Cerebellar hemorrhages in very preterm infants: presence, involvement of the dentate nucleus, and cerebellar hypoplasia are associated with adverse cognitive outcomes
摘要
Impaired cognition is a frequent complication of prematurity, closely related to patients’ outcomes. Imaging features of cerebellar hemorrhages (CBH) related to impaired cognition are not well studied. This study evaluated the relationship between cMRI-derived CBH characteristics and clinical risk factors for adverse cognition.
MethodsOur analysis is threefold: (1) We included very preterm infants (2009–2018) undergoing cMRI, and compared clinical and cMRI findings between infants with and without CBH. (2) In the CBH cohort, we associated clinical and imaging findings with cognitive outcomes (Bayley Score of Infant Development at two years corrected age, impaired outcomes: < 85) using uni- and multivariable logistic regression analyses. (3) We conducted a matched pair case-control analysis (CBH vs. no CBH) matching for gestational age (GA) and supratentorial injury.
ResultsAmong the 507 infants (52% male; mean GA 26.8 ± 2.7 weeks), 53 (10.5%) presented with CBH. Cognition was impaired in those with CBH (case-control: 88 (IQR: 75–110) vs. 105 (IQR: 90–112), p < 0.001), even in those with CBH < 5 mm (case-control: 95 (IQR: 77.5–115) vs. 105 (IQR: 91–113), p = 0.037). In infants with CBH, red-blood-cell-transfusion requirement (odds ratio (OR) 1.32, 95% CI: 1.01–1.72, p = 0.037), dentate nucleus involvement (OR 17.61, 95% CI: 1.83–169.83, p = 0.013) and moderate-to-severe cerebellar hypoplasia (OR 26.41, 95% CI: 1.11–626.21, p = 0.043) were independent predictors of impaired cognition. Adding dentate nucleus involvement to cerebellar hypoplasia increased the discriminatory capacity (AUC 0.85 vs. 0.71, p = 0.004).
ConclusionCBH (even < 5 mm) impact cognitive outcomes of very preterm infants, underlining the cerebellum’s importance for cognition. In infants with CBH, involvement of the dentate nucleus and moderate-to-severe cerebellar hypoplasia are independent structural risk factors for impaired cognition.
Key Points