Press.
Chasnoff, I.J. (1989). Cocaine, pregnancy, and the neonate.
Women & Health, 15, 23-35.
Chasnoff, I.J*, Burns, K.A., & Burns, W.J. (1987). Cocaine
use in pregnancy: perinatal morbidity and mortality.
Neurotoxicology and Teratology. 9, 291-293.
Chasnoff, I.J., Burns, W.J., Schnoll, S.H., & Burns, K.A.
(1985). Cocaine use in pregnancy. The New England
Journal gf Medicine, 313, 666-669.
Chasnoff, I.J., Chisum, G.M., Kaplan, W.E. (1988). Maternal
cocaine use and genitourinary tract malformations.
Teratology, 37, 201-204.
Chasnoff, I.J*, Griffith, D.R., Freier, C., & Murray, J.
(1992). Cocaine/polydrug use in pregnancy: two-year
follow-up. Pediatrics. 89, 284-289.


30
In a study with variable outcomes, Eisen, Field,
Bandstra, Roberts, Morrow, Larson, and Steele (1991) studied
26 target and 26 control infants for the effects of maternal
cocaine use on the Brazelton Neonatal Behavior Assessment
Scale (BNBAS). Infants were excluded if their mothers used
opiates? and mothers were matched for maternal age, ethnicity,
gravida, previous abortions, and hepatitis. Cocaine-using
mothers were more likely to be tobacco and marijuana smokers
and alcohol drinkers.
Results showed no differences between controls and
cocaine-exposed infants in sex distribution, gestational age,
chronological age, birth weight, birth length or postnatal
complications. However, cocaine-exposed infants had smaller
head circumferences and more obstetric complications than the
nonexposed infants. In addition, cocaine-exposed infants
showed more stress behaviors defined as abnormal reflex
behavior and autonomic instability on the Neonatal Stress
Scale. However, regression analysis showed obstetric
complications and maternal alcohol use were the only
significant variables that contributed to the variance on the
Neonatal Stress Scale. Finally, the cocaine group
demonstrated impaired ability to habituate responses to
repeated stimuli; regression analysis showed cocaine exposure


100
Table 15
Means and Standard Deviations of Tested Sample with Normative Sample DPICS-II
Parent Directed Interaction
Normative Normative
Sample Clinic-Referred Nonreferred
M
sc
M
M
£D
Direct Command
25.24*
15.50
11.50
8.41
6.75
5.62
Indirect Command
4.15
3.79
6.60
4.00
4.75
3.89
Compliance
10.35*
7.30
3.60
2.32
3.90
3.29
Noncompliance
2.50
2.82
6.10
6.18
1.30
2.29
No Opportunity
16.54*
10.07
8.20
7.89
6.35
5.58
Laugh
.31
1.23
-
-
-
-
Yell
.19
.87
.95
3.34
.00
.00
Physical Positive
.48
1.14
--
--
-
-
Physical Negative
.11
.42
.55
2.23
.00
.00
Destructive
.22
.63
.15
.49
.00
.00
* Sample group significantly different from Clinic Referred and Nonreferred normative
group.


12
maternal blood pressure and decreases in uterine blood flow
accompanied by fetal hypoxemia, hypertension, and tachycardia.
Cocaine administration to the fetus directly resulted in
relatively smaller increases in fetal heart rate and blood
pressure than those observed following maternal
administration, and no changes in fetal arterial blood gas
values. These results were interpreted to indicate that
maternal administration of cocaine alters fetal oxygenation by
reducing uterine blood flow and impairing oxygen transfer to
the fetus and that resulting fetal cardiovascular changes may
reflect fetal hypoxemia, increased fetal levels of cocaine, or
a combination of these events.
Birth outcome studies with animals demonstrate a range of
postnatal results following cocaine exposure in tero.
Henderson and McMillen (1990) studied postnatal development in
rats exposed to cocaine daily in tero. The cocaine-exposed
group weighed less, had more stillbirths, and more birth
defects when compared to a nonexposed group. In addition,
cocaine-exposed pups had delayed righting reflexes although no
delay was noted in opening their eyes, both indices of
developmental integrity. Their findings led Henderson and
McMillen (1990) to conclude that cocaine exposure in tero


72
priority dependent variables tested in a univariate ANOVA.
Conduct Problem was chosen as the highest priority dependent
variable since the literature suggests that this may be a
marker of prenatal cocaine exposure.
The results of this analysis are shown in Table 17. The
Hotelling's criterion for the combination of dependent
variables was not significant with F(6,51) = 1.26, p > .05.
Findings indicate that there are no differences between
exposed children and nonexposed children on this combination
of variables by parent report. Even in a univariate context
at the p < .05 level, there are no significant differences
between exposed and nonexposed children on these variables.
Specifically, no significant differences were found between
groups for conduct problem F((l,56) = 1.06, p > .05, learning
problem F(l,55) = 1.22, p > .05, psychosomatic F(l,54) = .74,
p > .05, impulsivity F(l,53) = .55, p > .05, anxiety F(l,52)
= 3.25, p > .05, or hyperactivity F(l,51) = .71, p > .05.
Hypothesis 3
As before, it was hypothesized that behavioral
difficulties would be more pronounced in the exposed group.
Descriptive data for the exposed and nonexposed children are
summarized on Table 16. To test this, a multivariate analysis


32
over the first few weeks of life for the cocaine-exposed
infant (Black, Schuler, & Nair, 1993? Coles, Platzman, Smith,
James, & Felix, 1992).
Summary of Literature Review
A review of the literature concerning cocaine effects on
fetal development indicates several serious methodological
problems in human clinical studies, including probable
underreporting of cocaine use and the increased likelihood
that cocaine users also use more alcohol and other drugs.
There is also the likelihood of confounding of other maternal
risk factors that are more common in cocaine-using groups than
nonusers such as sexually transmitted diseases (including
HIV); previous spontaneous and elective abortions, and less
prenatal care; low birth weight infants? polydrug use; poor
health and nutrition; and poverty (Dow-Edwards, 1991). Other
methodological problems endemic to the literature include a
preponderance of unblinded evaluations. Further, most
research has concentrated on urban populations and
inappropriate control groups and analyses which frequently
ignore important environmental and maternal factors.
In terms of specific animal research findings, cocaine
generally has no effect on gestational length in the rat, a


27
developmental outcome of children prenatally exposed to
maternal substances of abuse. Their subjects included 93
children exposed prenatally to cocaine and other drugs, 24
children exposed to polydrugs without cocaine and 25 children
who were nonexposed. Drug exposed children had smaller head
circumferences than nonexposed children; the
polydrug/noncocaine group performed worse than nonexposed
children on tasks of abstraction and visual reasoning; the
cocaine/polydrug group performed worse on a task of verbal
reasoning; and a marijuana group performed more poorly on a
task of abstract/visual reasoning. Caregivers also rated drug
exposed children as more aggressive than nonexposed children.
The authors concluded that not all substance exposed
children suffer the same poor prognosis, and that
generalizations about outcome for drug-exposed children need
to be qualified pending more thorough investigations of the
roles of maternal and environmental factors such as SES
levels. Recognizing that cocaine may not account for all
negative findings and that bias on the part of researchers and
even parents could convolute findings was an important pivot
point, not only for this group of researchers but for other
investigators in the field as well.


28
Studies focusing on the behavioral outcome of cocaine-
exposed infants present a range of findings and methodology.
In a study of fetal behavioral state as a predictor of
neonatal outcome, Hume, O'Donnell, Stanger, Killam, and
Gingras (1989) performed fetal assessments which included
ultrasonographic examination, videotaping and scoring of a
behavioral protocol developed by the authors. Abnormal or
delayed state behavior was identified in 13 of 20 fetuses
exposed to cocaine. State organization was also suspect or
abnormal for 16 of 20 exposed newborns, and the disorganized
behavioral states in fetuses successfully predicted abnormal
newborn behaviors. The authors concluded that cocaine
disrupts (CNS) development. Again, problems in this early
study included lack of a control group, small sample size,
unblinded examiners, and the use of unnormed scales which,
because they were developed by the authors for this study, may
have led to biased observations.
Davis, Fennoy, Laraque, Kanem, Brown and Mitchell (1992),
who were also interested in behavioral outcome, studied 70
children with cocaine exposure in tero who had been targeted
by positive urine screen, maternal report, or by doctor/agency
notation. All children in the study had been referred to a
large inner city hospital for developmental evaluation. Davis


MATERIALS AND METHODS
Subjects
Subjects were 30 children exposed to crack in tero and
30 nonexposed control children who were part of a large,
ongoing, prospective longitudinal research project conducted
at Shands Teaching Hospital through the Department of
Pediatrics, Division of Neonatology. Subjects were the
children of women who were originally recruited predominantly
from public health department (PHD) prenatal clinics in two
counties in an understudied rural area of north central
Florida. Recruitment began in the Fall of 1991. These women
represented a range of low to moderate reproductive risk and
all were scheduled to deliver at the referral hospital. There
was a wide range of drug use with most smoking crack cocaine
and few having access to drug treatment.
Criteria for inclusion in the original study were: 1)
women over 18 years of age to reduce the confounding influence
of perinatal risk known to be associated with pregnancy in the
young teenager and to eliminate problems with obtaining
informed consent from minors, 2) women with no major illnesses
37


104
Table 17
MANCO VA with Covariates Child Gender and Maternal Depression and Dependent
Variables, from the Connors
Univariate Stepdown
F df F df p-value
Conduct
1.06
(1.56)
1.06
(1,56)
.308
Learning
2.27
(1,56)
1.22
(1,55)
.273
Psychosomatic
1.53
(1,56)
.74
(1,54)
.393
Impulsivity
.09
(1,56)
.55
(1,53)
.460
Anxiety
3.89
(1,56)
3.25
(1,52)
.077
Hyperactivity
2.39
(1,56)
.71
(1,51)
.405
Significance not attained in either univariate or step-down context.


127
used for the sample to norm group comparisons highlighting
significant findings that may otherwise have been obscured.
The study was based on the literature and what is currently
understood about the effects of cocaine on neurodevelopment
and behavior. Measures reflected this understanding, and were
well normed with good psychometric properties. Examiners were
blinded to drug exposure status minimizing bias effects. As
much as possible, evaluations were standardized for each
child.
There were also several weaknesses to this study. The
sample was relatively small limiting the power of comparisons.
Comparisons based on population norms were done using
familywise error rates. While this contributes to meaningful
interpretation, potentially significant findings may have been
obscured. The scope of the study was broad and efforts were
made to control for large variable to sample ratios by
breaking analyses into conceptually related groups. This
resulted in seven separate familywise comparisons for the
total sample and four separate MANOVAs for between groups
comparisons which can inflate Type I error.
Within the MANOVAs, a hierarchical approach was used to
control for shared variance among measured variables. Shared
variance was assigned to one variable which can result in


3
reportedly shorter and more intense when smoking crack than
for either intranasally or intravenously administered cocaine.
Users may feel a greater compulsion to repeat the experience
when smoking crack both for its magnified euphoric effects as
well to avoid the subsequent crash (Howard et al., 1987).
Binges, characterized by frequent readministration of the
drug, reportedly may last 12 hours but may go on for several
days (Gawin & Kleber, 1985). In addition, the price of crack
continues to decrease, making it accessible to people of all
socioeconomic levels. A 'rock' may cost as little as five to
ten dollars (Howard, 1989). Combined, these factors
precipitate abuse.
While it is uncertain whether cocaine is physically
addictive, it clearly has powerful psychological effects. It
is estimated that five times as many people are addicted to
cocaine than to heroin (Grinspoon & Balkalar, 1980). Indeed,
treatment for cocaine use, and crack use in particular, is
escalating while age of first use appears to be dropping
(Adams, Gfroerer, Rouse, & Kosel, 1986). In reaction to
epidemic use, researchers are beginning to describe not only
the immediate effects of cocaine intoxication but also to
contemplate the long-term implications of using what had


107
Table 20
MANQVA with Dependent Variables from the DPlCS-II--Derived Variables
Univariate Stepdown
F df F df p-value
Commands
.26
(1,45)
.26
(1,45)
.612
Comply
.84
(1,45)
.86
(1,44)
.358
Noncomply
.02
(1,45)
.11
(1,43)
.744
No Opportunity
1.07
(1,45)
.02
(1,42)
.881
Significance not attained in either univariate or step-down context.


