Journal of Pediatric Psychology, Vol. 27, No. 3, 2002, pp. 235-244
© 2002 Society of Pediatric Psychology
Neurocognitive Development of Young Children With Sickle Cell Disease Through Three Years of Age
Duke University Medical Center
All correspondence should be sent to Robert J. Thompson, Jr., Duke University, 114 Allen Building, Box 90042, Durham, North Carolina 27708-0042. E-mail: bobt{at}asdean.duke.edu .
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Abstract |
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Objective: To determine (1) the neurocognitive development of children with sickle cell disease (SCD) from 6 months through 36 months of age, (2) the independent and combined contributions of biomedical risk and parenting risk to child neurocognitive functioning, and (3) the independent and combined contributions of biomedical risk, parent cognitive processes, and family functioning to parent adjustment.
Method: The study sample included 89 African American children and their parents served through the Duke University—University of North Carolina Comprehensive Sickle Cell Center. Measures of cognitive and psychomotor development were obtained at 6, 12, 24, and 36 months of age, and parents completed self-report measures of the cognitive processes of daily stress and attributional style, psychological adjustment, and family functioning.
Results: There was no significant decrease in psychomotor functioning (PDI) over time but cognitive functioning (MDI) declined, with a significant decrease occurring between the 12- and 24-month assessment points. At 24 months, poorer cognitive functioning was associated with parenting risk, in terms of a learned-helplessness attributional style, and biomedical risk, in terms of HbSS phenotype. Levels of psychological distress within the clinical range were reported by 24% of the parents, and poorer parent adjustment was associated with high levels of daily stress, less knowledge about child development, lower expectations of efficacy, and HbSC phenotype.
Conclusions: The findings indicate that young children with SCD are at risk for neurocognitive impairment and provide support for the initiation of early intervention studies to promote neurocognitive development.
Key words: sickle cell disease; neurocognitive functioning; parent adjustment; preschoolers.
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Introduction |
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Newborn screening for sickle cell disease (SCD) has enabled early entry into programs of comprehensive care that have reduced mortality and morbidity (Consensus Conference, 1987
).
However, children with SCD are still at high-risk status for neurocognitive
deficits and poor academic performance associated with the complications of
SCD that include infarction of major cerebral arteries or microvascular
systems, silent infarcts, and a chronic state of anemia and poor oxygenation
to the brain due to poor pulmonary function and oxygen saturation
(Brown, Armstrong & Eckman,
1993). Between 5% and 10% of children under age 15 with SCD are at
risk for experiencing a central nervous system infarct and between 16% and 22%
demonstrate radiologic evidence of silent infarct
(Balkaran et al., 1992;
Hindmarsh, Brozovic, Brook, & Davis, 1987;
Pavlakis et al., 1988;
Powers, Wilson, Imbus, Pegelow, &
Allen, 1978). For children with overt stroke, neurocognitive
impairment has been found to be pervasive and substantial
(Hariman, Griffith, Hurtig, & Keehn,
1991). For children with no history of stroke, subtle cognitive
and academic delays have been identified
(Swift et al., 1989), most
notably in the areas of visual motor integration, attention and concentration,
memory (Fowler et al., 1988;
Wasserman, Wilimas, Fairclough, Mulhern,
& Wang, 1991), math
(Wasserman et al., 1991), and
reading and spelling (Fowler et al.,
1988).
The purpose of this study is to extend the assessment of neurocognitive
functioning of children with SCD to the infancy and preschool period. This
research is guided by a cognitive and stress processing model of parenting
influences on child development (Thompson
& Gustafson, 1996) that reflects an integration of the
transactional stress and coping model of adaptation to chronic childhood
illness (Thompson & Gustafson,
1996) with Belsky's
(1984) process model of
parenting. In this model, parenting is affected by parental stress and
distress and child characteristics and, in turn, affects child development.
Components of the model, as depicted in
Figure 1, are applied to the
early cognitive development of children with SCD. SCD severity parameters are
considered child characteristics that constitute biomedical risk and
parent cognitive processes, distress, knowledge regarding child development,
and family functioning are parameters that constitute parenting
risk.
