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weight quintiles versus those in the 3 RESULTS boys and girls were similar up to about
middle quintiles were assessed with t the age of 15 years. Girls plateaued
Descriptive Statistics
tests. earlier than boys, and between the
The study population included 25 545 ages of 15 and 20 years boys tended to
Mortality children (56% male, aged 2–20 years) weigh more than girls. Gender differ-
who contributed 102 163 weight mea- ences were smaller in the more se-
Electronic death records were ob-
surements (Table 1). Age, gender, pre- verely affected groups. For example, at
tained from the California Department
maturity or low birth weight, and cal- age 20 years the difference in median
of Health Services. Individuals surviv-
endar year of CDER did not vary weights for boys and girls in GMFCS
ing 3 or more years after their last
significantly by GMFCS level. The most level I was 7.3 kg; the difference was
weight measure were censored at 3
frequent level in our study population only 1.8 kg in the GMFCS V-TF group.
years. All individuals surviving to De-
was GMFCS level II (31%). This was fol- Figure 2A shows a scatter plot of weight-
cember 31, 2002, were administra-
lowed by levels IV (24%), V (17%), I for-age data in boys from GMFCS level I,
tively censored at that date. (14%), and III (14%). The proportion along with estimated weight-for-age per-
We used Cox proportional hazards re- with severe feeding and cognitive dis- centiles and the CDC percentiles for boys
gression analysis with time-varying co- abilities increased with increasing in the general population. The 90th per-
variates28 to relate survival time to GMFCS level. For example, 2% of chil- centile in GMFCS level I closely tracked
weight percentiles. This enabled us to dren in GMFCS level I were either tube that of the general population. The me-
control for other variables, such as fed or orally fed by others compared dian was lower, and the difference in me-
feeding skills, that might confound or with 42% of children in GMFCS level IV dians increased with age. The 10th per-
modify the effect of low weight on mor- and 90% in GFMCS level V. Eleven percent centile was markedly lower at all ages.
tality. Separate models were fit for of children in GMFCS level I had severe or Children in GMFCS level V exhibited more
GMFCS levels I and II and GMFCS levels profound mental retardation compared linear growth patterns (ie, no growth
III through V because children in these with 50% of children in GMFCS level IV spurt), with a plateau in late adoles-
groups tend to be different with re- and 73% in GFMCS level V. cence (Fig 2B).
spect to functional skills beyond gross
motor function, feeding and cognition, Weight-for-Age Morbidity
age-specific weight values, age- In all but the most severe group The mean number of chronic major
specific mortality patterns, and secu- (GMFCS level V), weight-for-age data medical conditions increased mod-
lar trends. Low-weight cutoffs were se- exhibited nonlinear dependence on estly with GMFCS level. The most strik-
lected on the basis of maximum age, with a visible growth spurt be- ing marker for chronic medical condi-
likelihood. Data were managed in SAS tween ages 9 and 13 years and plateau tions was the presence of a feeding
version 9.12,29 and analyzed by using R in late adolescence. For each GMFCS tube. For example, children in GMFCS
version 2.9.30 level, weight-for-age percentiles for V-TF had, on average, twice as many
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FIGURE 5
Clinical growth charts for children with cerebral palsy.
my patient? And, if so, for how long?” The primary limitation of the study is ment of Developmental Services be-
The evidence presented here is the lack of information regarding the cause of a perceived lack of need.
generally applicable to all children etiology of low weight. Low weight is a Thus, our GMFCS level I findings may be
with cerebral palsy, but additional known marker for nutritional deficits valid only for children with ongoing
patient-specific features should al- and general frailty, which is a reason- needs for services.
ways be considered. One potentially able mechanism for increased mor-
The study has a number of strengths. The
benign reason for low weight may bidity and mortality. On the other hand,
simply be small parental stature. In children may lose weight or have trou- findings represent the first evidence-
cases where benign etiology has ble gaining it as a result of chronic or based link between low weight and mor-
been ruled out, the excess risks as- acute illness. A secondary limitation is tality risk in children with cerebral palsy.
sociated with low weight should be the apparent underrepresentation of The large sample size allowed percentile
interpreted as persistent for as long GMFCS level I (14%) in our study popu- estimates that are robust to modeling
as the child remains in the low- lation. In other population-based cere- assumptions. For example, the charts
weight category. On the other hand, bral palsy registries, the proportion of presented here have estimated weight-
for the reasons stated above clini- those in level I ranged from 30% to for-age percentiles that are consistent
cians should not take the findings of 40%.35–37 It may be that the most mildly with those in Day et al.4 The GAMLSS
this study to infer that overweight is affected individuals in California dis- growth chart methodology used here is
not a significant health risk in chil- proportionately choose not to seek consistent with that of both the CDC
dren with cerebral palsy. long-term services from the Depart- and World Health Organization. It al-
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