Child Behavior Inventory. Child behavior was also assessed by
direct objective observation using the Dyadic Parent-Child
Interaction Coding System-II. Administered instruments
intended to determine whether a) scores for the total sample
conformed to norms provided by psychological measures, and b)
whether behavioral or adaptive deficits were present in the
crack-exposed preschoolers when compared to same-aged
nonexposed peers. Results showed significant differences
between the total study cohort which included exposed and
nonexposed children and normative groups on which many
standardized psychological measures are based. For example,
the total sample was more likely to display elevations in
conduct problems, learning problems, hyperactivity, and
impulsivity compared to normative groups. Second, at three
years of age, no differences were found between a prenatally
crack-exposed cohort on parent and objective measures of
behavior and adaptive functioning when compared with
nonexposed matched peers. Thus elevations on disordered
behavior compared to normative groups cannot be attributed to
exposure status. Implications of findings and possible
explanation for nonsignificant between groups findings are
discussed.
ix


92
Table 9 - (Continued)
ALCOHOL
Low
M
(n = 25)
High
M
(n = 29)
P
DPICS-1I (Derived Scores)
Total Commands*
42.1600
49.4138
.291
Percent Comply6
.3690
.3329
.410
Percent Noncomply6
.0846
.1000
.524
Percent No Opportunity6
.5464
.5671
.611
* = p < .05
* frequency data
b percentages


60
environments. Findings indicated that the group representing
children from less enriched environments had more conduct
problems t = 2*57, p < .013, learning problems t = 2.25, p <
.028, worse socialization t = -2.75, p < .008, and reduced
communication skills t = -2.07, p < .043 compared to children
from relatively more enriched environments (Table 6).
When groups were defined by foster care status, children
who were with their biological mothers (n = 44) tended to have
significantly more conduct problems t = 2.25, p < .028 than
children living away from their biological mothers (n = 16)
(Table 7). Further, when groups were defined by child gender,
boys (n = 26) were significantly more likely to display
learning problems t = -2.38, p < .021, and have poorer
communication skills than girls t = 2.05, p < .045. Girls (n
= 34) were significantly more likely to feel anxious t = 2.17,
p < .034 than boys (Table 8). Interestingly, although alcohol
use was significantly different between exposed and nonexposed
groups, no significant differences were found on any parent
report measure using alcohol as the independent variable
(Table 9).
In terms of observational measures and covariates, no
between groups differences were found on the four derived
DPICS-II scores when groups were defined by either maternal


115
parent report measures may be further compounded by the use of
an inappropriate control group. For example, there are
studies in the cocaine exposure literature that have used no
control group or were comprised of mother-child dyads which
were unmatched on a number of important variables such as
race, parity, SES, etc. (Little et al., 1989; Oro & Dixon,
1987).
Alternately, some systematic variation in the sample
group may account for elevations on these scales and
significant differences when compared to norms. Our original
hypothesis proposed that any elevations in disordered
behaviors by parent report or by observation, or reductions in
adaptive functioning would be at least partially accounted for
by drug exposure status. Thus, the ultimate finding of no
differences between exposed and nonexposed groups on all
administered measures is especially intriguing. In other
words, variability due to drug exposure status does not
account for differences between the total sample and norms.
The first critical finding of this study, then, is to
highlight the possible deviation from standardized normative
samples for reasons other than drug exposure status, and
second, to emphasize the danger of basing conclusions on test


123
years of age. However, no significant relationships were
noted between drug exposure status and any dependent variable.
No significant relationships were noted between alcohol
exposure and any dependent variable. No significant
relationships were noted between fostercare status and any
dependent variable.
Remaining covariates were not significantly related to
drug exposure status. However, maternal depression was
positively related to Conduct, Learning, and Hyperactivity on
the Connors and to the Problem scale of the ECBI. In other
words, children of depressed caregivers were more likely to
display a range of disordered behaviors than children of
nondepressed caregivers. Interestingly, maternal depression
was negatively associated with fostercare status. Thus,
caregivers who were not biological mothers were less likely
to be depressed than biological mothers.
How this relates to ultimate performance on measures of
behavior, particularly with regard to the tendency for
nonexposed children to display more disordered behavior, is
unclear. One suggestion might be to study child outcome based
on parenting differences between depressed biological mothers
and other less depressed caregivers. Finally, HOME inventory
was significantly related to the Communication subscale of the


90
Table 8 - Continued
GENDER
Low
M
(n = 30)
High
M
(n = 24)
P
DPICS-II (Derived Scores)
Total Commands*
44.1333
48.4583
.532
Percent Comply1*
.3746
.3183
.198
Percent Noncomplyb
.0801
.1089
.233
Percent No Opportunity1*
.5453
.5728
.500
* = p < .05
* frequency data
b percentages


125
independent variables. Findings showed that the group with
higher maternal depression demonstrated more conduct problems,
learning problems, hyperactivity, and increased intensity of
problem behaviors. This finding mirrors these results already
discussed. The group with high HOME inventory scores had
fewer conduct problems, learning problems, socialization and
communication difficulties. Children with their biological
mothers tended to have more conduct problems than children
living away from their biological mothers. Finally, boys were
significantly more likely to display learning problems and
have poorer communication skills than girls, and girls were
more likely to feel anxious. No differences were noted by
groups when defined by alcohol use versus no alcohol use.
These findings are sensible given our understanding of
the effects of parenting and environmental variables on child
behavior. Given the complexity of possible interactions
between these variables and outcome based on drug exposure,
their inclusion as covariates in the study appeared
appropriate. Although not relevant to the current study,
questions about the interactions between covariates, drug
exposure and ultimate behavior and adaptive functioning
remain. With the continued collection of data, modeling with
regression analysis can help to clarify the relationships


25
exposed infants, Schneider and chasnoff (1992) found
significant differences between groups in muscle tone,
primitive reflexes and volitional movement with cocaine-
exposed infants performing more poorly. Results demonstrated
that motor differences were evident in cocaine-exposed infants
at a postnatal period beyond the first month of life. As in
other studies from the Chasnoff group, mother/infant
involvement in a drug treatment program was known by
investigators, and subjects in the cocaine group included
polydrug users.
In a two year followup, Chasnoff, Griffith, Freier and
Murray (1992) investigated the growth and developmental
outcome of cocaine-exposed infants. Comparing a cocaine-
exposed group (with marijuana and alcohol exposure), a
marijuana/alcohol exposed group, and a nonexposed control
group, they found that cocaine-exposed children no longer
lagged behind nonexposed children in terms of length and
weight although the cocaine group and marijuana/alcohol group
both lagged in head growth. No differences in performance on
the Bayley Scales of Infant Development (BSID) were noted
between the three groups. Again, these children were all
known to the researchers through a drug treatment program, and
polydrug use was a confound. Further, the study sample had a


PURPOSE OF RESEARCH
While the particular results of studies vary somewhat,
reports consistently portray cocaine as an agent strongly
implicated in a host of negative outcomes. Further, crack has
been singled out as the most potent form of cocaine both in
terms of abuse potential and morbid impact (Kaye, Elkind,
Goldberg, & Tytun, 1989). Clearly research on the
implications of in tero exposure to cocaine, and especially
crack, needs to be ongoing and continually refined from a
methodological, medical and psychosocial perspective.
At present, long-term followup on the effects of prenatal
exposure to cocaine and cocaine derivatives is extremely
limited. Because of the variability in outcome cited in the
neonatal literature, it remains unclear what long-term impact
in tero cocaine exposure may have on the developing child.
In the past, the media have portrayed cocaine-exposed infants
and toddlers as behaviorally disordered, impulsive,
nonempathetic, and autistic, generally without benefit of
sound empirical evidence. These prejudices have frequently
been supported by biased investigations making hasty
unwarranted projections as to future status while ignoring the
35


UNIVERSITY OF FLORIDA
II in 1
3 1262 08554 8955


RESULTS
Descriptive Analysis
First, means and standard deviations were calculated for
the total sample for parent report dependent variables
including: 1) the Vineland (Sparrow et al.# 1984) subscales
Communication, Daily Living, Motor Skills, and Socialization,
2) the Connors' (Connors, 1990) subscales Conduct Problem,
Learning Problem, Psychosomatic, Impulsive-Hyperactive,
Anxiety, and Hyperactivity Index, and 3) the ECBI (Eyberg &
Colvin, 1994) Intensity and Problem scales.
Parent Report Measures
Normality assumptions for parent report dependent
variables were then tested by graphing and computing skewness
scores. One subscale of the Connors' scale (Psychosomatic)
and one subscale of the Vineland (Daily Living) were found to
be skewed. These were corrected for further analyses using
log transformations. All other dependent variables on
standardized parent report measures were found to approximate
normality. Data were missing for two children on all Connors
subscales, and for one child on all Vineland subscales. Data
were missing for four children on the ECBI subscales. Missing
53


84
Table 5 - Continued
MATERNAL
DEPRESSION
Low
M
(n = 18)
High
M
(n = 36)
P
DPICS-II (Derived Scores)
Total Commands*
46.0256
46.1333
.989
Percent Complyb
.3460
.3514
.908
Percent Noncomplyb
.0996
.0896
.696
Percent No Opportunity11
.5544
.5591
.915
* = p < .05
* frequency data
b percentages


11
controls. Weese-Mayer and Barkov (1993) studied the responses
of rabbit pups to hypoxia following exposure to 30 mg/kg of
cocaine from days seven to 15 gestation. They found the
cocaine-exposed pups had more significant oxyhemoglobin
desaturation and pulse deceleration during exposure to severe
hypoxia than controls, suggesting that cocaine exposure in
tero may reduce the normal defense mechanisms for metabolic
adjustment to low oxygen.
These results supported findings from an earlier study by
Weese-Mayer, Klemka-Walden, Barkov, and Gingras (1992) who
also found that, while baseline ventilation did not differ
significantly among study groups, cocaine-exposed pups had a
deficient ventilatory response during an hypoxic challenge.
Weese-Mayer et al. (1992) argued that these findings may
represent perturbed maturation of respiratory control. Other
researchers have found similar results which suggest that
infants exposed to cocaine have an impaired repertoire of
protective responses to hypoxia and hypercapnia during sleep
which may play a role in increased risk for SIDS (Ward,
Bautista, Woo, Chang, Schuetx, Wachsman, Sehgal, & Bean,
1992).
Similarly, Woods, Plessinger, and Clark (1987) found that
pregnant ewes exposed to cocaine produced increases in


ACKNOWLEDGMENTS
I would like to thank my cochairs, Eileen B. Fennell,
Ph.D., ABPP, and Fonda D. Eyler, Ph.D., for their support and
guidance throughout this project. The breadth of their
combined expertise in the world of child psychology and
development is substantial. I would also like to thank my
committee members, Marylou Behnke, M.D., Michael Conlon,
Ph.D., Steven Boggs, Ph.D., and Sheila Eyberg, Ph.D., for
their advice and practicality in the management of the
research.
I would particularly like to thank Drs. Eyler, Behnke, and
Conlon for making this project possible by generously allowing
me to in participate on their research grant. My association
with their group was among the best of my graduate school
experiences. I would also like to thank Kathie Wobie, M.A.
and Lisa Maag for the all the help and friendship they have
offered before and during the course of this project. My
thanks are also extended to Annie, Kristen, Lorraine, Bruce,
Bridget, Jack and others who, at various times over the past
five years, have been the mainstay of the grant's success.
ii


91
Table 9
Between Group Differences Defined by Alcohol Use
ALCOHOL
No Use
M
(n = 29)
Use
M
(n = 31)
U
CONNORS
Conduct
63.0000
56.8387
.107
Learning
57.1724
53.4839
.287
Psychosomatic
56.5172
48.9355
.056
Impulsive
59.0000
56.8710
.334
Anxiety
50.7931
51.0968
.895
Hyperactivity
61.8966
56.4839
.105
ECBI
Problem
11.7931
8.4839
.132
Intensity
127.4438
113.2903
.075
VINELAND
Socialization
99.1724
98.5806
.865
Communication
100.4483
104.0000
.284
Daily Living
102.6897
106.3226
.410
Motor Skills
96.0690
97.0968
.797
(Continued)


67
scores on any of these measured domains were significantly
different from provided norms (Table 13).
Observational Ratings
The final two conceptual groupings were comprised of
basic objective observational data including: 1) direct
commands, indirect commands, compliance, noncompliance and no
opportunity to comply, and 2) laugh, yell, physical positive,
physical negative, and destructive behavior over the total ten
minute play period in two situations including both child-
directed and parent-directed play. These results are
summarized on Tables 14 and 15.
Using the SMM familywise rate for five comparisons,
significant differences were noted in sample scores in the
child-directed interaction when compared to normative data.
Specifically, the caregivers in the present sample tended to
have a higher rate of direct commands than either the clinic
referred or nonreferred normative group where y = 8.61, p <
.01 and y = 9.35, p < .01 respectively. The rate of indirect
commands was similarly elevated in the sample compared to
clinic referred and nonreferred normative groups where y =
4.01, p < .01 and y = 3.37, p < .01 respectively. Not
surprisingly given the higher rates of commands, the rate of


20
methodological shortcomings in this study which may impact the
reliability of the authors' conclusions. Mothers were self
reported drug users whose neonates were automatically referred
to a high risk nursery for observation of withdrawal symptoms
compromising blind evaluations. Furthermore, the cocaine
using mothers were generally older, more likely to be black,
and use tobacco and other illicit drugs when compared to
controls. Controls were not matched to drug using mothers,
and it is unclear whether other risk variables were controlled
adequately in the analysis.
In a subsequent study, Little and Snell (1991) studied
the pattern of brain growth in cocaine-exposed newborn infants
where brain growth was defined as head circumference in
addition to other growth variables including birth weight,
length, and gestational age. Groups were cocaine-exposed
infants without alcohol exposure, alcohol but no cocaine
exposure, and neither cocaine nor alcohol exposure. Results
showed significant differences in head size between unexposed
and cocaine-exposed infants. Head circumference was reduced
proportionately more than birth weight in cocaine-exposed
infants. Cocaine and alcohol exposed groups were not
statistically different in terms of head size. Little and
Snell (1991) concluded that cocaine exposure results in a


51
Hypothesis 2
It was hypothesized that the performance of the cocaine-
exposed group would be impaired compared to the nonexposed
group in terms of behavior as measured by parent report on the
six subscales of the Connors (Connors, 1990). After graphing
to inspect relationships between scales, MANCOVA with
Hotelling's T2 was used to analyze between group differences.
Hypothesis 3
It was hypothesized that the performance of the cocaine-
exposed group would be impaired compared to the nonexposed
group in terms of behavior as measured by parent report on the
two subscales of the ECBI (Eyberg & Colvin, 1994). After
graphing to inspect relationships between scales, MANCOVA with
Hotellings T2 was used to analyze between group differences.
Hypothesis 4
It was hypothesized that the performance of the cocaine-
exposed group would be depressed compared to the nonexposed
groups in terms of adaptive behaviors as measured by the four
subscales of the Vineland (Sparrow et al., 1984) by parent
report. After graphing to inspect relationships between


121
Perhaps the most intriguing explanation for the lack of
significant findings lies in the progression of
neurodevelopment. Briefly, cocaine works on the monamine
system in the brain including the neurotransmitter dopamine,
serotonin, and norepinephrine. The monamine pathways are
involved in early fetal development by innervating forebrain
regions. Cocaine may also have effects on brain development
that are region specific. For example, subcortical structures
including the basal ganglia, nigrostriatal, and mesolimbic
brain may be particularly vulnerable. These systems are
involved in cognition, arousal, attention, anxiety, and
reinforcement in addition to fine motor control. Subcortical
connections with the frontal lobes responsible for attention
and the modulation of behavior, are vast and reciprocal.
Critical here is the maturation of the frontal subcortical
connections by myelination, and in particular, the development
of the dopaminergic system which can continue into the third
decade of life (Yakovlev & Lecours, 1967). Thus, impairments
in subcortical to cortical connections and behavioral
correlates may not be fully realized until after puberty.