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Biomedical Risk
Recently, well-controlled studies have advanced our understanding of
neurocognitive functioning in children and adolescents with SCD. In a
cross-sectional study of 70 children (ages 2.5 to 17 years) with SCD compared
to 18 nondiseased siblings, the children with SCD had no overt evidence of
stroke but performed significantly less well on a sustained attention task
associated with frontal lobe impairment and a reading decoding achievement
test (Brown, Buchanan, et al.,
1993). Cognitive functioning did not decrease with age and did not
differ as a function of type of SCD. However, overall intellectual and
academic functioning were related to socioeconomic status (SES) and hemoglobin
level. In a subsequent study of 63 children and adolescents with SCD, magnetic
resonance imaging (MRI) indicated a high frequency of frontal lobe
abnormalities particularly with the subgroup with stroke
(Brown et al., 2000). Children
with stroke and silent infarcts performed more poorly than those without
central nervous system impairment on tasks requiring sustained attention or
that were associated with frontal lobe impairment.
The Cooperative Study of Sickle Cell Disease (CSSCD), a national natural
history study with patients from 15 clinical sites, included
neuropsychological and radiographic (MRI) assessment of children 6-12 years of
age (Armstrong et al., 1996).
For children with HbSS disease (sickle cell anemia), 6.6% had a clinical CVA
and 15.6% had a silent infarct for a combined 22.2% demonstrating an infarct
on MRI. For children with HbSC disease, none had evidence of CVA and 5.1% had
a silent infarct. For both types of disease combined, 4.6% had evidence of a
clinical stroke and 12.4% had a silent infarct, for an overall 17% incidence
of infarct on MRI. For children with HbSS disease, those with a history of
stroke had significantly lower verbal, performance, and full-scale IQ scores
and math achievement scores than children without MRI abnormalities and
significantly lower performance and full-scale IQ scores than children with
silent infarcts. Children with silent infarcts had significantly lower verbal
scale IQ scores with trends for lower full-scale IQ and reading and math
achievement scores than children without MRI abnormalities. The CSSCD also
included a cohort of 392 infants with sickle cell anemia or sickle
cell—B0—thalassemia who were monitored for
complications to 10 years of age (Miller
et al., 2000). An adverse outcome occurred for 18% (n =
70): death (n = 18), stroke (n = 25), frequent pain
(n = 17), or recurrent acute chest syndrome (n = 10).
However, assessment of early neurocognitive functioning was not included.
Parenting Risk
Caregiver stress and distress have been linked with both less optimal
caregiver-child interactions and family functioning and lower child
development competencies (Crnic &
Greenberg, 1990). Important in this regard are the findings that
13% to 20% of mothers of children with SCD have consistently high levels of
psychological distress related to high levels of daily stress and family
functioning characterized by less supportiveness and more control
(Thompson, Gil, et al., 1994;
Thompson, Gustafson, Gil, Kinney, &
Spock, 1999).
Findings based on the transactional stress and coping model of maternal
adaptation to chronic childhood illness indicate the particular role of the
cognitive processes of appraisal of daily and illness-related stress and
expectations of efficacy in maternal distress
(Thompson & Gustafson,
1996). In the situation of a child with SCD, there is reason to
believe that another cognitive process, attributional style, would be
important. The reformulated theory of learned helplessness
(Peterson & Seligman,
1984) postulates that exposure to uncontrollable events may lead
to expectations about the lack of contingency between responses and outcomes
and a pattern of cognitive, motivational, and emotional deficits referred to
as helplessness. This pattern includes an inability to perceive opportunities
to control outcomes; lower assertiveness, persistence, competitiveness, and
passivity; and depression and lowered self-esteem. Those who demonstrate a
cognitive attributional style, characterized by habitual explanations of bad
events as stable in time, global in effect, and internal to themselves, and
good events as unstable, specific, and external will be predisposed, upon
exposure to negative events, to helplessness. Given the genetic basis of SCD
and specific symptoms that are difficult to control, for example, painful
crises, we hypothesize that parents of children with SCD are at risk for
developing a learned helplessness attributional style that would negatively
affect parenting directly, as well as indirectly through impact on
psychological distress.
Parents' child-rearing cognitions and knowledge are also incorporated into
the model as parameters affecting parenting. There is evidence in support of
the association of more adaptive child-rearing behaviors with the
sophistication of beliefs about development and the accuracy of conceptions of
children's abilities (Miller,
1988).
