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Welcome to The Visible Embryo, a comprehensive educational resource on human development from conception to birth.

The Visible Embryo provides visual references for changes in fetal development throughout pregnancy and can be navigated via fetal development or maternal changes.

The National Institutes of Child Health and Human Development awarded Phase I and Phase II Small Business Innovative Research Grants to develop The Visible Embryo. Initally designed to evaluate the internet as a teaching tool for first year medical students, The Visible Embryo is linked to over 600 educational institutions and is viewed by more than one million visitors each month.

Today, The Visible Embryo is linked to over 600 educational institutions and is viewed by more than 1 million visitors each month. The field of early embryology has grown to include the identification of the stem cell as not only critical to organogenesis in the embryo, but equally critical to organ function and repair in the adult human. The identification and understanding of genetic malfunction, inflammatory responses, and the progression in chronic disease, begins with a grounding in primary cellular and systemic functions manifested in the study of the early embryo.

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Pregnancy Timeline by SemestersFetal liver is producing blood cellsHead may position into pelvisBrain convolutions beginFull TermWhite fat begins to be madeWhite fat begins to be madeHead may position into pelvisImmune system beginningImmune system beginningPeriod of rapid brain growthBrain convolutions beginLungs begin to produce surfactantSensory brain waves begin to activateSensory brain waves begin to activateInner Ear Bones HardenBone marrow starts making blood cellsBone marrow starts making blood cellsBrown fat surrounds lymphatic systemFetal sexual organs visibleFinger and toe prints appearFinger and toe prints appearHeartbeat can be detectedHeartbeat can be detectedBasic Brain Structure in PlaceThe Appearance of SomitesFirst Detectable Brain WavesA Four Chambered HeartBeginning Cerebral HemispheresFemale Reproductive SystemEnd of Embryonic PeriodEnd of Embryonic PeriodFirst Thin Layer of Skin AppearsThird TrimesterSecond TrimesterFirst TrimesterFertilizationDevelopmental Timeline
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Home | Pregnancy Timeline | News Alerts |News Archive Sep 10, 2013


Current findings indicate that poor fetal growth and birth
defects may greatly contribute to cerebral palsy and infant death,
suggesting that research should focus more on those specific risk factors.

WHO Child Growth Charts




Risk factors for cerebral palsy and infant death

Scientists from NIH and Australia investigate risk factors that contribute to cerebral palsy and early infant death.

Karin B. Nelson, M.D., scientist emeritus at the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health, and her colleagues from the University of Sydney, the University of Western Australia and Sydney Adventist Hospital in Australia examined the degree to which four specific risk factors contributed to cerebral palsy and young infant death.

The risk factors were asphyxial birth events (incidences during labor and delivery that had the potential to interfere with oxygen getting to the newborn's brain), inflammation (signs of infection), birth defects, and poor fetal growth (low birth weight plus some other factors related to expected size).

Cerebral palsy is a group of neurological disorders that appear in early childhood and affect body movement and muscle coordination. Movement problems associated with cerebral palsy include dyskinesia (uncontrollable writhing or jerky movements) and spastic quadriplegia (severe stiffness in the limbs).

In this study, published in Obstetrics & Gynecology, the researchers compared the medical records of children with cerebral palsy and infants who died within 1 month of birth with the records of healthy children to identify how often the risk factors occurred in the groups.

Among the cerebral palsy and infant death cases, birth defects and poor fetal growth were the most common risk factors. Birth defects and/or poor fetal growth were seen in almost half of the cerebral palsy cases. In addition, out of the four risk factors, only birth defects and/or poor fetal growth predicted dyskinesia or quadriplegia.

Many studies looking into the causes of cerebral palsy have concentrated on asphyxial birth events. However, the current findings indicate that poor fetal growth and birth defects may greatly contribute to cerebral palsy and infant death, suggesting that research should focus more on those specific risk factors.

OBJECTIVE: To examine the antecedents of cerebral palsy and of perinatal death in singletons born at or after 35 weeks of gestation.

METHODS: From a total population of singletons born at or after 35 weeks of gestation, we identified 494 with cerebral palsy and 508 neonates in a matched control group, 100 neonatal deaths, and 73 intrapartum stillbirths (all deaths in selected birth years). Neonatal death and cerebral palsy were categorized as without encephalopathy, after neonatal encephalopathy, or after neonatal encephalopathy considered hypoxic-ischemic. We examined the contribution of potentially asphyxial birth events, inflammation, fetal growth restriction, and birth defects recognized by age 6 years to each of these outcomes and to intrapartum stillbirths.

RESULTS: The odds of total cerebral palsy after potentially asphyxial birth events or inflammation were modestly increased (odds ratio [OR] 1.9, 95% confidence interval [CI] 1.1-3.2 and OR 2.2, 95% CI 1.0-4.2, respectively). However, potentially asphyxial birth events occurred in 34% of intrapartum stillbirths and 21.6% of cerebral palsy after hypoxic-ischemic encephalopathy. Inflammatory markers occurred in 13.9% and 11.9% of these outcomes, respectively. Growth restriction contributed significantly to all poor outcome groups. Birth defects were recognized in 5.5% of neonates in the control group compared with 60% of neonatal deaths and more than half of cases of cerebral palsy without hypoxic-ischemic encephalopathy. In children with cerebral palsy, a potentially asphyxial birth event, inflammation, or both were experienced by 12.6%, whereas growth restriction, a birth defect, or both were experienced by 48.6% (P<.001).

CONCLUSION: Fetal growth restriction and birth defects recognized by age 6 years were more substantial contributors to cerebral palsy and neonatal death than potentially asphyxial birth events and inflammation.


(C) 2013 by The American College of Obstetricians and Gynecologists.

For more information about cerebral palsy, please visit:

NINDS is the nation's leading funder of research on the brain and nervous system. The NINDS mission is to reduce the burden of neurological disease – a burden borne by every age group, by every segment of society, by people all over the world.

About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www.nih.gov.

Original press release:http://www.eurekalert.org/pub_releases/2013-09/nion-cio090413.php