61
depression (exposed n = 36, nonexposed n = 18) or HOME
inventory (exposed n = 29, nonexposed = 25). Further, no
differences were found on derived DPICS-II observational
scales when groups were defined by foster care status (exposed
n = 15, nonexposed n = 39), gender (exposed n = 24, nonexposed
n = 30), or alcohol use (exposed n 31, nonexposed n 29)
(Table 9). Together, these results suggest that chosen
covariates may have complex relationships with outcome on
behavioral measures, and that their selection for inclusion as
covariates was warranted.
Initial Correlations
Several additional analyses were done to clarify the
nature of relationships between covariates and dependent
variables, between pairs of covariates, and between pairs of
dependent variables. It should be noted that correlations
with nominal, ordinal, and interval data were done with
Pearson's Product Moment rather than point biserial
correlations as the outcome is identical (Weinberg & Goldberg,
1979).


7
Exposed infants have also been shown to exhibit decreased
length, weight and head circumference, higher rates of
congenital malformations, deviant neurobehavior, rapid shifts
between irritability and lethargy, and be at increased risk
for Sudden Infant Death Syndrome (SIDS) although many of these
outcomes remain controversial (Bingol et al., 1987; Chasnoff,
1989; Chasnoff, Burns, fit Burns, 1987; Oro fit Dixon, 1987).
However, negative findings are not consistently found in well
controlled studies. Reports of investigations into the
behavioral and long-term developmental outcome of cocaine-
exposed infants remain unclear.


2
insufflatted cocaine. Cocaine in powder form is also
frequently diluted or cut before sale further limiting plasma
drug concentrations in the body.
Crack on the other hand is almost 70% pure cocaine, made
by precipitating alkaloidal cocaine from an aqueous solution
of cocaine HC1. Unlike the powder form of cocaine, crack is
not destroyed by moderate heating and vaporizes at
temperatures over 98 degrees celcius (Medical Letter, 1986).
Crack, named for the popping sound it makes when heating, may
be smoked via freebasing with a base pipe or rolled with
tobacco in a cigarette. Crack may also be injected. Smoking
crack delivers large quantities of cocaine directly to the
vascular bed of the lungs. The plasma drug concentration in
this instance is substantially higher than for insufflatted
cocaine and rises almost instantaneously producing an effect
more intense than that experienced with intravenous injection
(Medical Letter, 1986).
Crack when smoked reaches the brain in approximately
eight seconds producing an intense, immediate euphoria
(Howard, Mofenson, & Caraccio, 1987). These euphoric effects
are short lived, lasting approximately 45 minutes followed by
a severe crash (dysphoria) during which the user becomes
depressed and agitated (Howard, 1989). This cycle is


17
a cocaine and methamphetamine group, a narcotic group and a
drug free group. Findings in this study were plentiful and
dramatic. The researchers found significantly lower birth
weight, length, occipitofrontal head circumference (OFC), and
gestational ages in both the cocaine/methamphetamine and
narcotics groups compared to the illicit drug free group.
They also found significantly higher incidence of prematurity,
intrauterine growth retardation, fetal distress, and
complications during the neonatal period in both the
cocaine/methamphetamine and narcotics groups compared to the
illicit drug free group.
Significant increases in neurologic and physiologic
problems in the cocaine/methamphetamine group were also
reported including (in order of decreasing significance)
abnormal sleep patterns, tremors, poor feeding, hypertonia,
vomiting, sneezing, high pitched crying, frantic fist sucking,
tachypnea, loose stools, fever, yawning, hyperreflexia, and
excoriation. Physician and nurse descriptions of the behavior
of these exposed infants included disorganization, poor visual
processing of faces and objects, random sucking and long dull-
alert periods with eyes open. Decreased spontaneous activity
and fixed catatonic postures were seen in four of the
cocaine/methamphetamine group. Even accounting for various


120
more direct and indirect commands, and for their children to
display proportionally higher incidence of compliance,
noncompliance, and no opportunity to comply. However, when
looking at percentages rather than frequency, exposed children
had higher rates of noncompliance and no opportunity to
comply, but a lower rate of compliance when compared to
nonexposed children. Thus, while exposed children tend to
look better by parent report, objective observation suggests
that the behavior of exposed children may be worse than
nonexposed children. One explanation for this dissociation is
that caregivers of exposed children relax their expectations
for compliance. Although these are trends only and do not
represent significant differences, they suggest parenting
styles and rates of compliance between the two groups may be
different.
When evaluating remaining child behaviors, such as laugh,
yell, physical negative, physical positive or destructive
behavior, no obvious pattern emerges. Again, observed trends
do not represent significant differences between groups and
must be discussed with caution. Alternately, trends are
useful when considering direction for future research. It is
possible that with larger samples and more statistical power,
significant differences might emerge.


Last but not least, I would like to thank my parents for
their constant encouragement and support, and Tiffany,
Samantha, and Ben, who make the rest of my life better.
This research was supported in part by NIDA grant
R01DA05854 and GCRC grant M01RR00082.
iii


13 Means and Standard Deviations of Tested
Sample with Age-Based Norms Parent
Report 98
14 Means and Standard Deviations of Tested
Sample with Normative Sample DPICS-II
Child Directed Interaction 99
15 Means and Standard Deviations of Tested
Sample with Normative Sample DPICS-II
Parent Directed Interaction 100
16 Dependent Variables Means and Standard
Deviations for Exposed and Nonexposed
Children for the Total Sample 101
17 MANCOVA with Covariates Child Gender and
Maternal Depression and Dependent
Variables from the Connors 104
18 MANOVA with Dependent Variables from the
ECBI 105
19 MANOVA with Dependent Variables from the
Vineland 106
20 MANOVA with Dependent Variables from the
DPICS-II - Derived Variables 107
vii


83
Table 5
Between Group Differences Defined by Maternal Depression
MATERNAL
DEPRESSION
Low
M
(n = 21)
High
M
(n = 39)
a
CONNORS
Conduct
53.4286
63.2564
.013*
Learning
48.3810
58.9744
.003*
Psychosomatic
49.2381
54.4103
.217
Impulsive
55.9524
58.9487
.193
Anxiety
49.9048
51.5128
.502
Hyperactivity
53.5714
62.0769
.014*
ECBI
Problem
7.3810
11.5385
.069
Intensity
107.5238
126.9231
.019*
VINELAND
Socialization
102.6190
96.8462
.108
Communication
102.6190
102.1026
.882
Daily Living
105.4286
104.1026
.775
Motor Skills
97.0952
96.3333
.856
(Continued)


34
abnormal orientation, sensory and motor functions. Most of
these problems appear to resolve by six months of age. Some
studies have found exposed infants at risk for SID whereas
others have not found a significant association with cocaine.
Additionally, neonates exposed in tero to cocaine do not
appear to suffer from addiction to cocaine which is unlike
infants exposed to opiates in tero.
At the present time, reduced length and head
circumference appear to be the most consistent findings
reported for neonates exposed prenatally to cocaine, and
again, these deficiencies are usually resolved by one year of
age. There does not appear to be a clinical syndrome which
adequately captures the impact of cocaine exposure in tero on
the developing human. Individual variation in outcome appears
to be the most consistent finding. The methodological
difficulties of working with a drug-using population,
exaggerated media portrayals of 'crack babies,' and the need
to control for investigator bias in studies have added to the
confusion evident in the cocaine literature. Thus, while
cocaine exposure in tero may reasonably be expected to have
deleterious effects on some children, it is not possible at
this time to define a syndrome in any, even globally,
meaningful way.


29
et al. (1992) found significant neurodevelopmental
abnormalities including language delay and a high frequency of
autism (11.4%) in the cocaine-exposed group. Since autistic
disorders have not been linked to alcohol or opiate exposure
alone, Davis et al. (1992) attributed their findings to
cocaine use. There are obvious deficiencies in this study
including the nonblinded status of clinical evaluators, the
skewed sampling of clinically referred children, the polydrug
use status of the mothers, and the conclusion that results
must be narrowly attributed to cocaine exposure in tero.
In a study of 51 cocaine-exposed infants and 60
nonexposed infants targeted by maternal report or positive
infant urine screening, Neuspiel, Hochberg, Greene, and
Campbell (1991) found no differences on the Brazelton Neonatal
Behavioral Assessment Scale (BNBAS) administered between one
and three days of age. A second examination at 11 to 30 days
of age showed a significant difference in motor functioning in
the cocaine-exposed group. However, this difference
disappeared when researchers controlled for confounding
variables such as perinatal and social factors. No
differences were detected in observed maternal or infant
behaviors indicating that prenatal cocaine use had no
significant impact on maternal/infant interactions.


LIST OF TABLES
Table P-age
1 Demographic Characteristics of the Total
Sample 79
2 Covariate Characteristics of the Total
Sample 80
3 Reliability of Video Coding of Selected
DPICS-II Categories in the Child-Directed
Interaction 81
4 Reliability of Video Coding of Selected
DPICS-II Categories in the Parent-
Directed Interaction 82
5 Between Group Differences Defined by
Maternal Depression 83
6 Between Group Differences Defined by Home
Inventory 85
7 Between Group Differences Defined by
Foster Care Status 87
8 Between Group Differences Defined by
Gender 89
9 Between Group Differences Defined by
Alcohol Use 91
10 Correlations between Covariates and
Behavioral and Adaptive Variables 93
11 Correlations between Covariates 95
12 Correlations between Dependent Subscales 96
vi


36
very significant presses of poverty, malnutrition and a
caregiving environment compromised by addiction. While the
potential toxicity of cocaine exposure should be in no way
minimized, it has been the recent onus of researchers in this
area to produce methodologically sound and conservatively
interpreted accounts of the impact of cocaine on the
developing infant and toddler. Only recently has sound
research on the infant and toddler been possible as
prospectively enrolled cohorts mature to preschool age and
older. Thus, there are a number of interesting questions to
be investigated. Whether the effects linked to cocaine
exposure in tero are stable over time, and how they translate
behaviorally and developmentally will require increasing
attention as these infants mature.
The present study is intended as an initial exploration
of some of these developmental issues within improved
methodological design. Addressed here is whether toddlers
exposed in tero to crack differ from same aged unexposed
peers in their level of behavioral and adaptive development.


113
completed with composite (derived) scores. For the child-
directed interactions, the study sample had a significantly
higher incidence of direct commands and indirect commands when
compared to both referred and nonreferred normative groups.
Given the higher incidence of commands, it is not surprising
that the incidence of child compliance, noncompliance and no
opportunity for compliance was also elevated in the total
study sample when compared to both referred and nonreferred
normative groups.
For the parent-directed interactions, the study sample
had a significantly higher incidence of direct commands, and
subsequently, child compliance and no opportunity for
compliance when compared to both referred and nonreferred
normative groups. No significant differences were noted
between the incidence of indirect commands and noncompliance
during the parent-directed portion of the DPICS-II. These
findings indicate that caregivers in the total sample tended
to use more commands (and especially direct commands in the
parent-directed context) regardless of the play situation,
which in turn seemed to increase the incidence of child
behaviors such as compliance.
It is of particular interest that in the parent-directed
context, no differences between indirect commands and


80
Table 2
Covariate Characteristics of the Total Sample
NOMINAL/
ORDINAL
Non-
Exposed
Exposed
%
df p-value
Child Gender*
Female
18
16
56.7
Male
12
14
43.3
1 .7945
Fostercare*
Yes
2
14
26.7
No
28
16
73.3
1 .0013*
Alcohol*
Yes
8
23
51.7
No
22
7
48.3
1 .0003*
Non-
INTERVAL
Exposed
Exposed
t
p-value
Maternal
18.4
20.9
.99
.326
Depression11
HOME
37.6
36.5
-.52
.605
Inventory**
* Using Fisher's Chi-Square with the Yates correction for small sample sizes
b Using Students t-test
* = p < .05


50
unequal n and Studentized Maximum Modulus (SMM) tables for
familywise error rates to control for multiple comparisons at
the .05 significance level. Dependent variables were grouped
conceptually for comparison to norms as follows: 1) the six
subscales of the Connors (Connors, 1990) including Conduct
Problem, Learning Problem, Psychosomatic, Impulsive-
Hyperactive, Anxiety, and Hyperactivity Index, 2) the ECBI
(Eyberg & Colvin, 1994) Problem and Intensity scales, and 3)
the four subscales of the Vineland (Sparrow et al, 1984)
including Socialization, Communication, Daily Living, and
Motor Skills.
The ten DPICS-II basic observation frequency variables
were broken into two groups for analysis. The first group
included compliance information including frequency of direct
and indirect commands, compliance, noncompliance, and no
opportunity for compliance. The second group consisted of
child behaviors including frequency of laugh, yell-whine,
physical positive, physical negative, and destructive. Scores
were compared to normative data using Welch's V for unequal n
and Studentized Maximum Modulus (SMM) tables for familywise
error rates. Comparisons to normative groups were not
performed for DPICS-II derived summary scores as norms are not
available.


