Locus: The Seton Hall Journal of Undergraduate Research Locus: The Seton Hall Journal of Undergraduate Research

Volume 3 Article 2

October 2020

The Adaptationist View: Ambiguity in Infant Withdrawal after The Adaptationist View: Ambiguity in Infant Withdrawal after

Prenatal Cocaine Exposure Prenatal Cocaine Exposure

Angelo Cadiente

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Recommended Citation Recommended Citation Cadiente, Angelo (2020) "The Adaptationist View: Ambiguity in Infant Withdrawal after Prenatal Cocaine Exposure," Locus: The Seton Hall Journal of Undergraduate Research: Vol. 3 , Article 2. Available at: https://scholarship.shu.edu/locus/vol3/iss1/2

The Adaptationist View:Ambiguity in Infant WithdrawalAfter Prenatal Cocaine Exposure

Angelo CadienteSeton Hall University

Abstract

Neonatal Abstinence Syndrome is a set ofsymptoms that result from prenatal exposure to ad-dictive drugs. This syndrome is often attributedto opiate withdrawal; yet, there is a controversywithin the literature as to whether cocaine, an ad-dictive stimulant, leads to a variant, which I term“cocaine-based Neonatal Abstinence Syndrome.”In this paper, I contrast the evidence that supportsthe presence of cocaine withdrawal in neonateswith the opposing evidence that supports its ab-sence. I offer an intermediary explanation throughthe “Adaptationist View,” which attributes the sup-posed symptoms of cocaine infant withdrawal tothe neonate adapting to extreme changes in its en-vironment. Moreover, I introduce the Addictive-ness of Cocaine Conclusion to serve as a logicalmeans to bridge the addiction cycle with the Adap-tationist view.

1. Introduction

Neonatal Abstinence Syndrome (NAS), his-torically known as “infant addiction” and “con-genital addiction,” describes a body of symptomsexperienced by an infant as a result of maternaldrug abuse over the course of a pregnancy (Jones& Fielder 2015). The symptoms that arise arethe result of defects in the central nervous system(CNS), autonomic nervous system (ANS), gas-

trointestinal (GI) system, and respiratory system.Specifically what symptoms arise and their sever-ity are dependent on the drugs used and when thepregnant mother uses them. Historically, NAS hasbeen diagnosed in the context of opiates, yet itis controversial as to whether infants experiencewithdrawal when they have been exposed to co-caine prenatally (Jones & Fielder 2015). In pursu-ing the possible existence of infant cocaine with-drawal, I will refer to cocaine-based neonatal ab-stinence syndrome as “cNAS.”

While the focus of this paper is to discuss therelationship between neonates and cocaine with-drawal, it is important to describe the effect of co-caine on neurotransmitters and the placenta; un-derstanding the physiological effects of cocainewill provide context for symptoms. Cocaineis a CNS stimulant that inhibits norepinephrinetransporters, serotonin transporters and dopaminetransporters, preventing the reuptake of synap-tic norepinephrine, serotonin, and dopamine re-spectively (Cain, Bornick, and Whiteman 2013).As these neurotransmitters are not removed in atimely manner, they remain in excess in the synap-tic cleft and elicit a signal upon binding to theircorresponding receptors on post-synaptic neurons.This signal, known as an action potential, ulti-mately leads to effects that are dependent on theneurotransmitter. The high concentration of neu-rotransmitters lead to the overstimulation of post-synaptic neurons; hence cocaine’s classification as

