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Maturation of rod function in preterm infants with and without retinopathy of prematurity
Ruth Hamilton1, Michael S Bradnam, John Dudgeon
1Department of Clinical Physics, Royal Hospital for Sick Children, and Princess Royal Maternity, Glasgow, United Kingdom.
Insights
Preterm birth slows rod sensitivity maturation, while retinopathy of prematurity (ROP) further reduces retinal sensitivity. Treatment for ROP also impairs retinal responsivity in infants.
Area of Science:
- Ophthalmology
- Neonatology
- Developmental Neuroscience
Background:
- Rod electroretinograms (ERG) are crucial for assessing retinal function.
- Understanding normal ERG development in preterm infants is essential for early detection of visual impairments.
- Retinopathy of prematurity (ROP) is a significant cause of visual loss in premature infants.
Purpose of the Study:
- To establish normative data for rod electroretinogram development in preterm infants.
- To evaluate the impact of retinopathy of prematurity (ROP) on rod ERG maturation.
- To compare ERG outcomes between control, untreated ROP, and treated ROP groups.
Main Methods:
- Measured Naka-Rushton functions from 41 preterm infants (30-72 weeks postmenstrual age).
- Assessed key outcomes: log sigma, retinal sensitivity, and V(max) (retinal responsivity).
- Compared outcomes across three groups: no ROP, untreated ROP, and treated ROP.
Main Results:
- In controls, retinal sensitivity increased with postmenstrual age but remained lower than term-born infants.
- Retinal responsivity accelerated in preterm infants, exceeding that of term-born infants by 40 weeks PMA.
- Infants with ROP showed reduced retinal sensitivity, with further decreases in treated ROP cases. Responsivity was unaffected in untreated ROP but reduced in treated ROP.
Conclusions:
- Preterm birth appears to slow the maturation of rod sensitivity.
- Maturation of rod responsivity is accelerated in preterm infants.
- ROP significantly impairs retinal sensitivity, and treatment further diminishes both sensitivity and responsivity.
Objectives:
To establish normal development of rod electroretinograms in preterm infants and to assess the effects of retinopathy of prematurity (ROP).
Study Design:
We measured 88 Naka-Rushton functions from 41 preterm infants at maturities from 30 to 72 weeks postmenstrual age (PMA). Outcomes (log sigma, retinal sensitivity and V(max), retinal responsivity) were compared between control (no ROP), untreated ROP, and treated ROP.
Results:
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 microV to 90 microV between 30 and 40 weeks PMA and was 35 muV 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.
Conclusions:
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.
