Claire
B. Kopp & Sandra R. Kaler
American Psychologist
Copyright 1989 by the American Psychological
Association, Inc.
Volume 44(2) February 1989 p 224230
Risk in Infancy: Origins and Implications
[Health and Development]
Kopp, Claire B.1,2;
Kaler, Sandra R.1
1University
of California, Los Angeles.
2Correspondence
concerning this article should be addressed to Claire B. Kopp,
Department of Psychology, Franz Hall, University of California,
Los Angeles, CA 90024.
Support for writing this article was provided in
part by National Science Foundation Grant BNS 8710028 and
Department of Education Grant G0086 35232 to Claire B. Kopp.
Outline
· ABSTRACT:
· Origins
and Implications of Risk
·
Risk Factors, Development, and Timing
·
Prepregnancy risks.
·
Prenatal period.
·
Perinatal period.
·
Postnatal risks.
·
Concluding comment.
·
Epidemiology
·
Assessments and Interventions
·
Assessment of Infant Developmental Status
·
Interventions for Infants
·
Future Directions
·
REFERENCES
ABSTRACT:
This article focuses on biological risks that can adversely
influence development during infancy and later. In the first
part of the article, the origins of risks and their potential
consequences are discussed relative to prepregnancy, prenatal,
perinatal, and postnatal periods. Epidemiological data are
presented. The second part of the article addresses issues
pertaining to assessment of infant development and interventions
provided for infants whose development may be in jeopardy.
Finally, goals for prevention are highlighted and the need for a
nationally derived data base on risk and outcomes is emphasized.
Infancy, the foundation period of our species, is no more and no
less important than other phases of life. Still, infancy marks
the beginning of our contacts with the outside world, and for
this reason it has been accorded special status by some
philosophers, scientists, and lay people. There are others, we
among them, who prefer to think of infancy as a way-point in
childhood's journey. Important, developmentally related events
occur before birth, and many more will occur long after. When
genetic heritage and prenatal life are favorable, the infant's
roots are securely anchored and sound development should occur.
If physical or psychological adversities arise later on, there
is potential for resiliency given that rearing conditions are
reasonably supportive. Alternatively, unfavorable genetic or
prenatal factors set the stage for vulnerabilities. Sometimes an
adverse condition is so profound that development is
irreversibly impaired. In other instances, risk factors may
disrupt processes of growth but not conclusively alter them. In
this case development is less predictable and depends on both
the nature of early risks and the child's ensuing life
experiences. Often supportive caregiving can buffer the child
and facilitate development, whereas rearing that is neglectful,
uncaring, or abusive compounds earlier vulnerabilities. Exposed
to multiple and continuing liabilities, a few children manage to
adapt, many more marginally accommodate to educational and
social demands, and still others ultimately fail and deteriorate
mentally, behaviorally, and socially.
Risks that compromise development are diverse and complex. They
include those that are (a) biological in origin; (b) from the
environment, primarily adverse rearing conditions; and (c) from
a combination of the two. Our focus is on biological risk, and
where appropriate, combined risks are mentioned as well. Topics
discussed include the origins of risks and their effects on
development, epidemiology, assessment of status in infancy, and
interventions for infants whose development may be problematic.
Origins and Implications of Risk
Risk Factors, Development, and Timing
The phrase
biological risk
encompasses different kinds of adverse conditions; these are
discussed relative to prenatal, perinatal, and postnatal life
along with implications for development.
Biological risks stem from genetic conditions (e.g., mutant
recessive genetic material) as well as from exposure to harmful
nonsocial environmental factors. Viral infections or use of
drugs during pregnancy are examples of the latter. Biological
risks pose serious threats to the developing organism and can
result in death or outcomes that include physical malformations,
growth retardation, neurological (e.g., cerebral palsy) and
physiological problems, mental retardation, sensory disorders
(e.g., blindness or deafness), learning disabilities and other
educational difficulties, psychiatric disorders, and social
deviancy. Some professionals also consider preterm birth and low
birth weight as negative outcomes.
Biological risks may show developmental effects early in life or
later, may lead to severe impairments or subtle dysfunctions,
and may influence all aspects of human behavior or only one or
two. Because development is a lifelong process, problems
observed in infancy are not necessarily those manifested in
subsequent years. On the other hand, particularly during early
life, development, whether proceeding as expected or not, is
associated with increasing maturation of brain structures and
functions. The immature brain is adaptive to new experiences
and, equally important, often has potential for recovery should
certain kinds of brain insult occur.
Developmental risk,
a term frequently used by professionals, is reserved for
immature organisms and refers to a statistical probability that
ongoing development will be compromised in some way. Statistical
probabilities are expectations about the percentage of children
that will have developmental problems.