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a stimulant.Every neurotransmitter has a correspond-

ing effect. Due to the inhibition of mecha-nisms that reuptake norepinephrine, serotonin,and dopamine, cocaine creates an imbalance inthese neurotransmitters. This dysregulation leadsto the symptoms of cocaine-use. Norepinephrineis responsible for activating the sympathetic ner-vous system. The activation of the sympatheticnervous system increases blood flow that is di-rected from the GI tract and reproductive systemto the heart, brain, and skeletal muscles (Buckley2015). Serotonin is the prominent neurotransmit-ter that affects mood. Like cocaine, selective sero-tonin reuptake inhibitors (SSRIs) keep serotoninin the synaptic cleft. Due to its function in main-taining high serotonin levels within the synapticcleft, there are similar arguments as to whetherSSRIs lead to neonate withdrawal when used overthe course of a pregnancy (Jones & Fielder 2015).Dopamine is attributed to the feeling of euphoria,colloquially known as a “high” (Cain, Bornick &Whiteman 2013; Kuczkowski 2003, 2004, 2005).Excess dopamine in the nucleus accumbens is thebiologically evident site of addiction. Cocaine in-creases the production of enzymes that decreasedopamine levels. This increase in enzymes is aresponse to the abnormally high concentration ofdopamine in the synaptic cleft. The body adaptsand synthesizes more enzymes in order to coun-teract future imbalances. Thus, the body becomesless sensitive to dopamine; more precisely, it nowtakes more dopamine to experience euphoria. Inthe context of cocaine addiction, the user nowrequires more cocaine in order to attain a highenough dopamine concentration to experience eu-phoria.

As an extension to neurotransmitters, cocainedirectly affects the placenta. The placenta isthe site of maternal-fetal exchange. Within thisexchange, the placenta transfers nutrients frommother to fetus, eliminates fetal metabolic waste,mediates fetal gas exchange, and produces steroidhormones. Effectively, the placenta serves as the

fetal equivalent to the kidneys, the liver, and thelungs (De Giovanni & Marchetti 2012). Consid-ering its wide-ranging utility, the placenta is themedium through which the mother prenatally pro-vides the neonate with the necessary nutrients tosupport its growth and development (Coyle, et al.2018).

Cocaine acts on the placenta due to the pres-ence of surface norepinephrine and serotonin re-ceptors. The surface norepinephrine receptors actin tandem with the mother’s sympathetic nervoussystem. This connection is one of the reasons thatcocaine-use during pregnancy has an increasedrisk for preterm rupturing of the membranes—colloquially known as “the water breaking early.”This risk is due to the overstimulation of nore-pinephrine receptors that line the face of the pla-centa. As cocaine activates the sympathetic ner-vous system and there is an increase in nore-pinephrine, uterine contractions occur as the preg-nant mother enters preterm labor (De Giovanni& Marchetti 2012). The constant stimulation ofthe sympathetic nervous system effectively pushesthe neonate into delivery. The increase in nore-pinephrine is characteristic of a “catecholamine 1

surge” that occurs during birth and is speculatedto be the mechanism in which the infant adaptsto hypoxia during delivery (Buckley 2015). Addi-tionally, there are higher levels of catecholaminesin umbilical arterial blood during vaginal deliv-ery than in caesarean sections, indicative of itsuse during stressful environments (Faxelius, et al.1983). Regarding the use of serotonin, this neu-rotransmitter is transported to the fetus to reg-ulate brain development, namely thalamocorticalwiring in the forebrain, cortical development, andlong-term behavior (Velasquez, et al. 2013).

Considering the potent effects of cocaine inboth the placenta and the fetus, the presence ofwithdrawal from prenatal maternal cocaine use,

1The term catecholamine describes a class of structurallysimilar monoamine neurotransmitters. Among these neuro-transmitters, norepinephrine and dopamine are a part of thisclass. Serotonin is not.

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i.e. cNAS, is a point of controversy within the lit-erature (Jones & Fielder 2015). It is logical to de-duce that infants that were prenatally exposed tococaine experience withdrawal. A deductive argu-ment that aptly represents this view can structuredsuch that:

