Diámetro transverso del cerebelo fetal en la restricción del crecimiento intrauterino / Fetal cerebellum transverse diameter in intrauterine growth restriction

Evaluar el comportamiento de la biometría del cerebelo fetal en su diámetro transverso, en los casos con restricción del crecimiento intrauterino. Servicio de Perinatología, Hospital "Dr. Adolfo Prince Lara", Puerto Cabello. Estudio transversal, de correlación. En 1 569 fetos se realizó la biometría del diámetro transverso del cerebelo, para la construcción del nomograma del mismo. Se estableció una comparación entre los valores del diámetro transverso del cerebelo de 77 fetos con restricción del crecimiento fetal y los valores del nomograma, para establecer si existía o no afectación de este en la restricción del crecimiento fetal. Se observó un alto grado de correlación entre el diámetro transverso del cerebelo fetal y la edad gestacional r = 0,994732287, t= 6,36 P<0,001, se determinó el coeficiente de determinación r²= 0,9947, que indica que la variación de la edad gestacional explica el 99 por ciento de la variación del DTC. Se realizó el cálculo del coeficiente de regresión lineal, obteniéndose la ecuación siguiente: Y = 2,123082 +1,12981 x X, lo que deduce que el DTC aumenta 1,12 mm por cada semana de gestación. Las dos variables están linealmente relacionadas F = 97,8325 P<0,001. El error típico del diámetro transverso del cerebelo previsto para cada semana de gestación es ± 2,4 mm. No hubo diferencias entre el diámetro transverso del cerebelo de los fetos con restricción del crecimiento y los de peso adecuado, t = 0,84 P>0,05. El diámetro transverso del cerebelo no se afecta con los trastornos del crecimiento, por lo que resulta de gran utilidad en la determinación de la edad gestacional

Evaluate the modifications of the transverse diameter cerebellar biometry the IUGR cases. Perinatology Service, "Dr. Adolfo Prince Lara" Hospital, Puerto Cabello, Venezuela. It is a correlation transversal study. We did in 1 569 fetuses the transverse diameter cerebellar biometry, which helped us for the realization of the fetal. We established a comparison between the transversediameter cerebellar of the normal growing fetuses in relation with the gestational age to establish if there is affectation in the IUGR. We observed a high degree of correlation between the transverse diameter cerebellar and gestational age r = 0.994732287, t= 6.36 P<0.001. Determine the coefficient of determination r² = 0.9947, which indicates that the variation in gestational age explained 99 percent of the variation of the DTC. Is the coefficient of linear regression, yielding the following equation: Y= 2.123082 + 1.12981 x X, which permit deduct that the transverse diameter cerebellar increase 1.12 mm each week of gestation. The two variables are linear relationated F = 97.8325 P< 0.001, the preview typical mistake for each week of gestation is ± 2.4 mm. There were no observed differences between the transverse diameter cerebellar of the IUGR and the adequate weight fetuses t = 0.84 P>0.05. The transverse diameter cerebellar is not affected with the growing disorder which gives the great value of the utilization in the gestational age determination

Auditory neural maturation after exposure to multiple courses of antenatal betamethasone in premature infants as evaluated by auditory brainstem response.

OBJECTIVE: Our goal was to determine if multiple courses of antenatal betamethasone affect auditory neural maturation in 28 to 32 weeks' gestational age infants. PATIENTS AND METHODS: A retrospective cohort study was performed to compare auditory neural maturation between premature infants exposed to 1 course of betamethasone and infants exposed to > or = 2 courses of betamethasone. Inclusion criteria included all 28 to 32 weeks' gestational age infants delivered between July 1996 and December 1998 who had auditory brainstem response testing performed (80-dB click stimuli at a repetition rate of 39.9/second) within 24 hours of postnatal life as part of bilirubin-auditory studies. Infants with toxoplasmosis, rubella, cytomegalovirus, herpes infections, chromosomal disorders, unstable conditions, exposure to antenatal dexamethasone, and exposure to < 1 complete course of betamethasone were excluded. Auditory waveforms were categorized into response types on response replicability and peak identification as types 1 through 4 (type 1 indicating most mature). Absolute and interpeak wave latencies were measured when applicable. Categorical and continuous variables were analyzed by using the chi2 test and Student's t test, respectively. RESULTS: Of 174 infants studied, 123 received antenatal steroids. Of these, 50 received 1 course and 29 received > or = 2 courses of betamethasone. There were no significant differences in perinatal demographics between the 2 groups. After controlling for confounding variables, there was no significant difference in mean absolute wave latencies, mean interpeak latencies, or distribution of response type between the 2 groups. There also was no significant difference in any auditory brainstem response parameters between infants exposed to 1 course of betamethasone (n = 50) and infants exposed to > 2 courses of betamethasone (n = 17). CONCLUSION: Compared with a single recommended course of antenatal steroids, multiple courses of antenatal betamethasone are not associated with a deleterious effect on auditory neural maturation in 28 to 32 weeks' gestational age infants.