Timing
refers to the particular period in early development when a risk
event occurs, that is, before pregnancy, at conception, during
prenatal life, at the perinatal period, or after birth
(postnatal life). Consideration of timing leads to inferences
about the effects a risk event can have when the developing
organism is at age Χ as opposed to one that is at age y (Freeman,
1985;
Hagberg, 1978; Kopp, 1983).
In the remainder of this section, risks, developmental outcomes,
and timing are interrelated, and illustrative examples are
provided. We use chronological order beginning with risks that
occur before pregnancy and end with those that arise after
birth.
Prepregnancy risks.
Data unequivocally show that deleterious factors occurring years
before a pregnancy may have developmental implications for the
conceptus, throughout infancy and beyond. Prepregnancy risks
include maternal chronic illness, history of drug use,
inadequate nutrition during childhood and adolescence, genetic
vulnerability within the family, previous numerous closely
spaced pregnancies, and female age (extremes) at time of
conception.
Among the economically disadvantaged, prepregnancy risks may run
through generations. Poor nutrition and lack of health care
during childhood are often compounded by adverse pregnancy
conditions (e.g., lack of prenatal care, drug use, or exposure
to infections). Combinations such as this portend
constitutionally vulnerable infants who become vulnerable
children and then high-risk childbearing adults. All too often,
health and developmental disorders such as poor school
achievement and social deviancy arise. Unfortunately, the extent
of these problems is unknown.
Of course, conditions other than poverty give rise to
prepregnancy risks. In our culture, social and economic forces
have moved increasing numbers of women into the job market.
Concomitantly, these women are postponing first pregnancies
beyond the optimal childbearing period (20 to 30 years). The
largest growth in fertility rates has occurred among women in
their early 30s, with first births among 30to34year-olds
almost doubling between 1970 and 1979 (Dorfman,
1986).
A substantial number of these births were to educated women who
were not in economic distress. This trend in later pregnancies
will likely continue.
Concerns have heightened about child outcomes. In addition to
the well-established association between maternal age and
chromosomal abnormalities (e.g., the risk for Down syndrome for
women over 40 years is manyfold greater than for women in their
20s), there has been worry about other forms of nonoptimal
development. Earlier studies suggested that maternal age was a
risk factor in and of itself; however, conditions that coexist
with increasing age such as hypertension or diabetes may explain
previous findings. Recently completed, well-designed studies are
optimistic. In a comparison of 511 pregnancies of women over 40
with 26,000+ pregnancies of women between 2030 years,
controlling for maternal weight, cigarette smoking, and parity,
there were no higher risks for older women (Spellacy,
Miller, & Winegar, 1986).
Undeniably, entering pregnancy with good overall health status
and having access to careful prenatal monitoring are critically
important.
Prenatal period.
In the aggregate, risks that arise around the time of conception
or during the first weeks of pregnancy (when structures are
being formed) are associated with more serious developmental
ramifications than those that arise earlier or later.
Impairments tend to be both major and irreversible and include
malformations of head, face, limbs, and organs; sensory and
neurological disorders; and severe mental retardation (IQ of 50
or less). Brain disorders are often obvious at birth; later,
developmental delays and intellectual problems become apparent.
The seriousness of early prenatal risks is underscored by the
fact that few affected individuals escape long-term
difficulties, and many require lifelong assistance.
Adverse conditions and events related to prenatal risks include
mutant recessive genes and chromosomal disorders, environmental
agents (e.g., harmful agents such as drugs, chemicals, and
toxins), maternal viral infections such as rubella, and chronic
and severe maternal health conditions that continue into
pregnancy (e.g., major kidney disease and cardiac anomalies).
Multiple biological factors and adverse environmental events are
also likely to be involved.
The developmental picture for later pregnancy risks is less
clear. It is known that some children develop normally, a few
will have major handicapping conditions, and others will show
various kinds of less severe intellectual and social
impairments. For some indeterminate number, there will be a
variety of dysfunctions involving physiological and
psychological systems (Vorhees,
1986).
The relatively new research discipline called behavioral
teratology focuses on behavioral effects subsequent to stress or
damage to the developing brain. Intellectual and behavioral
dysfunctions that occur in the absence of malformations can be
as important as those that occur with them. Researchers are
examining behavioral effects of alcohol, chemicals, pollutants,
and other agents using a variety of animal models and human
studies. There is evidence that methylmercury, alcohol, lead,
and high doses of ionizing radiation
are
disruptive to children's development, and there is suspicion
that nicotine, narcotics, some pollutants, hormones, and lower
doses of ionizing radiation
may
affect development (Vorhees
& Mollinow, 1987).