1. Some drugs are addictive.

2. Users of addictive drugs become addicted af-ter repeated use.

3. Removal of addictive drugs from an addicteduser leads to withdrawal.

4. Cocaine is an addictive drug.

5. Therefore, the removal of cocaine from anaddicted user leads to withdrawal.

I will label this argument the Addictiveness ofCocaine Conclusion (ACC). This argument iscommonsensical; if an addictive substance is re-moved from its timely abuser, then withdrawalfollows. The ACC is described in part from theaddiction cycle, which considers three intercon-nected phases: intoxication, withdrawal, and pre-occupation (Herman & Roberto 2015). In in-toxication, the addictive substance is consumed,prompting psychological and physiological ef-fects, e.g. pleasure that stimulates the reward cir-cuit in the brain. In withdrawal, an unpleasurablestate is sustained after the addictive substance isremoved for a period of time. Preoccupation is thestate in which an addicted user craves the addictivesubstance after a period of abstinence. While ad-diction has been heavily researched in both humanand non-human subjects (Koob & Le Moal 1997),there still remains a discrepancy as to whethercocaine-exposed neonates experience withdrawal.I will consider the ACC in response to whetherwithdrawal exists in cocaine-exposed infants.

In this paper, I will present two viewpoints,labeled “Study A” and Study “B”. In StudyA, I discuss evidence derived from a retrospec-tive case-control study that concludes that with-drawal occurs in infants prenatally exposed to

cocaine; their conclusion is derived through asymptom-based definition of withdrawal (Ogun-yemi & Hernandez-Loera 2004). In Study B, Idiscuss evidence derived from a cross-sectionalcase-control study that concludes that withdrawaldoes not occur in infants prenatally exposed to co-caine; their conclusion is derived through a stan-dardized scale (Eyler, et al 2001). The purposeof defining each view as “Study A” and “StudyB” is to utilize a representative argument in favorof each perspective. Among the different articlessupporting either side of the argument, the arti-cle by Ogunyemi & Hernandez-Loera in 2004 andEyler, et al in 2001 were used as exemplars to sup-port the presence and absence of cocaine neonatewithdrawal respectively. Figure 2 under Conclu-sion and Discussion provides explicit differencesbetween the two representative studies. Addition-ally, other supporting articles were considered inorder to supplement both arguments provided inStudies A and B. In light of these opposing views,I conclude with the “Adaptationist View” to uniteboth views while responding to the ACC.

2. Comparison of Methods between ParentStudies

Study A: Source of Data, Definition of With-drawal, and Methodology

Study A utilizes a retrospective case-controlstudy. In this study, cNAS was defined as“neurobehavioral abnormalities, including greaterirritability, hypertonicity, tremulousness, moodalterations and inconsolability” (Ogunyemi &Hernandez-Loera 2004). Thus, the presence of co-caine neonate withdrawal is determined on the ba-sis of observed symptoms.

Study A’s cases included 253 pregnant womenwith neonates that were diagnosed with prenatalcocaine exposure and selected from the study’sDivision of Obstetrics database. The controlgroup was determined through a random selectionof 237 pregnancies with neonates that have no his-

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tory of prenatal cocaine exposure from the samedatabase. Of the selected, 53 cocaine-exposed and37 non-exposed maternal-neonatal charts were ex-cluded from the analysis as a result of incom-plete records. Each chart of the selected maternal-neonate pair was then reviewed for the follow-ing pieces of information: maternal age, gravid-ity, parity, race, onset of prenatal care, medicalhistory, obstetric and gynecological history, ed-ucational level, employment, marital status, le-gal problems, living conditions, urine toxicologyresults, routine prenatal laboratory data, obstet-ric complications, delivery records and neonatalcomplications. If the maternal-neonatal chart didnot possess these variables, they were excludedfrom the analysis and were considered incomplete(Ogunyemi & Hernandez-Loera 2004).

Data analysis was undertaken through anSPSS statistical program with categorical variablerelationships being tested for significance throughchi squared analysis. T-tests, variance, andlinear regression were used as needed. Multiplelogistic regression was also used for multivariableanalysis. A p-value less than 0.05 and a 95%confidence interval was considered statisticallysignificant (Ogunyemi & Hernandez-Loera 2004).

Study B: Source of Data, Definition of With-drawal, and Methodology

Study B was a cross sectional case-controlstudy. In this study, cNAS was defined as thelack of improvement or the worsening of cocainemetabolite-positive infants following the removalof cocaine (Eyler, et al 2001). Thus, the pres-ence of cocaine neonate withdrawal is determinedfrom significantly lower scores for varying quali-tative data of cocaine metabolite-positive neonatescontrasted with the data from an exposed cocainemetabolite-negative group and non-exposed con-trol group.

