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Abstract
BackgroundCerebellar hemorrhagic injury (CHI) is being recognized more frequently in premature infants. However, much of what we know about CHI neuropathology is from autopsy studies that date back to a prior era of neonatal intensive care. To update and expand our knowledge of CHI we reviewed autopsy materials and medical records of all live-born preterm infants (<37 weeks gestation) autopsied at our institution from 1999–2010 who had destructive hemorrhagic injury to cerebellar parenchyma (n = 19) and compared them to matched non-CHI controls (n = 26).ResultsCHI occurred at a mean gestational age of 25 weeks and involved the ventral aspect of the posterior lobe in almost all cases. CHI arose as a large hemorrhage or as multiple smaller hemorrhages in the emerging internal granule cell layer of the developing cortex or in the nearby white matter. Supratentorial germinal matrix hemorrhage occurred in 95% (18/19) of CHI cases compared to 54% (14/26) of control cases (p = 0.003). The cerebellar cortex frequently showed focal neuronal loss and gliosis (both 15/19, 79%) in CHI cases compared to control cases (both 1/26, 4% p < 0.0001). The cerebellar dentate had more neuronal loss (8/15, 53%) and gliosis (9/15, 60%) in CHI cases than controls (both 0/23, 0%; p < 0.0001). The inferior olivary nuclei showed significantly more neuronal loss in CHI (10/17, 59%) than in control cases (5/26, 19%) (p = 0.0077). All other gray matter sites examined showed no significant difference in the incidence of neuronal loss or gliosis between CHI and controls.ConclusionsWe favor the possibility that CHI represents a primary hemorrhage arising due to the effects of impaired autoregulation in a delicate vascular bed. The incidences of neuronal loss and gliosis in the inferior olivary and dentate nuclei, critical cerebellar input and output structures, respectively were higher in CHI compared to control cases and may represent a transsynpatic degenerative process. CHI occurs during a critical developmental period and may render the cerebellum vulnerable to additional deficits if cerebellar growth and neuronal connectivity are not established as expected. Therefore, CHI has the potential to significantly impact neurodevelopmental outcome in survivors.
Highlights
Cerebellar hemorrhagic injury (CHI) is being recognized more frequently in premature infants
In this study we examined a modern cohort of premature infants with CHI, we sought to determine: 1) the extent and region of the cerebellum involved by CHI; and 2) if CHI is associated with additional neuropathology, especially gray matter lesions that may provide insight into the neurodevelopmental impairments encountered in surviving premature infants
The incidence of pulmonary hemorrhage, a sign of a hemodynamically significant patent ductus arterious (PDA) was significantly increased in the CHI group (Table 1) [28]
Summary
Cerebellar hemorrhagic injury (CHI) is being recognized more frequently in premature infants. The largest series reported an overall incidence of approximately 3%, which increased to 8.7% in infants with a birth weight less than 750 gm, and decreased in infants of greater birth weight suggesting that the smallest and most premature infants are at greatest risk to develop CHI [4,13] During this developmental period the human cerebellum is undergoing rapid growth and many complex developmental processes are taking place that are essential to proper cerebellar function [14]. Other critical developmental events occurring in this time period include granule cell migration and the early establishment of cerebellar neuronal circuitry Because all of these important events occur within this time frame it is considered to represent a critical period of cerebellar development when the cerebellum is vulnerable to injury. Because CHI tends to affect the most premature infants during a time when the cerebellum is developmentally vulnerable, CHI could have significant neurodevelopmental impact on survivors, and there is a critical need to learn as much as possible about the neuropathology of CHI
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