Maturation of Rod Function in Preterm Infants with and without Retinopathy of Prematurity

• Published in: The Journal of pediatrics Vol. 153; no. 5; pp. 605 - 611
• Main Authors: Hamilton, Ruth, Bradnam, Michael S., Dudgeon, John, Mactier, Helen
• Format: Journal Article
• Language: English
• Published: Maryland Heights, MO Mosby, Inc 01.11.2008; Elsevier
• Subjects: Biological and medical sciences; Case-Control Studies; Electroretinography - methods; General aspects; Gestational Age; Humans; Infant, Newborn; Infant, Premature; Laser Therapy; Light Coagulation; Medical sciences; Ophthalmology; Pediatrics; Retina - physiopathology; Retinal Diseases - diagnosis; Retinal Diseases - physiopathology; Retinal Neovascularization; Retinal Rod Photoreceptor Cells - physiology; Retinal Rod Photoreceptor Cells - physiopathology; Retinopathies; Retinopathy of Prematurity - diagnosis; Retinopathy of Prematurity - physiopathology; Treatment Outcome; PMA; ROP; ERG; Electroretinography; Retinopathy of prematurity; Postmenstrual age; Human; Ripening; Premature; Pediatrics; Eye disease; Newborn diseases; Retinopathy; Prematurity; Rod; Infant; Comparative study
• ISSN: 0022-3476; 1097-6833; 1097-6833
• DOI: 10.1016/j.jpeds.2008.05.018

To establish normal development of rod electroretinograms in preterm infants and to assess the effects of retinopathy of prematurity (ROP). We measured 88 Naka-Rushton functions from 41 preterm infants at maturities from 30 to 72 weeks postmenstrual age (PMA). Outcomes (log σ, retinal sensitivity and V max, retinal responsivity) were compared between control (no ROP), untreated ROP, and treated ROP. In control infants, sensitivity increased by 1.5 log units from 30 to 40 weeks PMA and by a further 0.5 log units by 50 weeks PMA but was 0.5 log units less than in similarly-mature, healthy, term-born infants. Average retinal responsivity increased from 23 μV to 90 μV between 30 and 40 weeks PMA and was 35 μV greater at 40 weeks PMA than in similarly-mature term-born infants. At around 36 weeks PMA, (when onset of ROP peaks), infants with untreated ROP had average retinal sensitivity 0.2 log units lower than control infants; sensitivity was reduced further in infants treated for ROP. Retinal responsiveness did not differ between control subjects and untreated infants with ROP but was greatly reduced in infants treated for ROP. Maturation of rod sensitivity appears to be slowed by preterm birth whereas maturation of rod responsivity is accelerated. ROP reduces retinal sensitivity, and treated ROP reduces both sensitivity and responsivity.