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Research Library
In this section you will find a compilation
of recent Cerebral Palsy research article summaries called
‘abstracts’. There are no commentaries attached to these
articles; if you would like to read articles with
comments/interpretation provided by the CPON team please
click here.
Blair, E. and F. Stanley (1992).
"Intrauterine growth and spastic cerebral palsy II. The
association with morphology at birth." Early Hum Dev 28(2):
91-103.
This study tests the hypothesis that
children with spastic cerebral palsy had different birth
morphologies, defined in terms of their weight, length, head
circumference, ponderal index and length to head
circumference ratio, from that of the normal liveborn
population. An earlier study showed a highly significant
association of spastic cerebral palsy with low birthweight
for gestational age in infants over 34 weeks gestation at
delivery. This analysis defines morphological measurements
as "abnormal" if not within the 10th-90th percentile ranges
of appropriate total liveborn populations. The proportions
with combinations of such measurements in 104 cases of
spastic cerebral palsy from a population register of
cerebral palsy are compared with those in a total liveborn
population. Categories of 'abnormal' measurements associated
with increased risk contained 44.4% of cases in excess of
the proportion observed in the total population. More than
half these excess cases were short for their gestation
(suggesting size deficits originating before the 3rd
trimester) and tended to have more severe forms of cerebral
palsy. A further excess of 7.4% of cases had a head
circumference above their 90th percentile: these generally
developed mild cerebral palsy.
Blair, E. and F. Stanley (1993). "When can
cerebral palsy be prevented? The generation of causal
hypotheses by multivariate analysis of a case-control
study." Paediatr Perinat Epidemiol 7(3): 272-301.
Causal hypotheses for spastic cerebral palsy
were sought by comparing a population based sample of 183
cases with 549 matched controls. A time- ordered
multivariate analysis was used to distinguish confounders
and consequences of disease from possible causes, which
could be single factors or sequences of factors. Eighteen
factors were identified as having an association with
spasticity that did not arise by confounding with other
identified factors nor as a consequence of the disease.
Nearly half the cases (48.6%) but only 14.4% of controls
experienced one or more of these factors, but no one factor
was experienced by > 11%, and most by < 5%, of cases. Those
factors identified as occurring before labour commenced
affected 35% of all cases. The proportion of cases
experiencing identified factors and the distribution of
those factors between epochs varied with gestation of
delivery and with description and severity of impairment.
The possible timing of causes in cases without identified
factors and the role of preterm birth and poor intrauterine
growth are discussed. We conclude that there were many
pathways to spastic cerebral palsy many of which could not
be identified. Each contributed only a small proportion and
many may have been multifactorial. Intrapartum initiation of
the aetiological pathway was relatively unimportant, being
likely in about 9% of cases, but the majority of pathways
commenced predelivery.
Blair, E. and F. J. Stanley (1988). "Intrapartum
asphyxia: a rare cause of cerebral palsy." J Pediatr 112(4):
515-9.
Data on all children with spastic cerebral
palsy (N = 183) and on a matched group of control children
(N = 549) born in Western Australia between 1975 and 1980
were compared to investigate the relationship between birth
asphyxia and spastic cerebral palsy. Information on
perinatal events for both the children with cerebral palsy
and the control subjects was collected by means of
epidemiologic methods to reduce bias. An association between
clinically observed perinatal signs of birth asphyxia and
spastic cerebral palsy was found (relative risk 2.84; 95%
confidence interval 1.85 to 4.37). The population-
attributable risk proportion was 14.1%. The likelihood of
birth asphyxia's causing perinatal brain damage was assessed
by two independent observers using defined criteria. It was
estimated that in only about 8% (15/183) of all the children
with spastic cerebral palsy was intrapartum asphyxia the
possible cause of their brain damage. The contribution of
intrapartum events and obstetric mismanagement to overall
cerebral palsy rates is probably less than was previously
thought.
Boyle, C. A., P. Decoufle, et al. (1994).
"Prevalence and health impact of developmental disabilities
in US children." Pediatrics 93(3): 399-403.
OBJECTIVE. Data from the 1988 National
Health Interview Survey--Child Health Supplement were used
to examine the prevalence of selected developmental
disabilities and their impact among children ages 0 through
17 years. DESIGN. The following conditions, identified
through a structured in-person interview with a parent or
other adult household member, were examined: deafness or
trouble hearing, blindness, epilepsy or seizures, stammering
and stuttering, other speech defects, cerebral palsy, delay
in growth or development, learning disabilities, and
emotional or behavioral problems. The impact was defined by
measures of perceived health status, school performance and
attendance, and health care utilization. RESULTS. Seventeen
percent of children in the United States were reported to
have ever had a developmental disability. The prevalence of
the individual disabilities ranged from 0.2% for cerebral
palsy to 6.5% for learning disabilities. These conditions
taken together had a substantial impact on the health and
educational functioning of affected children: 1.5 times more
doctor visits, 3.5 times more hospital-days, twice the
number of school-days lost, and a 2.5-fold increase in the
likelihood of repeating a grade in school compared with
children without these conditions. The extent of this impact
was much greater among children with multiple disabilities
or with either cerebral palsy, epilepsy or seizures, delays
in growth and development, or emotional or behavioral
problems. The impact on school performance was most
pronounced for children reported to have learning
disabilities. CONCLUSIONS. Future research efforts should be
focused on ways to reduce the impact of these developmental
disabilities on quality of life.
Breart, G. and C. Rumeau-Rouquette (1996).
"[Cerebral palsy and perinatal asphyxia in full term newborn
infants]." Arch Pediatr 3(1): 70-4.
Actual data on the frequency of
cerebral palsy (CP) and "infirmite motrice cerebrale" (IMC),
and their relationship with perinatal asphyxia and perinatal
managements, are presented. In France, the frequency of IMC
at 9 years of age, approximates 1 per thousand, for the
1972, 1976, 1981 generations. Three surveys, two English and
one Australian, show an association between perinatal
asphyxia and CP. However computation of percent attributable
risk indicates that asphyxia can explain only one case of CP
out of six among term neonates. These surveys show also that
10% of CP only could be prevented by improving perinatal
managements. This, in addition to other factors such as the
increase in survival of very preterm babies, explains the
absence of a significant reduction of CP frequency despite
improvements in the perinatal care.
Burns, Y. R., M. O'Callaghan, et al. (1989).
"Early identification of cerebral palsy in high risk
infants." Aust Paediatr J 25(4): 215-9.
This study of high risk infants aimed to
identify which signs at the corrected ages of 1, 4 and 8
months were important for distinguishing those infants who
later developed hypertonic cerebral palsy (CP). From a total
cohort of 450 infants (350 of birthweight less than 1500 g
and 100 of birthweight greater than 1500 g), 26 infants were
later diagnosed as having CP and formed the study group. A
control group of 26 infants from the same initial cohort who
did not develop CP was matched to the study group. Both
groups were followed for a minimum of 2 years. At each
assessment (1, 4, 8, 24 months corrected age), all children
were assessed using a standard medical examination and a
detailed neurosensorimotor developmental scale that
evaluated neurological signs, motor attainments, primitive
reflexes and postural reactions. Each test response was
graded as normal, suspect or abnormal and the results for
the two groups were compared. Assessment at 1 month failed
to identify a number of the CP infants whereas at 4 months
there was some overidentification. At 8 months, assessment
was highly predictive of cerebral palsy. Individual signs of
abnormality were found to be of limited value but the
presence of three or more abnormal signs at 8 months was
highly predictive of CP.