The challenge for behavioral teratology is substantial because
long-term effects as well as transient ones must be demonstrated
while controlling for variables other than the risk agents, and
it is important that the reason underlying variability in
outcome effects be ascertained. A case in point is alcohol: Not
all children born to alcoholic mothers show fetal alcohol
syndrome or even less severe symptomatology.
Other research approaches yield promising findings. Drawing on
suggestive data linking pregnancy illnesses and schizophrenia,
Mednick, Machon, Huttunen,
and Bonett (1988)
examined the incidence of schizophrenia in a 1957 Finnish birth
cohort in which pregnant women were exposed to a widespread
severe type Az
influenza epidemic. Using a variety of procedures, the authors
were able to ascertain that second-trimester viral exposure was
significantly linked to a greater percentage of offspring who
were later admitted to psychiatric hospitals with a diagnosis of
schizophrenia. Expressing caution about their findings, the
authors nonetheless argue for an association between
mid-pregnancy risk and psychiatric vulnerability. Moreover, they
suggest that second-trimester risk may hold implications for
brain functioning in that risks may interfere with the
development of late appearing cortical neurons, destruction of
existing cells, or disruption of cell migration. The
implications of this research are profound for defining
long-term effects, particularly those that pertain to emotional
dysfunction rather than intellectual impairment.
Perinatal period.
This third time frame overlaps prenatal and postnatal life and
extends from the seventh prenatal month to the end of the first
postnatal month. Illustrating the importance ascribed to this
period, perinatal mortality statistics are used as one measure
of the health and well-being of nations.
Perinatal trends in the United States show a 1985 mortality rate
of 10.6 deaths per 1,000 live births, contrasted with the 7 to 9
per 1,000 rates found in Scandinavian and some European
countries (Miller,
1987; National Center for Health Statistics [NCHS],
1987).
Part of the United States's high rate is due to higher mortality
for certain minority groups (for Blacks the 1984 rate was 18.4,
whereas for Whites it was 9.4 per 1,000 [NCHS,
1987]).
Poverty, teenage pregnancies, and lack of prenatal care are
implicated (Hughes,
Johnson, Rosenbaum, Butler, & Simons, 1988).
What are perinatal risks? Historically, they have been defined
as any symptom or condition that may stress the fetus or
newborn. Thus preterm birth, congenital malformations,
undergrowth in the newborn period whether observed in full-term
or preterm babies, respiratory distress, newborn seizures,
asphyxia, birth trauma, and newborn infections have been labeled
perinatal risks.
Although categorizing these risks as perinatal has been
effective for deriving general mortality statistics, the
category is less useful for estimating developmental outcomes.
More recently, attempts are being made to separate conditions
that had their origins in prenatal life from those that
originate solely within the perinatal period. Profound growth
retardation observed in either preterm or full-term newborns is
an example of a risk that began in the prenatal period, whereas
an infection acquired from the mother during the birth process
exemplifies a de novo perinatal risk. These distinctions
encourage more precise diagnosis and treatment. Moreover,
evidence also suggests that early or late pregnancy risks
predispose the fetus to additional perinatal stresses (Freeman,
1985),
and a combination of prenatal-perinatal risks has more adverse
developmental consequences than de novo perinatal risks (Rosen,
1985).
Even if definitional problems did not exist, perinatal risks
pose difficult challenges for understanding and determining
outcomes. For one, nationally derived statistics for nondeath
outcomes are virtually nonexistent. Developmental estimations
are generated by different research and clinical teams.
Moreover, documented outcomes for infancy and childhood vary
widely and are a function of quality of medical care in the
newborn period, the risk condition that is studied, criteria
selected as measures of outcome, and social class and family
rearing conditions.
Second, despite evidence that the environment in which the
infant lives is a continuing influence on development, the
interaction of biological risk and rearing milieu is largely
unspecified. It is clear that perinatal risks combined with
nonoptimal rearing conditions portend poor developmental
outcomes, whereas good rearing ameliorates the risk (Sameroff
& Chandler, 1975; Werner & Smith, 1982).