94
Table 10 - Continued
Exposure
Status
Alcohol
Exposure
Foster
Care
Gender
Maternal
Dep
Home
Invent
DPICS-II (Derived Scores)
Total Commands .0759
.0274
.0160
.0406
.0333
.0198
Percent Comply
-.1351
-.1070
-.1405
-.1981
-.0207
.0467
Percent Noncom
-.0229
-.0033
.1437
.1883
.1261
.0232
Percent No Opp
.1524
.1110
.0489
.0783
-.0615
-.0627
DPICS-II (Basic Observations)
Direct Com
.0717
.0236
.0118
.0084
-.0796
.1580
Indirect Com
.1154
-.0155
-.0770
-.0289
-.0576
.2318
Comply
.0415
-.0521
-.0575
-.0656
-.0939
.2127
Noncomply
.0528
-.0094
.0367
.1606
.0543
.0424
No Opp
.1384
.0640
.0162
.0015
-.0890
.1632
Laugh
-.1836
-.0433
-.1050
-.1149
-.1760
-.2549
Yell
-.1523
-.1600
-.0555
.1000
.1736
-.1499
Physical Pos
.0000
.1953
-.0178
-.0642
-.0954
-.0193
Physical Neg
.2432
.2174
.0922
.0700
-.1296
-.0243
Destructive
.0669
-.1305
-.1646
.1516
.2883
-.1774
* p < .01
** p < .001


122
Covariate Findings
To reiterate the major finding, the results of this study
showed no significant differences in the behavior or adaptive
functioning between children exposed to crack prenatally and
nonexposed matched counterparts. If anything, there is a
tendency by parent report for nonexposed children to exhibit
slightly worse behavior than exposed children. It was
presumed at the outset of the study that scores on measures of
child behavior and adaptive functioning by parent report and
by direct observation would reflect effects of a complex
combination of home, caregiver, and child variables in
addition to the possible influence of drug exposure. For this
reason, multiple covariates were considered in the analysis
including prenatal exposure to alcohol, home environment,
maternal depression, foster care status, and child gender.
Initial exploration of the relationships between covariates
and outcome variables confirmed the appropriateness of their
inclusion in the study.
First, drug exposure status was positively related to
foster care status and alcohol use during pregnancy. In other
words, children exposed to crack in tero were more likely to
be exposed to alcohol and to be in a foster care placement
(defined as someone other than the biological mother) at three


86
Table 6 - Continued
HOME
INVENTORY
Low
(n = 25)
High
M
(n = 29)
Me
DPICS-II (Derived Scores)
Total Commands*
45.8000
46.2759
.945
Percent Complyb
.3316
.3651
.445
Percent Noncomplyb
.0947
.0914
.892
Percent No Opportunityb
.5738
.5435
.458
* p < .05
* frequency data
b percentages


105
Table 18
MANO VA with Dependent Variables from the ECBI
Univariate Stepdown
F
df
E
df
p-value
Problem Scale
2.63
(1,58)
2.63
(1,58)
.110
Intensity Scale
.88
(1,58)
.05
(1,57)
.819
Significance not attained in either univariate or step-down context.


LITERATURE REVIEW
Physiological and Behavioral Effects
The physiological impact of in tero cocaine exposure has
been extensively modelled in animal investigations. The
underlying assumption in such studies is that cocaine may
affect development in two principle ways: 1) by disturbing
dopaminergic functioning in the developing fetus, and/or 2)
via hypoxic effects.
The dopamine system is implicated in the modulation of
reward systems, reinforcement, sensorimotor integration, and
environmental responding. Cocaine acts as an inhibitor of
dopamine reuptake presynaptically, serving to increase the
amount of amines in the synaptic cleft. There is evidence
that repeated cocaine administration decreases the amount of
dopamine synthesis presynaptically and increases the number of
dopamine receptors postsynaptically (Fung, Reed, & Lau, 1989).
The dopaminergic system is developing in the third trimester
of human fetal development and is functional and capable of
mediating behaviors in rat fetuses towards the end of their
gestational period. Moody, Robison, Spear, and Smotherman,
8


33
few studies report an increase in stillbirth rate, and cocaine
appears to reduce litter size but only at the most toxic doses
which may not be relevant to human studies. In animals, odor-
associated learning appears to be impaired in some studies.
Altered neuronal circuits, including nigrostriatal pathway
(fine motor tuning) and mesolimbic dopaminergic system
(reinforcement), have been also demonstrated. Head size in
animals does not appear to be associated with prenatal cocaine
use.
While some reports in the human clinical literature
suggest that cocaine use during pregnancy is associated with
smaller babies, others do not find statistically significant
effects on fetal growth. Evidence of decreased length in
human fetal growth has been found, but it is unclear whether
these results can be attributed to cocaine or to other factors
such as maternal malnutrition and hypoxia. Further, no
specific constellation of fetal malformations is found with
prenatal cocaine use although case reports of craniofacial
defects, missing digits, and genitourinary malformations exist
(Dow-Edwards, 1991).
Transient neurological deficits have been noted in
neonates exposed to cocaine in tero which have included
tremors, rigidity, hyperactivity, abnormal EEG, seizures,


93
Table 10
Correlations between Covariates and Behavioral and Adaptive Variables
Exposure
Status
Alcohol
Exposure
Foster
Care
Gender
Maternal
Dep
Home
Invent
CONNORS
Conduct
-.0410
-.1558
-.2830
-.0992
.3358*
.2237
Learning
-.0552
-.0567
-.0522
.2985
.3977*
-.1751
Psychosomatic
-.0825
-.2544
-.1669
-.1093
.3139
-.0869
Impulsive
-.0419
-.0449
-.0962
.1188
.3298
.0158
Anxiety
-.2271
.0114
-.1397
-.2738
.1451
-.1449
Hyperactivity
-.1026
-.1075
-.0961
.2062
.3534*
.1181
ECBI
Problem
-.1729
-.1245
-.2034
-.0167
.3387*
-.0680
Intensity
-.0114
-.2002
-.1755
-.0468
.3109
-.0656
VINELAND
Social
.0642
.0123
-.1142
-.1266
-.2017
.3209
Commun
.1101
.1655
-.0704
-.2598
-.0851
.3488*
Daily
-.0794
.1615
-.1373
-.0817
-.1414
.0295
Motor
.1776
.0782
.1078
.0895
-.0737
.2688
(Continued)


114
noncompliance were noted from normative groups, but that the
higher incidence of direct commands occurred together with an
increase in child compliance. These results suggest that
basic parenting styles may be different when comparing the
study group to the normative sample. Observations suggest
that the caregivers in the study group may simple talk more
than the caregivers included in the normative samples. These
findings may reflect cultural or ethnic differences which may
play an important role in parenting style and subsequent child
behavior independent of drug use or exposure status.
Measures used in this study were chosen for their good
standardization properties and ability to distinguish between
groups (Connors, 1990; Eyberg, 1992; Eyberg et al., 1994;
Sparrow et al., 1984). Thus, significant differences between
the total sample and the normative group on these subscales
may be interpreted in several ways. First, the total sample
regardless of drug exposure status may not conform to
normative groups. If this is the case, measures which
commonly form the basis for behavioral and adaptive
evaluation, such as the Connors or Vineland, may be misleading
when used with this sample or other similar samples comprised
largely of poor, undereducated, rural, minority caregivers and
their children. The danger of misinterpretation of outcome on


70
for certain comparisons may have been diminished by the use of
familywise comparisons which tends to reduce power.
Hypothesis 2
It was hypothesized that behavioral difficulties would be
more pronounced in the exposed group. Descriptive data for
the exposed and nonexposed children are summarized on Table
16. To test this hypothesis, a multivariate analysis of
covariance was performed on the six dependent variables that
comprise the Connors: Conduct Problem, Learning Problem,
Psychosomatic, Impulsive-Hyperactive, Anxiety and
Hyperactivity. In the initial analysis, adjustment was made
for five covariates including alcohol, maternal depression,
foster care, HOME inventory, and child gender. The
independent variable was exposure status (exposed to crack
versus not exposed). SPSSX (Norusis, 1987) MANCOVA was used
for the analyses with the sequential adjustment for
nonorthogonality.
With the use of Hotelling's criterion, the dependent
variables were significantly related to the combined
covariates, with £(30,232) = 1.70, p < .05. To investigate
more specifically the power of the covariates to adjust the
dependent variables, multiple regressions were run with


52
scales, MANCOVA with Hotellings T2 was used to analyze between
group differences.
Hypothesis 5
It was hypothesized that the performance of the cocaine-
exposed group would be depressed compared to the nonexposed
groups in terms of observed disordered behaviors as measured
on the DPICS-II (Eyberg et al., 1994). Because data for
individual behaviors are observed at very low frequencies, the
basic ten observed behaviors were compared for between group
differences using t-tests. The four derived summary scores
including Total Commands, Percent Compliance, Percent
Noncompliance and Percent No Opportunity for Compliance, were
treated like parent report variables. After graphing to
inspect relationships between scales, MANCOVA with Hotellings
T2 was used to analyze between group differences.


TABLE OF CONTENTS
Page
ACKNOWLEDGMENTS i i
LIST OF TABLES vi
ABSTRACT V
INTRODUCTION 1
LITERATURE REVIEW 8
Physiological and Behavioral Effects 8
Summary of Literature Review 32
PURPOSE OF RESEARCH 35
MATERIALS AND METHODS 37
Subjects 37
Parent Report Measures 43
Behavioral Observation Measures 45
Procedures 47
ANALYSES 49
Descriptive Analyses 49
Hypothesis 1 49
Hypothesis 2 51
Hypothesis 3 51
Hypothesis 4 51
Hypothesis 5 52
RESULTS 53
Descriptive Analyses 53
Initial Between Groups Analyses 57
Initial Correlations 61
Hypothesis 1 65
iv


46
from 38% to 99% (Bessmer, 1993). The DPICS-II includes three
situations that may be coded. For this study, we selected
five minutes of child directed play between caregiver and
child (CDI) and five minutes of parent-directed play (PDI).
Administration and scoring criteria for the standardized
protocol were not altered. The DPICS-II code categories
selected for observation were child behaviors that others have
suggested might differentiate between cocaine-exposed children
and nonexposed children. Exposed children may demonstrate
conduct disordered behaviors. Alternately, the exposed child
may be withdrawn in interactive situations. To capture a
potential range of child behaviors, both positive and
negative, included here were: 1) yell and whine, 2) laugh, 3)
destructive, 4) physical negative, and 5) physical positive.
These variables were measured by frequency over two, five
minute periods. Compliance data were drawn from several
variables as follows: 1) compliance or 2) noncompliance to a
3) direct or 4) indirect command, or 5) no opportunity for
compliance. Total frequency of commands were calculated for
each child. The five compliance variables were also combined
to derive a percentage representing the rate of compliance,
noncompliance, and no opportunity for compliance for each
child. These behaviors are defined in detail in the DPICS-II


74
The results of this analysis are shown in Table 18. The
Hotelling's criterion for the combination of dependent
variables was not significant with F(2,57) = 1.32, p > .05.
Findings indicate that there are no differences between
exposed and nonexposed children on this combination of
variables by parent report. Inspection of univariate and
stepdown results at the p < .05 level reveal no significant
differences between exposed and nonexposed children on these
variables. Specifically, groups were not significantly
different on either the ECBI problem scale F(l,58) = 2.63, p
> .05, or intensity scale F(l,57) = .05, p > .05.
Hypothesis 4
It was also hypothesized that adaptive difficulties would
be more pronounced in the exposed group. Descriptive data for
the exposed and nonexposed children are summarized on Table
16. To test this, a multivariate analysis of covariance was
performed on the four dependent variables that comprise the
Vineland: Socialization, Communication, Daily Living, and
Motor Skills. In the initial analysis, adjustment was made
for five covariates including alcohol, maternal depression,
foster care, HOME inventory, and child gender. The
independent variable was exposure status (exposed to crack


