Amblyopia or lazy eye is the most common cause of uniocular blindness in adults. It is caused by a disruption to normal visual development as a consequence of unmatched inputs from the two eyes in early life, arising from a turned eye (strabismus), unequal refractive error (anisometropia) or form deprivation (e.g. cataract). Animal models based on extracellular recordings in anesthetized animals suggest that the earliest site of the anomaly in the primate visual pathway is the primary visual cortex (corresponding to the striate cortex, cytoarchitectonic area 17 and area V1), which is where inputs from the two eyes are first combined in an excitatory fashion, whereas more distal and monocular processing structures such as the retina and lateral geniculate nucleus (LGN) are normal. Using high‐field functional magnetic resonance imaging in a group of human adults with amblyopia, we demonstrate that functional deficits are first observable at a thalamic level, that of the LGN. Our results suggest the need to re‐evaluate the current models of amblyopia that are based on the assumption of a purely cortical dysfunction, as well as the role for the LGN in visual development.

Background:  To report the incidence of retinopathy of prematurity (ROP) in a subgroup of extremely premature infants admitted to an Australian tertiary centre over an 18‐year period.Design:  Retrospective study. Royal Brisbane and Women's Hospital Neonatal Intensive Care Unit.Participants:  Five hundred and fifty‐four infants admitted between 23 and 25.6 weeks gestational age (GA).Methods:  The 18‐year study was divided into three 6‐year periods for analysis: period 1 (1992–1997), period 2 (1998–2003) and period 3 (2004–2009). Infants were compared based on their week of GA and by the study period in which they were born.Main Outcome Measures:  GA, birthweight, incidence and severity of ROP.Results:  Three hundred seventy‐three (67.3%) infants survived until ROP screening, and 351 (63.4%) survived until discharge. ROP incidence increased from 78.2% in period 1 to 86.1% in period 3. Over the entire study, 90.5% of 23‐week GA infants had ROP compared with 89.7% of 24‐week GA infants and 76.1% of 25‐week GA infants. Mean birthweight was significantly lower in infants with any ROP (725.1 g) and ROP of at least stage 3 (720.8 g) compared with infants without ROP (806.5 g) (P < 0.0001). Twenty‐three–week GA infants had more severe ROP (28.6%) than 24 weeks (18.3%) and 25 weeks GA (11.9%).Conclusions:  There has been increased survival and incidence of ROP in extremely premature infants over the past 20 years. Lower birthweight and GA are both associated with higher incidence and more severe ROP.