Because nonoptimal rearing is relatively more common among
socially and economically distressed individuals than among
affluent individuals, social economic status (SES) is a
frequently used index of rearing conditions. However, SES is not
a pure measure. Nominally it is a descriptor of education and
occupational status, but SES actually subsumes considerable
heterogeneity within middle and lower class categories in terms
of caregiver knowledge and attributes, family atmosphere, and
home density. Furthermore, accumulating evidence suggests more
extensive variation exists in today's society among lower class
families than in our recent past. This appears to result from
increased levels of joblessness, poverty, homelessness, drug
use, and caregiver emotional disturbance. Until more systematic
documentation is made of child characteristics, specific rearing
conditions, and home atmosphere factors it will be difficult to
further specify the influences of combined biological and social
risks on development.1
No discussion of perinatal risks is complete without calling
attention to
low birth weight;
this is one of the most highly visible perinatal risks. Low
birth weight is the designation given to infants born weighing
less than 5 lb; most often, low birth weight goes along with
preterm birth, that is, birth at or before the 37th week of
pregnancy. Low-birth-weight infants are further differentiated
by their size in relation to gestational age; if
disproportional, prenatal stresses were encountered.
Multiple factors contribute to low birth weight, including
social and economic conditions, maternal size, maternal health,
smoking during pregnancy, lack of prenatal care, geographic
locale, ethnicity, toxic exposure during pregnancy, poor
pregnancy histories, and more (e.g.,
Kramer, 1987).
However, there is great discrepancy among our population.
Healthy, economically comfortable, White women between 20 and 30
years of age can have a 3% low birth weight rate, whereas
economically distressed ethnic teenagers often have rates that
are three times higher (NCHS,
1987).
During the recent past, major improvements have occurred in
long-term outcomes for larger low-birth-weight infants as a
result of modern medical technology and skill found in newborn
intensive-care nurseries.2
Sophisticated care is also permitting increased rates of
survival for the tiniest low-birth-weight infants; however,
developmental appraisals suggest a greater proportion of
developmental, neurological, and health problems among this
group than with their heavier preterm counterparts. In terms of
numbers, approximately 6% to 8% of the larger low-birth-weight
infants, and perhaps twice that number for the smallest, will
show major developmental sequelae although there is considerable
variability across samples (e.g.,
Hoy, Bill, & Sykes, 1988).
Given this extraordinary complexity, what generalizations can be
made about perinatal outcomes? Assuming differentiation in
diagnosis, with de novo perinatal risks most children develop
normally, some have mild to moderate dysfunctions, and a few are
seriously handicapped. It is considerably more difficult to
repeat even this most general statement with respect to outcomes
for children exposed to dual prenatal-perinatal risks. More
research with carefully defined groups is needed.
Postnatal risks.
The postnatal period extends from the end of the first month of
life to the end of the first year. Postnatal risks include
respiratory disorders, infections, accidents, exposure to
environmental contaminants, and nutritional deficiencies. In
some cases, such as meningitis, a short, acute episode may be as
devastating as a chronic, debilitating condition such as anemia.
Postnatal risk events contribute only a small amount to major
handicapping conditions among infants and children (Hagberg,
1978).
Their contribution to less severe developmental problems is
unknown. (Discussion of postnatal risks of nutritional factors
and accidents is provided by
Lozoff (pp. 231236)
and
Christopherson (pp.
237241),
respectively, in this issue.
Concluding comment.
There is little doubt that risk events hold serious consequences
for development. Steps can be taken to prevent risks from
occurring or, in some cases, to ameliorate their effects.
Preventions and interventions are discussed later in this
article.
Epidemiology
In this section, we discuss the number of infants born each year
who have discernible problems and mention the types and
percentages of developmental disorders that are noted after
infancy. With the exception of birth and mortality statistics,
all figures represent approximations as a result of differences
in reporting methods, sampling criteria, selection of outcome
variables, and definition of mental retardation and handicap.3
During 1985, more than 3,700,000 births were recorded in the
United States. Of these, 3% showed evidence of major
malformations (Kalter
& Warkany, 1983).
In real numbers, this means more than 100,000 infants were born
with problems that will interfere with their own lives and those
of their families. A precise cause for malformations can be
identified only 40% of the time (Vorhees,
1986).
Examples include Fetal Alcohol Syndrome, with an overall
incidence of I to 2 cases per 1,000 births (Abel,
1984)
and Down syndrome, with a similar overall incidence rate.4
Six to seven percent of all births in this country are of low
birth weight (250,000 infants in 1985). Included in this figure
are the 1% of infants who are born with a birth weight of 3.5 lb
or less (Hughes
et al., 1988).
Excluding those with major malformations, from 1985 births
15,000 of the larger infants and 3,500 smaller ones have major
handicapping conditions.
