Lack of short-latency-potentials in the VEP reflects immature extra geniculate visual function in delayed visual maturation (DVM).
OBJECTIVE
To investigate children with delayed visual maturation (DVM) and correlate the electrophysiological findings to visual development.


METHODS
Three children, one from each of the DVM-classification groups, were subjected to routine ophthalmological examinations and electrophysiological examinations: flash visual evoked potential (VEP) and skin electrode electroretinography (ERG).


RESULTS
All three children had normal ERGs but initially abnormal VEP-recordings with marked delay of latency or grossly altered VEPs. When visual interest developed with responsive smiling at 4, 4.5 and approximately 12 months of age, a maturation in the VEPs also appeared, with development of a short-latency complex (approximately 70 ms). In the normal neonatal development of the VEP, a negativity at approximately 60-70 ms (N1) emerged at four to six weeks of postnatal life when the child started responsive smiling and showing raised visual interest. According to animal experimental research and human studies, the development of the specific response (the short-latency complex) represents the gradual onset of cortical activity mediated via the specific retino-geniculo-striatal pathway. Thus, when the short-latency complex of the VEP cannot be identified, the visual function is mainly of subcortical origin. Since the VEP developed in the same way in the children with DVM as in normal subjects, the pathophysiological dysfunction and origins of DVM can partly be understood.


CONCLUSIONS
The results show that i) children with DVM has a period of visual inattentiveness at a time when normal children show visual interest, ii) the VEP is abnormal in children with DVM at the time of visual inattentiveness, iii) the improvement of vision in DVM can be measured with VEP and iiii) the extra-geniculate system(s) provides for the visual function early neonatally in the normal child and in a prolonged period in the DVM-child as long as the VEPs are abnormal.
Kraemer
M
M
Department of Ophthalmology, Institute of Clinical Neuroscience, Göteborg University.
Sjöström
A
A
D004596:Electroretinography; D005074:Evoked Potentials, Visual / Q000502:physiology*; D005183:Failure to Thrive / Q000150:complications; D005260:Female; D005829:Geniculate Bodies / Q000503:physiopathology*; D006801:Humans; D007223:Infant; D008297:Male; D014786:Vision Disorders / Q000209:etiology / Q000503:physiopathology*; D015348:Vision, Binocular / Q000502:physiology*; D014793:Visual Cortex / Q000503:physiopathology*; D014795:Visual Pathways / Q000503:physiopathology*