Chaplais, J. D. and J. A. Macfarlane (1984).
"A review of 404 'late walkers'." Arch Dis Child 59(6):
512-6.
A survey of all known 18 month old
Oxfordshire children who had not yet walked unassisted and
who were born in the four year period between July 1, 1976
and June 30, 1980 was carried out. A total of 275 children
aged 18 months with no previously suspected cause for late
walking were referred by health visitors; 257 of these
children were assessed neurologically and developmentally by
a paediatrician at home. Nine cases of cerebral palsy (3 X
5%) and 6 cases of minor neurological abnormality (2 X 3%)
were newly diagnosed. A register of all other 18 month old
'late walkers' (129) who were already known to
paediatricians and were either normal (17) or had known
causes for late walking (112) was compiled for the same four
year period. The total incidence of pathology among all late
walkers (404) in these two groups was 32%.
Dite, G. S., R. Bell, et al. (1998).
"Antenatal and perinatal antecedents of moderate and severe
spastic cerebral palsy." Aust N Z J Obstet Gynaecol 38(4):
377-83.
Routinely collected perinatal morbidity data
were abstracted for 204 cases of moderate and severe spastic
cerebral palsy and 816 matched controls. Separate analyses
were conducted for cases with birth-weight > or = 2,500 g
and birth-weight < 2,500 g. The presence of a congenital
abnormality was an important risk factor for cerebral palsy
in both groups and further analyses were conducted after
dividing the groups according to presence or absence of a
congenital abnormality. In the < 2,500 g group,
resuscitation needed was clearly identified as a risk factor
for cerebral palsy in the group with no congenital
abnormalities (adjusted OR=3.4; 95% CI=1.6-7.5) while in the
group with congenital abnormalities, none of the risk
factors were clearly associated with an increased risk of
cerebral palsy. Among the cases with birth-weight > or =
2,500 g, intrauterine hypoxia/birth asphyxia was clearly
associated with an increased risk of cerebral palsy
(adjusted OR=18.1; 95% CI=1.8-186) in the group with no
congenital abnormalities while in the group with congenital
abnormalities, none of the factors were clearly associated
with an increased risk of cerebral palsy.
Dowding, V. M. and C. Barry (1990).
"Cerebral palsy: social class differences in prevalence in
relation to birthweight and severity of disability." J
Epidemiol Community Health 44(3): 191-5.
STUDY OBJECTIVE--The aim of the study was to
examine the possible influence of social class on the
prevalence of cerebral palsy. DESIGN-- The study was a
retrospective population based survey of all cases of
cerebral palsy. SETTING--The study involved all cases of
cerebral palsy born to residents in the Eastern Health Board
area of the Republic of Ireland between 1976 and 1981
inclusive. PATIENTS--There were 289 cases of cerebral palsy
during the study period. Thirty one were excluded because
they were attributable to postneonatal brain damage, leaving
258 children for analysis. Cases with uncertain diagnosis
were excluded. MAIN RESULTS--There was a clear social class
gradient in the overall prevalence of cerebral palsy, also
evident in the individual syndromes of hemiplegia and
diplegia. No such gradient was detected in the other
syndromes, either singly or in combination. Among cases of
low birthweight (less than or equal to 2500 g), the
prevalence was the same across the social class range after
allowing for the increased low birthweight rate in the lower
social class categories. Among normal birthweight cases
there was a strong positive association with decreasing
social class. Intrauterine growth retardation seemed to be a
factor in cerebral palsy in all social class groups.
Prevalence of cerebral palsy severe enough to prevent
walking by the fourth birthday, but not of cases ambulant by
this age, increased with socioeconomic disadvantage.
CONCLUSIONS--The clear social class gradients in hemiplegia
and diplegia suggest that environmental factors play an
important role in the aetiology of these syndromes, but
there was no evidence of a contribution from this type of
factor in the remaining types of cerebral palsy.
Freeman, J. M. and K. B. Nelson (1988).
"Intrapartum asphyxia and cerebral palsy." Pediatrics 82(2):
240-9.
Signs of presumed hypoxia/asphyxia of the
fetus are not uncommon and can be detected during labor, in
the delivery room, and during the early neonatal period.
Virtually no single sign or symptom has sufficient
correlation to enable prediction of later cerebral palsy
with a reasonable degree of medical certainty. To attribute
cerebral palsy to prior asphyxia with reasonable certainty,
there must be evidence that a substantial hypoxic injury
occurred and that a sequence of events ensued which would
prove the clinical impact of that hypoxic insult. Few cases
of cerebral palsy meet these criteria.
Gaudet, L. M. and G. N. Smith (2001).
"Cerebral palsy and chorioamnionitis: the inflammatory
cytokine link." Obstet Gynecol Surv 56(7): 433-6.
Cerebral palsy remains a significant cause
of perinatal morbidity in medically developed countries.
Human epidemiologic data suggest a relationship between
cerebral palsy and chorioamnionitis mediated by
proinflammatory cytokines. This association has been
confirmed by experimental data from human and animal
research that demonstrate an increase in cytokine levels in
the amniotic fluid of cases of white matter damage. Recent
evidence suggests this damage is the result of a fetal
inflammatory response initiated in response to placental
inflammation. The strong association between cerebral palsy
and chorioamnionitis warrants additional investigation into
the mechanisms by which white matter damage is initiated and
into possible neuroprotective treatments to prevent the
development of cerebral palsy.
Grether, J. K., S. K. Cummins, et al.
(1992). "The California Cerebral Palsy Project." Paediatr
Perinat Epidemiol 6(3): 339-51.
The California Cerebral Palsy Project (CACP)
is a population-based study of 192 children with moderate or
severe congenital cerebral palsy who were born between 1983
and 1985 in four San Francisco Bay area counties and who
were alive and residing in California at age 3 years.
Initial ascertainment of cases was based on records of two
agencies known to enrol virtually all CACP-eligible
children. Final case status was established by standardised
clinical examination in 67% of cases and extensive record
review in 33%. The 192 cases gave a prevalence at age 3 of
1.23/1000 survivors. Twins were 10% of the cases with a
prevalence of 6.7/1000. Overall, 53% of the cases had
birthweight greater than or equal to 2500 g and 28% had
birthweight less than 1500 g. There was no association
between birthweight and severity of functional impairment
and no consistent association between birthweight and the
presence of associated disabilities. The CACP prevalence is
lower than that reported in other studies and is believed to
be due to the more stringent case inclusion criteria
employed for this research data base.
Grether, J. K. and K. B. Nelson (1997).
"Maternal infection and cerebral palsy in infants of normal
birth weight." Jama 278(3): 207-11.