Study B selected 74 cocaine-exposed neonatesand 81 nonexposed neonates. The selectivity ofthe study is described in Table 1.

Table 1. Study B’s selection of controls and co-caine exposed infants.

Urine toxicology was used to differentiate co-caine exposed neonates at birth. Infants testing“cocaine–” for cocaine metabolites was indicativeof the fact that cocaine was not found in the in-fant’s system. Infants testing “cocaine+” for co-caine metabolites was indicative of the fact thatcocaine was found in the infant’s system. Thereason why urine toxicology is nominally usedis because cocaine, after consumption, is even-tually broken down in the body and removedthrough the infant’s excretory system. Of the co-caine exposed neonates, 47 tested cocaine– and 27tested cocaine+ at birth. Neonates that were bornpreterm or by cesarean section were disqualifiedto avoid confounding factors (Table from Eyler, etal 2001).

Data analysis was undertaken to compare cat-egorical variable relationships for significancethrough chi squared analysis and t-tests. In par-ticular, these variables were graded using theBrazelton Neonate Behavior Assessment Scale(NBAS). Significant differences in correlativestudies among mean levels by group or by timewere determined through ANOVA (Eyler, et al2001).

3. Results

Study A indicated that cocaine-users, on aver-age, delivered their infants earlier than the con-trols, i.e. at 36 weeks versus 39 weeks, with

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birth weights significantly lower than their controlcounterparts, i.e. 2660 grams versus 3305 grams.Fetal death had only occurred in the cocaine-usingsample. 131 cocaine-exposed infants tested co-caine+ in the womb with 75 of these infants fittingthe criteria to be diagnosed with neonatal absti-nence syndrome after birth. The average time thatcocaine metabolites remained in the urine toxicol-ogy tests was 3.16 days after birth (Ogunyemi &Hernandez-Loera 2004).

Study B revealed that only autonomic reg-ulation scores differed significantly between thegroups at birth. The data that was not controlledfor the effects of other drugs—i.e. marijuana, al-cohol, and tobacco—indicated that there were sig-nificant differences in alert responsiveness, reg-ulatory capacity, state regulation, and reinforce-ment value as shown in Table 2.

Table 2. The results of Study B that did not controlfor the effects of other drugs. In controlling theireffects, the data reveals that autonomic regulationwas the only source of significant difference fromone another. (Table from Eyler, et al. 2001)

Of the 27 cocaine+ infants, 79% remainedpositive between Days 2–4 with none testing posi-tive between Days 5–7. In analyzing NBAS scoresover time, the regulation state was the only statisti-cally significant change over time when contrastedbetween the cocaine-exposed groups and the con-trol group. Figure 1 depicts the actual NBASscores and a pictorial representation of tested reg-ulation state scores of the groups over time.

Within the data depicted in Figure 1, it is im-portant to note that on Day 1, there was no sig-

Table 3. Chart depicting the mean regulation statescores for each of the three groups over time.State regulation score is also given as a functionof time in a graphical representation. (Figures fromEyler, et al. 2001)

nificant difference among the three groups. FromDays 2 to 4, the cocaine+ group had a significantlyhigher regulation state score than both the controlgroup and cocaine– group. For the data betweenDays 5 to 7, the cocaine+ group was significantlylower than the control group but not significantlydifferent than the cocaine– group.