Early Identification and Intervention
Assessment of early neurocognitive functioning of children with SCD is
important for two reasons. First, it is imperative to ascertain when deficits
in neurocognitive functioning are initially manifested and to differentiate
the independent and combined contributions of biomedical and psychosocial
processes. As reflected by standardized tests, cognitive functioning of
children reared in low-income families, and African American children
specifically, is characterized by average functioning in infancy and gradual
declines during early childhood, with a disproportionate number of children
functioning one or more standard deviations below the mean by kindergarten age
(Burchinal, Campbell, Bryant, Wasik, &
Ramey, 1997). Furthermore, ethnicity and poverty are confounded.
Consequently, the deficits in neurocognitive functioning that affect some
children with SCD occur within the context of early declines in functioning
associated with economic disadvantage. Second, it is essential to delineate
processes that affect cognitive functioning over time and that, in turn, can
serve as targets for early intervention efforts to promote development.
Studies with predominantly African American economically disadvantaged
children have demonstrated that cognitive performance is associated with
mothers' cognitive functioning and democratic, nonauthoritarian parental
attitudes; infants' responsiveness; and the responsiveness and stimulation of
the family environment (Burchinal et al.,
1997). In general, intervention programs aim to foster child
development by enhancing parenting skills in terms of expectations for, and
interactions with, their children that can promote cognitive and behavioral
development. There are now applications of this intervention strategy, for
example, through the Infant Health and Development Program, for children at
risk not only as a result of chronic poverty but also at higher biological
risk due to low birthweight (Ramey et al.,
1992). The demonstration of early deficits in neurocognitive
functioning associated with biomedical and parenting risk would provide
support for the initiation of early intervention with children with SCD.
The three interrelated objectives of this study are to determine (1) the neurocognitive development of children with SCD through 36 months of age; (2) the independent and combined contributions of biomedical risk and parenting risk to child neurocognitive functioning; and (3) the independent and combined contributions of biomedical risk, parent cognitive process, and family functioning to parent adjustment. We hypothesize that (1) neurocognitive functioning will decline over time; (2) biological risk and parenting risks will make independent and combined contributions to child neurocognitive functioning; and (3) parent distress will not be related to biomedical risk, but will be related to higher levels of daily and illness-related stress, lower expectations of efficacy, and more conflicted family functioning.
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Method |
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Participants
Through a statewide newborn screening program, infants with a confirmed diagnosis of sickle cell disease are entered into a case management and health care system to provide early initiation of prophylactic penicillin, education regarding the management of symptoms, and regular medical follow-up. Those infants, and their parents, who reside in the catchment areas served by Duke University Medical Center constitute the sample for this study. Patients are seen for an initial visit within 1 month of the infant's birth through the Duke outpatient clinic and for follow up every 3-4 months in their first 3 years at Duke or at clinics in Greensboro, Greenville, and Fayetteville, North Carolina.
The institutional review board approved study protocol included assessment of the infant's functioning during follow-up clinic visits at 6, 12, 24, and 36 months of age and parent self-reports of cognitive processes, distress, and family functioning. With a 5-year project period (4/93 to 8/97), patients enrolled early could be followed through 36 months, whereas those enrolled later could be followed only through 12 months. During the enrollment period, 96 African American infants with confirmed diagnoses of SCD were entered into the medical follow-up system and were invited, at the time of their initial clinic visit, by a member of the clinic staff to participate in the developmental follow-up study. Six parents declined, one of whom was the mother of twins. Informed consent was obtained for 89 (93%) infants and their parents (85 mothers and 4 fathers), who constitute the sample for this study. Mothers' marital status was as follows: single (66%), married (27%), divorced or separated (4%), and unknown (2%).
Demographic Parameter
Parent education was used as a marker of SES potentially associated with
child outcome and was classified in three levels: 24% (n = 21) had
post—high school education (with n = 5 
16 yrs), 52%
(n = 46) were high school graduates, and 25% (n = 22) had
less than a high school education (M = 10.0 yrs.).
Biomedical Risks
Biomedical risk was reflected through two measures of illness severity,
obtained from the infants' medical records, that have been previously
associated with outcomes: SCD phenotype and percentage hematocrit. In terms of
phenotype, 55 infants were HbSS, 27 were HbSC, and 7 had other types.
Percentage hematocrit ranged from 19.8 to 39.0 (M = 27.72,
SD = 3.90) for the subgroup with SS and 25.0 to 38.0 (M =
30.05, SD = 3.22) for the subgroup with SC or other. Increased
severity of SCD is associated with HbSS and lower percentage hematocrit.
