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Paired associates learning is impaired in both schizophrenia and amnestic mild cognitive impairment (aMCI), which may reflect hippocampal pathology. In addition, schizophrenia is characterized by the dysfunction of the retino-geniculo-striatal magnocellular (M) visual pathway. The purpose of this study was to investigate the interaction between visual perceptual and memory dysfunctions. We administered a modified version of the CANTAB paired associates learning task to patients with schizophrenia (n = 20), aMCI (n = 20), and two groups of matched healthy controls (n = 20 for each patient group). The stimuli in the paired associates learning task biased information processing toward the M pathways (low contrast, low spatial frequency) and parvocellular (P) pathways (high contrast, high spatial frequency). Results revealed that patients with schizophrenia exhibited a more pronounced learning deficit for M-biased relative to P-biased stimuli. In aMCI, there were similar memory deficits for both types of stimuli. Orientation discrimination for M- and P-biased stimuli was intact in both groups of patients. The number of errors in the M-biased memory condition significantly and inversely correlated with the volume of the right hippocampus in schizophrenia. These results suggest an interaction between M-biased perceptual processing and short-term relational memory in schizophrenia, which may be associated with the structural alteration of the right hippocampus. (Contains 3 tables and 3 figures.)

Previous studies reported impaired visual information processing in patients with fragile x syndrome and in premutation carriers. In this study, we assessed the perception of biological motion (a walking point-light character) and mechanical motion (a rotating shape) in 25 female fragile x premutation carriers and in 20 healthy non-carrier controls. Stimuli were moving stimulus dots embedded among a cloud of noise dots. Sensitivity (d) for motion detection was determined. Emotional symptoms were assessed by Hamilton's depression and anxiety rating scales. Results revealed that the premutation carriers displayed lower sensitivities for biological and mechanical motion relative to the non-carriers. This deficit was more pronounced in the case of biological stimuli. The premutation carriers displayed higher depression and anxiety scores relative to the non-carriers. Higher depression, but not anxiety, scores were associated with decreased sensitivity for biological, but not mechanical, motion in the carrier group. These results suggest that motion perception deficits are detectable in fragile x premutation carriers, and that the impairment of biological motion perception is associated with depressive symptoms. (Contains 4 figures and 2 tables.)

Previous studies indicated impaired magnocellular (M) and relatively spared parvocellular (P) visual pathway functioning in patients with fragile X syndrome. In this study, we assessed M and P pathways in 22 female fragile X premutation carriers with normal intelligence and in 20 healthy non-carrier controls. Testing procedure included visual contrast sensitivity and vernier threshold measurements. Results revealed that carriers were selectively impaired on tests of M pathways (low spatial/high temporal frequency contrast sensitivity and frequency-doubling vernier), whereas they showed intact performance on P pathway tests. These results suggest that the deficit of the M pathway is an endophenotype of fragile X syndrome. (Contains 3 figures.)