CONTEXT: Exposure to maternal or placental
infection is related to risk of preterm birth and, in
premature infants, of brain lesions predictive of cerebral
palsy (CP). Few studies have investigated whether maternal
infection is associated with risk of CP in children of
normal birth weight. OBJECTIVE: To investigate maternal
infection during the admission for delivery as a possible
risk factor for CP in infants born weighing 2500 g or more.
DESIGN: Population-based case-control study. SETTING: All
hospitals in 4 northern California counties, 1983 through
1985. PARTICIPANTS: A total of 46 children with disabling
spastic CP who had no recognized prenatal brain lesions and
378 randomly selected control children weighing 2500 g or
more at birth and surviving to age 3 years. MAIN OUTCOME
MEASURES: Disabling spastic CP and signs of neonatal
morbidity. RESULTS: Maternal fever exceeding 38 degrees C in
labor was associated with increased risk of unexplained CP
(odds ratio [OR], 9.3; 95% confidence interval [CI],
2.7-31.0), as was a clinical diagnosis of chorioamnionitis.
One or more indicators of maternal infection were present in
2.9% of control children, 22% of children with CP (OR, 9.3;
95% CI, 3.7-23.0), and 37% of those with the spastic
quadriplegic subtype of CP (OR, 19.0; 95% CI, 6.5-56.0).
Newborns exposed to maternal infection, both cases and
controls, had 5-minute Apgar scores below 6 more often than
those unexposed. Among children with CP, those born to
infected women were more often hypotensive, needed
intubation, had neonatal seizures, and received a clinical
diagnosis of hypoxic-ischemic encephalopathy. CONCLUSION:
Intrauterine exposure to maternal infection was associated
with a marked increase in risk of CP in infants of normal
birth weight. Maternal infection was also linked with low
Apgar scores, other evidence of hypotension [corrected] and
need for resuscitation, and neonatal seizures-signs commonly
attributed to birth asphyxia.
Grether, J. K., K. B. Nelson, et al. (1996).
"Prenatal and perinatal factors and cerebral palsy in very
low birth weight infants." J Pediatr 128(3): 407-14.
OBJECTIVE: To identify prenatal
and perinatal characteristics associated with cerebral palsy
(CP) in infants born weighing < 1500 gm (very low birth
weight, VLBW). DESIGN: All 42 VLBW singleton infants with CP
born in the period from 1983 to 1985 in a defined population
were compared with 75 randomly selected VLBW control
infants. RESULTS: Birth in a level I facility was associated
with increased risk of CP (odds ratio (OR) 6.3, 95%
confidence interval (CI) 1.8, 19), as was birth within 3
hours of the mother's first admission for delivery (OR 3.2,
CI 1.4, 7.4). Delivery occurred within 3 hours of admission
to a level I facilty in 24% of VLBW children with CP and no
control children (OR (0.5 added to each cell of 2 x 2 table)
49, CI 3.1, 204). Chorionitis was associated with increased
risk in children born more than 5 hours after admission (OR
4.3, CI 1.1, 13). Chorionitis followed by neonatal seizures
occurred in 14% of VLBW children with CP (in 25% with
spastic diplegia) and in no control child (OR (0.5 added to
each cell of 2 x 2 table) 26, CI 1.6, 116). Preeclampsia was
associated with decreased risk (OR 0.08, CI 0.02, 0.67), as
was use of magnesium sulfate (OR 0.14, CI 0.05, 0.51)
administered for preeclampsia or preterm labor. Other risk
factors for CP included gravidity greater than one (OR 3.9,
CI 1.2, 11), short interbirth interval (OR 4.1, CI 1.3, 12),
and vaginal bleeding on the day of admission (OR 2.9, CI
1.2, 7.4). CONCLUSIONS: In this population-based study,
almost one fourth of the CP in VLBW children occurred in
infants delivered in level I facilities soon after their
mothers' admissions. Another 14% was in children who had
neonatal seizures after birth to women with chorionitis. No
control subject experienced either of these sequences.
Hagberg, B. and G. Hagberg (1989). "The
changing panorama of infantile hydrocephalus and cerebral
palsy over forty years--a Swedish survey." Brain Dev 11(6):
368-73.
The time trends and background
of infantile hydrocephalus (IH) and cerebral palsy (CP) are
surveyed. The changes in live birth prevalence, disability
patterns, associated neuroimpairments and distribution of
etiologies are analysed. Both the risk of IH and that of CP
sharply increase with decreasing birth weight and
gestational age. It is concluded that the remarkably
enhanced survival of particularly very preterm infants,
those at the highest risk of long-term morbidity, implies an
increasing number of impaired children as long as the
outcome of survivors is not drastically improved. The data
presented are thought to be of relevance as to
reconsideration of the effectiveness of perinatal care for
preterm babies.
Hardt, N. S., M. Kostenbauder, et al.
(1985). "Influence of chorioamnionitis on long-term
prognosis in low birth weight infants." Obstet Gynecol
65(1): 5-10.
The contribution of obstetric
management to quality of life of surviving low birth weight
infants is unclear. A possible association between maternal chorioamnionitis and development outcome was evaluated. One
hundred twenty-seven mother/infant pairs with infant birth
weight less than 2000 g were studied. The antenatal course
was complicated by chorioamnionitis, premature rupture of
membranes without chorioamnionitis, premature labor, or
abruptio placenta. Analysis of variance was performed using
these four diagnosis groups. After potentially confounding
variables were taken into account, the overall difference in
the four groups in Mental Development Index (Bayley Scales)
was borderline (P = .138). However, significant differences
remained between the group with chorioamnionitis and the
group with premature rupture of membranes without
chorioamnionitis (P = .017). The potential advantage of
leaving infants in utero after premature rupture of
membranes may be offset by disadvantage of chorioamnionitis
with respect to future development in surviving infants.
Harris, S. R. (1987). "Early neuromotor
predictors of cerebral palsy in low-birthweight infants."
Dev Med Child Neurol 29(4): 508-19.
The purpose of this study was to
analyze retrospectively which neuromotor behaviors in a
sample of four-month-old low-birthweight infants were most
predictive of later cerebral palsy. The infants were
evaluated at four months corrected age on the Movement
Assessment of Infants (MAI) and were followed to between
three and eight years of age. For the CP group as a whole,
17 neuromotor items from the MAI were highly significant (p
less than 0.001) predictors of cerebral palsy. A further 15
items also were significant, but less highly so (p less than
0.01 to p less than 0.05). Seven items were predictive of
later spastic diplegia, seven of spastic hemiplegia, and 35
items differentiated quadriplegic infants. A shorter version
of the MAI should be developed to increase its over-all
reliability and validity in the early detection of cerebral
palsy. Only then would it be possible to implement early
therapeutic intervention and to evaluate its efficacy.
Harris, S. R. (1989). "Early diagnosis of
spastic diplegia, spastic hemiplegia, and quadriplegia." Am
J Dis Child 143(11): 1356-60.
