Effect of Intraventricular Hemorrhage on Cerebellar Growth in Preterm Neonates

Abstract

The aim of this study is to evaluate cerebellar growth of preterm infants with intraventricular hemorrhage. Vermis height (VH) and transverse cerebellar diameter (TCD) were measured by cranial ultrasound in 18 preterm infants (26-30 weeks) with intraventricular hemorrhage (IVH) at first 3 days of life and at term equivalent age (TEA). IVH was diagnosed by ultrasonography and scaled in accordance with the definitions by Papile et al. Measurements were compared with 18 preterm (26-30 weeks) infants without IVH. Both VH and TCD of preterm infants with IVH were significantly lower than those of preterm ones without IVH at TEA (p < 0.001). No significant difference was found for head circumference (p = 0.158) and weight (p = 0.092). In subgroup analysis, preterm infants with grades 3-4 IVH had significantly lower TCD (p = 0.008) and head circumference (p = 0.033) than the ones with grades 1-2 IVH. However, VH (p = 0.102) and weight (p = 0.480) did not show any difference between these subgroups. IVH may have a significant impact on cerebellar growth on preterm infants at TEA, specially those with a severe IVH. TCD is affected more than VH.

Germinal Matrix-Intraventricular Hemorrhage of the Preterm Newborn and Preclinical Models: Inflammatory Considerations

“…In normally growing fetuses, between 25 to 37 weeks of gestation total brain volume increases by 230%, brain stem volume increases by 134% and the cerebellum volume increases by 384% [15]. Other authors describe that the volume of the cerebellum increases fivefold between weeks 24-40 [22]. Besides, from 24 weeks gestation on, cortical gray matter matures, radial glia disappear, the complexity of the connections increases, and cortical folding and gyrification become progressively more complex.…”

“…Moreover, brain abnormalities are directly related to an increased risk of sensory [7,23,35], cognitive and motor [33,41] impairments. PTNB with severe GM-IVH commonly suffer developmental delay [23,35,48], associated to cerebelum abnormalities [22], as well as a consequent cerebral palsy [7,23]. Previous studies have reported that approximately 10% of PTNB with severe GM-IVH will develop cerebral palsy [49] and these children will frequently suffer spastic dysplasia where both legs are affected [5].…”

Ultrasound of acquired posterior fossa abnormalities in the newborn

“…5 The disturbance in development is inversely related to gestational age at birth 29 and again different mechanisms are involved: hypoxia-ischemia, infection-inflammation, poor nutrition, and glucocorticoid exposure, as well as indirect remote effects related to hemosiderin deposits originating from IVH. 5,[30][31][32] At the MF transverse cerebellar diameter can be measured in both axial and coronal plane, to be compared with nomograms available for different gestational ages for detecting cerebellar hypoplasia or atrophy. [33][34][35] Cerebellar hemorrhage in the term infant Cerebellar hemorrhagic lesions are less common but may also occur in (near) term infants and include both small or punctate hemorrhages deep within the cerebellum and large hemispheric or vermian hemorrhage.…”

A Closer Look at a Small Brain: Transnuchal Ultrasound Facilitates High-Resolution Imaging of the Cerebellum in Preterm Infants

“…Impairment of cerebellar growth occurs even without direct cerebellar lesions. Hemosiderin deposits on the surface of the cerebellum are associated with smaller cerebellar volumes at term-equivalent age, likely caused by a neurotoxic effect of free hemoglobin or iron within the cerebrospinal fluid [13][14][15]. Due to disruption of the trophic cerebro-pontine-cerebellar pathways, a remote atrophy of one cerebellar hemisphere can result, for example, after contralateral periventricular hemorrhagic infarction in the cerebrum, thus the mechanism known as crossed cerebrocerebellar diaschisis.…”