4. Conclusion and Discussion

Study A concluded that 75 of the 131cocaine-exposed infants were afflicted with cNAS.Namely, this diagnosis of cNAS was undertakenthrough the observation of specific symptoms.These symptoms focused on neurobehavioral ab-normalities such as hyperirritability, hypertonic-ity, tremulousness, mood alterations and incon-solability (Ogunyemi & Hernandez-Loera 2004).Concurrent with these observations, Ogunyemi &Hernandez-Loera found that cocaine– infants of-

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ten did not meet the criteria to be diagnosed withcNAS. Instead, they proposed the idea of an “inutero withdrawal,” i.e. the concept that cocaine–infants at birth did not display withdrawal symp-toms because they had already experienced with-drawal in the womb. The authors came to thissuggestion by analyzing both maternal urine tox-icology and neonatal urine toxicology. In findingtrends within neonatal toxicology, they found thatif the urine sample had resulted in a positive testfor only one day or outright negative for cocainemetabolites postnatally, withdrawal was unlikelyto be observed. In contrast, if the urine sample hadresulted in a positive test for two days or longerpostnatally, neonatal withdrawal was more likelyto be observed. The authors attribute this discrep-ancy to the time taken between the last adminis-tration of cocaine and delivery. If the infant wascocaine+ for one day or cocaine– at birth, it is sug-gested that the mother’s last dose was one weekor earlier prior to delivery. In this instance, with-drawal would have occurred in utero. If the in-fant was cocaine+ for greater than two days post-natally, it is suggested that the mother’s last dosewas two to seven days prior to delivery. Thus,the infant would exhibit symptoms that resemblewithdrawal postnatally (Ogunyemi & Hernandez-Loera 2004).

Study A is particularly convincing in that itprovides an explanation as to why some cocaine-exposed neonates do not display withdrawalsymptoms. The study draws a distinction betweencocaine+ and cocaine– infants, where the formergroup is proposed to experience withdrawal inutero and the latter experiences withdrawal post-natally. The results of Study A are also sup-ported by other studies that have diagnosed mildto moderate withdrawal based on observed behav-ior (Cherukuri, et al. 1988; va de Bor, et al. 1990;Mastrogianis, et al. 1990). Studies have alsosupported Study A’s conclusion through a stan-dardized scale, i.e. Finnegan’s Neonatal Absti-nence Scoring System (Fulroth, Phillips & Du-rand 1989; Terri, et al. 1995). It is important to

recognize, however, that this system is nominallyused to diagnose opioid NAS, which bears differ-ent symptoms than cocaine addiction and cocainewithdrawal (Eyler, et al. 2001). Thus, the reliabil-ity of these results are questionable as to whetherthe scores were the result of cNAS or simply anoverall effect of cocaine.

Study B suggests otherwise. While StudyA concludes with the presence of neonate with-drawal in utero and postnatally, Study B statis-tically concludes that cocaine– and cocaine+ in-fants are not significantly different from one an-other as denoted by their NBAS score; thus, theevidence supports the idea that the generally lowerscores of cocaine-exposed infants relative to thenonexposed infants is an overall effect of co-caine. This approach is convincing because NBASis a standardized evaluation that has the capac-ity to measure behaviors that are commonly at-tributed to cocaine exposure. Thus, the usage ofthis evaluation provides a standardized means fordiagnosing cNAS. In analyzing the results, thelack of a statistical significance between cocaine+and cocaine– symptoms leads to the conclusionthat withdrawal does not occur within neonatesexposed to cocaine. Instead, the results indi-cate that, when contrasted with the behavior ofthe control group, cocaine-exposed groups expe-rience intransient defects due to the influence ofcocaine on an infant’s neurobehavioral pattern.This view is supported through observational stud-ies (Chiriboga 1993; Hadeed & Siegel 1989) andthrough Finnegan’s Neonatal Abstinence Scor-ing system (Ryan, Ehrlich, and Finnegan 1987).Again, it is important to note that Finnegan’s sys-tem was primarily used to diagnose opiate NASrather than cNAS. Moreover, it is also noteworthythat the creator-namesake of this system, LorettaFinnegan, also concluded the lack of cocaine with-drawal in infants (Ryan, Ehrlich, and Finnegan1987). Both views are outlined and contrasted inFigure 2.