A retrospective study examined
early neurodevelopmental behaviors of children with spastic
diplegia, spastic hemiplegia, and quadriplegia (spastic,
athetoid, or mixed) who had been followed up longitudinally
in a high-risk infant follow-up clinic. Compared with peers
with normal outcomes, children with all three types of
cerebral palsy had significantly lower scores on the Bayley
Mental Scale at 4 months of age; children with hemiplegia
and quadriplegia also scored significantly lower on the
Bayley Motor Scale. On the Movement Assessment of Infants at
4 months of age, the children with hemiplegia and
quadriplegia showed significantly higher risk scores than
the nonhandicapped group. The Movement Assessment of Infants
was more than three times as sensitive as the Bayley Motor
Scale in detecting motor abnormalities in 4-month-old
infants with diplegia and more than twice as sensitive in
detecting early abnormalities of hemiplegia. At 1 year of
age, however, the Bayley Motor Scale was extremely sensitive
in picking up motor deficits in children with all three
types of cerebral palsy.
Harris, S. R., S. M. Haley, et al. (1984).
"Reliability of observational measures of the Movement
Assessment of Infants." Phys Ther 64(4): 471-7.
This study was conducted to
examine the reliability of the Movement Assessment of
Infants (MAI), a recently published neuromotor assessment
tool. Interobserver and test-retest reliability data were
collected on 27 full-term and 26 preterm 4-month-old
infants. Reliability coefficients (Pearson r) were
calculated for both the total-risk scores and the
section-risk scores on the MAI. The total-risk score was
calculated by summing the questionable or abnormal ratings
on each of the 65 test items. For each of the four sections
of the test, tone, primitive reflexes, automatic reactions,
and volitional movement, an individual section-risk score
was computed in a similar manner. Fair reliability was
demonstrated for the total-risk scores (interobserver: r =
.72; test-retest: r = .76). Section-risk score coefficients
yielded a wide range of values for both interobserver and
test-retest reliabilities (poor to good reliability). These
measures provide needed technical data for therapists using
this test and will assist the authors of the MAI in their
attempts to improve the clinical validity of this assessment
tool.
Hutton, J. L., T. Cooke, et al. (1994).
"Life expectancy in children with cerebral palsy." Bmj
309(6952): 431-5.
OBJECTIVE--To determine life
expectancy of children with cerebral palsy. DESIGN--Cohort
analysis, by means of register compiled from multiple
sources of ascertainment, of all children with cerebral
palsy born during 1966-84 to mothers resident in Mersey
region. Status of children was determined by flagging
through NHS central register. SUBJECTS--1258 subjects with
idiopathic cerebral palsy, of whom 1251 were traced and
included in analysis. MAIN OUTCOME MEASURES--Effect of
functional ability (ambulation, manual dexterity, and mental
ability), sex, birth weight, and gestational age on
survival. RESULTS--20 year survival for whole cohort was
89.3% for females and 86.9% for males. For subjects with no
severe functional disabilities 20 year survival was 99% (95%
confidence interval 98% to 100%), while subjects severely
disabled in all three functional groups had 20 year survival
of 50% (42% to 58%). Subjects with birth weight < or = 2500
g had 20 year survival of 92% (89% to 95%), while those with
birth weight > 2500 g had survival of 87% (84% to 89%).
Subjects with gestational age of > 37 weeks had 20 year
survival of 93% (91% to 96%), while those with gestational
age > or = 37 weeks had survival of 85% (83% to 88%). Birth
weight and gestational age were less predictive of survival
than functional disability. Best statistical model used
gestational age and number of severe functional disabilities
as predictors. CONCLUSIONS-- Life expectancy of this cohort
of children with cerebral palsy was greater than has been
suggested in some previous studies. This has important
implications for social, educational, and health services.
Jarvis, S. N., J. S. Holloway, et al.
(1985). "Increase in cerebral palsy in normal birthweight
babies." Arch Dis Child 60(12): 1113-21.
A register has been compiled of
the 421 children with congenital cerebral palsy born between
1960 and 1975 from a defined geographical area of North East
England (population 770 000). There was a fall in the rate
of cerebral palsy among very low birthweight babies between
1964 and 1975 and also in the small group with dyskinetic
cerebral palsy. The rate rose, however, among babies
weighing more than 2.5 kg at birth in the second half of the
study, in parallel with changes in perinatal mortality. The
net effect is that the overall congenital cerebral palsy
rate (mean 1.64 per 1000 livebirths) showed a gradual rise
between 1968 and 1975. This conclusion is reinforced by
evidence of a rise in incidence among the subgroup of
patients with severe cerebral palsy (as defined by an
interval measurement of handicap) during the same period.
Jaw, T. S., Y. J. Jong, et al. (1998).
"Etiology, timing of insult, and neuropathology of cerebral
palsy evaluated with magnetic resonance imaging." J Formos
Med Assoc 97(4): 239-46.
To define the patterns of
pathologic changes in cerebral palsy (CP) and to assess the
etiology and time of brain damage, we reviewed the magnetic
resonance images and clinical records of 86 pediatric CP
patients seen over 8 years. Patients were divided into two
groups, based on the gestational age at birth. The majority
of CP patients (69) had spasticity. In the premature group
(< 37 wk gestational age) n = 27), spastic diplegia (12
patients) and quadriplegia (8) were the major subtypes. In
the term group (> or = 37 wk gestational age) ( n = 59),
spastic hemiplegia (23) and quadriplegia (12) were most
common. The other main clinical manifestations in the two
groups were seizures (36) and mental retardation (15).
Magnetic resonance (MR) imaging provided significant
findings in 82 patients (95%). In the 27 patients born
prematurely, MR imaging revealed periventricular
leukomalacia (17), multicystic encephalomalacia (3),
cortical and subcortical atrophy (4), migration disorders
(2), and basal ganglia injury (1). Among the patients born
at term, the MR imaging findings were more heterogeneous;
they included cortical and subcortical atrophy (17), brain
malformations (17), periventricular leukomalacia (6),
multicystic encephalomalacia (5), porencephaly (4),
hemiatrophy (3), delayed myelination (3), and none (4). MR
imaging alone could define the time of brain insults in 73
of our 86 CP patients. Combined with clinical histories, MR
imaging could help assess the time of insult in 93% of
patients. The brain insults occurred prenatally in 34 of our
patients, perinatally in 37, and postnatally in eight. The
time of insult could not be determined in six patients. In
the premature patients, the insult occurred most frequently
perinatally (74%), whereas in the term group it occurred
most frequently prenatally (54%). MR imaging was found to be
very helpful in the evaluation of the various
neuropathologic changes in CP, in the depiction of the
etiology, and in the determination of the time of brain
injury.
Kuban KCK, Leviton A. Cerebral Palsy. N Engl
J Med 1994;330:188-195.
More than 100,000 Americans under the age of
18 years are estimated to have some degree of neurologic
disability attributed to cerebral palsy1. Approximately 25
percent of the people with cerebral palsy identified by
registries in France and the United Kingdom are unable to
walk (even with help), and 30 percent are classified as
mentally retarded2,3. In the United States, the total annual
cost to society of cerebral palsy has recently been
estimated by the Advisory Council of the National Institute
of Neurological Disorders and Stroke at $5 billion.
Emotional suffering and lost opportunities . . .
Blair, E. and F. Stanley (1990).
"Intrauterine growth and spastic cerebral palsy. I.
Association with birth weight for gestational age." Am J
Obstet Gynecol 162(1): 229-37.
