Web neck anomaly and its association with congenital heart disease.

To investigate the relationship between congenital heart disease and jugular lymphatic obstruction as manifested in web neck anomaly, we used the Iowa Birth Defects Registry to determine the incidence of congenital heart defects (CHD) in infants with and without web neck. Sixty percent of infants with web neck had CHD, with a high incidence of flow-related defects such as hypoplastic left heart, coarctation, and secundum atrial septal defect. Sixty-eight percent of infants with web neck had a genetic syndrome (37% Down syndrome, 13% Ullrich-Turner syndrome, and 5% Noonan syndrome), and 24% had dysmorphic features consistent with lymphatic obstruction sequence. When infants with Down, Ullrich-Turner, and Noonan syndrome and web neck were compared to infants with the same syndrome but without web neck, those with web neck were significantly more likely to have flow-related heart defects. Infants with Ullrich-Turner syndrome and web neck had an 11-fold higher incidence of coarctation, compared to those with a normal neck. Our data suggests web neck is associated with both flow and nonflow-related heart defects. This association implies a pathogenetic relationship and appears to be independent of causal factors. The finding of web neck or nuchal cystic hygroma on a prenatal ultrasound or newborn examination should prompt a search for CHD.

Role of amniotic fluid homocysteine level and of fetal 5, 10-methylenetetrahydrafolate reductase genotype in the etiology of neural tube defects.

A mutation in the gene 5,10-methylenetetrahydrofolate reductase (MTHFR), leading to altered homocysteine metabolism, has been identified in parents and fetuses with fetal neural tube defects. We sought to determine which is of greater importance in fetal neural tube defect formation: the fetal MTHFR mutation or elevated amniotic fluid homocysteine level. We retrieved stored amniotic fluid from cases of isolated fetal neural tube defect diagnosed from 1988 to 1998 (n = 80), and from normal controls matched for race, month and year of amniocentesis, and maternal age. The presence or absence of the 677C-->T mutation of MTHFR was determined and homocysteine levels were measured; cases and controls were compared. Significantly more cases than controls were heterozygous or homozygous for the 677C-->T MTHFR mutation (44% vs 17%, P < or = 0.001). Cases were also significantly more likely than controls to have an amniotic fluid homocysteine level above the 90th centile (>1.85 micromol per liter); 27% vs 10%, P = 0.02. Thirty one cases and 12 controls had an abnormal genotype; however, amniotic fluid homocysteine levels were not significantly different between these two groups (6/31, or 19% of cases had an elevated homocysteine compared to 1/12, or 8% of controls; P = 0.65). In contrast, 40 cases and 60 controls had a normal genotype; the neural tube defect cases had significantly higher homocysteine levels (13/40, or 32% of cases had an elevated homocysteine level compared to only 6/60, or 10% of controls; P = 0.008). Although both abnormal fetal MTHFR genotype and abnormal amniotic fluid homocysteine concentration are significantly associated with neural tube defects, the association with amniotic fluid homocysteine concentration is significant regardless of the fetal MTHFR genotype. The relationship between maternal and fetal homocysteine metabolism is complex.

Unique phenotype associated with a pericentric inversion of chromosome 6 in three generations.

We observed a pericentric inversion of chromosome 6 in three generations of one family. Carriers had several phenotypic alterations including congenital cataracts, hearing loss, dental anomalies, ear anomalies, premature graying, unilateral strabismus, coloboma, and mild mental retardation. These manifestations may all be explained by a failure or delay in development of tissues derived from neural crest cells and are similar to these seen in the Rieger syndrome. The description of this family extends the known phenotypic abnormalities associated with alterations of chromosome 6.

Amniotic fluid homocysteine levels, 5,10-methylenetetrahydrafolate reductase genotypes, and neural tube closure sites.

