Abstract
The retina is part of the CNS and provides a window into brain structure and function that has been useful in examining schizophrenia and other neuropsychiatric disorders. Several prior flash electroretinogram (fERG) studies have demonstrated that ERG amplitudes are reduced in schizophrenia, and that latencies are prolonged. In this study we used fERG to determine which retinal cell types (photoreceptor, bipolar, ganglion) demonstrate impaired signaling, and under which conditions (scotopic vs. photopic) the impairments are most pronounced. In addition, we examined relationships between abnormal ERG values and performance on measures of visual acuity, contrast sensitivity, and contour integration. Data were collected on 25 schizophrenia patients and 25 healthy controls. The primary variables of interest were a-wave activity (reflecting photoreceptor response), b-wave activity (reflecting primarily bipolar cell activity) and the photopic negative response (PhNR) (reflecting ganglion cell activity). On light-adapted tests, schizophrenia patients demonstrated significantly weaker photoreceptor response when a flash was presented against an unlit background, and during a steady-state flicker test. On dark-adapted tests, the rate of photoreceptor response gain per unit of intensity increase was significantly weaker for patients than controls. In dark-adapted conditions, patients also demonstrated weaker signaling of bipolar cells. The schizophrenia group was characterized by a marginally weaker PhNR. ERG latencies were generally normal in all tests. Correlations between ERG indices and other test scores were generally not significant and were not consistent across ERG trials. Overall, these data suggest that both reduced signaling of photoreceptor and bipolar cells, as well as attenuated response gain, are associated with schizophrenia. Moreover, both rod and cone responses appear to be affected. However, weakened retinal signaling is not consistently related to visual task performance, perhaps due, in part, to compensatory LGN or cortical gain control mechanisms.
Meeting abstract presented at VSS 2017