Considering both studies aptly describe differ-ent perspectives regarding the existence of cNAS,

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Table 4. A Comparison of Study A (Ogunyemi & Hernandez-Loera 2004) and Study B (Eyler, et al. 2001).Notice the conclusion column for a summary of both studies’ main point.

the question arises as to whether both views can beunited. Study A is reasonable when a symptom-centric perspective is considered, where specificdefects are a result of cNAS. The downfall fromthis study, however, is the inability to distinguishthe symptoms of withdrawal from the direct ef-fects of cocaine. Likewise, Study B is reasonablewhen a scale-centric perspective relative to a con-trol is considered, where lower NBAS scores com-pared to controls are the result of cocaine’s directeffects rather than withdrawal. The concern forStudy B, however, is that this conclusion is coun-terintuitive. Recall the logic behind the ACC: theremoval of an addictive drug from a user leadsto withdrawal. Neonates are exposed to cocainewith the substance flowing in and out of their sys-tem; how can the exposed infant seemingly be im-mune to withdrawal from cocaine, an addictivesubstance? The answer is that they are not im-mune to withdrawal and this question can be ap-proached by uniting both perspectives through the“Adaptationist View”.

The Adaptationist View begins with thematernal-fetal connection of the placenta. Theeffects of cocaine stimulate the sympathetic ner-

vous system. As a result of the active sympatheticnervous system, less blood flows to the placenta.Thus, less oxygen, hormones, and nutrients arriveat the fetus (Messiah, et al. 2011; Nathanielsz& Hanson 2003). Due to this low supply, theexposed neonate does not possess comparativeamounts of nutrients or oxygen in order to grow ata similar rate to unexposed neonates; this conceptis evident in that cocaine exposed neonates, onaverage, weigh less than nonexposed neonates asbirth (Ogunyemi & Hernandez-Loera 2004; Chiri-boga et al., 1999; Bandstra et al., 2001; Bada etal.,2002; Nordstrom-Klee et al., 2002). Thus, thefetus adapts to this state by growing accustomedto its low-resource environment. It is of inter-est to note that as hypoxia occurs during labor,norepinephrine is in high concentration as part ofthe catecholamine surge in order to adapt to thisstate (Buckley 2015). Though I am not claimingthat cocaine-exposed infants become hypoxic perse, they do utilize a comparatively lower supplyof oxygen; thus, neonates are forced into makingnecessary adjustments, i.e. less expenditure of en-ergy and devoting less resources for growth. Nore-pinephrine is the principal hormone for long-term

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adaptation. Moreover, dopamine has recently be-come a prominent treatment for neonate hypoten-sion due to its capacity to increase blood pressure,circulating more oxygen (Bhayat, et al 2016). Inthis low-resource state, the neonate adapts to co-caine use at the expense of size and neurobehav-ioral development.

Upon birth, this adapted, maintained state isdisturbed. In particular, the neonate is not re-liant on the mother’s blood supply and is thusexposed to an excess of environmental oxygen.With this significant amount of oxygen, the in-fant is overstimulated and ill-informed as to whathe or she ought to do with this excess energy.Thus, the symptoms of hyperirritability, hyper-tonicity, and tremulousness arise. With an excessamount of oxygen, the body also must readjustto the higher concentrations of usable dopamine,readapting from its adapted cocaine-exposed state.This excess dopamine leads to the observed moodalterations and inconsolability described in StudyA.

Upon the excretion of the cocaine metabolites,the Adaptationist View would posit that the bodyattempts to recalibrate a set point, indicative ofthe stark increase in state regulation followed bya stark decrease as shown in Eyler, et al.’s study(2001). As the infant seeks a set point for homeo-static function, the final result would, when com-pared to unexposed infants, be lower in NBASscores. Due to the distressing environment inutero and the change of environment postnatally,a decrease in the state of regulation is an expectedresult of adaptation when contrasted with the un-exposed controls. This result is in accordance withEyler, et al.’s study (2001), indicative of an overalleffect of cocaine rather than cocaine withdrawal.

