Disrupted cerebellar development in preterm infants is associated with impaired neurodevelopmental outcome.

The unfavorable impact of prematurity on the developing cerebellum was recently recognized, but the outcome after impaired cerebellar development as a prematurity-related complication is hitherto not adequately documented. Therefore we compared 31 preterm patients with disrupted cerebellar development to a control group of 31 gender and gestational age matched premature infants with normal cerebellar development. Supratentorial brain injuries during the neonatal period were comparable between the groups. At a minimum age of 24 months motor and mental development was assessed by standardized tests. Disrupted cerebellar development was associated with significantly poorer scores both in the subtests for neuromotor (p < 0.001) and mental development (p < 0.001), respectively. Mixed CP was diagnosed in 48% of affected patients, whereas none of the patients of the control group had mixed CP. Microcephaly and epilepsy were significantly related to disrupted cerebellar development. Preterm patients with disrupted cerebellar development exhibit poorer outcome results in all investigated variables. The role of the cerebellum in neurodevelopment after prematurity seems to be underestimated so far.

Preterm birth and disruptive cerebellar development: assessment of perinatal risk factors.

OBJECTIVE: Abnormal cerebellar development was recently recognized to be related to prematurity. Aim of the present study was to evaluate preterm birth and possible peri- and postnatal risk factors associated with this type of brain injury. PATIENTS AND METHODS: We report on a series of 35 very low birth weight infants (birth weight 986+/-257g S.D.) born between 24 and 32 weeks of gestation (27.0+/-1.8 weeks of gestation S.D.) sustaining disruption of cerebellar development after preterm birth. Perinatal medical records of study patients were compared to 41 preterm control infants (birth weight 900+/-358g S.D., gestational age 26.3+/-2.1 weeks S.D.) with normal cerebellar development on MRI scan. RESULTS: A severely compromised postnatal condition with consecutive intubation and catecholamine support was found to be significant risk factor. Additional supratentorial hemorrhagic brain injury followed by posthemorrhagic hydrocephalus, neurosurgical interventions and hemosiderin deposits on the cerebellar surface were significantly related to disruptive cerebellar development. No other differences in perinatal factors were found between the groups. CONCLUSION: Premature birth between 24 and 32 gestational weeks associated with poor postnatal conditions and complicated supratentorial hemorrhagic brain lesions represents a high-risk situation for disruption of cerebellar development.

Disruption of cerebellar development: potential complication of extreme prematurity.

BACKGROUND AND PURPOSE: Infants with very low birth weight are at high risk for cerebral lesions. Although supratentorial brain damage is a common radiologic finding, posterior fossa pathologies are rare. We studied the morphology of cerebellar involvement in a large series of 28 premature infants born before the 30th week of gestation to define typical patterns and identify possible risk factors for this pathology. METHODS: Cranial sonograms were obtained in the early neonatal period. MR imaging was performed between the 2nd month and the 6th year of life. Morphologic patterns of cerebellar involvement were evaluated. RESULTS: Three morphologic patterns of cerebellar involvement were recognized: (1) symmetric volume reduction of the cerebellar hemispheres, which were floating immediately beneath the tentorium, and a small vermis with preserved shape; (2) symmetrical reduction in hemispheric volume with an enlarged, balloon-shaped fourth ventricle and a small, deformed vermis; and (3) normal overall cerebellar shape with extensive reduction of its dimensions. A small brain stem with flattened anterior curvature of the pons and loss of supratentorial white matter was present in all patients. CONCLUSION: Symmetric cerebellar volume reduction was found as a consequence of extreme prematurity. Selective vulnerability of the developing cerebellum in the window of 24-30 weeks of gestation, combined with several additive perinatal risk factors (eg, hemosiderin deposits) seems to lead to destruction of immature structures and developmental arrest. Therefore, the resulting condition is the consequence of disrupted cerebellar development.