Parenting Risks
The overall rubric of parenting risk included three sets of parameters:
cognitive processes, psychological adjustment, and knowledge regarding child
development.
Cognitive Processes. Daily stress was assessed with the 117-item
Hassles Scale (Kanner, Koyne, Schaefer, & Lazarus, 1981) that yields a
summary measure reflecting both frequency and severity ratings. A structured
interview provided summary scores for parent appraisals of stress and
expectations of efficacy across three illness-related tasks: dealing with
medical problems and symptoms, maintaining emotional well-being, and preparing
for an uncertain future (Thompson et al.,
1999). Cognitive attributional style
(Peterson & Seligman,
1984) was assessed through the Kastan-Parent's version of the
Children's Attributional Styles Questionnaire
(Kaslow, Tannenbaum, & Seligman,
1978). Twenty-four items describe situations that happen to
children, for example, "your child breaks a glass." Two possible
reasons for why this situation might have happened are provided, for example:
(A) "My child is not careful enough"; (B) "Sometimes my
child is not careful enough." Parents are asked to choose the most
likely reason to explain why the situation happened to their child. The 24
items include positive and negative outcomes across three attributional
dimensions (internal, stable, global) and yield an overall composite score
(the score for positive events minus the score for negative events). The lower
the composite score, the more the attributional style is characterized as
"learned-helplessness." A Cronbach alpha of.58 was obtained with
this study sample.
Knowledge of Child Development. Knowledge was assessed through the
58-item Knowledge of Infant Development Inventory (KIDI;
MacPhee, 1981). Each item
describes behavior of a typical infant or caregiver that could affect a baby's
growth and behavior: for example, "Infants understand only words they
can say"; "Talking to a child about things he (she) is doing helps
its mental development." Parents respond by indicating whether they
"agree," "disagree," or are "not sure" for
each item. The KIDI yields a total score across four subscales: Knowledge of
Norms and Milestones; Principles of Development; Parenting Strategy; and
Health and Safety Knowledge and Beliefs. Reported reliability includes
Cronbach alpha of.82, split half reliability of.85 and 2-week test retest
stability of.92.
Psychological Adjustment. Adjustment was assessed with the 53-item
Brief Symptom Inventory (BSI; Derogatis
& Melisaratos, 1983), which yields a Global Severity Index
(GSI) that combines information on number of symptoms and intensity of
distress, using standard scores for nonpatient norms. Parental distress was
classified as clinically significant (yes/no) if GSI was greater than the 90th
percentile (i.e., GSI T63: nonpatient norms).
Family Functioning
Family functioning was assessed with the Family Environment Scale (FES;
Moos & Moos, 1981). The
FES contains 90 true/false items that cover 10 subscales, which cluster into
three empirically derived higher-order components: Supportive, Conflicted, and
Controlling (Kronenberger & Thompson,
1990). The component structure of the FES has been replicated with
two samples drawn from the normative FES data
(Kronenberger & Thompson,
1990) and with the families of children included in the CSSCD
study (Thompson et al.,
1999).
Cognitive and Neuromotor Functioning
The Bayley Scales of Infant Development II
(Bayley, 1993) were
administered by a psychologist during a regular clinic visit. The Mental
Developmental Index (MDI) and Psychomotor Development Index (PDI) were
obtained and scores < 85 were classified as high neurocognitive risk
status. Because children were enrolled during the first 4 years of the 5-year
project period, some were able to complete the four assessments through the
36-month assessment point, whereas those who were enrolled later could be
followed only through the 12-month assessment point. The number of assessments
completed by the 89 children who were enrolled in the study is as follows:
none (n = 5, 6%), one (n = 16, 18%), two (n = 28,
32%), three (n = 23, 26%), and four (n = 17, 19%). The
number of assessments completed at each of the four assessment points and the
mean and standard deviations of age in months when the evaluation was
completed are as follows: 6 months (n = 66, M = 7.3,
SD = 1.5); 12 months (n = 68, M = 13.6, SD
= 2.6); 24 months (n = 42, M = 25.4, SD = 3.1); and
36 months (n = 26, M = 38.2, SD = 3.0).
