Cerebral damage and retinopathy of prematurity appear to be independently associated with visual impairment among preschool children who were born extremely premature, according to a report published Online First by Archives of Ophthalmology.
Retinopathy of prematurity (ROP; an eye disease in very premature infants) is considered the main cause of visual impairment in extremely preterm children, however cerebral damage is also a cause of visual impairment (often referred to as cerebral visual impairment) among extremely preterm children, according to background information in the study.
To examine the importance of cerebral damage and retinopathy of prematurity for visual impairment in preschool children who were born extremely premature, Carina Slidsborg, M.D., from Copenhagen University Hospital, Glostrup Hospital and Rigshospitalet, Denmark, and colleagues conducted a clinical follow-up study of a Danish national cohort of children.
The authors included 178 extremely premature children (gestational age <28 weeks) born between February 13, 2004 and March 23, 2006, and a matched control group of 56 term-born children (gestational age 37 to <42 weeks) in the analysis.
Analysis found that global developmental deficits (an indicator for cerebral damage) and foveal sequelae (abnormalities involving the fovea, a small area of the retina responsible for sharp vision) occurred more often in extremely preterm children than in term-born children, and increased with ROP severity. The authors also found that global developmental deficits, moderate to severe foveal abnormality, and ROP treatment were independently associated with visual impairment.
"In conclusion, we herein demonstrate that, in Denmark, cerebral damage and ROP sequelae are independent risk factors for VA loss among preschool children born extremely premature and that the presence of cerebral damage is the primary risk factor of the two," the authors conclude.
Explore further: Vision loss more common in people with diabetes
Arch Ophthalmol. Published online June 11, 2012. doi:10.1001/archophthalmol.2012.1393