Birth weight, gestational age at delivery,
and other factors were collected for 171 white children with
spastic cerebral palsy. Their birth weights were compared
with the birth weight distribution expected for a population
of the same race, gestation, sex, maternal height, and
parity, born in the same geographic area, and during the
same time period. Birth weights of children with spastic
cerebral palsy tended to be significantly lower than the
median birth weight of their comparison population. Analysis
stratified by gestation at delivery suggested that if the
reduced birth weight were causally associated with the
spastic cerebral palsy, 22% of cases were attributable to
being below the 10th percentile of the comparison population
birth weight distribution. The risk of spastic cerebral
palsy associated with poor intrauterine growth was dependent
on gestation at delivery; poorly grown infants delivered
between 34 and 37 weeks' gestation were at highest risk.
Some probable pathways by which growth retardation could
result in brain damage (intrapartum hypoxia, hypoglycemia,
and hypothermia) were investigated. Only intrapartum hypoxia
may have played a causal role but probably accounted for
less than 2% of all cases. These data suggest that spastic
cerebral palsy is associated with poor intrauterine growth
in infants of more than 33 weeks' gestation, but no
important causal mechanism has yet been identified.
Meberg, A. and H. Broch (1995). "A changing
pattern of cerebral palsy. Declining trend for incidence of
cerebral palsy in the 20-year period 1970-89." J Perinat Med
23(5): 395-402.
In a population-based study
cerebral palsy (CP) was diagnosed in 110 cases (2.4 per
1000) among children live born with birth weight > or = 500
g (n = 45,976) during the 20-year-period 1970-89 (CP cases
with a postneonatal etiology excluded). The CP-incidence
showed a linear trend of decline from 2.8 per 1,000 in the
first 5-year-cohort born 1970-74, to 2.0 per 1,000 in
children born 1985-89 (p = 0.17). Birth weight specific
CP-incidence showed a trend of decline in very low birth
weight infants (500-1,499 g) and in infants > or = 2,500 g
from the first 10-year-cohort born 1970-79 to the second
born 1980-89. The same trend occurred for the incidence of
spastic diplegia in total and in children born preterm.
These trends of decline did not achieve statistical
significance (p > 0.05). The CP-incidence was 36.7 and 11.3
times higher among infants with birth weight 500-1,499 g and
1,500- 2,499 g respectively compared to infants > or = 2,500
g (p < 0.01). 15.9% of the decline in CP-incidence from the
first to the second 10- year-cohort could be explained by a
decreased low birth weight rate (500-2,499 g) in the
population, from 4.2% 1970-79 to 3.8% 1980-89 (p < 0.05).
The origin of CP was considered prenatal in 22 (20%),
perinatal in 47 (42.7%), and undifferentiated in 41 (37.3%)
of the cases. More CP- children born in the 10-year-period
1980-89 were treated with mechanical ventilation in the
neonatal period (13/46; 28.3%) than those born in the
10-year-period 1970-79 (4/64; 6.3%) (p < 0.01). The neonatal
mortality rate declined significantly from 7.2 per 1,000 in
the first to 3.9 per 1,000 in the last 10-year-cohort
respectively (p < 0.01). Birth weight-specific neonatal
mortality rates declined more than 50% in all weight groups
(p < 0.01). The results are contradictive to other
investigations showing increased CP-incidence following
improved survival rates in low birth weight infants, and may
reflect a different pattern for development of perinatal
care (organization, intensive care). The overall effect of
mechanical ventilation may be improved survival and
prevention of brain damage, though the percentage of
ventilated CP-children increased. Preventing low birth
weight should be a main strategy for preventing CP.
Murphy, D. J., P. L. Hope, et al. (1997).
"Neonatal risk factors for cerebral palsy in very preterm
babies: case- control study." Bmj 314(7078): 404-8.
OBJECTIVE: To identify neonatal
risk factors for cerebral palsy among very preterm babies
and in particular the associations independent of the
coexistence of antenatal and intrapartum factors. DESIGN:
Case- control study. SETTING: Oxford health region.
SUBJECTS: Singleton babies born between 1984 and 1990 at
less than 32 weeks' gestation who survived to discharge from
hospital: 59 with cerebral palsy and 234 randomly selected
controls without cerebral palsy. MAIN OUTCOME MEASURES:
Adverse neonatal factors expressed as odds ratios and 95%
confidence intervals. RESULTS: Factors associated with an
increased risk of cerebral palsy after adjustment for
gestational age and the presence of previously identified
antenatal and intrapartum risk factors were patent ductus
arteriosus (odds ratio 2.3; 95% confidence interval 1.2 to
4.5), hypotension (2.3; 1.3 to 4.7), blood transfusion (4.8;
2.5 to 9.3), prolonged ventilation (4.8; 2.5 to 9.0),
pneumothorax (3.5; 1.6 to 7.6), sepsis (3.6; 1.8 to 7.4),
hyponatraemia (7.9; 2.1 to 29.6) and total parenteral
nutrition (5.5; 2.8 to 10.5). Seizures were associated with
an increased risk of cerebral palsy (10.0; 4.1 to 24.7), as
were parenchymal damage (32; 12.4 to 84.4) and appreciable
ventricular dilatation (5.4; 3.0 to 9.8) detected by
cerebral ultrasound. CONCLUSION: A reduction in the rate of
cerebral palsy in very preterm babies requires an integrated
approach to management throughout the antenatal,
intrapartum, and neonatal periods.
Naeye, R. L., E. C. Peters, et al. (1989).
"Origins of cerebral palsy." Am J Dis Child 143(10):
1154-61.
Analyses were undertaken to
determine the causes of cerebral palsy in a prospective
study of 43,437 full-term children. Presumed causes were
found for about 71% of the 34 quadriplegic and 40% of the
116 nonquadriplegic patients with cerebral palsy. Risk
estimates based on predictive models, adjusted for multiple
factors, suggest that 53% of the quadriplegic patients with
cerebral palsy could be attributed to congenital disorders,
14% to birth asphyxia, and 8% to other identified disorders.
Thirty-five percent of the nonquadriplegic patients with
cerebral palsy could be attributed to congenital disorders
and 6% to other disorders. In the victims of cerebral palsy,
characteristic consequences of birth asphyxia were more
often the result of nonasphyxial disorders. These included
meconium in the amniotic fluid, low 10-minute Apgar scores,
neonatal apnea spells, seizures, persisting neurologic
abnormalities, and slow head growth after birth.
Nelson, K. B. and S. H. Broman (1977).
"Perinatal risk factors in children with serious motor and
mental handicaps." Ann Neurol 2(5): 371-7.
Fifty children with marked
neurological abnormality manifested by moderate or severe
motor disability and severe mental retardation were compared
with a large control population with respect to
prospectively ascertained perinatal characteristics. None of
60 prenatal factors distinguished the affected group from
controls. In labor and delivery, lowest fetal heart rate in
the second stage of labor, arrested progress of labor, and
use of midforceps discriminated between the two groups.