44
words or "Feeds self with spoon without spilling."
Administration time is approximately 15 minutes. Split-half
coefficients and test-retest reliabilities for the Adaptive
Behavior Composite are .94 and .95 respectively and factors
reportedly load in appropriate subdomains of each of the four
areas. Scores are percentile ranks, means, and standard
deviations.
Connors Parent Rating Scale
The Connors (1990) is a parent rating report of
hyperactive and attentional problems in children aged three to
17. It was normed on 383 children and consists of 48
questions which load into six factors including Conduct
Problem, Learning Problem, Psychosomatic, Hyperactivity Index,
Impulsive-Hyperactive, and Anxiety. Higher scores indicate
increased problems in the tested area. Administration time is
approximately 15 minutes. Factors loadings of the CPRS-48
range form .41 to .82 and appear stable over time. Scores are
percentile ranks, means and standard deviations.
Eyberg Child Behavior Inventory (ECBI)
The ECBI (Eyberg, 1992) is a parent report screening
measure for disruptive behaviors in children ages two through


75
versus not exposed to crack in tero). SPSSX MANCOVA was used
for the initial analyses with the sequential adjustment for
nonorthogonality.
With the use of Hotelling's criterion, the dependent
variables were not significantly related to the combined
covariates, with £(20,194) = 1.55, p > .05. Thus, all five
covariates were dropped from further analyses. The effects of
exposure status on the dependent variables without inclusion
of covariates were investigated in univariate and stepdown
analysis using SPSS* MANOVA. Dependent variables were entered
in the following order: Socialization, Communication, Daily
Living, and Motor Skills. In the stepdown analysis, each
dependent variable was analyzed in turn with higher priority
dependent variables treated as covariates and with the highest
priority dependent variables tested in a univariate ANOVA.
Socialization was chosen as the highest priority dependent
variable as the literature suggests that social relatedness
may be disturbed by prenatal cocaine exposure.
The results of this analysis are shown in Table 19. The
Hotelling's criterion for the combination of dependent
variables was not significant with F(4,50) = 1.17, p > .05.
These findings suggest that there are no differences between
exposed and nonexposed children on this combination of


DISCUSSION
Background
This study was designed to explore differences in
behavioral and adaptive functioning between toddlers who were
prenatally exposed to crack cocaine and their matched
nonexposed peers. Results showed that children in the total
sample tended to display more conduct problems, learning
problems, impulsivity, and hyperactivity than normative
samples. Higher intensity of problem behaviors was noted in
the total sample compared to norms. During the child-directed
interaction portion of the DPICS-II, caregivers in the total
sample tended to have a higher incidence of direct commands
and indirect commands in conjunction with higher incidence of
child compliance, noncompliance, and no opportunity to comply
than the normative group. Similarly, during the parent-
directed interaction portion of the DPICS-II, caregivers
tended to have a higher incidence of direct commands in
conjunction with higher incidence of child compliance and no
opportunity to comply.
108


19
among the three groups, stillbirth rates were significantly
higher in the cocaine only group compared to the no drug
group. Also, there were significantly more congenital
malformations in the cocaine only group compared to both
contrast groups. Five of fifty infants in the cocaine only
group had major congenital malformations including
exencephaly, intraparietal encephalocele, and parietal bone
defects. Although complications occurred in women after all
three routes of cocaine administration, the sequelae were more
frequent in those who smoked crack regularly or injected it
intravenously. These findings are dramatic and suggest that
cocaine is a powerful teratogen to the developing fetus.
However, this study was conducted in a large inner city
hospital where the confound of polydrug use was common among
the cocaine-using group, and it is unclear whether examiners
were blinded as to the drug status of the infants.
Little, Snell, Klein, and Gilstrap (1989) also examined
perinatal outcome following maternal cocaine use during
pregnancy in 53 exposed infants compared to a 100 infant
control group. Cocaine use in their study was associated with
preterm labor; birth complications including meconium
staining, tachycardia, and lower birth weight; and an excess
of congenital cardiac anomalies. There were several


66
learning problems were also more frequent in the sample than
the normative group with y = 2.98, p < .05. Children in the
sample tended to be more impulsive than the normative group
where y 6.76, p < .01. Similarly, parent report indicated
increased hyperactivity in the total sample than in the
normative population where y = 5.30, p < .05 (Table 13).
Eyberq Child Behavior Inventory
The second conceptual grouping was comprised of the two
ECBI scores including: Problem and Intensity. Using the SMM
familywise rate for two comparisons, the total sample was
significantly more likely to display a high intensity of
problem behaviors than the normative group where y = 2.637, p
< .05. Despite the high intensity of problem behaviors,
caregivers did not endorse items indicating that the behavior
posed a significant problem in the home (Table 13).
Vineland Adaptive Behavior Scales
The third group was comprised of the four subscales of
the Vineland related to adaptive functioning: Socialization,
Communication, Daily Living, and Motor Skills. Using the SMM
familywise rate for four comparisons, none of the sample


110
warranted. Although researchers have speculated about the
presence of disordered behavior with cocaine exposure, there
has been no long-term followup of exposed children which
addresses this issue (Davis et al., 1992? Griffith et al,
1994; Hume et al., 1989). Further, methodological problems in
the literature have made interpretation of results difficult.
Whether disordered behavioral or adaptive outcome can be
attributed to cocaine exposure remains an open question (Dow-
Edwards, 1991).
Comparison to Norms
As a starting point, the present study was interested in
investigating whether clinical norms provided with
standardized psychological measures could be appropriately
applied to a study sample which, at least in this case, was
comprised of primarily poor, undereducated, African Americans.
Thus, hypothesis one was concerned with total sample
performance compared to norms. Significant differences were
noted. For example, the total sample was more likely to
display behaviors consistent with conduct problems, learning
problems, impulsivity, and hyperactivity than normative
samples. In general, these difficulties were worse with
increased maternal depression.


141
Developments in Pharmacological Therapeutics, 18, 116-
124.
Weinberg, S.L., & Goldberg, K.P. (1979). Corelationspecial
cases of the Pearson Correlation Coefficient. In S.L.
Weinberg & K.P. Goldberg, Basic statistics for education
and behavioral sciences (pp. 93-95). Boston: Houghton
Mifflin Co.
Wise, R.A. (1984). Neural mechanisms of the reinforcing
action of cocaine. National Institute of Drug Abuse
Research Monograph Series. 50, 15-33.
Woods, N.S., Eyler, F.D., Behnke, M., & Conlon, M. (1993).
Cocaine use during pregnancy: maternal depressive
symptoms and infant neurobehavior over the first month.
Infant Behavior and Development. 1£, 83-98.
Woods, J.R., Plessinger, M.A., & Clark, K.E. (1987). Effect
of cocaine on uterine blood flow and fetal oxygenation.
Journal of the American Medical Association, 257, 957-
961.
Yakovlev, P.I., Lecours, A.R. (1967). The myelogenetic
cycles of regional maturation of the brain. In Regional
Development of the Brain in Early Life (A. Minkowski,
Ed). Philadelphia: F.A. Davis, pp 3-70.


65
group and correlational findings suggest complex relationships
between measured scales (Table 12).
Hypothesis 1
It was hypothesized that the performance of both groups
would be depressed on all measures compared to age-based
norms. Analyses were performed with sample scores and
population norms. To test this, Welch's V for unequal sample
size was calculated comparing total sample scores on dependent
variables to standardized norms. Dependent variables were
grouped conceptually a'priori' and Studentized Maximum Modulus
(SMM) tables for familywise error rate were used to control
for multiple comparisons at the .05 significance level.
Tables 13, 14, and 15 summarize these results.
Connors Parent Rating Scale
The first group was comprised of the six subscales of the
Connors including: Conduct Problem, Learning Problem,
Psychosomatic, Impulsive, Anxiety, and Hyperactivity Indices.
Using the SMM familywise rate for six comparisons, Conduct
Problem was significantly different from the population norm
y = 5*03, e < .01 where the mean for the sample was higher
than the population mean. According to parent report,


31
to account for a significant amount of the variance in
habituation scores. Maternal polydrug use may confound
findings somewhat in this study.
In an attempt to improve upon the methodology in the
prenatal cocaine exposure literature, Woods, Eyler, Behnke,
and Conlon (1993) longitudinally assessed infant behavior
using the BNBAS at birth and again at one month. Mothers
enrolled in this study were from a rural, low income
population with little or no drug treatment. All examinations
were performed blindly. Woods et al. (1993) found cocaine-
exposed infants had lower birth weights and shorter gestations
than controls, a finding typical of many investigations.
However, there were no differences in neonatal performance on
the BNBAS at birth or at one month of age. These results
indicate that not all cocaine-exposed infants show
neurobehavioral deficits in the neonatal period.
Again, studies of infant neurobehavior report varying
results. For example, Mayes, Granger, Frank, Schottenefeld,
and Bornstein (1993) reported that exposed infants had poorer
orientation than nonexposed infants, while Richardson and Day
(1991) reported no differences on any Brazelton scale. In
general, studies documenting birth outcome using repeated
BNBAS assessments report a pattern of developmental recovery


116
outcome without using an appropriate (read matched) control
group.
Between Groups Comparisons
When accounting for nonsignificant findings between
groups, there are several possible explanations. The most
parsimonious is that there are in fact no measurable
differences in the behavior or adaptive functioning between
children exposed to crack prenatally and their nonexposed
counterparts at three years of age. Given the level of
scientific and popular press focus on the disordered behavior
of cocaine-exposed children, support of the null hypothesis in
this case is extremely interesting. This finding suggests that
when an appropriate control group is used, group differences
potentially attributed to cocaine exposure disappear.
A review of the literature indicates that the most
reliable findings in the neonatal period is smaller head
circumference and reduced length and birthweight (Chiroboga,
1993? Eyler, Behnke, Conlon, Woods, & Frentzen, 1994? Little
& Snell, 1991? MacGregor et al. 1987? Oro & Dixon, 1987).
Notably, these differences tend to diminish with time until by
one year of age, generally no growth differences remain with
the possible exception of head circumference (Chiriboga et


134
Eisen, L.N., Field, T.M. Bandstra, E.S., Roberts, J.P.,
Morrow, C., Larson, S.K., & Steele, B.M. (1991).
Perinatal cocaine effects on neonatal stress behavior and
performance on the Brazelton Scale. Pediatrics. 88# 477-
480.
Ellinwood, E.H. (1974). The epidemiology of stimulant abuse.
In: Josephson F., Carroll, E., eds. Drug use:
epidemiological and sociological approaches. Washington,
D.C.: Hemisphere, 1974, 303-329.
Eyberg, S. (1992). Parent and teacher behavior inventories
for the assessment of conduct problem behaviors in
children. In: L. VandeCreek, S* Knapp, & T.L. Jackson
(Eds.), Innovations in clinical practice,: A source book
(Vol. 11). Sarasota, FL: Professional Resource Press.
Eyberg, S., Bessmer, J., Newcomb, K., Edwards, D. & Robinson,
E. (1994). Dyadic Parent-Child Interaction Coding
System-Il. Gainesville, FL: University of Florida.
Eyberg, S., & Colvin, A. (1994, August). Restandardization
of the Eyberg Child Behavior Inventory. Poster presented
at the annual meeting of the American Psychological
Association, Los Angeles.
Eyler, F.D., Behnke, M., Conlon, M., Wobie, K., & Woods, N.S.
(in preparation). Birth outcome from a longitudinal
study of prenatally matched cocaine-using and non-using
women.
Eyler, F.D., Behnke, M., Conlon, M., Woods, N.S., Frentzen, B.
(1994). Prenatal cocaine use: A comparison of neonates


97
Table 12 - Continued
VINELAND Communication Daily Living Socialization Motor Skills
ECBI
Problem -.2361
-.1958
-.1177
-.1680
Intensity -.0862
-.0669
-.1817
-.1364
DPICS-II (Derived Scores)
Total Commands .0739
.0544
.0652
.0817
Percent Comply .2592
.2774
.4384*
.0111
Percent Noncomp -.2685
-.4229*
-.2757
-.1140
Percent No Opp -.1637
.0432
-.2942
-.0051
ECBI Problem Intensity
DPICS-II (Derived Scores)
Total Commands
-.1174
-.0110
Percent Comply
-.1527
-.0747
Percent Noncomp
.2771
.1489
Percent No Opp
.0287
-.0250
* p < .01
** p < .001


88
Table 7 - Continued
FOSTER CARE
No
M
(n = 39)
Yes
M
(n = 29)
P
DP1CS-II (Derived Scores)
Total Commands*
46.0256
46.1333
.989
Percent Comply6
.3592
.3247
.481
Percent Noncomply6
.0836
.1170
.212
Percent No Opportunity6
.5572
.5583
.981
* = p < .05
frequency data
b percentages


55
The Total Commands score was derived by adding together
total direct command comply, total direct command noncomply,
total direct command no opportunity to comply, total indirect
command comply, total indirect command noncomply, and total
indirect command no opportunity to comply. Percent Compliance
was the sum of total direct command comply and total indirect
command comply divided by the sum of total direct command
comply, total indirect command comply, total direct command
noncomply, total indirect command noncomply, total direct no
opportunity to comply, and total indirect no opportunity to
comply. Percent Noncompliance was the sum of total direct
command noncomply and total indirect command noncomply divided
by the sum of total direct command noncomply, total indirect
command noncomply, total direct command comply, total indirect
command comply, total direct command no opportunity to comply,
and total indirect command no opportunity to comply. Finally,
Percent No Opportunity to Comply was the sum of total direct
command no opportunity and total indirect command no
opportunity divided by total direct command no opportunity,
total indirect command no opportunity, total direct command
comply, total indirect command comply, total direct command
noncomply, and total indirect command noncomply.