A specific gene mutation leading to altered homocysteine metabolism has been identified in parents and fetuses with neural tube defects (NTDs). In addition, current animal and human data indicate that spine closure occurs simultaneously in five separate sites that then fuse. We sought to determine whether either this mutation or abnormal amniotic fluid homocysteine levels are associated with all five neural tube closure sites. We retrieved stored amniotic fluid from cases of isolated fetal neural tube defect diagnosed from 1988 to 1998 (n = 80) and from normal controls matched for race, month and year of amniocentesis, and maternal age. Cases were categorized according to defect site by using all available medical records. The presence or absence of the 677C-->T mutation of 5, 10-methylenetetrahydrafolate reductase (MTHFR) gene was determined, and homocysteine levels were measured; case and controls were compared. Significantly more cases than controls were heterozygous or homozygous for the 677C-->T MTHFR mutation (44% vs. 17%, P < or = 0. 001). Likewise, cases were significantly more likely than controls to have amniotic fluid homocysteine levels >90th centile (>1.85 micromol/L), 27% vs. 10%, P = 0.02. Most (83%) of control cases had both normal MTHFR alleles and normal amniotic fluid homocysteine levels (normal/normal), whereas only 56% of NTD case were normal/normal (P = 0.001). When evaluated by defect site, only defects involving the cervical-lumbar spine, lumbosacral spine, and occipital encephalocele were significantly less likely to be normal/normal than controls (P = 0.007, 0.0003, and 0.007, respectively), suggesting a strong association with the 677C-->T allele. In contrast, anencephaly, exencephaly, and defects confined to the sacrum included many cases that had both normal MTHFR alleles and normal homocysteine and were not significantly different from controls. The 677C-->T MTHFR mutation and elevated homocysteine levels appear to be disproportionately associated with defects spanning the cervical-lumbar spine, lumbosacral spine, and occipital encephalocele. In contrast, anencephaly, exencephaly, and defects confined to the sacrum may not be related to altered homocysteine metabolism.

The prevention of meconium aspiration in labor using amnioinfusion.

In an effort to improve maternal and fetal outcome in patients laboring with thick meconium, 85 patients presenting with thick meconium were randomized to receive either amnioinfusion with 1000 mL normal saline initially and every 6 hours until delivery, or routine care. Meconium was discovered on initial examination during labor, after artificial rupture of membranes, through the use of an intrauterine pressure catheter, or on amniocentesis. Labor management was otherwise routine. Forceps operations and cesarean sections were for distress or failure to progress, as indicated. Patients receiving amnioinfusion had significantly fewer low 1-minute Apgar scores, less meconium below the cords, and a significantly lower incidence of operative delivery. The only three cases of meconium aspiration syndrome occurred in infants delivered of patients receiving routine management. No adverse side effects of amnioinfusion were detected. Amnioinfusion is a simple, inexpensive, and safe technique that reduces the incidence of meconium below the cords and improves obstetric outcome in patients laboring with thick meconium.

Determination of the seroprevalence of human immunodeficiency virus infection in gravidas by non-anonymous versus anonymous testing.

From February 16, 1988 to July 15, 1988, a prospective study was undertaken at the University of Illinois Hospital in Chicago to do the following: 1) determine the seroprevalence of human immunodeficiency virus (HIV) infection among our gravid patients, 2) test the hypothesis that methodical counseling would elicit a more thorough recounting of risk factors, and 3) test the hypothesis that those patients who self-identify risk factors represent only a fraction of HIV-positive gravidas. After educational counseling regarding HIV infection, 349 clinic patients (34%) requested non-anonymous HIV testing (group I). Risk factor histories were recorded from these women. Simultaneously, 849 women admitted to labor and delivery were queried with regard to the same risk factors but without preliminary counseling, and then tested anonymously (group II). Nineteen percent (63 of 349) of group I reported risk factors, whereas only 9.6% (82 of 849) of group II reported similar risks (P less than .0001). Two HIV-positive patients were identified in group I, both of whom reported risk factors (seroprevalence 0.6%). Nine HIV-positive patients were detected in group II, but only four reported risk factors (seroprevalence 1.1%). We conclude that methodical counseling may elicit increased reporting of HIV risk factors as compared with questioning without preliminary counseling. Because many HIV-positive patients may be unable or unwilling to report risk factors, selective voluntary testing will not identify all HIV-positive gravidas.

Second-trimester maternal serum CA-125 versus estriol in the multiple-marker screening test for Down syndrome.

