Potentially asphyxiating conditions and spastic cerebral palsy in
infants of normal birth weight
Karin B. Nelson, MD, and Judith K. Grether, PhD
Bethesda, Maryland, and Emeryville, California
OBJECTIVE: Our purpose was to examine the association of cerebral palsy with conditions that can inter-
rupt oxygen supply to the fetus as a primary pathogenetic event.
STUDY DESIGN: A population-based case-control study was performed in four California counties, 1983
through 1985, comparing birth records of 46 children with disabling spastic cerebral palsy without recognized
prenatal brain lesions and 378 randomly selected control children weighing ≥2500 g at birth and surviving to
age 3 years.
RESULTS: Eight of 46 children with otherwise unexplained spastic cerebral palsy, all eight with quadriplegic
cerebral palsy, and 15 of 378 controls had births complicated by tight nuchal cord (odds ratio for quadriplegia
18, 95% confidence interval 6.2 to 48). Other potentially asphyxiating conditions were uncommon and none
was associated with spastic diplegia or hemiplegia. Level of care, oxytocin for augmentation of labor, and
surgical delivery did not alter the association of potentially asphyxiating conditions with spastic quadriplegia.
Intrapartum indicators of fetal stress, including meconium in amniotic fluid and fetal monitoring abnormalities,
were common and did not distinguish children with quadriplegia who had potentially asphyxiating conditions
from controls with such conditions.
CONCLUSION: Potentially asphyxiating conditions, chiefly tight nuchal cord, were associated with an appre-
ciable proportion of unexplained spastic quadriplegia but not with diplegia or hemiplegia. Intrapartum abnor-
malities were common both in children with cerebral palsy and controls and did not distinguish between
them. (Am J Obstet Gynecol 1998;179:507-13.)
Key words: Birth asphyxia, tight nuchal cord, maternal infection, Apgar scores, neonatal seizures,
Approximately 1 of 1500 infants born weighing ≥2500 g
has disabling cerebral palsy.
Cerebral palsy in infants of
normal birth weight has greatly influenced medical practice
because of the assumption that this disorder is chiefly the
result of asphyxial birth and is preventable if detected early.
This assumption has been an important factor in the devel-
opment and widespread use of electronic fetal monitoring
and other forms of antenatal and intrapartum surveillance
and has influenced the rate of surgical delivery.
In spite of
these changes in medical management, the cerebral palsy
rate in term infants has not declined in recent decades.
Assessment of the contribution of asphyxial events to
cerebral palsy is complicated by the fact that there is no
generally available tool for direct measurement of birth
asphyxia. In the absence of a validated means for its
recognition, birth asphyxia is commonly diagnosed on
the basis of fetal or neonatal signs such as abnormalities
on electronic fetal monitoring, low Apgar scores, need
for respiratory support, and neonatal encephalopathy.
The specificity of these signs to asphyxial states has not
It is not known how much of perinatal hypoxia or is-
chemia, when present, is primary and how much is a
downstream consequence of other initiating pathologic
features. This distinction is potentially important be-
cause identification of factors that initiate pathogenesis
may influence strategies for primary prevention.
In a large cohort of births in the mid-1980s we
sought to evaluate the contribution of birth asphyxia to
From the Neuroepidemiology Branch, National Institute of Neurological
Disorders and Stroke,
and the California Birth Defects Monitoring
Program, California Department of Health Services.
Supported in part by a cooperative agreement with the Center for
Environmental Health and Injury Control, Centers for Disease
Control and Prevention, in part by funds from the Comprehensive
Environmental Response, Compensation, and Liability Act Trust Fund
through an interagency agreement with the Agency for Toxic Substances
and Disease Registry, Public Health Services, and in part by a contract
with the National Institute for Neurological Disorders and Stroke, con-
tract No. 263-95-CO255.
Received for publication October 15, 1997; revised January 10, 1998;
accepted January 15, 1998.
Reprint requests: Judith K. Grether, PhD, California Birth Defects
Monitoring Program, 1900 Powell St, Suite 1050, Emeryville, CA