5
findings are mirrored in clinical observations of protracted
anhedonia and anergia in some cocaine users (Gawin & Kleber,
1986). Generally, these symptoms resolve over time. However,
there are sporadic reports of high dose users with chronic
anhedonia, anergia and a craving for stimulants that does not
remit (Ellinwood, 1974; Schuster & Fischman, 1985).
Pregnant women are not immune to either the pleasurable
effects of crack or to the physiological consequences of use.
Over the last several years researchers have turned their
attention to the possible impact of in tero exposure to
cocaine and cocaine derivatives on the neonate. This interest
has accelerated due partially to shifting attitudes towards
drug use in general as well as justified alarm at the recent
explosion in crack use (Grinspoon & Balkalar, 1980). Still,
the toxic effects of cocaine use are only beginning to be
understood, and focus has been almost entirely on adult users.
Early reports concerning infant outcomes of in tero exposure
to cocaine has been limited, often anecdotal, contradictory
and predominantly focused on medical outcomes (Ryan et al.,
1987) Thus, while reports in the popular media of antisocial
or hyperactive toddlers created by in tero exposure to
cocaine make sensational copy, they are distinctly premature.


140
chronic prenatal cocaine dosing. Neurotoxicology and
Teratology, 11, 35-38.
Sparrow, S.S., Balia, D.A., & Cicchetti, D.V. (1984).
Vineland Adaptive Behavior Scales, Interview Edition,
Survey Form Manual. American Guidance Service, Inc.,
Minnesota.
Spear, L.P., Kirstein, C.L., & Frambes, N.A. (1989). Cocaine
effects on the developing central nervous system:
behavioral, psychopharmacological, and neurochemical
studies. Annals New York Academy of Science. 362, 290-
307.
Spear, L.P., Kirstein, C.L., Bell, J., Yoottanasumpun, V.,
Greenbaum, R., O'Shea, J., Hoffmann, H., & Spear, N.E.
(1989). Effects of prenatal cocaine exposure on behavior
during the early postnatal period. Neurotoxicology and
Teratology. 11, 57-63.
Ward, S.L.D., Bautista, D.B., Woo, M.S., Chang, M., Schuetz,
S., Wachsman, L. Sehgal, S., & Bean, X. (1992).
Responses to hypoxia and hypercapnia in infants of
substance-abusing mothers. Journal of Pediatrics, 121,
704-709.
Weese-Mayer, D.E., & Barkov, G.A. (1993). Effect of cocaine
in early gestation: physiologic responses to hypoxia in
newborn rabbits. American Review of Respiratory
Diseases. 148. 589-596.
Weese-Mayer, D.E., Klemka-Walden, L.M., Barkov, G.A., &
Gingras, J.L. (1992). Effects of prenatal cocaine on
the ventilatory response to hypoxia in newborn rabbits.


137
Little, B.B., & Snell, L.M. (1991). Brain growth among
fetuses exposed to cocaine in tero: asymmetrical growth
retardation. Obstetrics & Gynecology. 77, 361-364.
Little, B.B., Snell, L.M., Klein, V.R., & Gilstrap, L.C.
(1989). Cocaine abuse during pregnancy: maternal and
fetal implications. Obstetrics & Gynecology. 73., 157-
160.
MacGregor, S.N., Keith, L.G., Chasnoff, I.J., Rosner, M.A.,
Chisum, G.M., Shaw, P., & Minogue, J.P. (1987). Cocaine
use during pregnancy: adverse perinatal outcome.
American Journal of Obstetrics and Gynecology. 157, 686-
690.
Mayes, L.C., Granger, R.H., Frank, M.A., Schottenfeld, R., &
Bornstein, M.H. (1993). Neurobehavioral profiles of
neonates exposed to cocaine prenatally. Pediatrics f 91,
778-783.
Medical Letter (1986). Crack: The Medical Letter On Drugs
and Therapeutics, 28., 69-70.
Minabe, Y., Ashby, C.R., Heyser, C. Spear, L.P., & Wang, R.Y.
(1992). The effects of prenatal cocaine exposure on
spontaneously active midbrain dopamine neurons in adult
male offspring: an electrophysiological study. Brain
Research, 586. 152-156.
Moody, C.A., Robinson, S.R., Spear, L.P., & Smotherman, W.P.
(1993). Fetal behavior and the dopamine system:
activity effects of Dx and D2 receptor manipulations.
Pharmacology Biochemistry and Behavior. 44. 843-850.


22
Alternately, Hadeed, and Siegel (1989), when studying
neonates of 56 mothers who used cocaine prenatally, found no
differences in the frequency of maternal preeclampsia or
caesarian section (C/S) rate, teratogenicity, narcotic
withdrawal symptoms, or illnesses compared to a no illicit
drug control group. Alternately, weight, length and head
circumference growth curves of infants born to cocaine-using
mothers shifted below the 25th percentile, although this
finding was not thought to be clinically significant. In
addition, cocaine use did seem to precipitate more spontaneous
abortions, abruptio placentae, and meconium stained amniotic
fluid. Advantages of this study included the use of a cocaine
only group and blinded evaluations. In addition, maternal
factors were controlled for differences in age, parity,
socioeconomic status (SES), ethnicity, and smoking, making
findings apparently more reliable.
One of the most prolific researchers in this area, Ira
Chasnoff, consistently reported a number of negative outcomes
for infants exposed to cocaine in tero in his early
investigations. In addition to the effects described by both
Oro and Dixon (1987) and Ryan et al. (1987), Chasnoff (1989)
reported a higher incidence of significant genitourinary tract
malformations. In one study of a pool of 70 infants with


89
Table 8
Between Group Differences Defined by Gender
GENDER
Girls
M
(n = 34)
Boys
M
(n = 26)
P
CONNORS
Conduct
61.0882
58.1538
.451
Learning
51.8235
59.7692
.021*
Psychosomatic
54.0588
50.6923
.406
Impulsive
57.0294
59.0385
.366
Anxiety
53.0294
48.2308
.034*
Hyperactivity
56.7941
62.1154
.114
ECBl
Problem
10.2059
9.9231
.899
Intensity
121.3824
118.5000
.732
VINELAND
Socialization
100.3235
96.9615
.335
Communication
105.1471
98.5385
.045*
Daily Living
105.7647
103.0000
.535
Motor Skills
95.4118
98.1538
.496
(Continued)


13
impacted neonatal outcome and long term development in the
rats due to disruption of the dopamine system.
In a study designed to mimic moderate cocaine use by
humans during pregnancy, Fung et al. (1989) examined the
neurobehavioral responses and striatal dopaminergic system in
cocaine-exposed newborn rats. No change in length of
gestation, litter size, birth weight and length of pups, and
the ratio of male to female pups was noted. At 14 days old,
exposed and nonexposed pups showed similar locomotor
performance in righting reflex, position reflex and negative
geotaxic tests. Results demonstrated that prenatal exposure
to cocaine did not alter the development of motor coordination
suggesting no significant impact on the developing
dopaminergic and striatal systems with moderate exposure.
Spear, Kirstein, Bell, Yoottanasumpun, Greenbaum, O'Shea,
Hoffmann, and Spear (1989) also studied the early development
of cocaine-exposed rats. They found that when pups were
exposed a relatively large dose of cocaine daily (40 mg/kg)
late in gestation, there were no differences in maternal
weight gain, duration of pregnancy, or number of live
male/female pups per litter were found. Like Fung et al.
(1989), they found no differences in offspring body weights at
birth and weaning, physical maturation and reflex development.


69
and referred and nonreferred normative groups in the parent-
directed interactions (Table 15). Specifically, caregivers in
the sample group displayed significantly more direct commands
than either the referred or nonreferred normative groups with
y = 4.91, p < .01 and y = 7.64, p < .01 respectively.
Interestingly, no differences were noted in the rate of
indirect commands in the parent-directed interaction. As in
the child-directed interactions, the rate of compliance was
significantly higher in the sample group during the parent-
directed interactions than in either the referred or
nonreferred normative groups with y = 6.13, p < .01 and y =
5.28, p < .01 respectively. Similarly, the study sample
tended to have a significantly higher rate of no opportunity
to comply than either the referred or nonreferred comparative
group with y = 3.76, p < .01 and y = 5.55, p < .01
respectively.
Alternately, no significant differences were noted in the
rate of noncompliance between the study sample and normative
groups. It was not possible to test between groups
differences for child behaviors for laugh, yell, physical
positive, physical negative or destructive due to either the
absence of normative data or variance in the normative group
(Table 15). Finally, it should be noted that the significance


103
Table 16 - Continued
Exposed Non-Exposed
M
SD
M
SJB
(n =
30)
(n =
= 24)
DP1CS-II (Basic Observations)
Physical Negative
.2333
.626
.0000
.000
Destructive
.3667
.928
.4583
1.668
* = p < .05
** = p < .01


78
exposed and nonexposed children on this combination of
variables by parent report. Inspection of univariate and
stepdown results at the p < .05 level likewise reveal no
significant differences between exposed and nonexposed
children on these variables. Specifically, significant
differences were not found between groups for commands £(1,45)
= .26, p > .05, comply £(1,44) = .86, p > .05, noncomply
£(1,43) = .11, p > .05, or no opportunity £(1,42) = .02, p >
.05.


102
Table 16 - Continued
Exposed
M
(n = 30)
£D
Non-Exposed
M £D
(n = 24)
DPICS-II (Derived Scores)
Total Commands
48.6333
22.380
42.8333
28.013
Percent Comply
.3307
.132
.3731
.188
Percent Noncomply
.0981
.093
.0864
.081
Percent No Opportunity
.5711
.123
.5405
.175
DPICS-II (Basic Observations)
Direct Command
41.5000
21.463
37.5000
25.480
Indirect Command
7.1333
5.237
5.3333
6.418
Comply
16.1000
10.056
15.11672
2.383
Noncomply
4.2333
3.945
3.5417
4.681
No Opportunity
28.3000
15.063
23.6250
17.338
Laugh
.2667
.450
.5833
1.792
Yell
.1333
.434
.3750
1.439
Physical Positive
.9333
1.701
.8750
1.513
(Continued)


71
covariates acting as multiple predictors. None of the
covariates provided adjustment to the Conduct Problem or
Anxiety subscales of the Connors. However, two of the five
covariates, child gender and maternal depression, provided
significant adjustment to Learning Problems with beta values
of .34 t (53) = 2.75, p < .05 and .41 t(53) = 3.27, p < .05
respectively. Maternal depression also provided adjustment to
Psychosomatic with a beta value of .30 significantly different
from zero where t(53) = 2.13, p < .05. Similarly maternal
depression provided significant adjustment to Impulsivity and
Hyperactivity with beta values at .36 t(53) = 2.60, p < .05,
and .36 t(53) = 2.67, p < .05 respectively. For none of the
dependent variables did alcohol, foster care, or HOME
inventory provide significant adjustment. These covariates
were dropped from further analyses.
The effects of exposure status on the dependent variables
after adjustment for significant covariates were investigated
in univariate and stepdown analysis. Dependent variables were
entered in the following order: Conduct Problems, Learning
Problems, Psychosomatic, Impulsivity, Anxiety, and
Hyperactivity Indices. In the stepdown analysis, each
dependent variable was analyzed in turn with higher priority
dependent variables treated as covariates and with the highest


136
Henderson, M.G. & McMillen, B.A. (1990). Effects of
prenatal exposure to cocaine or related drugs on rat
developmental and neurological indices. Brain Research
Bulletin. 24, 207-212.
Howard, C. Mofenson, H.C., & Caraccio, T.R. (1987).
Cocaine. Pediatric Annals. 16, 864-874.
Howard, J. (1989). Cocaine and its effects on the newborn.
Developmental Medicine and Child Neurology, 31, 255-256.
Hume, R.F., O'Donnell, K.J., Stanger, C.L., Killam, A.P., &
Gingras, J.L. (1989). In tero cocaine exposure:
observations of fetal behavioral state may predict
neonatal outcome. American Journal of Obstetrics and
Gynecology, 161, 685-690.
Hutchings, D.E., Fico, T.A., & Dow-Edwards, D.L. (1989).
Prenatal cocaine: maternal toxicity, fetal effects and
locomotor activity in rat offspring. Neurotoxicology and
Teratologyf 11. 65-69.
Kaye, K. Elkind, L., Goldberg, D. & Tytun, A. (1989).
Birth outcomes for infants of drug abusing mothers. New
YorK State Journal of Medicine, May, 259, 261.
Levine, S.R., Washington, J.M., Jefferson, M.F., Kieran, S.N.,
Moen, M., Feit, H., & Welch, K.M.A. (1987). "Crack"
cocaine-associated stroke. Neurology. 37., 1849-1853.
Link, E.A., Weese-Mayer, D.W., & Byrd, S.E. (1991). Magnetic
resonance imaging in infants exposed to cocaine
prenatally: a preliminary report. Clinical Pediatrics.
30, 506-508.