OBJECTIVE: To determine the ability of second-trimester maternal serum CA-125 levels to detect fetal Down syndrome. METHODS: From stored, second-trimester maternal serum analyzed previously with the multiple-marker screening test for fetal Down syndrome, we selected 306 samples from euploid pregnancies and 22 samples from Down syndrome pregnancies at 14-20 weeks' gestation. CA-125 levels were measured by enzyme-linked immunosorbent assay and converted to gestational week-specific multiples of the median (MoM). RESULTS: The mean maternal age (+/- standard deviation) of the study population was 35.5 +/- 5.3 years. The Down syndrome group CA-125 mean MoM was significantly higher than the euploid group mean MoM (1.47 +/- 0.51 MoM versus 1.05 +/- 0.44 MoM; P < .001). CA-125 at or above 1.5 MoM identified 10 of 22 (45%) Down syndrome cases. Substituting CA-125 for estriol (E3) in the multiple-marker screening test resulted in a lower screen-positive rate (67 of 328, 20% [95% confidence interval {CI} 16, 25] versus 91 of 328, 28% [95% CI 23, 33]) with a similar Down syndrome detection rate (18 of 22, 82%). Alternatively, when the screen-positive rate was held constant, the Down syndrome detection rate improved (20 of 22, 91% [95% CI 71, 99] versus 18 of 22, 82% [95% CI 60, 95]). CONCLUSIONS: Down syndrome pregnancies have higher second-trimester maternal serum CA-125 levels than euploid pregnancies. CA-125 may be superior to E3 in the multiple-marker screening test for fetal Down syndrome.

Ultrasound findings and multiple marker screening in trisomy 18.

OBJECTIVE: To compare detection of trisomy 18 in the second trimester by ultrasound and multiple-marker testing. METHODS: A computerized genetics database was used to identify fetuses of 14-22 weeks' gestation who had comprehensive ultrasound examinations, multiple-marker screening tests (alpha-fetoprotein [AFP]), hCG, unconjugated estriol [E3], and trisomy 18 karyotype. A positive trisomy 18 screen was defined as AFP up to 0.75 multiples of the median (MoM), hCG up to 0.55 MoM, and unconjugated E3 up to 0.60 MoM. A risk of at least 1:190 defined a positive Down syndrome screen. Ultrasound abnormalities were diagnosed prospectively and were confirmed later by retrospective review of sonographic images. RESULTS: From 1988-1997, 30 trisomy 18 fetuses who had comprehensive ultrasounds and multiple-marker testing were identified. Twenty-one (70%) had abnormalities detected by ultrasound, of which the most common isolated finding was choroid plexus cyst. Eleven fetuses (37%) had positive trisomy 18 screens, and two had positive Down syndrome screens, for a total of 13 of 30 (43%) fetuses with positive multiple-marker screening tests. CONCLUSION: We found that ultrasound was more likely to be abnormal than multiple-marker screening tests in fetuses with trisomy 18 (70%) (95% confidence interval [CI] 54, 86 versus 43% CI 25, 61). However, combining the two testing methods yielded the highest detection rate (80% [CI 66%, 94%]).

Antenatal treatment of fetal alloimmune thrombocytopenia.

OBJECTIVE: To review our experience with, and to evaluate the efficacy of, antenatal pharmacologic treatment of pregnancies complicated by alloimmune thrombocytopenia. METHODS: We reviewed the records of six pregnancies complicated by alloimmune thrombocytopenia recently cared for at the University of Iowa Fetal Diagnosis and Treatment Unit. All patients had a history consistent with alloimmune thrombocytopenia in a previous gestation. All fetuses had thrombocytopenia on funipuncture at 20-32 weeks' gestation, and all patients and fetuses demonstrated a platelet antigen incompatibility. Three women initially received weekly gamma globulin infusions, two received gamma globulin and dexamethasone, and one had no initial treatment but was given gamma globulin and dexamethasone at 32 weeks' gestation. Repeat funipuncture was performed at 3.5- to 7-week intervals, and therapeutic modifications were made as necessary. RESULTS: In five cases, the last funipuncture before delivery documented platelet counts adequate for vaginal delivery. One woman, who received gamma globulin alone with good initial response, was delivered by cesarean for a platelet count of 25,000/microL at 39 weeks. Following delivery, all infants were thoroughly evaluated, and none had evidence of intracranial hemorrhage or other alloimmune thrombocytopenia-associated morbidity. All had normal platelet counts at discharge from the hospital. CONCLUSIONS: Our experience confirms the efficacy of gamma globulin treatment, but indicates that not all fetuses will respond to it alone. Serial funipunctures are essential to evaluate patient response and allow appropriate therapeutic modifications. Randomized studies are needed to determine the optimal antenatal pharmacologic therapy for this disease.

Diverse maternal and fetal pathology associated with absent diastolic flow in the umbilical artery of high-risk fetuses.

