This paper provides a brief description of amblyopia and discusses current research regarding the motion pathway in individuals with amblyopia.

Amblyopia is a condition in which visual acuity in one eye is greatly reduced. It is caused by lack of stimulation or disuse during visual development (Rose, 1998). Because the eye is not fully developed at birth (Jarvis, 1992, as cited in Rose, 1998), infants need stimulation to complete the visual neural pathway. When one or both eyes are inhibited, for example due to misalignment of one eye (strabismus) or a large difference in refractive power between two eyes (anisometropia), the neural pathway for the inhibited eye develops abnormally, or does not develop at all. At approximately six years of age eye development is complete (Stager, 1990, as cited in Rose, 1998). Before visual development is complete amblyopia can be treated. If it is caught and treated at an early age, normal vision can be preserved (Rose, 1998).

There are several types of amblyopia. Researchers must be aware of the various types of amblyopia because the effects for each are not always consistent. Strabismic amblyopia is caused when the two eyes are out of alignment due to weak musculature. Anisometropic amblyopia is a result of a large difference in refractive power of an individual's eyes. Another form of amblyopia results when visual information does not reach the retina. This is called stimulus deprivation amblyopia. Meridional amblyopia is a result of the diffused images caused by astigmatism. Researchers often discover that there are differences between groups of amblyopes based on type. For example, Levi and his colleagues (1994) discovered differences in vernier acuity between anisometropic amblyopes and strabismic amblyopes.

To better understand amblyopia: how it works, what its causes are, and how it is best treated, current research looks for the underlying brain mechanisms that are implicated in the deficits in visual acuity of amblyopes. This information is important because it could provide meaningful insight into the nature of the underlying problems involved (Hess & Anderson, 1993).

There is a general consensus that amblyopes have reduced contrast sensitivity, grating acuity, and spatial resolution in one eye and a loss of binocular vision (Levi, 1991; Sireteanu et al., 1977, as cited in Fahle & Bachmann, 1996). Amblyopes also suffer from "crowding" (Levi & Klein, 1985, as cited in Fahle & Bachmann, 1996) which causes difficulty, for example, in comprehending a letter found in text rather than an isolated letter. The mechanisms delegating positional information are also disabled in amblyopes (Rentschler & Hilz, 1985, as cited in Fahle & Bachmann, 1996).

Even though amblyopia results in a profusion of visual obstacles, there is one area for which amblyopia may actually provide beneficial. Arguments have been made that while fine spatial detail has been affected in amblyopes, the motion pathway has not been affected (Chung & Levi, 1997; Kubova, Kuba, Juran, & Blakemore, 1996), and may even be more acute (Fahle & Bachmann, 1996). It has been proposed that in amblyopes the parvocellular pathway is impaired resulting in loss of fine spatial detail (Kubova, et al., 1996). On the other hand, parasol cells that lie in the magnocellular layers of the lateral geniculate nucleus (LGN) and are likely to influence perception of motion may be excluded from impairment. It is believed that information then projects to an extrastriate area, where motion is analyzed. Along this motion pathway, it has been proposed, amblyopes are less impaired than along the parvocellular pathway.

Partial evidence to support this hypothesis comes from a study conducted by Kubova and her colleagues (1996). In this study, visual evoked potentials (VEPs) were brought about by either pattern reversal or motion onset and compared between the amblyopic eye and the normal or visually corrected eye in amblyopes. It was found that amplitude and latency were worse for the amblyopic eye in the pattern-reversal VEP, however these measures did not differ significantly between the two eyes during the motion onset induced VEP. Area of fixation seemed to play a minor role as well. Amblyopes with parafoveal or peripheral fixation had motion induced VEPs that were slightly larger than those of the amblyopes with central fixation. This seems to coincide with previous evidence that central vision is more affected in amblyopia than is peripheral (Hess, 1978; Hess & Howell, 1978; Hess & Pointer, 1985, as cited in Kubova et al, 1996). Results in the Kubova (1996) study were, however, confined to high contrast and low spatial frequency. Kubova and her colleagues suggest that more research be conducted to determine whether the ocular dominance and spatial properties of neurons in the MT area of the visual pathway have been affected in individuals with amblyopia.

