Visual Contrast Sensitivity

Visual contrast sensitivity (VCS) is a function that is not commonly tested by neurologists, yet it is an important sensory function that pervades many activities of daily living. It is probably a more meaningful reflection of functional vision than standard visual acuity tests as measured in most clinical settings. VCS has consistently been found to be abnormal in Parkinson's disease. VCS is measured by determining the minimal contrast required to distinguish objects from one another presented at a given spatial frequency. Visual targets spaced very closely together are said to have a high spatial frequency, and those spaced farther apart represent a low spatial frequency. Spatial frequency is expressed in cycles per degree of visual angle. The spectrum of contrast can be thought of as ranging from black on white (high contrast) to white on white (low contrast), with all shades of grey on black or grey on white in between. Another way to depict the concept of VCS is to ask how low in contrast adjacent images displayed at a given spatial frequency (distance apart) must be before they appear to be indistinguishable from a visually homogeneous field. The lower the contrast at which one can still detect a difference between adjacent objects, the higher the contrast sensitivity. Sinusoidal gratings of various spatial frequencies are among the most sensitive visual stimuli for testing VCS in humans. In this context, the term "sinusoidal" refers to the gradual diminution and then reconstitution of contrast between adjacent targets rather than a precipitous contrast change such as would be seen between adjacent black and white squares on a checkerboard. The peak of normal human contrast sensitivity is found at intermediate spatial frequencies. In Parkinson's disease, VCS is most reduced at these intermediate spatial frequencies.43-45 This VCS abnormality is most exaggerated when the gratings are temporally modulated at medium frequencies of 4 to 8 Hz.43 In addition, VCS is sometimes less attenuated at lower spatial frequencies in PD than it is in normal individuals.46 These abnormalities are different from the declining VCS function associated with normal aging.47 In some studies, VCS loss has been found to correlate with the overall severity of PD,48 but in others it has not.45 However, during the course of an individual day, there appears to be a more consistent correlation with the underlying severity of parkinsonian symptoms. VCS has been shown to exhibit a circadian variability that conforms to the common pattern of improved morning and worsened afternoon motoric disability seen in PD.45 Recent evidence demonstrating a distinct circadian cycle of retinal dopamine content is consistent with this observation.16,17 Similarly, VCS function can change in parallel to motor symptoms during transient "on" and "off' phases in fluctuating PD patients49 and can be improved by the administration of levodopa.50 Whether the basic abnormality underlying abnormal VCS in PD resides in the retina, the visual cortex, or in both is still unclear. The fact that there are interocular differences in VCS45,51 suggests the presence of retinal pathology. Moreover, the pattern electroretinogram, which largely reflects retinal ganglion cell activity, has been found to be abnormal in PD5253 with a characteristic amplitude loss at intermediate spatial frequencies similar to those associated with the greatest abnormality of VCS in PD.52 As is the case with VCS, levodopa therapy improves the PERG abnormality in PD.5253 Langheinrich et al.54 demonstrated that contrast discrimination threshold in PD patients correlated with frequency-specific PERG abnormalities (a retinal phenomenon) but not VEP impairment (a cortical phenomenon) and viewed these findings as further evidence that the VCS abnormality in PD is predominantly a result of retinal dysfunction. However, there is also evidence suggesting that cortical dysfunction may contribute to the VCS abnormality in PD. VCS impairment in PD patients has been found to be ori entation specific in that the VCS deficit is more severe for horizontally oriented patterns than those arrayed vertically.43,44 Other dopamine deficiency syndromes, such as drug-induced parkinsonism, are also associated with VCS loss that is orientation dependent.55 Although orientation specificity may be partially subserved by the lateral geniculate, 56 this perceptual function is felt to largely reside in the orientation-tuned receptive fields of the visual cor-tex.57 While the presence of orientation specific VCS loss clearly raises the possibility of a central contribution to the VCS abnormality in PD, other investigators have noted that the cortically mediated function of contrast adaptation is preserved in PD and consider this finding evidence that cortical pathology is not significant in these patients and is not likely to play a major role with respect to reduced contrast sensitivity.58

Like the color vision abnormality in PD, VCS impairment progressively increases over time as the underlying neurologic condition worsens.36 This worsening is accelerated at the intermediate spatial frequencies that are known to be most affected in PD, rather than at higher spatial frequencies, which would be expected to show the greatest rate of decline if the progressive worsening were solely due to aging.59 As VCS worsens over time in PD, there is a contemporaneous progressive reduction in amplitude and lengthening of latency of the ERG, once again supporting the notion that abnormal VCS in this patient population is linked to retinal dysfunction.60

The use of low-contrast letter charts in patients with PD and other medical conditions has been found to detect visual dysfunction that was not appreciated through the use of standard visual acuity charts, which are confined to extremely high-contrast, high-spatial-frequency visual stimuli.6162 Parkinson's disease patients and their physician are usually unaware of this contrast sensitivity abnormality, but the patient may have noticed an inexplicable impairment in everyday visual tasks. This subtle abnormality, largely affecting VCS at the intermediate spatial frequencies, can impair such critical functions as facial recognition or proper and early identification of highway signs.63 Additional functional correlates of this VCS deficit are possible.64,65 Abnormal VCS might impair the ability to drive a motor vehicle in a low-contrast environment such as might exist at dusk or dawn. Intact spatiotemporal vision is functionally important on a day-to-day basis, since much of the visual world is periodic in array,66 and is important for the normal perception of depth and depth discrimination.67 It has been suggested that, in PD, abnormal contrast sensitivity might predispose to gait freezing. Mestre et al.68 described a PD patient exhibiting increased contrast sensitivity to low and intermediate spatiotemporal frequencies who experienced gait freezing in the presence of environmental stripes arrayed at these low frequencies but not at higher spatial frequencies or with his eyes closed. They postulated that a hypersensitivity to low frequency visual stimuli resulted in an adaptive "braking" reflex leading to gait freezing. Of interest is the observation that levodopa therapy may preferentially increase VCS at these low spatial frequencies,69 a fact that is consistent with the observation that dopaminergic therapy can paradoxically worsen gait freezing in some patients. Other investigators have demonstrated that the gait of PD patients improves in the presence of well illuminated periodic stimuli (lines) in the visual environment,70 and that parameters of gait such as stride length are related to visual cues.71

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