Twenty-two of approximately 450 high-risk pregnancies referred to a regional center for a level II sonographic examination after 20 weeks' gestation were characterized by absent or reversed diastolic flow in the umbilical artery. Ten fetuses had congenital malformations or were aneuploid. Ten were growth-retarded in association with other problems: maternal hypertension, preeclampsia, cyanotic heart disease, elevated maternal serum alpha-fetoprotein levels, or twin gestation. In two cases, no etiology could be identified. Knowledge of the fetal karyotype, fetal anatomy, gestational age, maternal disease, and fetal status as determined by other tests of fetal well-being was required to optimize outcome in each case. In view of the heterogeneous etiologies of absent or reversed diastolic flow, management of such cases must be individualized.

Prognostic significance of unexplained elevated amniotic fluid alpha-fetoprotein.

OBJECTIVE: To compare the prognostic values of unexplained elevated amniotic fluid alpha-fetoprotein (AF AFP > or = 2.0 multiples of the median [MoM]) and unexplained elevated maternal serum alpha-fetoprotein (MSAFP > or = 2.5 MoM). METHODS: We accessed a data base containing the results of MSAFP screening tests, genetic amniocenteses, and pregnancy outcome data on all women undergoing second-trimester genetic amniocentesis from October 1988 through August 1994. After excluding all patients whose elevated AFP levels had any identifiable cause (positive AF acetylcholinesterase, AF blood contamination, fetal malformation or aneuploidy, multiple gestation, etc), 5743 cases were analyzed. Relative risks (RR) for selected pregnancy complications were determined. RESULTS: Elevated MSAFP, with any AF AFP, was associated with fetal growth restriction (RR 2.5, 95% confidence interval [CI] 1.4-4.4), stillbirth (RR 3.5, 95% CI 1.4-8.3), preeclampsia (RR 2.8, 95% CI 1.1-7.0), and preterm delivery (RR 2.8, 95% CI 2.3-3.4). Elevated AF AFP, with any MSAFP, was associated with preeclampsia (RR 4.4, 95% CI 2.0-10.0) and preterm delivery (RR 1.7, 95% CI 1.3-2.4). Elevation of both AF AFP and MSAFP was associated with preterm delivery (RR 4.0, 95% CI 2.8-5.7). When elevated AF AFP was found in association with a normal MSAFP, the RR to develop preeclampsia was 4.6 (95% CI 1.9-11.2). CONCLUSION: Maternal serum alpha-fetoprotein is a better predictor of late pregnancy complications than AF AFP. However, unexplained elevated AF AFP appears to be especially predictive of preeclampsia.

Antenatal screening for factor V Leiden mutation: a critical appraisal.

Thromboembolic disease is a leading cause of maternal mortality in the United States. Recently, inherited resistance to activated protein C has been recognized as a major risk factor for thrombosis and has been demonstrated in 20-60% of patients with clinically evident thrombosis. The factor V Leiden mutation, which is readily detectable by molecular DNA techniques, is responsible for 90-95% of cases of activated protein C resistance. Because 5% of whites and 1% of blacks in the United States are heterozygous for the Leiden mutation, at least one group has suggested that screening of asymptomatic gravidas for the mutation should be considered. Therefore, we conducted a combined MEDLINE and bibliographic literature search for relevant data and evaluated screening for the factor V Leiden mutation in the context of well-elucidated desirable characteristics for a successful screening program. Based on this evaluation, we conclude that routine antenatal screening for the factor V Leiden mutation cannot be recommended at the present time.

Free beta-hCG subunit versus intact hCG in Down syndrome screening.

OBJECTIVE: To assess the ability of second-trimester maternal serum free beta-hCG to detect fetal Down syndrome and to compare free beta-hCG to intact hCG in the multiple-marker screening test for Down syndrome. METHODS: From our bank of stored maternal sera, we selected 40-50 samples from euploid pregnancies at each week of gestation from 14 to 20 weeks and 31 samples from Down syndrome pregnancies. Free beta-hCG was measured by enzyme-linked immunosorbent assay, and week-specific multiples of the median (MoM) were derived. The free beta-hCG Down syndrome detection and false-positive rates were determined. Free beta-hCG was then substituted for intact hCG in the multiple-marker screening test, and the Down syndrome detection and false-positive rates at various risk cutoffs were compared. RESULTS: The mean (+/-standard deviation) maternal age of all study samples was 35.6 +/- 5.3 years. The mean Down syndrome free beta-hCG MoM was significantly higher than the mean euploid MoM (2.4 +/- 1.1 versus 1.2 +/- 1.0; P < .001). A free beta-hCG level of at least 1.7 MoM identified 68% of Down syndrome pregnancies at a false-positive rate of 20%. When intact hCG was replaced with free beta-hCG in the multiple-marker screening test, a higher Down syndrome detection rate was achieved at a lower false-positive rate at each of several screen positive risk cutoffs. CONCLUSION: Elevated free beta-hCG levels identify Down syndrome pregnancies. Replacing intact hCG with free beta-hCG in the multiple-marker screening test results in a higher Down syndrome detection rate at a lower false-positive rate.