Another study that provides evidence to support the hypothesis that the motion pathway is unaffected in amblyopes also provides evidence that amblyopes show better performance in a specific area of motion perception than individuals with normal vision. Fahle and Bachmann (1996) demonstrated that amblyopes performed better on vernier acuity at high-speed interpolation. In other words, when presented with vertical lines bisected and offset that were presented in a way that is similar to television (perception of motion resulting from stationary images), at high velocities amblyopes performed at a lower threshold. Fahle and Bachmann propose that amblyopes suppress input from smaller receptive fields which in turn aids their performance on the interpolation task by eliminating irrelevant information.

Chung and Levi (1997) conducted a further study that in addition compares amblyopic vision to normal peripheral vision. Chung and Levi state that vernier acuity in both amblyopic and normal peripheral vision is degraded. Vernier acuity is dependent on stimulus contrast when stationary stimuli is produced (Levi, Klein, & Wang, 1994), which for amblyopes would result in low visual acuity. However, in accordance with the previously mentioned study by Fahle and Bachmann (1996), Chung and Levi found that in amblyopic eyes vernier thresholds are lower with regard to image motion. This is understandable, they say, because in amblyopic (and normal peripheral) vision the spatial scale for vernier discrimination is already larger compared to normal foveal vision, therefor image motion does not exert any detrimental effect on the vernier threshold. The increased tolerance to image motion in amblyopic eyes may be beneficial to amblyopes, because they show higher eye drift velocities when fixating with their amblyopic eyes than do normal observers (Ciuffreda et al., 1980 as cited in Chung and Levi, 1997).

Even though several studies support the hypothesis that the motion pathway remains unimpaired in amblyopia, other research continues to show deficits in motion perception. Hess, Demanins, and Bex (1997) conducted research using motion aftereffects (MAEs) to determine whether motion processing is impaired. The researchers found that amblyopes experienced reduced MAEs for both stationary and moving stimuli. It was reported that no interocular transfer was exhibited in amblyopes. The researchers considered the possibility that the reduced MAEs resulted from spatial scrambling and tested this possibility also. Even when spatial scrambling was accounted for, there was a reduction in duration of MAE. Also considered was the effect of naso-temporal asymmetry. This too was accounted for providing similar results. Unstable fixation of amblyopes was also taken into account; however the method used incorporated individuals with normal vision who were instructed to voluntarily make rapid eye movements in an attempt to simulate the unstable fixation of amblyopia. Hess and his colleagues suggest that stationary and moving stimuli reflect activity of different aspects or sites of motion processing.

One study using drifting sine-wave gratings showed that at high and low frequencies, amblyopes could discriminate direction of motion at detection threshold (Hess & Anderson, 1993). However, Hess and Anderson did not attribute the ability to discriminate motion direction to the motion pathway. This is, in part, a conclusion based on the lack of evidence for significant spatial undersampling in the central field of amblyopes. Hess and Anderson propose that the motion-sensitive pathway of the amblyopic visual system is a spatially scaled version of the normal visual system. The researchers do acknowledge that the possibility exists that a motion deficit may result from a spatio-temporal deficit that does not include the motion pathway.

Even though it is still controversial as to whether the motion pathway is unaffected in humans with amblyopia, treatments have been implicated and though they may not be the potentially most effective, they do help moderate amblyopia or allow dealing with amblyopia less difficult for people who exhibit symptoms. Various forms of treatment of amblyopia include occlusion, penalisation (institution of fog in the "good" eye), use of drugs, and in some cases surgery. According to Campos, (1997) of these methods occlusion is the ideal treatment because it has more positive results with fewer side effects.

Despite lack of consensus in certain areas, research of amblyopia has made significant headway. For example, Levi and Polat (1996) argue that even as adults, the effects of amblyopia can be somewhat corrected. In an experiment measuring acuity, adults were found to improve after practice entailing a Vernier acuity test. They concluded that the involved type of learning indicated alterations in early neural processes.

As researchers continue to isolate the areas of the brain involved in image motion, amblyopia and its causes and effects will become more easily evaluated. One of the primary causes for conflict is that researchers in this field seem to only loosely categorize types of motion. Perhaps the motion pathway is segregated with regard to the types of motion allowing amblyopes to exhibit deficits in specific areas while others remain unimpaired. Another area for conflict is variation in attribution of the causative factors involved in motion impairment. Researchers are unsure as to whether the deficits in motion-related tasks are a result of impairment of the motion pathway or are a result of deficits, such as contrast sensitivity, earlier in the visual pathway that affect subsequent motion analysis.

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