Evaluation of hippocampal infolding using magnetic resonance imaging.

To investigate developmental morphological variation of the hippocampal formation, we evaluated the degree of hippocampal infolding in cross-sectional oblique coronal images of the cerebral peduncle and the superior cerebellar peduncle. We defined the hippocampal infolding angle as the angle between the vertical midline and the straight line connecting the medial superior margin of the subiculum with the lateral margin of the cornu ammonis. The angle increased slightly with age, and was larger in the superior cerebellar peduncle than in the cerebral peduncle and larger in the right superior cerebellar peduncle than in the left superior cerebellar peduncle. This suggests that this angle and its variation with age and location merit our attention in morphological evaluation of the hippocampal formation.

Analysis of aberrant neuronal migrations in the hereditary cerebellar vermis defect (CVD) rat using bromodeoxyuridine immunohistochemistry.

The hereditary cerebellar vermis defect rat (CVD) is a new neurological mutant characterized by cerebellar vermis defect and a dysplastic cerebellum, especially in the cerebello-pontine junctions. In this study, the cytokinetics of neuronal migrations in the CVD were analyzed using 5-bromo-2'-deoxyuridine (BrdU) as a labeling marker. From embryonic day 21, the CVD cerebellum was small in size with retarded foliation, but no significant differences were detected in the migration pattern of the BrdU-labeled cells between the unaffected controls and the CVD during the prenatal period. On postnatal day 0 (P0), heterotopic Purkinje cells, demonstrable by calbindin immunohistochemistry, were seen in the dorsal pons of the CVD. From P4, BrdU-positive external granule cells (EGCs), which were labeled by BrdU injection on P2, began to penetrate the pons. From P5, the EGCs aggregated around the blood vessels, leading to a disturbance of the cerebellar lamination both in the cerebello-pontine junctions and in the cerebellar hemispheres. Thereafter, the BrdU-labeled cells in the perivascularly aggregated EGCs migrated radially, and formed internal granular layers around the vessels, indicating an aberrant perivascular migration of the EGCs. These findings suggest that the EGC dislocation was preceded by an aberrant settlement of the Purkinje cells, and that the perivascularly aggregated EGCs resulted in cerebellar dysplasia in the CVD.

Maduración histológica de las neuronas del tronco encefálico en víctimas del síndrome de muerte súbita infantil / Histological maturation of the neurons of the brainstem in victims of sudden death syndrome of children

Se examinaron los cerebros de tres niños fallecidos con diagnóstico de síndrome de muerte súbita infantil (SMSI), con el propósito de determinar el patrón de maduración histológico de los núcleos del puente, oliva bulbar e hipogloso mayor, núcleos del tonco encefálico que no están directamente vinculados con la función cardiorrespiratoria y compararla con el patrón observado en tres niños que fallecieron de causa conocida usando el método de Golgi-Cox y morfometria. Los niños fallecidos del SMSI presentan una reducción significativa de la arborización dendrítica neural en los tres núcleos estudiados, comparado con el grupo control. Estos hallazgos sugieron un retardo de la maduración neuronal de todo el tronco encefálico y no sólo de los centros cardiorrespiratorios como ha sido demostrado en niños que fallecieron del SMSI. Se sugiere que este retardo en la maduración del tronco encefálico representa un sustrato anatómico anormal en la multifactorial patogénesis de este síndrome