Abstract

It is new well documented that an attenuation of spatial contrast sensitivity is to be expected in most multiple sclerosis (MS) patients (1-3). Further, it has been reported that patients contrast sensitivity functions can be influenced by modulating the grating in time as well as in space (4-7). The specific consequences of using flickering gratings, however, has been a matter of some conjecture. For example, Marx et al. (5) concluded that temporally modulating stimulus gratings causes a uniform reduction in contrast sensitivity across all spatial frequencies, while Medjbeur and Tulunay-Keesey (6) concluded that flickering the grating stimuli caused a number of distinct deficit patterns to emerge. Although these discrepancies could be due to the way in which the pathology manifested itself in the particular groups of patients sampled in these studies, they may also have been due to the uncontrolled and unknown response criteria that were adopted by the observers (8). An example of how this factor can influence the conclusions that are drawn has been offered by Brussell et al. (2). They observed similar contrast sensitivity deficit patterns in 15 MS patients for both flickering and non–flickering grating stimuli. The most parsimonious explanation of these data was that a single diseased pathway was carrying information about both the spatial and temporal characteristics of the stimulus. In addition to assessing contrast sensitivity, observers were also asked on each trial to state whether detection was based upon seeing a pattern or upon seeing flicker. A summary of these data indicated that the patients reported detecting patterns more often than controls. This additional information led to quite a different conclusion: the patients relied upon the output of a pattern mechanism more often than the controls because it was less impaired than a mechanism responsible for processing information about flicker.

© 1987 Optical Society of America