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Results |
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Table I presents the Bayley MDI and PDI scores and the percentage of children with high risk status (MDI < 85; PDI < 85) at each of the four assessment times for the total sample and phenotype subgroups. Repeated measures analysis of variance was used to assess hypothesis 1 regarding decline in neurocognitive functioning over time. The findings indicated no significant change over time for PDI scores, F(3, 39) = 1.39, but there was a significant decrease in MDI scores over time, F(3, 39) = 9.09, p <.0001, and Duncan contrast analysis indicated that a significant decrease in scores occurred between the 12- and 24-month assessment times, F(1, 18) = 9.19, p <.01. In terms of neurocognitive risk status, by 24 months 29% of the children have MDI scores and 24% have PDI scores more than one standard deviation below the mean for the normative group. Although there was a significant phenotype subgroup difference in percentage hematocrit, F(1, 84) = 8.09, p <.01, with the HbSC/other subgroup having a higher level (M = 30.05, SD = 3.22) than the HbSS subgroup (M = 27.72, SD = 3.90), cross-sectional analysis of variance indicated no significant phenotype subgroup differences in MDI or PDI at any assessment time.
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We used multiple regression analysis to assess hypothesis 2 regarding the independent and combined contributions of biomedical risk and parenting risk to developmental outcome as reflected in MDI and PDI scores. The 24-month assessment point was utilized rather than the 36-month assessment point to maximize the sample size. It is important to note that the significant declines in functioning had occurred by this point, and the 24-month subsample did not differ from the study sample in demographic, biomedical, or parenting parameters. In a forward, stepwise procedure, the following variables were allowed to enter if they accounted for a significant increment (p <.05) in variance of MDI or PDI: parent education; phenotype; caregiver cognitive processes of daily stress, illness stress, illness efficacy, and attributional style; knowledge of child development; parent distress (GSI); and the supportive, conflicted, and controlling factors of family functioning. The summary analyses are presented in Table II. In terms of PDI, only one variable, phenotype, entered and accounted for 15% of the variance. With regard to MDI, learned helplessness attributional style entered first and accounted for 20% of the variance followed by phenotype, which accounted for a 22% increment in variance. Together, these two variables accounted for 42% of the variance in MDI. Thus, the regression analyses indicated that poorer developmental outcome, as reflected in both MDI and PDI, is associated with HbSS phenotype and also with learned helplessness attributional style for MDI.
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In terms of the psychological adjustment of parents, 19 (24%) had GSI
scores indicating clinically significant levels of distress (GSI: T 63).
Parent adjustment status (clinical level: yes/no) did not differ significantly
as a function of phenotype (
2 [1, N = 80] = 2.54) or
as a function of child risk status at 24 months (2 [1,
N = 41] = 1.82). Forward, stepwise multiple regression analysis was
used to assess hypothesis 3 regarding the independent and combined
contribution of biomedical, demographic, and parent variables to parent
distress (GSI). The summary analysis is presented in
Table III. Parent daily stress
entered first and accounted for 33% of the variance, followed by phenotype
(7%), and knowledge of child development (4%) and parent expectations of
efficacy (4%). Together these four variables accounted for 49% of the variance
in parent distress. Thus, the regression analysis indicates that parent
distress was related to HbSC phenotype, high levels of daily stress and lower
expectations of efficacy, and less knowledge of child development.
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Discussion |
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This study is one of the first to trace the early neurocognitive functioning of children with SCD and to examine the independent and combined contribution of biomedical and parenting risks to neurocognitive functioning. Of particular importance is that impairment in neurocognitive functioning, previously reported in children with SCD (Armstrong et al., 1996
;
Brown, Armstrong, & Eckman,
1993), is also evident in early childhood. As hypothesized, there
was a significant decline in neurocognitive functioning during the first 36
months of life. However, this decline was manifested in cognitive (MDI) but
not psychomotor (PDI) functioning, and the significant decline in cognitive
functioning occurred between 12 and 24 months of age. This pattern is
consistent with findings from studies of poor and African American children
without chronic illness (Burchinal et al.,
1997). Guided by a cognitive and stress processing model of parenting, the hypothesized contribution of biomedical risk and parenting risk to neurocognitive functioning (Figure 1) was examined through multiple regression analysis. The results demonstrate that phenotype did account for 15% of the variance in psychomotor functioning (PDI) and 20% of the variance in cognitive functioning (MDI) at 24 months. These findings suggest the presence of subtle effects of biomedical risk on neurocognitive functioning by 24 months of age, which, in turn, provides impetus for MRI studies that would further delineate biomedical risk and the relationship of functional deficits with neurological impairment. The evidence for additional psychosocial effects on cognitive, but not psychomotor functioning, stems from the contribution of the parenting parameter of cognitive attributional style to neurocognitive functioning. Together, biomedical risk and parenting risk parameters account for 42% of the variance in cognitive functioning (MDI) of children with SCD at 24 months of age.