Insulin-like growth factor binding protein-3 in the detection of fetal Down syndrome pregnancies.

OBJECTIVE: To study the usefulness of maternal serum insulin-like growth factor binding protein-3, a potential cell growth inhibitor, in second trimester prenatal screening for fetal Down syndrome. METHODS: Three hundred and forty-two samples from normal pregnancies and nine fetal Down syndrome pregnancies were analyzed for insulin-like growth factor binding protein-3 levels by radioimmunoassay. Data were converted to multiples of median (MoM) and analyzed statistically to compare the differences between control and Down syndrome pregnancies. RESULTS: The mean insulin-like growth factor binding protein-3 MoM of Down syndrome-affected pregnancies (1.09) was significantly higher than that of the normal pregnancies (1.00) (P < .01). Insulin-like growth factor binding protein-3, in combination with maternal serum alpha-fetoprotein (MSAFP), hCG, and maternal age, detected 89% of Down syndrome pregnancies at a screen positive rate of 2.1%. This compares favorably to the standard combination of MSAFP, hCG, and unconjugated estriol (E3), which had a 66.7% Down syndrome detection rate and a 4.1% screen positive rate in our study samples. CONCLUSION: This retrospective analysis suggested that the inclusion of insulin-like growth factor binding protein-3 into the triple screen program to replace unconjugated E3 might enhance the detection rate of fetal Down syndrome pregnancies. These data need to be confirmed by a larger prospective study.

Value of perinatal autopsy.

OBJECTIVE: To determine how often a perinatal autopsy identified the cause of death, and how frequently this information changed recurrence risk estimates or altered parental counseling. METHODS: We reviewed all autopsies of fetal stillbirths and briefly viable neonates performed by one perinatal pathologist at the University of Alabama Hospital from 1992 to 1994. RESULTS: Four hundred sixteen fetal and early neonatal deaths occurred at our hospital from January 1, 1992, to June 1, 1994. Consent for an autopsy examination was granted for 139 of these (33%), and all autopsies were performed by a single perinatal pathologist. Abnormalities likely to be the cause of death were identified in 130 of 139 cases (94%). Ninety-one subjects did not have structural anomalies: In 14 cases autopsy revealed previously unsuspected pathology that altered parental counseling; in 68 cases autopsy findings were consistent with the clinical obstetrical diagnosis; and in nine cases the cause of death could not be identified. Forty-eight subjects were anomalous. Thirty-seven of these (79%) had been evaluated by antenatal ultrasonography, and autopsy identified additional abnormalities in 51% (19 of 37). In the 11 deaths evaluated neonatally, a previously unsuspected diagnosis likely to be the cause of death was identified in three. Overall, autopsy findings changed recurrence risk estimates and/or parental counseling in 36 of 139 cases (26%). CONCLUSION: The cause of fetal or perinatal death was determined by autopsy in 94% of cases in our series. Counseling and recurrence risk estimates were altered by autopsy findings in 26%.

Frequency, distribution, and theoretical mechanisms of hematologic and weight discordance in monochorionic twins.