Unfortunately, these numbers do not convey the magnitude of the
problem. Only the severest and most obvious difficulties are
diagnosed in the first two years of life. After infancy, 3
individuals per 1,000 members of our population show evidence of
major developmental disorders. It is thought that most of these
stem from prenatal risks. Roughly 35% are due to chromosomal
disorders including Down syndrome, 20% to multiple anomalies, 8%
to inadequate fetal supply, 5% to adverse drug and chemical
effects, around 4% to single gene defects (e.g., biochemical
disorders that result in Tay Sachs disease, phenylketonuria, or
other conditions associated with mental retardation), and about
3% to 4% for early prenatal infections; unknown causes,
presumably prenatal in origin, are felt to be instrumental
factors in 10% or more. Perinatal risks account for
approximately 10% and postnatal risks less than 5% of severe
developmental problems (Hagberg,
1975, 1978; Susser, Hauser, Kiely, Paneth, & Stein, 1985).
Less severe developmental problems (e.g., IQs in the 5070 range
or minor neurological and sensory disorders) are found in
approximately 10 individuals per 1,000 (Haskins,
1986).
In contrast to the major developmental disorders, it is believed
that only about 20% are due to biological causes; the majority
are linked to deleterious social and economic circumstances or
to a combination of biological and social vulnerabilities (Haskins,
1986).
Many of the less severe developmental difficulties are primarily
intellectual and social and are not identified until the child
enters educational settings. Sometimes intelligence is in the
normal range, but school achievement is lower than expected;
this occurs, for example, among some low-birth-weight children
and most frequently among boys (Kopp,
1983).
Problematic intellectual functioning and difficulty in school
are serious matters for society. Increasingly, data indicate
that intellectual problems, irrespective of cause, can be
associated with a variety of social and emotional ills (e.g.,
Olweus, Block, & Radke-Yarrow, 1986).
Assessments and Interventions
Assessment of Infant Developmental Status
Infants are typically categorized as those with an uneventful
early course and whose development is normal, those exposed to
risk events and whose development is either suspect or requires
observation, and those exposed to risks that are invariably
associated with mental retardation and whose development is
delayed. Assessment of developmental status, and the
implications thereof, for each of these groups has been fraught
with challenges. Nonetheless, assessment takes on heightened
meaning because of recently enacted Education of the Handicapped
Act Amendments of 1986 (PL
99457),
which provide financial assistance to states for implementing
intervention services for infants and families (birth to two
years) where a known handicapping condition exists or where
development is perceived to be at risk. Developmental assessment
is mandated prior to provision of preventive or remedial
services. The following discussion focuses primarily on
developmental testing for infants whose development may be
suspect or at risk.
Assessment by a good clinician provides a reasonable evaluation
of infant capability; this is an ongoing process in which infant
and toddler (up to age three years) performance is observed and
a judgment is made about developmental status at the time of
testing (e.g., normal, suspect, delayed, or abnormal).
Typically, assessment involves clinical evaluation and use of a
developmental test, for example the Gesell Schedules (Gesell
& Amatruda, 1941)
or the Bayley Scales (Bayley,
1969).
The tests are based on normative trends, that is, the kinds of
mental, motor, language, and social abilities most infants
demonstrate at one or another month. A few items ask for
primitive problem solving, reasoning, and memory.
Developmental tests are not comparable to the intelligence and
achievement tests given to school-aged children. The latter ask
for practical and abstract intelligence, factual knowledge,
arithmetic skills, and sophisticated use of social language. The
differences between developmental assessments and intelligence
tests highlight the differences between infant capability and
the capabilities demonstrated and needed by more mature children
and adults.
Developmental tests have limitations. They do not evaluate the
efficiency by which mental processes are used; how effectively
particular behaviors are produced, controlled, or terminated;
the characteristics defining growth of adaptive behaviors; or
even why a minor deviation from an expected response might be
developmentally significant.
The most vocal challenge to developmental tests has surfaced
around the issue of prediction from infancy to later childhood
capabilities. Repeatedly, research findings from these tests
indicate that predictive accuracy is dubious unless the infant
has a known handicap (e.g., Down syndrome) invariably associated
with later mental retardation or repeated assessments yield
moderate to severe developmental delays (Kopp
& McCall, 1982).
Attempts have been made to enhance predictions by combining
infant test scores with social class indexes and family
conditions or by cumulating or weighting medical, behavioral,
and performance variables. Increases in levels of success have
been modest (Goodman,
in press).
Recently, a new type of infant test has garnered considerable
publicity because of claims for prediction. The procedure
involves measurement of infant information processing abilities
such as visual attention to and memory for patterns and
photographs. Because infants have some ability to process
incoming information from the earliest months of life, it is
suggested that continuity may exist between the processing
abilities of infants and children. Further, it is assumed that
individual differences in infant processing capability will be
related to differences in child information-processing
performance. In this regard, several researchers report moderate
associations between infancy and preschool language/intelligence
test performance.