Neonatal characteristics of children who were later severely
handicapped differed from controls, particularly with
respect to difficulty in initiating and maintaining
respiration, intracranial hemorrhage, neonatal seizures, low
birth weight and small head circumference, lowest hemoglobin
or hematocrit, and overall neurological status. Multivariate
analysis, including factors from all epochs, indicated that
intracranial hemorrhage and neonatal seizures were the
strongest independent discriminators between the
neurologically impaired children and controls.
Nelson, K. B., J. M. Dambrosia, et al.
(1996). "Uncertain value of electronic fetal monitoring in
predicting cerebral palsy." N Engl J Med 334(10): 613-8.
BACKGROUND. Electronic
monitoring of the fetal heart rate is commonly performed, in
part to detect hypoxia during delivery that may result in
brain injury. It is not know whether specific abnormalities
on electronic fetal monitoring are related to the risk of
cerebral palsy. METHODS. Among 155,636 children born from
1983 through 1985 in four California counties, we identified
singleton infants with birth weights of at least 2500 g who
survived to three years of age and had moderate or severe
cerebral palsy. The children with cerebral palsy were
compared with randomly selected control children with
respect to characteristics noted in the birth records.
RESULTS. Seventy-eight of 95 children with cerebral palsy
and 300 of 378 controls underwent intrapartum fetal
monitoring. Characteristics found to be associated with an
increased risk of cerebral palsy were multiple late
decelerations in the heart rate, commonly defined as slowing
of the heart rate well after the onset of uterine
contractions (odds ratio, 3.9; 95 percent confidence
interval, 1.7 to 9.3), and decreased beat-to- beat
variability of the heart rate (odds ratio, 2.7; 95 percent
confidence interval, 1.1 to 5.8); there was no association
between the highest or lowest fetal heart rate recorded for
each child and the risk of cerebral palsy. Even after
adjustment for other risk factors, the association of
abnormalities on fetal monitoring with an increased risk of
cerebral palsy persisted (adjusted odds ratio, 2.7; 95
percent confidence interval, 1.4 to 5.4). The 21 children
with cerebral palsy who had multiple late decelerations or
decreased variability in heart rate on fetal monitoring
represented only 0.19 percent of singleton infants with
birth weights of 2500 g or more who had these fetal-
monitoring findings, for a false positive rate of 99.8
percent. CONCLUSIONS. Specific abnormal findings on
electronic monitoring of the fetal heart rate were
associated with an increased risk of cerebral palsy.
However, the false positive rate was extremely high. Since
cesarean section is often performed when such abnormalities
are noted and is associated with risk to the mother, our
findings arouse concern that, if these indications were
widely used, many cesarean sections would be performed
without benefit and with the potential for harm.
Nelson, K. B. and J. H. Ellenberg (1979).
"Neonatal signs as predictors of cerebral palsy." Pediatrics
64(2): 225-32.
Signs of neonatal neurologic
dysfunction, recorded in approximately 40,000 infants, were
evaluated prospectively for their ability to predict later
motor handicap. Tenfold to 33-fold increases in risk of
cerebral palsy (CP) were observed in surviving children with
any one of the following characteristics: birth weight less
than 2,000 gm, head circumference more than 3 SD above or
below the mean, five minute Apgar score of 3 or less,
diminished activity or diminished cry lasting for more than
one day, thermal instability, need for gavage feeding,
hypotonia or hypertonia, single or multiple apneic episodes,
or hematocrit less than 40%. Of worse portent, with relative
risks exceeding 50, were neonatal seizures or Apgar scores
of 3 or less at ten minutes or later. These characteristics
were also markers of considerable risk of early death. For
0.5% of surviving infants, an overall impression of
abnormality of brain function during the nursery period was
recorded by the attending physician; there was a 99-fold
increase in CP among these children.
Nelson, K. B. and J. H. Ellenberg (1982).
"Children who "outgrew' cerebral palsy." Pediatrics 69(5):
529-36.
A diagnosis of cerebral palsy
was made for 229 one-year-old children enrolled in a large
longitudinal study. Of these children, 118 were free of
motor handicap at the age of 7 years. Mild early cerebral
palsy, and the monoparetic, ataxic/dyskinetic, and diplegic
forms of the disorder, resolved with high frequency.
Normalization of motor signs was observed more frequently in
black than in white children. However, 13% of white children
and 25% of black children whose motor signs resolved were
mentally retarded (IQ below 70) at 7 years of age.
Nonfebrile seizures, abnormalities in speech articulation
and extraocular movements, and certain abnormalities of
behavior were more frequent among children who "outgrew"
cerebral palsy than in the general population of the study.
Nelson, K. B. and J. H. Ellenberg (1986).
"Antecedents of cerebral palsy. Multivariate analysis of
risk." N Engl J Med 315(2): 81-6.
We examined prenatal and perinatal factors predicting cerebral palsy, using
multivariate analysis to investigate which factors were most
important and the proportion of cases for which they
accounted. Maternal mental retardation, birth weight below
2001 g, and fetal malformation were among the leading
predictors. Breech presentation was also a predictor, but
breech delivery was not. A third of the children with
cerebral palsy who had breech presentations had a major
noncerebral malformation. Among 189 children with cerebral
palsy, 40 (21 percent) had at least one of three clinical
markers suggestive of asphyxia; only 17 of these 40 children
(9 percent of all cases) lacked major congenital
malformation or other intrinsic defects that might have
contributed to an unfavorable outcome. When all the
principal risk factors present by the time labor began were
considered, the 5 percent of the population at highest
estimated risk was seen to have contributed 34 percent of
the cases. When all the risk factors present during the
period beginning before pregnancy and extending through the
nursery stay were included, the 5 percent at highest risk
was seen to have contributed 37 percent of the cases. Thus,
the inclusion of information about the events of birth and
the neonatal period accounted for a proportion of cerebral
palsy only slightly higher than that accounted for when
consideration was limited to characteristics identified
before labor began.
Nelson, K. B. and J. H. Ellenberg (1987).
"The asymptomatic newborn and risk of cerebral palsy." Am J
Dis Child 141(12): 1333-5.
We investigated whether infants
weighing over 2500 g who had experienced one or more of 14
late pregnancy or birth complications, but who were free of
certain signs in the nursery period were at increased risk
of cerebral palsy (CP). The signs evaluated were decreased
activity after the first day of life, need for incubator
care for three or more days, feeding problems, poor suck,
respiratory difficulty, or neonatal seizures. More than 90%
of the infants weighing over 2500 g had none of these signs.
In asymptomatic infants with one or more birth
complications, the rate of CP by 7 years of age was
2.3/1000; among asymptomatic infants whose births were
uncomplicated, the rate of CP was 2.4/1000. The risk for CP
rose with number of abnormal neonatal signs, and children
with sustained neonatal abnormalities were at higher risk
than those whose abnormalities were transient. Most children
with CP did not derive from groups at increased risk. The
full-term infant whose birth was complicated but who was
free of certain abnormal signs in the newborn period was not
at increased risk of CP.
Niswander, K., G. Henson, et al. (1984).
"Adverse outcome of pregnancy and the quality of obstetric
care." Lancet 2(8407): 827-31.
The case-control method was used
to study the relation between four possibly preventable
adverse outcomes of pregnancy and suboptimal antepartum and
intrapartum obstetric care defined by clinical consensus.