Abstract of the Dissertation Presented to the Graduate
School of the University of Florida in Partial Fulfillment
of the Requirements for the Degree of Doctor of Philosophy
DEVELOPMENTAL OUTCOME FOR TODDLERS PRENATALLY EXPOSED TO
CRACK COCAINE: BEHAVIORAL AND ADAPTIVE SEQUELAE
By
Karen Anne Holler
August, 1996
Chairpersons: Eileen B. Fennell, Ph.D., ABPP
Fonda D. Eyler, Ph.D.
Major Department: Clinical and Health Psychology
Early studies indicated that infants exposed prenatally
to cocaine and cocaine derivatives may be at risk for
increased spontaneous abortions, fetal death, preterm labor,
abruptio placentae, decreased length, weight, and head
circumference, congenital malformations, and deviant
neurobehavior. However, very little long-term followup has
been done to assess the functioning of these children as they
mature. The present study compared two groups of three-year
old preschoolers who were a) exposed in tero to crack, or b)
not exposed in tero to crack. Information about child
behavior and adaptive functioning was collected by primary
caregiver report using the Vineland Adaptive Behavior Scales
Survey Form, the Connors Parent Rating Scale, and the Eyberg
viii


59
maternal depression at the three year visit and HOME (Caldwell
& Bradley, 1984) inventory total score at the time of the
three year visit. No differences were found in terms of
maternal depression or HOME inventory total scores at three
years of age using exposure status as the independent variable
(Table 2).
Group Differences using Covariates as Independent Variables
Notably, significant differences were found on parent
report measures when the groups were defined by covariates.
For example, groups were defined by maternal depression based
on provided clinical cutoffs (Radloff, 1977), the low group
with scores of 16 or less (n = 21) and a the high group with
scores over 16 (n = 39) representing elevated depression. The
elevated maternal depression group demonstrated more conduct
problems t = -2.57, p < .013, learning problems t = -3.16, p
< .003, hyperactivity t = -2.55, p < .014, and increased
intensity of problem behaviors t = -2.42, p < .019 (Table 5).
Similarly, HOME inventory scores were divided based on a
provided normative mean of 37 (Caldwell & Bradley, 1984). The
first group (low) was comprised of scores of 37 or less (n =
29) and a second group (high) was comprised of scores of
greater than 37 (n = 31) representing more enriched


96
Table 12
Correlations between Dependent Subsets
CONNORS Conduct Learning Psycho
somatic
Impulsive
Anxiety Hyperactivity
ECBl
Problem .5569**
.5586**
.2387
.4915**
.1621
.6089**
Intensity .6635**
.5827**
.2427
.6014**
.0808
.6331**
VINELAND
Socialization -.0861
-.4672**
-.1739
-.1941
-.0539
-.3343*
Communication -.0604
-.3768*
-.1786
-.0780
-.1292
.2737
Daily Living .0059
-.2056
-.1040
-.2864
-.0352
-.2706
Motor Skills -.0246
-.1588
-.2236
-.0876
-.3104
-.2185
DPCIS-II (Derived Scores)
Total Commands .1053
-.0397
-.0328
-.0731
-.0080
-.0074
Percent Comply -.0022
-.3005
.0751
-.2315
.1761
-.1646
Percent Noncom -.1059
.3578*
.2806
.2133
.0304
.2336
Percent No Opp .0476
.0676
-.2406
.0820
-.1757
.0082
(Continued)


98
Table 13
Means and Standard Deviations of tested Sample with Age-Based Norms Parent Report
Sample
M
SD
Norms
M
SD
CONNORS
Conduct
59.82**
14.78
50
10
Learning
55.27*
13.30
50
10
Psychosomatic
52.60
15.39
50
10
Impulsive
57.90**
8.45
50
10
Anxiety
50.95
8.76
50
10
Hyperactivity
59.10*
12.89
50
10
ECBI
Problem
10.08
8.47
7
8
Intensity
120.13*
30.77
97
35
VINELAND
Socialization
98.87
13.26
100
15
Communication
102.28
12.70
100
15
Daily Living
104.56
16.90
100
15
Motor Skills
96.60
15.31
100
15
* = p < .05
** = p < .01


14
However, cocaine-exposed pups were deficient in learning and
odor/milk association and showed enhanced locomotion. The
researchers concluded that prenatal cocaine exposure impacts
behavioral and cognitive function during the early postnatal
period even in the absence of overt physiological changes.
A review of studies of postnatal integrity of animals
exposed to moderate amounts of maternal cocaine administration
reveals some consistencies. Generally studies have found no
differences in dam weight gain, litter size or weight, or
early postnatal behavioral tests (Smith, Mattran, Kurkjian,
and Kurtz, 1989; Hutchings, Fico, & Dow-Edwards, 1989; Spear,
Kirstein, & Frambes, 1989). However, drug effects have been
noted on the level of locomotion, exploratory behavior, tail
flick, footshock sensitivity and some learning and/or
retention tasks. Arguments explaining significant results are
generally dependent on altered neurodevelopment during
critical prenatal periods, poor maternal nutrition, and
hypoxia.
While animal models for cocaine exposure in tero may be
useful, there are several difficulties in extrapolating the
effects found in animals to humans. In addition to the
obvious problem of equating human and rat, sheep, or rabbit
neurodevelopment, results of animal studies also tend to vary


106
Table 19
MANOVA with Dependent Variables frpm the Vineland
Univariate Stepdown
F df F df p-value
Socialization
.40
(1,58)
.40
(1,58)
.526
Communication
.91
(1,58)
.51
(1,57)
All
Daily Living
.16
(1,58)
1.12
(1,56)
.293
Motor Skills
2.67
(1,58)
1.67
(1,55)
.201
Significance not attained in either univariate or step-down context.


45
16. It includes an Intensity Scale, which indicates how often
the behaviors presently occur, and a Problem Scale, which
identifies the specific behaviors that are currently problems
for the caregiver. There are a total of 36 items.
Clinically, a Problem Scale score of 11 or greater and an
Intensity Scale score of 127 or greater are used as cutoffs
for disordered conduct. The normative sample was 798 parents
of children drawn from six pediatric health care settings
sampled so as to approximate the demographic composition of
the Southeast. Split-half correlations for both scales were
.93. Administration time is approximately 5 minutes.
Behavioral Observation Measure
Dyadic Parent-Child Interaction Coding Svstem-II (DPICS-II)
The DPICS-II (Eyberg, Bessmer, Newcomb, Edwards, &
Robinson, 1994) is a direct, objective observation measure to
discriminate normal from conduct-disordered child/parent
interactions. The system provides a measure of both child and
parent behaviors and was originally normed on 20 families
referred for treatment of a conduct-problem child and 22
families without such a conduct-problem child. Problem
behaviors include disobedience, aggression, destructiveness,
or hyperactivity. Reliability for DPICS-II by behavior ranged


43
10.41. Alcohol use, calculated as average number of 4-ounce
drinks per day over three trimesters, ranged from zero to 3.66
(M = .253, £D = .649). In the nonexposed group, average
maternal depression score was 20.9 (SD = 9.5), and average
home inventory score was 36.5 (SD = 8.1). Alcohol use in the
nonexposed groups averaged .2667 drinks per day (SD = .450).
In the exposed group, average maternal depression score was
18.4 (SD = 10.1), and average home inventory score was 37.6
(SD 8.7). Mean drinks per day in the exposed group was
.9333 (SD = .640). For purposes of further analyses, alcohol
was coded as a dichotomous variable, either present or absent
in the prenatal period.
Parent Report Measures
Vineland Adaptive Behavior Scales
The Vineland (Sparrow, Balia, & Cicchetti, 1984) is a
nationally normed measure of adaptive behavior for children
birth to adulthood and assesses competency in four skill
areas: Socialization, Communication, Motor Skills, and Daily
Living. The Survey Form used in this study consists of 297
guestions administered to the primary caregiver. Items to be
answered on a range from 'yes, usually' to 'don't know'
include such examples as "Uses sentences of four or more


38
diagnosed prior to pregnancy that are known to affect
pregnancy or developmental outcome or maternal interaction or
caregiving, such as diabetes, chronic hypertension, immune
complex disease, seizure disorders, mental illness or
retardation, etc., 3) women with no history of illegal drug
use other than marijuana and cocaine, 4) English speaking, and
5) women who did not use any of the following drugs without a
prescription or chronically with prescription: amphetamines,
benzodiazepines, barbiturates, opiates, methadone, and
methaqualone.
Target subjects were selected during a screening
interview from those who admitted any prenatal use of cocaine
or had a full toxicology screen positive for metabolites of
cocaine; maternal urine specimens were taken at two
unanticipated times, study enrollment and delivery. Any
patient who during the screening interview denied the use of
cocaine, the illicit substances and drugs listed above, and
had a negative cocaine toxicology screen were retained in the
subject pool as a potential match for a cocaine-using subject.
Matching was done within each county health department to
equate level of prenatal risk and included the following
subject conditions: 1) maternal race: black vs. nonblack? 2)
parity: primiparity vs. multiparity? and 3) socioeconomic


130
Conclusion
The major findings of this study were two fold. First,
there were significant differences between the total study
cohort and normative groups on which standardized
psychological measures are based. Second, at three years of
age, no differences were found between a prenatally crack-
exposed cohort on measures of behavior and adaptive
functioning when compared to nonexposed matched peers
regardless of whether evaluation was by parent report or by
objective observation.
These findings have implications for the critical
evaluation of previous (and future) studies which fail to
employ an appropriate control group, and serve as a caution
for the common presumption that toddlers prenatally exposed to
crack will automatically display disordered behavioral and
adaptive functioning. It will be important to continue to
follow this population to determine whether prenatal cocaine
exposure has any sleeper effects on the behavior or adaptive
functioning of children and to clarify the contribution of a
variety of factors to child outcome.


138
Neuspiel, D.R., Hamel, S.C., Hochberg, E., Greene, J., &
Campbell, D. (1991). Maternal cocaine use and infant
behavior. Neurotoxicology and Teratology. 13., 229-233.
Norusis, M.J. (1987). The SPSS Guide to Data Analysis for
SPSS*. Chicago, IL: SPSS, Inc.
Oro, A.S., & Dixon, S.D. (1987). Perinatal cocaine and
methamphetamine exposure: maternal and neonatal
correlates. The Journal of Pediatrics. Ill, 571-578.
Page, T.J., & Iwata, B.A. (1986). Interobserver agreement:
history, theory, and current methods. In: A. Poling,
R.W. Fugua, (Eds.). Research,Methods in Applied Behavior
Analysis Issues and Advances. New York: Plenum Press.
Radloff, L.S. (1977). The CES-D scale: a self-report
depression scale for research in the general population.
Applied Psychological Measurement, 1, 385-401.
Richardson, G.A., & Day, N.L. (1991). Maternal and neonatal
effects of moderate cocaine use during pregnancy.
Neurotoxicology and Teratology. 13, 455-460.
Ryan, L., Ehrlich, S., & Finnegan, L. (1987). Cocaine abuse
in pregnancy: effects on the fetus and newborn.
Neurotoxicology and Teratology. 9, 295-299.
Schneider, J.W., & Chasnoff, I.J. (1992). Motor assessment
of cocaine/polydrug exposed infants at age 4 months.
Neurotoxicology and Teratology. 14, 97-101.
Schnoll, S.H., Karrigan, J., Kitchen, S.B., Daghestani, A., &
Hansen, T. (1985). Characteristics of cocaine abusers


16
substances may not be as significant as some studies have
suggested.
Doberczak, Shanzer, Senie, and Kandall (1988) likewise
examined 39 infants with in tero exposure to cocaine for
neurologic and electroencephalographic (EEG) abnormalities.
During the first week of life, 17 of the infants had abnormal
EEGs and abnormal behavior characterized by irritability. By
the second week of life, nine of the 17 EEGs remained
abnormal. By three to 12 months of age, however, findings had
normalized, suggesting effects attributed to cocaine may be
transient. There was no control group utilized in this study
and it is unclear whether examiners were blinded to drug
status. Despite these methodological flaws, it may be
significant that EEG findings could not be predicted by
neurologic dysfunction or perinatal variables, and ultimately,
findings normalized for all infants.
Preliminary study of human infants indicates that cocaine
exposure results in worse outcomes than nonexposed infants in
terms of birth weight, length and head circumference,
spontaneous abortion, fetal death, and sudden infant death
syndrome (SID) (Ryan et al., 1987). In an early study, Oro
and Dixon (1987) examined neonatal growth, behavior and
physiologic organization in 104 mother/infant pairs including


40
significantly with infant/toddler development. Placement in
foster care was chosen post hoc to be included as a covariate
in the analysis due to the difference in frequency between the
two groups and due to the potential impact of foster placement
on child outcome at three years of age. Foster care was
defined as a child being placed in a home away from, or with
a relative other than, their biological mother. Thus, five
variables (alcohol use, maternal depression, child gender,
home environment, and foster placement) were included as
covariates in the initial analyses between groups.
In order to further strengthen the analyses, subjects
were excluded from the study based on several birth
characteristics which could significantly skew results. These
included any child born with a birth weight below 2,500 grams
and/or a congenital malformation. Children exposed to cocaine
in any form other than crack were also excluded from the
study. It was decided a'priori to exclude children from the
study who suffered any accident or illness (such as sickle
cell anemia) that might seriously affect their performance on
developmental measures independent of crack exposure in tero.
Altogether, 90 children from the longitudinal study were
evaluated between July 1, 1995 and January 30, 1996. Subjects
were assessed in the order that they came in for their three


129
Suggestions for Further Study
As the children in the study sample grow, it will be
interesting to note whether current trends in the data become
significant. Alternately, it seems unlikely that clinically
significant findings would emerge even with an increase in
power. Findings strongly suggest that maternal and
environmental variables other than prenatal cocaine exposure
may be the most significant contributors to behavioral and
adaptive outcome at three years old. Modelling the
relationships of maternal and environmental variables in
addition to exposure status via regression would be
interesting as well as studying the possible interactive
effects of current covariates and exposure status to outcome.
Examining effects of alcohol exposure, fostercare status, etc.
just within the cocaine exposure group would also be
interesting. Exploring the relationship of multiple foster
placements and types of foster placements on child outcome
would also be of interest. In addition, the effect of tobacco
use on outcome should be included in further study. Finally,
examining the possible dissociation between parent report and
observed child behavior may prove very interesting as study
continues.