Despite these promising data, caution is warranted before the
more traditional developmental tests are discarded. Some
methodological and design issues have yet to be addressed.
However, developmental tests could also be improved.
In the interim, sufficiently valuable judgments of ongoing
infant capability can be made with traditional developmental
tests if well-trained, developmentally knowledgeable individuals
do the assessments. For the long term, it is unlikely that any
test will provide absolute definitions of future capabilities
for all infants. This would require skills that science does not
havedetermining the degree of learning a brain is capable of
and the ability of children to produce adaptive behaviors and
predicting whether ameliorative or adverse factors will surface
in a child's life.
Interventions for Infants
Programs of intervention are based on the assumption that there
are recognizable conditions in infancy that, if not dealt with
appropriately, will result in poor developmental prospects.
Interventions may involve services geared exclusively to
infants, to their caregivers, or to both. Examples include the
carefully controlled introduction of social experiences for
preterm infants still in isolettes, provision of counseling and
support services for parents who have an infant with a diagnosed
handicapping condition, and interventions aimed at teaching an
adolescent mother how to provide play opportunities for her
toddler whose development is moving along slowly because of a de
novo perinatal risk.
All interventions have increased in the past decade. Although
few would quarrel with the need for program services, concerns
have risen about effective implementation and evaluation (e.g.,
Shonkoff & Hauser-Cram, 1987).
In fact, interventions per se are being examined for directions
and effectiveness (e.g.,
Casto & Mastropieri, 1986;
Dunst & Snyder, 1986;
Guralnick & Bennett, 1987; Marfo & Kysela, 1985).
The issues, particularly for infant interventions, do not lend
themselves to easy resolution. Aside from challenges that arise
because of differences in program goals and orientation,
characteristics of the recipients of intervention, and methods
of evaluation, infancy presents its own contradictions. At the
age when the brain is considered to be most open to learning and
experiences, many infant behaviors are remarkably resistant to
modification. Driven by strong biological givens, they have
their own timetable for growth. Thus teasing out effects
requires analysis of the content of intervention in terms of
processes targeted for change along with an understanding of
processes that are most susceptible to change (Horowitz,
1987; Keogh & Kopp, 1978).
Because Public Law 99457 provides financial assistance for
infant interventions when development is or might be
compromised, there is opportunity to service more needy infants
and families than ever before. Yet policies to determine who
should be served vary widely. In some instances, decisions are
based on assessment data and include inferences about when to
intervene, the nature of the interventions that should be
provided, and the kinds of outcomes that can be anticipated.
Other times, services are provided on the basis of infant
diagnosis (e.g., known handicap or risk condition), because of
group membership (e.g., economic distress), or even intervenor
philosophy (e.g., that all preterm infants require stimulation).
This unsystematic approach has ramifications for training and
certification of personnel, quality programming, and
availability of resources at the state and community levels (Burke,
McLaughlin, & Valdivieso, 1988, provide a timely discussion
of personnel issues).
The content and techniques of intervention should differ
relative to age and condition of the infant at risk, the
circumstances of risks, caregiver information and emotional
needs, program models, and personnel and program resources. This
diversity leads to questions about how to measure program
outcomes. Several have argued for more focus on adaptive
characteristics of families, analysis of infant behavioral
processes, and measurement of infant social performance rather
than extensive reliance on developmental or intelligence test
performance. We would also add measures that capture growth of
infant adaptive skills, including those related to
self-regulatory abilities, emotional control, and anticipatory
planning. These are skills often found wanting among children
with developmental, educational, and social difficulties. Use of
well-defined sample groups for study of outcomes and long-term
follow-ups is also advised (Dunst
& Snyder, 1986; Shonkoff & Hauser-Cram, 1987).
Although this brief discussion has highlighted stumbling blocks
for infant intervention, it should not obscure the real and
important progress made in the field. Infant intervention is a
fact, multiple services are available, and researchers and
clinicians are working together toward clarifying the meaning of
infant growth and development in the face of risk. All of this
did not exist a generation ago.
Future Directions
This article has focused on the origins of biological risk,
influences on infancy and later, assessment of infant
developmental status, and interventions for infants. We have
called attention to progress that has been made as well as to
challenges that remain. Our discussion of risks and
developmental outcomes underscores the importance of
establishing policies so that this nation's infants and children
can optimally function in tomorrow's society. Although it is
unlikely that biological risks will be completely eradicated, we
can set reasonable goals for prevention and thereby reduce the
incidence of adverse outcomes. Accordingly, prevention of
avoidable prenatal, perinatal, and postnatal risks should be a
high priority.