Fetuses whose deaths were ascribed to asphyxia or trauma,
and babies born at term who had seizures within 48 h of
delivery, were significantly more likely than controls to
have received suboptimal care during pregnancy. Babies with
seizures, as well as those with terminal apnoea, were also
substantially more likely than controls to have been born
after a failure to react appropriately to signs of severe
fetal distress during labour. Most of the babies who
received suboptimal obstetric care, however, did not have
any of these adverse outcomes. In addition, most babies with
these adverse outcomes had apparently received satisfactory
obstetric care. No relation was detected between cerebral
palsy and suboptimal obstetric care.
O'Shea, T. M., K. L. Klinepeter, et al.
(1998). "Intrauterine infection and the risk of cerebral
palsy in very low- birthweight infants." Paediatr Perinat
Epidemiol 12(1): 72-83.
Very low-birthweight infants
constitute more than one-quarter of all new cases of
cerebral palsy. We performed a case-control study of
associations between antenatal maternal infection and
cerebral palsy in very low-birthweight infants. Cases and
controls were selected from a cohort of 1238 consecutive
infants who: (1) had birthweights between 500 and 1500 g and
no major congenital anomaly; (2) were born 1 January 1986 to
31 December 1993 to a mother residing in 1 of 17 counties in
north-west North Carolina; and (3) were delivered at the
only tertiary obstetric referral centre in those same 17
counties. A total of 984 of these infants (79%) survived to
1 year of age (adjusted for degree of prematurity) and were
scheduled for a multidisciplinary examination; 815 (83%)
came as scheduled. Excluding two cases attributable to post-
neonatal events, 62 cases of cerebral palsy were identified.
Controls were the two infants, without cerebral palsy, born
closest in time to each case. Medical records were reviewed
by a nurse who was not aware of which subjects were cases.
Among possible markers of intra-amniotic infection, those
associated most strongly with cerebral palsy were
chorioamnionitis diagnosed by an obstetrician (odds ratio
[OR] adjusted for gestational age [95% confidence limits] =
2.6 [1.0, 6.5]), antepartum maternal temperature > 37.8
degrees C (OR = 2.6 [1.1, 6.0]), uterine tenderness (OR =
2.6 [0.8, 9.3]), maternal receipt of antibiotics (OR = 2.2
[1.0, 4.7]) and neonatal sepsis in the first week of life
(OR = 2.9 [0.9, 8.9]). All of these associations were
stronger for diplegia than the other clinical subtypes of
cerebral palsy. The association with chorioamnionitis and
spastic diplegia persisted when adjusted for maternal
magnesium sulphate receipt, maternal betamethasone receipt,
method of delivery (vaginal vs. abdominal), acidosis on the
neonate's initial arterial blood gas, systolic blood
pressure < 30 mmHg and the diagnosis of major neonatal
neurosonographic abnormality.
Paneth, N. (1986). "Etiologic factors in
cerebral palsy." Pediatr Ann 15(3): 191, 194-5, 197-201.
A variety of insults can cause
cerebral palsy, but the dominant mechanism of damage is
ischemic and/or asphyxial. Table 2 provides a rough estimate
of the relative contribution of each of the several risk
factor groups to the total burden of cerebral palsy. This
table is only approximate both because of our lack of
knowledge, and because risk factors often interact with one
another. Cerebral palsy is frequently multifactorial in
nature. For example the small-for-gestational age infant is
both more likely to experience labor asphyxia, and is also
more susceptible to its effects. The numerically largest
etiologic grouping in cerebral palsy consists of
pre-term/low birthweight infants, many of whom have
experienced ischemic damage perinatally. The second largest
grouping is infants born at term experiencing severe
perinatal asphyxia. Congenital infections, and metabolic
conditions such as hyperbilirubinemia certainly play some
role in the genesis of cerebral palsy but genetic conditions
as such rarely cause cerebral palsy. Some infants, if
carefully studied, will prove to have a congenital brain
malformation. The role of intrauterine ischemic events is at
present not well understood, but is probably significant.
Paneth, N. and R. I. Stark (1983). "Cerebral
palsy and mental retardation in relation to indicators of
perinatal asphyxia. An epidemiologic overview." Am J Obstet
Gynecol 147(8): 960-6.
Although intrapartum asphyxia is
established as an important cause of perinatal loss, there
is little consensus as to how much of the burden of
neurologic handicap in the community is attributable to
intrapartum and neonatal asphyxia, as measured clinically. A
review of the available epidemiologic information suggests
that the role of perinatal events in the genesis of severe
mental retardation and cerebral palsy is not as large as
popularly thought. Of all neurologic handicaps, cerebral
palsy bears the closest relationship to adverse perinatal
events, but at least 50% of all cases have no documented
depression at the time of birth. No more than 15% of severe
mental retardation can be attributed to perinatal events.
Severe mental retardation without cerebral palsy does not
appear to be attributable to birth asphyxia. The majority of
even quite severely asphyxiated babies suffer no detectable
neurologic or intellectual sequelae. These epidemiologic
observations suggest that resuscitative efforts in mature
newborn infants ought not to be too quickly abandoned for
fear of late sequelae. At the same time, obstetric
intervention based solely on concern for later neurologic
development cannot be justified. The most appropriate
justification for antenatal and intrapartum monitoring of
fetal condition are the established associations of
indicators of fetal asphyxia with fetal and neonatal death,
and with morbidity in the neonatal period.
Petridou, E., M. Koussouri, et al. (1998).
"Diet during pregnancy and the risk of cerebral palsy." Br J
Nutr 79(5): 407-12.
The role of maternal diet in the
development of the fetal brain has not been adequately
explored. Marine n-3 fatty acids have, however, been
proposed to be important for brain development. The present
case- control study aimed to investigate the relationship
between dietary intake during pregnancy and the occurrence
of cerebral palsy (CP) in the offspring. Children with CP (n
109), born between 1984 and 1988 to mothers residing in the
Greater Athens area, were identified at any time in 1991 or
1992 through institutions delivering care and
rehabilitation. Successful nutritional interviews were
conducted with ninety-one of these children. Controls were
chosen among the neighbours of the CP cases or were healthy
siblings of children with neurological diseases other than
CP, seen by the same neurologists as the children with CP. A
total of 278 control children were chosen, and 246 of them
were included in the nutritional study. Guardians of all
children were interviewed in person on the basis of a
questionnaire covering obstetric, perinatal socioeconomic
and environmental variables. A validated semiquantitative
food-frequency questionnaire of 111 food items was used to
estimate maternal dietary intake during pregnancy.
Statistical analysis was done by modelling the data through
logistic regression. Food groups controlling for energy
intake were alternatively and simultaneously introduced in a
core model containing non-nutritional confounding variables.
Consumption of cereals (mostly bread) and fish intake were
inversely associated with CP (P < 0.05 and P < 0.09
respectively) whereas consumption of meat was associated
with increased risk (P < 0.02). A protective effect of fish
consumption and a detrimental effect of meat intake have
been suggested on the basis of earlier work and appear to be
biologically plausible. If corroborated by other studies,
these results could contribute to our understanding of the
nutritional influences on fetal brain development.