OBJECTIVE: The purpose of this study was to determine the frequency, distribution, and most likely etiology of hematologic and weight discordance in pathologically proven monochorionic twins, and to use this information to reevaluate the neonatally derived definition of the twin-twin transfusion syndrome. METHODS: We reviewed our experience with 97 pathologically proven monochorionic twin pregnancies. The frequency and distribution of weight and hemoglobin-hematocrit (hb-hct) discordance were determined for all twin pairs. Factors that may have contributed to the discordance were identified, and theoretical mechanisms were proposed. RESULTS: All combinations of weight and hb-hct discordance were observed. Thirty-four twin pairs (35%) were discordant for weight. In half of these (17 of 34), the hb and hct were concordant. In 18% (six of 34), the smaller twin had the higher hb-hct, and in 32% (11 of 34), the smaller twin had the lower hb-hct. Twenty-three of 63 size-concordant pairs (36%) were discordant for hb-hct. Ten infants were infected at birth, eight had malformations, and 25 likely suffered an acute transfusion event. CONCLUSIONS: Any combination of weight and hb-hct discordance can occur in monochorionic twins. Acute and chronic twin-twin transfusion, uteroplacental insufficiency, infection, malformations, or other factors may have accounted for the discordance observed. Thorough antenatal evaluation with invasive testing and marker studies (to identify a physiologically unbalanced placental anastomosis) may be necessary to establish an accurate diagnosis. We conclude that weight and/or hb-hct discordance is relatively common in monochorionic twins and in itself is not sufficient to diagnose twin-twin transfusion.

Second-trimester cystic hygroma: prognosis of septated and nonseptated lesions.

OBJECTIVE: To compare karyotypic, ultrasonographic, and prognostic features of septated cystic hygromas and nonseptated cystic hygromas in second-trimester fetuses. METHODS: A computerized ultrasound data base was used to identify fetuses diagnosed with cystic hygromas at 14-22 weeks' gestation. Photographs from the initial ultrasound were reviewed retrospectively for hygroma type (septated or nonseptated) and any abnormal structural findings. Fetal karyotypes were obtained from amniotic fluid, aspiration of hygroma pouches, or fetal tissue culture. Pregnancy outcome information was obtained from hospital charts and physician office records. Ultrasound findings were then compared with fetal karyotype results and pregnancy outcome data. RESULTS: From 1990 to 1995, 61 fetuses with cystic hygromas were identified. Karyotypes were obtained in 55 fetuses, and pregnancy outcome was available for 59. Abnormal karyotype was present in 42 of 55 fetuses (76%). The most common chromosomal abnormality in septated hygromas was the 45,X karyotype. Trisomy 21 was the most common chromosomal abnormality in nonseptated hygromas. Compared with fetuses with nonseptated cystic hygromas, those with septated cystic hygromas were more likely to be aneuploid (33 of 39 [85%] versus nine of 16 [56%]; P = .03), more likely to develop hydrops (27 of 45 [60%] versus three of 16 [19%]; P = .005), and less likely to be live-born (one of 44 [2%] versus four of 15 [27%]; P = .01). CONCLUSIONS: Fetuses with septated cystic hygromas are more likely to be aneuploid and to develop hydrops, and thus are less likely to be survive than fetuses with nonseptated hygromas.

Amniotic fluid embolism after saline amnioinfusion: two cases and review of the literature.

BACKGROUND: Amnioinfusion is an intrapartum intervention with proven benefit in certain clinical situations. It is thought to be a safe treatment with few adverse effects. CASES: Two cases of fatal amniotic fluid (AF) embolism occurred in women who were treated during labor with a saline amnioinfusion. In both cases, amnioinfusion was administered after finding thick meconium staining of the AF. In addition to the amnioinfusion, common factors in these cases and three previously reported AF embolisms associated with amnioinfusion are the presence of rapid labor, meconium-stained fluid, or both. CONCLUSIONS: Amniotic fluid embolism is a rare cause of maternal morbidity and mortality. It is not known whether amnioinfusion increases the rate of its occurrence in laboring patients. No change in clinical practice is warranted on the basis of these reports; however, future reports must be examined so that any common factors can be identified.

Magnetic resonance imaging of fetuses with intracranial defects.

Thirteen women whose fetuses had intracranial defects on ultrasound examination were offered magnetic resonance imaging (MRI) without charge. All fetuses were paralyzed with pancuronium before the study, which lasted approximately 1 hour. With the mother in the left lateral decubitus position to minimize transmitted maternal aortic pulsation, T1-weighted images were obtained using a Picker 0.5-tesla superconductive unit. Magnetic resonance imaging provided excellent detail of intracranial anatomy in all cases. In four of the 13 fetuses, the MRI diagnosis differed from that of ultrasound and ultimately proved correct. In another three, MRI added greatly to the ultrasound diagnosis by delineating intracranial anatomy more precisely. In the remaining six cases, MRI confirmed the ultrasound impression. For circumstances in which the ultrasound diagnosis is unclear or antenatal intervention might require exact knowledge of anatomical detail, the additional information provided by MRI may justify its cost.