We studied contrast sensitivity function in 10 parkinsonian patients before and after levodopa treatment. Pretreatment contrast sensitivity function was abnormal in 16 of the 20 eyes. After treatment, only high-frequency loss was observed in 6 eyes. All other types of deficit disappeared under treatment. These changes of contrast sensitivity function following treatment suggest that dopamine is a functional transmitter in the visual pathways.
We studied the effect of stimulus orientation on contrast sensitivity function in 21 patients with Parkinson's disease and in 10 normal subjects. This was done by measuring contrast sensitivity over a range of spatial frequencies for vertical and horizontal sine wave grating stimuli. There was a great test-retest consistency in normal subjects and patients. Fifteen of the 21 patients showed contrast sensitivity deficit in at least one eye. Orientation-specific loss was demonstrated in 17 of the 25 "affected" eyes. The most frequent type of orientation-specific loss was a notch defect, which preferentially affected the middle spatial frequencies. We attribute orientation-specific and spatial frequency-selective loss in Parkinson's disease to a functional disruption of neurons on the visual cortex.
We studied contrast-sensitivity function in 39 patients with Parkinson's disease. Sixty-four percent of the patients showed contrast-sensitivity loss in one or both eyes. The abnormality was not related to the first symptom or the severity of disease. Sensitivity loss at intermediate frequencies (notch loss) in 30% of the "affected" eyes suggested a cortical component. These findings support the belief that there is a widespread neurotransmitter deficiency in Parkinson's disease.
White stimulus training-induced VFE can lead to improved color and shape perception and to increased reading speed in and beyond the pretraining transition zone if ECSG is sufficiently large. The latter depends on the eccentricity of the VFE.
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