Pharoah, P. O. and T. Cooke (1996).
"Cerebral palsy and multiple births." Arch Dis Child Fetal
Neonatal Ed 75(3): F174-7.
AIM: To compare the birthweight
specific prevalence of cerebral palsy in singleton and
multiple births. METHODS: Registered births of babies with
cerebral palsy born to mothers resident in the counties of
Merseyside and Cheshire during the period 1982 to 1989 were
ascertained. RESULTS: The crude prevalence of cerebral palsy
was 2.3 per 1000 infant survivors in singletons, 12.6 in
twins, and 44.8 in triplets. The prevalence of cerebral
palsy rose with decreasing birthweight. The birthweight
specific prevalence among those of low birthweight < 2500 g
was not significantly different in singleton than in
multiple births. Among infants weighing > or = 2500 g, there
was a significantly higher risk in multiple than in
singleton births. The higher crude cerebral palsy prevalence
in multiple births is partly due to the lower birthweight
distribution and partly due to the higher risk among normal
birthweight infants. CONCLUSIONS: Multiple birth babies are
at increased risk of cerebral palsy. There is also an
increased risk of cerebral palsy within a twin pregnancy if
the co-twin has died in utero.
Redline, R. W. and M. A. O'Riordan (2000).
"Placental lesions associated with cerebral palsy and
neurologic impairment following term birth." Arch Pathol Lab
Med 124(12): 1785-91.
OBJECTIVE: The aim of this study
was to determine the association of placental findings with
cerebral palsy and related forms of neurologic impairment
(NI) following birth at > or =37 weeks gestation (term).
DESIGN: In a retrospective comparison, placentas from 40
term infants with NI ascertained on the basis of clinicopathologic review for medicolegal consultation were
compared with placentas from 176 consecutive meconium-stained
term infants at low risk for NI. RESULTS: After
stratification for severity, 9 lesions were significantly
increased in placentas from infants with NI: 5 lesions
generally considered to occur within days of the time of
labor and delivery (meconium-associated vascular necrosis,
severe fetal chorioamnionitis, chorionic vessel thrombi,
increased nucleated red blood cells, and findings consistent
with abruptio placenta) and 4 lesions generally believed to
have their onset long before labor and delivery (diffuse
chronic villitis, extensive avascular villi, diffuse
chorioamnionic hemosiderosis, and perivillous fibrin).
Findings independently associated with NI by logistic
regression in this descriptive study were severe fetal
chorioamnionitis (odds ratio [OR], 13.2; 95% confidence
interval [CI], 1.2-144); extensive avascular villi (OR, 9.0;
95% CI, 1.6-51); and diffuse chorioamnionic hemosiderosis
(OR, 74.8; 95% CI, 6.3-894). The risk of NI increased as a
function of the number of lesions present (OR, 10.1; 95% CI,
5.1-20 for each additional lesion), particularly when
lesions generally considered to occur near the time of labor
and those believed to occur well before labor were found in
the same placenta (OR, 94.2; 95% CI, 11.9-747). CONCLUSIONS:
These findings suggest that placental pathology can
contribute to an understanding of the mechanisms that
contribute to NI at term.
Stanley, F. J. (1997). "Prenatal
determinants of motor disorders." Acta Paediatr Suppl 422:
92-102.
Cerebral palsies (CP) are the
commonest childhood motor disorders, originating in early
childhood as a result of interference in the developing
brain. Identifying prenatal factors in CP is a challenge
because there is a considerable period of time (years)
between the causal event(s) and diagnosis. Four fascinating
"natural" situations provided a unique opportunity to
identify and measure prenatal exposures in relation to motor
disorders, thus establishing the unequivocal role of some
factors. However, the majority of studies determining
adverse reproductive effects of environmental factors
require a retrospective case-control approach, which present
considerable problems. Studies based on the Western
Australian CP register suggest that prenatal factors singly
or in complex sequences are more common as causes than those
occurring perinatally or postnatally. In future, better
diagnosis of motor disorders, use of sophisticated
scientific techniques to identify markers of neuronal
development and the accurate linkage of these findings to
clinical patterns of motor dysfunction are required.
Yokoyama, Y., T. Shimizu, et al. (1995).
"Prevalence of cerebral palsy in twins, triplets and
quadruplets." Int J Epidemiol 24(5): 943-8.
BACKGROUND. Twins and triplets
are at higher risk of cerebral palsy than singletons. This
study investigated the degree of risk for cerebral palsy in
twins, triplets and quadruplets, and identified factors
associated with the increased risk. METHODS. The subjects
were recruited from the Kinki University Twin and Higher
Order Multiple Births Registry. RESULTS. The subjects were
705 twins pairs (1410 twins), 96 sets of triplets (287
triplets excluding one infant death), and 7 sets of
quadruplets (27 quadruplets excluding one infant death), who
were born after 1977. The prevalence of cerebral palsy was
0.9% among 1410 twins, 3.1% among 287 triplets, and 11.1%
among 27 quadruplets. Furthermore, the risks of producing at
least one child with cerebral palsy were 1.5%, 8.0%, 42.9%
in twin, triplet, quadruplet pregnancies, respectively.
After adjusting for each associated factor using logistic
regression, the risk of cerebral palsy was significantly
associated with decrease in gestational age and asphyxia.
The odds ratio indicated that infants whose gestational age
was < 32 weeks were 20 times more likely to develop cerebral
palsy than infants whose gestational age was > or = 36
weeks. CONCLUSIONS. The prevalence of cerebral palsy in
triplets and quadruplets was higher than that in twins.
Lower gestational age was associated with a greater risk of
cerebral palsy.
Yudkin, P. L., A. Johnson, et al. (1995).
"Assessing the contribution of birth asphyxia to cerebral
palsy in term singletons." Paediatr Perinat Epidemiol 9(2):
156-70.
In a geographically-based study,
we investigated the risk of cerebral palsy following intrapartum asphyxia at term, and the contribution of
intrapartum asphyxia at term to the overall rate of cerebral
palsy. We used stringent criteria for identifying
intrapartum asphyxia, while recognising that the initial
hypoxial insult might have occurred in the antenatal period.
In the first part of the investigation, a cohort of 160
term, singleton infants, with a low (< or = 3) 1-minute
Apgar score, was followed to the age of 5 years. Six infants
in the cohort had presumed intrapartum asphyxia, of whom two
died in the neonatal period, three had spastic
quadriparesis, profound developmental delay and visual
impairment, and one was unimpaired. The frequency of
cerebral palsy associated with birth asphyxia was estimated
as one in 3700 full-term livebirths. To assess the impact of
birth asphyxia on the overall rate of cerebral palsy, all
cases of cerebral palsy born in the study period were
identified. Of the 30 cases, the three identified in the
follow-up study were the only ones whose impairment could be
attributed to birth asphyxia in a full-term birth. Birth
asphyxia at term therefore was associated with 10% [95%
confidence interval (CI) 2.1, 26.5] of all cases of cerebral
palsy and with 20% (95% CI 4.3, 48.1) of the 15 cases of
cerebral palsy in children born at term.
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