Cognitive outcomes in late childhood and adolescence of neonatal hypoxic-ischemic encephalopathy

Abstract

Hypoxic-ischemic encephalopathy (HIE) is the most common cause of neonatal encephalopathy with a global incidence of approximately 1 to 8 per 1,000 live births. Neonatal encephalopathy can cause neurodevelopmental and cognitive impairments in survivors of hypoxic-ischemic insults with and without functional motor deficits. Normal neurodevelopmental outcomes in early childhood do not preclude cognitive and behavioral difficulties in late childhood and adolescence because cognitive functions are not yet fully developed at this early age. Therapeutic hypothermia has been shown to significantly reduced death and severe disabilities in term newborns with HIE. However, children treated with hypothermia therapy remain at risk for cognitive impairments and follow-up is necessary throughout late childhood and adolescence. Novel adjunctive neuroprotective therapies combined with therapeutic hypothermia may enhance the survival and neurodevelopmental outcomes of infants with HIE. The extent and severity of brain injury on magnetic resonance imaging might predict neurodevelopmental outcomes and lead to targeted interven tions in children with a history of neonatal encephalopathy. We provide a summary of the long-term cognitive outcomes in late childhood and adolescence in children with a history of HIE and the association between pattern of brain injury and neurodevelopmental outcomes.

Keywords: Brain magnetic resonance imaging; Cognition; Hypoxic-ischemic encephalopathy; Neonatal encephalopathy; Outcomes.

Fig. 1.

Two major patterns of neonatal hypoxic-ischemic brain injury; the watershed predominant pattern (A, B) and basal ganglia/thalamus predominant pattern (C, D). (A) Axial diffusion-weighted magnetic resonance imaging (MRI) of neonatal brain demonstrates reduced diffusion in periventricular white matter and corpus callosum (white arrows). (B) Apparent diffusion coefficient map of brain MRI shows hypointensity of multifocal areas in right parietal area (white arrowhead). (C) Moderately increased T1 hyperintensity involving the ventral lateral thalamus, posterior putamen, and globus pallidus (black arrow) can be seen. (D) Apparent diffusion coefficient map shows involvement of the bilateral thalamus (black arrowhead).