Delayed luminance and chromatic contrast sensitivity in infants with spontaneously regressed retinopathy of prematurity

Abstract

Background The current study assessed whether contrast sensitivity is affected in preterm infants with a history of spontaneously regressed retinopathy of prematurity (ROP, Stages 1–3). Specifically, we employed luminance (light/dark) and chromatic (red/green) stimuli, which are mediated by the magnocellular (M) and parvocellular (P) subcortical pathways, respectively. Methods Contrast sensitivity (CS) was measured using forced choice preferential looking testing in 21 infants with a history of ROP and 41 control preterm infants who were born prematurely but did not develop ROP, tested between 8 and 47 weeks (2–11 months) postterm age. Infants were presented with chromatic and luminance drifting sinusoidal gratings, which appeared randomly on the left or right side of the monitor on each trial. The contrast of the stimuli varied across trials and was defined in terms of root mean squared cone contrast for long- and medium-wavelength cones. Results Between 8 and 25 weeks postterm, ROP infants had significantly worse CS, and there was a trend for greater impairment for Luminance than Chromatic CS. This delay was not seen at older ages between 26 and 47 weeks postterm. Conclusions These findings are consistent with the concept that early maturation of the M pathway is vulnerable to biological insult, as in the case of ROP, to a greater extent than is the P pathway.

Identifying and characterising cerebral visual impairment in children: a review

“…Studies have shown that there is a differential development of the magnocellular and parvocellular pathways in premature children. This affects the chromatic contrast sensitivity in these children . Colour boundaries of low contrast can be difficult to discern, while boundaries with more contrasting colours and shades may be seen.…”

“…This affects the chromatic contrast sensitivity in these children. 106,107 Colour boundaries of low contrast can be difficult to discern, while boundaries with more contrasting colours and shades may be seen. It is important to look out for what is seen when not expected and what is not seen when it is expected.…”

The immunological link between neonatal lung and eye disease

“…Further to this, it has also been shown that IL‐1β has a sustained negative impact on the choroidal endothelium leading to its involution 25 . Although ROP chiefly involves the inner retina, outer retinal dysfunction is being increasingly recognised as a consequence of ROP and this may account for reduced visual function 82–85 . For example, damage to the retinal pigment epithelium (RPE) and photoreceptor layers of the outer retina triggered by oxidative stress can lead to poor dark adaptation, abnormal cone function and retinal depigmentation 25 .…”

“… 25 Although ROP chiefly involves the inner retina, outer retinal dysfunction is being increasingly recognised as a consequence of ROP and this may account for reduced visual function. 82 , 83 , 84 , 85 For example, damage to the retinal pigment epithelium (RPE) and photoreceptor layers of the outer retina triggered by oxidative stress can lead to poor dark adaptation, abnormal cone function and retinal depigmentation. 25 In a rat model of OIR, intravitreal injection of IL‐1R antagonist to inhibit IL‐1β led to relative preservation of the RPE and choroid, reduced outer retinal hypoxia and improved retinal function.…”

Electrophysiological characteristics of the retina in children with cicatrical retinopathy of prematurity

“…Недоношенность сама по себе, а также «накопленные» в активный период ретинопатии нарушения структуры и функции сетчатки негативно влияют на остроту зрения в долгосрочной перспективе. В частности, ряд исследователей отмечают в отдаленный период заболевания снижение максимально корригированной остроты зрения, нарушения строения и функционирования центральных отделов сетчатки разной степени выраженности [3][4][5][6][7][8], снижение контрастной чувствительности [9,10], прогрессирование периферических витреохориоретинальных дегенераций, изменение структуры витреоретинального интерфейса и как следствиеразвитие поздней тракционно-регматогенной отслойки сетчатки [11].…”