76
variables by parent report. Inspection of univariate and
stepdown results at the p < .05 level likewise reveal no
significant differences between exposed and nonexposed
children on these variables. Specifically, no significant
between groups differences were noted for socialization
F(1,58) = .40, p > .05, communication F(l,57) = .51, p > .05,
daily living F(l,56) =1.12, p > .05, or motor skills F(l,55)
= 1.67, p > .05.
Hypothesis 5
Finally, it was hypothesized that disordered behaviors by
objective observation would be more pronounced in the exposed
group. Descriptive data for the exposed and nonexposed
children are summarized on Table 16 collapsed across parent-
and child-directed interactions. To test this, a multivariate
analysis of covariance was performed on the four dependent
variables derived from compliance data on the DPICS-II: Total
Commands (frequency data), and Percent Comply, Percent
Noncomply, and Percent No Opportunity to comply (percentages).
The ten basic DPICS-II frequency observation variables were
not tested as they were not normally distributed. In the
initial analysis, adjustment was made for five covariates
including alcohol, maternal depression, foster care, home


99
Table 14
Means and Standard Deviations of Tested Sample with Normative Sample,- DP1CS.-1I
Child Directed Interaction
Normative Normative
Sample Clinic-Referred Nonreferred
M
M
£D
M
SD
Direct Command
14.48*
9.97
1.90
2.75
1.60
1.60
Indirect Command
2.26*
3.32
.35
.59
.60
.99
Compliance
5.61*
5.13
1.21
1.88
.89
.90
Noncompliance
1.43*
2.24
.36
.63
.17
.51
No Opportunity
9.70*
7.35
1.50
1.40
1.33
1.41
Laugh
.11
.32
-
--
-
-
Yell
.04
.19
.15
.67
.20
.89
Physical Positive
.43
1.00
-
--
-
--
Physical Negative
.02
.14
.00
.00
.00
.00
Destructive
.19
.75
.05
.22
.05
.22
* Sample group significantly different from Clinic-Referred and Nonreferred normative
group.


ANALYSES
Descriptive Analyses
Means and standard deviations were calculated for the
total sample for dependent variables including: 1) the
Connors' (Connors, 1990) subscales Conduct Problem, Learning
Problem, Psychosomatic, Impulsive-Hyperactive, Anxiety, and
Hyperactivity Index, 2) ECBI (Eyberg & Colvin, 1994) Problem
and Intensity scales, 3) the Vineland (Sparrow et al., 1984)
subscales Socialization, Communication, Daily Living, and
Motor Skills, and 4) DPICS-II (Eyberg et al., 1994) variables.
For the DPICS-II, ten behaviors were chosen for basic
frequency observation. For purposes of higher level analyses,
four summary variables were derived from DPICS-II compliance
data. Normality assumptions for dependent variables were
tested by graphing and computing skewness scores. Covariates
were included in the initial analyses between groups only for
derived summary scores.
Hypothesis 1
To test whether the performance of the entire sample is
depressed compared to age-based norms, scores on well normed
measures were compared to age-based norms using Welch's V for
49


119
Learning, Psychosomatic, Impulsivity, Anxiety, and
Hyperactivity than the exposed groups. Higher scores on these
subscales are consistent with increased behavioral problems.
Similarly, both the Problem and Intensity scales on the ECBI
are relatively elevated in the nonexposed group indicating
higher rates and intensity of disordered behavior by parent
report. It should be noted that, although not significant,
the nonexposed children tended to be slightly older than
exposed children which may result in subtle differences in
baseline behavior.
When examining outcome on adaptive functioning, the
exposed group tended to have higher scores on Vineland
subscales of adaptive functioning such as Socialization,
Communication, and Motor Skills. The exception is Daily
Living Skills where the nonexposed group tended to display
more competence. The tendency for nonexposed groups to
display generally worse behavior and adaptive functioning is
counter intuitive. Although the differences between groups
are not significant, it is possible that with larger samples
and more statistical power, some significant differences might
emerge.
In terms of basic observational compliance data, there
was a tendency for caregivers of exposed children to issue



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PAGE 152

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117
al., 1993; Doberczak et al., 1988; Schneider & Chasnoff,
1992).
Similarly, the behavioral literature in the neonatal
period has suggested differences, albeit inconsistently,
between exposed and nonexposed children. For example,
increased risk for motor dysfunction, poor arousal, and
cognitive differences have been reported (Bingol et al., 1987;
Chasnoff, 1989; Chasnoff, Burns, et al., 1987;Griffith et
al., 1994; Oro & Dixon, 1987; Schneider & Chasnoff, 1992;
Singer, Yamashita, Hawkins, Cairns, Baley, & Kliegman 1994).
One explanation for nonsignificant differences based on drug
exposure in this study is that behavioral differences between
groups present in the neonatal period, like growth
differences, may be compensated by three years of age. This
explanation seems unlikely as no initial growth or behavioral
differences were noted between exposed and nonexposed children
in the larger study (Eyler, Behnke, Conlon, Wobie, & Woods, in
preparation).
Alternately, differences in the behavior or adaptive
functioning of exposed children at three years of age may
exist but be so subtle as to be either unmeasurable by gross
parent report or by observed categories of behavior. Along
similar lines, the instruments used in this study may not have


21
pattern of growth retardation similar to alcohol exposure and
that this retardation may be asymmetrical with head size more
involved. However, mothers in the cocaine group tended to be
polydrug users, control groups were not matched, nor were
statistical controls used for possible confounding maternal
variables.
Chiriboga, Bateman, Brust, and Hauser (1992) reported
that, compared to a no illicit drug exposure control group (n
= 16), cocaine-exposed infants (n = 14) had significantly
lower birth weights, lengths and head circumferences.
Neurologic abnormalities were also associated with exposure
and included hypertonia, plantar extension, tremors and gaze
abnormalities. These findings led researchers to conclude
that prenatal cocaine exposure results in tone and movement
abnormalities in newborn infants. Strengths of this research
were the blinded status of the neurologic examiners and the
fact that toxicology screens were used in addition to
histories to determine cocaine use. However, this study also
was conducted in an inner city hospital serving primarily low
socioeconomic status (SES) women and information on
confounding polydrug use by mothers was considered either
somewhat unreliable or was unavailable to the researchers.


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101
Table 16
Dependent Variable Means and Standard Deviations, for Exposed and Non-Exposed
Children for the Total Sample
Exposed Non-Exposed
M £D M £D
(n = 30) (n = 30)
CONNORS
Conduct 57.27
Learning 52.63
Psychosomatic 49.57
Impulsive 57.30
Anxiety 48.57
Hyperactivity 56.37
ECBI
Problem 8.33
Intensity 116.40
VINELAND
Socialization 100.20
Communication 104.07
Daily Living 103.10
Motor Skills 99.97
13.05
62.37
16.14
12.53
57.90
13.73
12.48
55.63
17.53
8.04
58.50
8.94
7.25
53.33
9.58
12.47
61.83
12.94
7.81
11.83
8.87
30.32
123.87
31.30
13.77
97.53
12.84
13.33
100.50
12.02
20.00
106.03
13.30
16.46
93.23
13.50
(Continued)


48
camera was concealed behind a three sided screen to limit
distractions and to maximize play opportunity. The three toys
were placed in the center of the floor before each video
session began. Verbal instructions to the parent for the free
play or child-directed play, and for the parent-directed
portion of taping were standardized and followed the format
provided with the DPICS-II manual.
Tapes were scored by two advanced graduate students
trained to reliability on pilot tapes using the DPICS-II
(Eyberg et al., 1994) scoring criterion. Examiners were
blinded to cocaine status to reduce possible bias.


54
data were substituted with group means to allow analysis of
these variables to be performed with equal sample size.
Observational Measures
Second, means and standard deviations were calculated for
the total sample for the ten basic frequency observational
variables including: 1) DPICS-II (Eyberg et al., 1994) five
compliance scores including direct and indirect commands,
compliance, noncompliance and no opportunity to comply, and
child behaviors including yell and whine, laugh, destructive,
physical negative, physical positive, and 2) DPICS-II derived
variables as described previously including commands,
compliance, noncompliance, and no opportunity to comply.
It was determined a'priori' that the ten DPICS-II
observational variables would be consolidated to derive
various scores because the frequencies of target behaviors
tended to be low. Thus, for the present analysis we were not
concerned with testing normality assumptions for the ten
individual observational scales. However, normality
assumptions for consolidated observational dependent variables
including Total Commands, Percent Compliance, Percent
Noncompliance, and Percent No Opportunity to comply were
tested by graphing and computing skewness scores.


112
reveals that none of the parent behavior rating subscales on
either the Connors or the ECBI fall in the clinically impaired
range despite some significant statistical differences from
normative groups. Thus, differences between the study sample
and normative groups may be largely irrelevant in a clinical
context.
The first hypothesis also proposed that the sample would
be depressed on measures of adaptive functioning compared to
normative groups as measured by the Vineland. No significant
differences were found between the study sample and normative
groups on subscales including Communication, Daily Living,
Socialization, and Motor Skills. Notably, Communication,
which is characterized by items such as 'uses sentences of
four or more words' and 'follows instructions in the if-then
format' was positively associated with a more enriched home
environment. Again, the impact of home environment on child
functioning is well recognized (Azuma & Chasnoff, 1993; Bee,
Barnard, Eyres, Gray, Hammond, Spiet2, Snyder, & Clark, 1982?
Breitraayer & Ramey, 1986).
Comparisons between the study sample and norms were more
complex for observational measures. First, differences were
broken out between child-directed and parent-directed
interactions. Due to the lack of norms, comparisons were not


39
status: level of Hollingshead Index. These are factors which
have been shown to mediate caregiving and affect outcome of
high risk infants.
All subject mothers were interviewed once or twice
prenatally and/or at the time of birth, and their surviving
infants were evaluated at each followup time. Detailed drug-
use histories and psychosocial interviews were done by
helpful, nonjudgmental, experienced interviewers. Calendars
were used to help women identify timing of use, and probing
for drug use details was done about past but not present use
in an effort to be less threatening. Infants were assessed
one to three times in their first week of life and six more
times over three years. Three followup assessments were made
in the homes and three in the clinics. All infant assessments
were performed by trained, reliable examiners blinded to drug
exposure history. Subjects in the present study were seen at
three years of age plus or minus eight weeks, and measures
included parent report instruments and behavioral observation.
Several variables were chosen for use as covariates
during statistical analysis in order to strengthen results
including maternal alcohol use, maternal depression, child
gender, and home environment. Covariates were chosen a'priori
based on literature that indicated such variables correlate


47
manual (Eyberg et al., 1994). Toys used in the play situation
were standard and included: 1) large primary-color blocks, 2)
a farm, and 3) and a gender-neutral stuffed animal.
Procedures
Parents and children were seen during their scheduled
visits as part of the ongoing, longitudinal project. Informed
consent was obtained from parents at the intake of the
original project approximately three years previously.
Maternal demographic and perinatal medical information was
obtained from interviews conducted prenatally and/or at the
time of birth. Parent report measures for the present study
were incorporated into the existing project interview
scheduled as part of a home visit when the children were three
years old. The play observation for this study was scheduled
separately from the parent interview as part of the three-year
clinic visit. The observation period was situated in the test
period before procedures considered aversive (e.g., physical
examination) and after generally nonaversive testing (e.g.,
Bayley II). Administration of materials was standard for each
caregiver/child dyad.
Observation periods were videotaped in a room at either
the Public Health Department or delivery hospital. The video


24
unexposed children died of SID. These results suggested to
Bauchner et al. (1988) no increased risk of SID among infants
exposed in tero to cocaine. They observed that cocaine-using
mothers tended to use other drugs and alcohol, and tended to
have low birth weight babies. They further noted that SID
usually accounts for one to two deaths in a thousand; in poor
black groups, the rate may be as high as five to six per
thousand.
MacGregor, Keith, Chasnoff, Rosner, Chisum, Shaw and
Minogue (1987) again examined the perinatal outcome data of 70
women receiving care at a large urban drug treatment center.
In this study, the use of cocaine during pregnancy was
associated with younger gestational age at delivery, increase
in preterm labor and delivery, lower birth weight and delivery
of smaller for gestational age infants. However, no cocaine
related differences were found in the incidence of abruptio
placentae and congenital anomalies. Further, no differences
were noted on the basis of patterns of substance use. Again,
problems in this study included the possible biases of
unblinded investigators and confounding of polydrug use.
Schneider and Chasnoff (1992) also investigated the motor
development of cocaine/polydrug infants at four months of age.
Assessing 50 nonillicit drug exposed infants and 74 cocaine-