It is our belief that prevention will be served best by
formulating information campaigns directed toward young
children, adolescents, high-risk family groups, pregnant women,
and new parents with a goal of informing without alarming.
Innovative, dynamic media messages about nutrition, personal
health care, drug and alcohol abuse, known and possible
environmental pollutants, contraceptive options, pregnancy
diagnosis, prenatal care, and infant development could be
systematically disseminated. Effective information models
currently exist (e.g., drugs and children, screening efforts for
Tay Sachs disease, and avoidance of rubella) and could be the
basis for additional efforts involving national agencies,
community groups, school systems, health clinics, and
recreational associations.
Finally, we suggest that the United States require a nationally
derived data base that would permit definition of the scope of
developmental problems, establishment of research and service
priorities based on that knowledge, and determination of
resource allocation for preventions and interventions. With
reference to infants at risk, a national data base would provide
better understanding of infants who have been exposed to risk
conditions, the nature of the risks, the percentage of infants
and children who have known handicapping conditions, the
percentage of infants whose development is considered to be at
risk, and the percentage of infants who subsequently develop
educational and social problems in childhood. The
multidisciplinary expertise required to mount such a coordinated
effort is available.
REFERENCES
Abel, E. L. (1984). Fetal
alcohol syndrome and fetal alcohol effects. New York:
Plenum.
Bayley, N. (1969). The Bayley
Scales of Mental Development. New York: Psychological
Corporation.
Burke, P. J., McLaughlin, M. J., & Valdivieso, C.
H. (1988). Preparing professionals to educate handicapped
infants and young children: Some policy considerations.
Topics in Early Childhood Special Education,
8, 7380.
Casto, G., & Mastropieri, M. A. (1986). The
efficacy of early intervention programs: A meta-analysis.
Exceptional Children,
52, 417424.
Christophersen, E. R. (1989). Injury control.
American Psychologisl,
44, 237241.
Dorfman, S. F. (1986). Age as a factor in
pregnancy. Contemporary OB/GYN,
24, 6477.
Dunst, C. J., & Snyder, S. W. (1986). A critique
of the Utah State University early intervention meta-analysis
research. Exceptional Children,
52, 269276.
The Education of the Handicapped Act Amendments
of 1986, Pub. L. No. 99457.
Freeman, J. M. (1985). Summary. In J. M, Freeman
(Ed.), Prenatal and perinatal factors
associated with brain disorders. (NIH Publication No.
851149, pp. 332). Washington, DC: U.S. Department of Health
and Human Services.
Gesell, A., & Amatruda, C. S. (1941).
Developmental diagnosis: Normal and abnormal
child development. New York: Hoeber.
Goodman, J. (in press). Infant intelligence: Do
we, can we, should we assess it? In C. R. Reynolds & R. Kamphaus
(Eds.), Handbook of psychological and
educational assessment. New York: Guilford.
Guralnick, M. J., & Bennett, F. C. (1987).
The effectiveness of early intervention for
at-risk and handicapped children. Orlando: Academic
Press.
Hagberg, B. (1975). Pre-peri-, and postnatal
prevention of major neuropediatric handicaps.
Neuropaediatrie, 6, 331338.
Hagberg, B. (1978). Severe mental retardation in
Swedish children born 19591970: Epidemiological panorama and
causative factors. In Major mental handicap:
Methods and costs of prevention (Ciba Foundation
Symposium No. 59, pp. 2951). Amsterdam: Elsevier.
Haskins, R. (1986). Social and cultural factors
in risk assessment and mild mental retardation. In D. C. Farran
& J. D. McKinney (Eds.), Risk in intellectual
and psychosocial development (pp. 2960). Orlando:
Academic Press.
Horowitz, F. D. (1987). Targeting infant
stimulation efforts: Theoretical challenges for research and
intervention. In N. Gunzenhauser (Ed.), Infant
stimulation: For whom, what kind, when, and how much?
(pp. 97108). Skillman, NJ: Johnson & Johnson.
Hoy, E. A., Bill, J. M., & Sykes, D. H. (1988).
Very low birthweight: A long-term developmental impairment?
International Journal of Behavioral
Development, 11, 3767.
Hughes, D., Johnson, K., Rosenbaum, S., Butler,
E., & Simons, J. (1988). The health of
America's children: Maternal and child health data book.
Washington, DC: Children's Defense Fund.
Kalter, H., & Warkany, J. (1983). Congenital
malformations: Etiologic factors and their role in prevention.
New England Journal of Medicine,
308, 424431491497.