The Adaptationist View connects the data pre-sented between Study A and Study B and alsosatisfies a logical basis through which symptomsarise from both studies. Yet, it formulates animportant objection to Study A: the presence ofin utero withdrawal. According to Ogunyemi &Hernandez-Loera’s study, their primary explana-

tion was that cocaine– neonates tended to lackwithdrawal symptoms due to the withdrawal phaseoccurring in utero (2004). When juxtaposing thisview with the Adaptationist view, there does notleave much room as to when the neonate wouldexperience withdrawal prenatally. Though it canbe argued that in utero withdrawal occurs as theneonate is adapting to the low resource environ-ment, this environment and subsequent adaptationis undertaken in the presence of cocaine; with-drawal, as considered in the addiction cycle, oc-curs when cocaine is absent (Herman & Roberto2015; Eyler, et al. 2001). The unpleasurablestate sustained is the result of cocaine affecting themother’s sympathetic system, hindering the opti-mal nutrients needed in neonate growth and devel-opment. Thus, in utero withdrawal is not compat-ible with the Adaptationist view.

When considering Study A, the argument infavor of withdrawal is supported as a pathophys-iological function, where each neurobehavioralsymptom can be derived when observing thisview. When considering Study B, the Adaptation-ist View can explain how cocaine leads to an over-all effect on the infants, i.e. lower amounts of oxy-gen and nutrients and rapid changes in environ-ment, rather than withdrawal specifically. Thus,in application, the Adaptationist View very aptlyconnects the differences within Studies A and Band lines up with the conclusion made by Study B.Yet, by rejecting the presence of in utero cocainewithdrawal, there is no explanation as to whywithdrawal-like symptoms are present in somecocaine-exposed neonates but not others. More-over, if the symptoms that were present postna-tally are the effects of neonate cocaine withdrawal,there must be an explanation as to why withdrawalis selective to one cocaine-exposed population butnot the latter.

Though I united the results of both studies tosupport the notion of an overall effect of cocaine,the following scenario must be addressed: Whenneonates are exposed to cocaine repeatedly overthe course of a pregnancy if cocaine is suddenly

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removed, as is the case after birth, shouldn’t theinfant experience withdrawal symptoms, consid-ering that cocaine is an addictive substance? Thisscenario falls in line with the ACC presented in theintroduction. As commonsensical as the argumentmay be, I will offer a solution that may circumventthis discrepancy between cocaine addiction andneonate withdrawal. The infant may experiencesome variant of selective attention, where thereis a stronger negative effect experienced directlyfrom cocaine than there is from withdrawal. Inessence, the negative stimuli attributed to the over-all effects of cocaine are perceived stronger thanthe negative distractor stimuli attributed to with-drawal (Johansen-Berg & Lloyd 2000). If there iswithdrawal within a cocaine-exposed neonate, itseffects are secondary to the direct effects of co-caine and the body physiologically reacts to thestronger stimulant. Thus, the ACC may be ac-cepted in this context. Note that this conclusiondoes not undermine the Adaptationist View butrather provides an explanation as to why somecocaine-exposed infants did not experience with-drawal symptoms. The complication that arises isthat the scales used to diagnose cNAS are actuallydiagnosing the overall effects of cocaine. In ef-fect, these scales are not sensitive enough to cap-ture less stimulating cNAS. Without any data onborderline cases of NAS, i.e. cases where theirscore was minutely below the threshold for diag-nosis, this concern may hold. More studies, how-ever, need to be done to verify that this complica-tion is present.

Both studies support the Adaptationist Viewby equating the symptoms commonly attributedto cNAS to the adaption of an infant to a new,higher oxygen environment. This view continuesby attributing the extreme increases and decreasesin NBAS scores for autonomic regulation to bethe result of seeking a setpoint for homeostasis.Thus, withdrawal is not primarily evident and bothstudies would support the presence of an adapta-tion mechanism that points to the direct effects ofcocaine. In introducing the ACC, the presence

of withdrawal may be still be possible but sec-ondary to the overall effects of cocaine, causingthe lack of an identifiable physiological responsefor NAS. When considering NAS in the context ofthe Adaptationist View and ACC, the argument infavor of the direct effects of cocaine on the infantis strengthened but the presence of withdrawal re-mains logically possible.

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