Deactivation of the rod response in retinopathy of prematurity

Hansen, Ronald M.; Harris, M. E.; Moskowitz, Anne; Fulton, Anne B.

doi:10.1007/s10633-010-9228-z

Cited by 13 publications

(8 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…ERG results in Mild ROP indicate that deactivation of the rod photoreceptor response is slower than in No ROP or term born subjects (Hansen et al, 2010). Perhaps use of a model of the a-wave that incorporates both activation and recovery from activation (that is, deactivation) in the rod outer segment (Robson and Frishman, 2014; Robson et al, 2003) will improve specification of the rod to rod-driven relationship in ROP.…”

Section: Assessment Of Rod and Rod-driven Retinal Functionmentioning

confidence: 86%

The neural retina in retinopathy of prematurity

Hansen

Moskowitz

Akula

et al. 2017

Progress in Retinal and Eye Research

Self Cite

View full text Add to dashboard Cite

Retinopathy of prematurity (ROP) is a neurovascular disease that affects prematurely born infants and is known to have significant long term effects on vision. We conducted the studies described herein not only to learn more about vision but also about the pathogenesis of ROP. The coincidence of ROP onset and rapid developmental elongation of the rod photoreceptor outer segments motivated us to consider the role of the rods in this disease. We used noninvasive electroretinographic (ERG), psychophysical, and retinal imaging procedures to study the function and structure of the neurosensory retina. Rod photoreceptor and post-receptor responses are significantly altered years after the preterm days during which ROP is an active disease. The alterations include persistent rod dysfunction, and evidence of compensatory remodeling of the post-receptor retina is found in ERG responses to full-field stimuli and in psychophysical thresholds that probe small retinal regions. In the central retina, both Mild and Severe ROP delay maturation of parafoveal scotopic thresholds and are associated with attenuation of cone mediated multifocal ERG responses, significant thickening of post-receptor retinal laminae, and dysmorphic cone photoreceptors. These results have implications for vision and control of eye growth and refractive development and suggest future research directions. These results also lead to a proposal for noninvasive management using light that may add to the currently invasive therapeutic armamentarium against ROP.

show abstract

Section: Assessment Of Rod and Rod-driven Retinal Functionmentioning

confidence: 86%

The neural retina in retinopathy of prematurity

Hansen

Moskowitz

Akula

et al. 2017

Progress in Retinal and Eye Research

Self Cite

View full text Add to dashboard Cite

show abstract

“…Severe retinopathy of prematurity often leads to long-term visual loss, with blindness in the most severe cases. 149 Without treatment, most non-proliferative retinopathy of prematurity regresses, but even non-proliferative disease is associated with visual deficits, 150 since preterm birth itself has lasting effects on the developing visual system. Retinopathy of prematurity is also associated with other eye problems.…”

Section: Long-term Outcomesmentioning

confidence: 99%

Retinopathy of prematurity

2013

View full text Add to dashboard Cite

The immature retinas of preterm neonates are susceptible to insults that disrupt neurovascular growth, leading to retinopathy of prematurity. Suppression of growth factors due to hyperoxia and loss of the maternal–fetal interaction result in an arrest of retinal vascularisation (phase 1). Subsequently, the increasingly metabolically active, yet poorly vascularised, retina becomes hypoxic, stimulating growth factor-induced vasoproliferation (phase 2), which can cause retinal detachment. In very premature infants, controlled oxygen administration reduces but does not eliminate retinopathy of prematurity. Identification and control of factors that contribute to development of retinopathy of prematurity is essential to prevent progression to severe sight-threatening disease and to limit comorbidities with which the disease shares modifiable risk factors. Strategies to prevent retinopathy of prematurity will depend on optimisation of oxygen saturation, nutrition, and normalisation of concentrations of essential factors such as insulin-like growth factor 1 and ω-3 polyunsaturated fatty acids, as well as curbing of the effects of infection and inflammation to promote normal growth and limit suppression of neurovascular development.

show abstract

“…In addition to the vascular abnormalities, reduced visual acuity [14,15] and neuronal changes [16][17][18][19] have also been reported. Alterations of electroretinographic (ERG) responses have been reported in infants and children with a history of ROP.…”

Section: Retinopathy Of Prematuritymentioning

confidence: 98%

Stem Cell Therapy for Retinopathy of Prematurity

Fu¹

2013

Anat Physiol

View full text Add to dashboard Cite

Retinopathy of Prematurity (ROP) is a leading cause of childhood blindness that severely affecting the quality of life of these children. Few treatment options are available but without favorable outcomes. Stem cell therapy, through its proven potential in tissue regeneration, provides an attractive therapeutic approach in treating ROP and thereby restoring vision. A n a to my & P h y s io logy: C u r r e n t Re sea rc h

show abstract

Deactivation of the rod response in retinopathy of prematurity

Cited by 13 publications

References 39 publications

The neural retina in retinopathy of prematurity

The neural retina in retinopathy of prematurity

Retinopathy of prematurity

Stem Cell Therapy for Retinopathy of Prematurity

Contact Info

Product

Resources

About