Keogh, B. K., & Kopp, C. B. (1978). From
assessment to intervention: an elusive bridge. In F. D. Minifie
& L. L. Lloyd (Eds.), Communicative and
cognitive abilities: Early behavioral assessment.
Baltimore: University Park Press.
Kopp, C. B. (1983). Risk factors in development.
In M. M. Haith & J. J. Campos (Eds.), Handbook
of child psychology: Vol. 2. Infancy and developmental
psychobiology (pp. 10811188). New York: Wiley.
Kopp, C. B., & McCall, R. B. (1982). Predicting
later mental performance for normal, at-risk, and handicapped
infants. In P. B. Baltes & O. G. Brim (Eds.),
Life-span development and behavior (Vol. 4, pp. 3360).
New York: Academic Press.
Kramer, M. S. (1987). Intrauterine growth
retardation and gestational duration determinants.
Pediatrics, 80,
502511.
Lozoff, B. (1989). Nutrition and behavior.
American Psychologist,
44, 231236
Marfo, K., & Kysela, G. M. (1985). Early
intervention with mentally handicapped children: a critical
appraisal of applied research. Journal of
Pediatric Psychology, 10,
305324.
Mednick, S. A., Machon, R. A., Huttenen, M. O., &
Bonett, D. (1988). Adult schizophrenia following prenatal
exposure to an influenza epidemic. Archives of
General Psychiatry, 45, 189192.
Miller, A, C. (1987). Maternal
health and infant survival. Washington, DC: National
Center for Clinical Infant Programs.
National Center for Health Statistics. (1987).
Advance report of final natality statistics,
1985 (Monthly vital statistics report.
Vol. 36). Washington, DC: Author.
Olweus, D., Block, J., & Radke-Yarrow, M. (1986).
Development of antisocial and prosocial
behavior: Research, theory, and issues. Orlando: Academic
Press.
Rosen, M. G. (1985). Factors during labor and
delivery that influence brain disorders. In J. M. Freeman (Ed.),
Prenatal and perinatal factors associated with
brain disorders (NIH Publication No. 851149, pp.
239262). Washington, DC: U.S. Department of Health and Human
Services.
Sameroff, A. J., & Chandler, M. J. (1975).
Reproductive risk and the continuum of caretaking casualty. In
F. D. Horowitz (Ed.), Review of child
development research (Vol. 4, pp. 187244). Chicago:
University of Chicago Press.
Shonkoff, J. P., & Hauser-Cram, P. (1987). Early
intervention for disabled infants and their families: A
quantitative analysis. Pediatrics,
80, 650657.
Spellacy, W. N., Miller, S. J., & Winegar, A.
(1986). Pregnancy after 40 years of age.
Obstetrics and Gynecology, 68,
452454.
Susser, M. B., Hauser, W. A., Kiely, J. L.,
Paneth, N., & Stein, Z. (1985). Quantitative estimates of
prenatal and perinatal risk factors for perinatal mortality,
cerebral palsy, mental retardation, and epilepsy. In J. M.
Freeman (Ed.), Prenatal and perinatal factors
associated with brain disorders (NIH Publication No. 851
149, pp. 359439). Washington, DC: U.S. Department of Health and
Human Services.
Vorhees, C. V. (1986). Origins of behavioral
teratology. In E. P. Riley & C. V. Vorhees (Eds.),
Handbook of behavioral teratology (pp.
322). New York: Plenum.
Vorhees, C. V., & Mollinow, E. (1987). Behavioral
teratogenesis: Long-term influences on behavior from early
exposure to environmental agents. In J. D. Osofsky (Ed.),
Handbook of infant development (2nd
ed., pp. 913971). New York: Wiley.
Werner, E. E., & Smith, R. S. (1982).
Vulnerable but invincible. New York:
McCraw-Hill.
1Werner
and Smith (1982) provided an
interesting picture of biological risk factors, child
characteristics, and home conditions that distinguish children
and adolescents who succeed versus those who fail.
2The
newborn intensive-care nursery is a relatively recent
development. Physicians who specialize in the care and treatment
of sick and tiny infants, called neonatologists, have additional
training in newborn function and care.
3There
are more similarities than differences in the rates that are
estimated to occur in major industrialized nations. However,
these rates generally are inapplicable to developing nations.
4The
average rate given for Fetal Alcohol Syndrome obscures the
considerable disparity found in the United States. The rate is
manyfold higher among Eskimos and Native Americans. The average
rate for Down syndrome also obscures actual rates by age of
pregnant women. The incidence for a woman in her 20s is often
given as 1 in 1,000 births, whereas for a woman over 40 the rate
is 1 in 50 births.
Accession
Number: 00000487-198902000-00020
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