The findings of this study are consistent with those from two lines of research that together provide support for the utility of the process model of parenting for reflecting the role of parent cognitive processes and distress in the neurocognitive functioning of children who are at biomedical risk. One line of research has related parental distress with parent cognitive processes of stress appraisal and efficacy expectations and with family functioning. The other line of research relates parental stress and distress to child neurocognitive functioning.
With regard to parental distress, the findings of this study of 24% of
parents of young children with SCD with clinical levels of psychological
distress is similar to that found in studies of mothers of children and
adolescents with SCD (Thompson &
Gustafson, 1996). Also consistent with previous studies in support
of the transactional stress and coping model
(Thompson & Gustafson,
1996), high levels of daily stress, but not illness stress, and
low levels of efficacy expectations accounted for significant portions of the
variance in parental distress. In addition, higher levels of parental distress
were associated with child biomedical risk, HbSC/other and not the more severe
HbSS, and less knowledge of child development. It is not clear why the
predicted association of parental distress to high levels of family control
and low levels of supportiveness was not supported.
These findings of the association of both biomedical risk and parenting
risk with neurocognitive outcome in children with SCD are notably consistent
with studies of another group of children, very low birthweight infants, who
are also at risk for neurocognitive impairment. In a study of developmental
outcome, biological risk, in terms of processes likely to cause brain injury,
accounted for significant portions of variance in MDI (13%) and PDI (21%) at
24 months of age, and psychosocial risk, in terms of maternal daily stress,
accounted for a significant portion (6%) of variance in MDI
(Thompson, Goldstein, et al.,
1994). At 6 months corrected age, distress within the clinical
range was demonstrated by 41% of mothers
(Thompson, Oehler, Catlett, &
Johndrow, 1993). With demographic and child biomedical parameters
and prior psychological adjustment controlled, significant increments in the
variance in the maternal distress were accounted for by high levels of daily
stress (2%), low expectations of efficacy (10%), and high levels of family
conflict (10%). Infants of mothers with high, compared with low, distress had
significantly lower MDI (M = 89.59 vs. 101.88) and PDI (M =
89.84 vs. 104.71) scores.
The findings of this study provide support for the initiation of early intervention studies to promote the neurocognitive development of children with SCD and furthermore provide preliminary evidence in support of salient intervention targets, in terms of processes likely to affect parenting, which, in turn, is postulated to affect child development. More specifically, increasing parental knowledge about child development and expectations of efficacy with regard to management of illness tasks and decreasing daily stress would serve to lessen parenting distress. Altering learned-helplessness attributional styles should increase perceptions of opportunities to control outcomes, assertiveness, persistence motivation, and self-esteem and thereby promote more effective parenting in general and parenting of children with the chronic illness of SCD in particular.
The limitations of this study are those typically associated with an initial, prospective, developmental follow-up conducted at one site, particularly moderate sample size. The project period of 5 years meant that infants enrolled later in the period could be followed only through the 12-month assessment. As a result, the study sample at 36 months of age was too small for appropriate analysis of within-group differences as a function of biomedical and parenting risks. Furthermore, although the study was conceptually guided by the cognitive and stress processing model of parenting, only selected elements of the model could be incorporated into this study. The study design was intentionally within-group; thus, direct contrasts with other chronic illness or healthy subgroups were not possible. With these limitations, the findings must be considered suggestive and require replication. However, the findings provide the necessary foundation for the next step: multisite, conceptually driven, well-controlled, longitudinal studies of the neurocognitive development of children with SCD with concurrent MRI assessment in the context of an intervention study designed to foster parenting effectiveness.
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Acknowledgments |
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This research was supported by Duke University-University of North Carolina Sickle Cell Center Grant P60 HL 28391. We thank D. Johndrow, R. Froh, and J. Lazarus for data analysis and L. Schumacher, C. Pietrucha, and J. Sayre for infant assessment.
Received October 10, 2000; revision received February 8, 2001; revision received June 5, 2001; accepted June 20, 2001
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