This paper provides a brief description of amblyopia anddiscusses current research regarding the motion pathway inindividuals with amblyopia.
Amblyopia is a condition in which visual acuity in one eye isgreatly reduced. It is caused by lack of stimulation or disuse duringvisual development (Rose, 1998). Because the eye is not fullydeveloped at birth (Jarvis, 1992, as cited in Rose, 1998), infantsneed stimulation to complete the visual neural pathway. When one orboth eyes are inhibited, for example due to misalignment of one eye(strabismus) or a large difference in refractive power between twoeyes (anisometropia), the neural pathway for the inhibited eyedevelops abnormally, or does not develop at all. At approximately sixyears of age eye development is complete (Stager, 1990, as cited inRose, 1998). Before visual development is complete amblyopia can betreated. If it is caught and treated at an early age, normal visioncan be preserved (Rose, 1998).
There are several types of amblyopia. Researchers must be aware ofthe various types of amblyopia because the effects for each are notalways consistent. Strabismic amblyopia is caused when the two eyesare out of alignment due to weak musculature. Anisometropic amblyopiais a result of a large difference in refractive power of anindividual's eyes. Another form of amblyopia results when visualinformation does not reach the retina. This is called stimulusdeprivation amblyopia. Meridional amblyopia is a result of thediffused images caused by astigmatism. Researchers often discoverthat there are differences between groups of amblyopes based on type.For example, Levi and his colleagues (1994) discovered differences invernier acuity between anisometropic amblyopes and strabismicamblyopes.
To better understand amblyopia: how it works, what its causes are,and how it is best treated, current research looks for the underlyingbrain mechanisms that are implicated in the deficits in visual acuityof amblyopes. This information is important because it could providemeaningful insight into the nature of the underlying problemsinvolved (Hess & Anderson, 1993).
There is a general consensus that amblyopes have reduced contrastsensitivity, grating acuity, and spatial resolution in one eye and aloss of binocular vision (Levi, 1991; Sireteanu et al., 1977, ascited 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 letterfound in text rather than an isolated letter. The mechanismsdelegating 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 providebeneficial. Arguments have been made that while fine spatial detailhas been affected in amblyopes, the motion pathway has not beenaffected (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 parvocellularpathway is impaired resulting in loss of fine spatial detail (Kubova,et al., 1996). On the other hand, parasol cells that lie in themagnocellular layers of the lateral geniculate nucleus (LGN) and arelikely to influence perception of motion may be excluded fromimpairment. It is believed that information then projects to anextrastriate area, where motion is analyzed. Along this motionpathway, it has been proposed, amblyopes are less impaired than alongthe parvocellular pathway.
Partial evidence to support this hypothesis comes from a studyconducted by Kubova and her colleagues (1996). In this study, visualevoked potentials (VEPs) were brought about by either patternreversal or motion onset and compared between the amblyopic eye andthe normal or visually corrected eye in amblyopes. It was found thatamplitude and latency were worse for the amblyopic eye in thepattern-reversal VEP, however these measures did not differsignificantly between the two eyes during the motion onset inducedVEP. Area of fixation seemed to play a minor role as well. Amblyopeswith parafoveal or peripheral fixation had motion induced VEPs thatwere slightly larger than those of the amblyopes with centralfixation. This seems to coincide with previous evidence that centralvision is more affected in amblyopia than is peripheral (Hess, 1978;Hess & Howell, 1978; Hess & Pointer, 1985, as cited in Kubovaet al, 1996). Results in the Kubova (1996) study were, however,confined to high contrast and low spatial frequency. Kubova and hercolleagues suggest that more research be conducted to determinewhether the ocular dominance and spatial properties of neurons in theMT area of the visual pathway have been affected in individuals withamblyopia.
Another study that provides evidence to support the hypothesisthat the motion pathway is unaffected in amblyopes also providesevidence that amblyopes show better performance in a specific area ofmotion perception than individuals with normal vision. Fahle andBachmann (1996) demonstrated that amblyopes performed better onvernier acuity at high-speed interpolation. In other words, whenpresented with vertical lines bisected and offset that were presentedin a way that is similar to television (perception of motionresulting from stationary images), at high velocities amblyopesperformed at a lower threshold. Fahle and Bachmann propose thatamblyopes suppress input from smaller receptive fields which in turnaids their performance on the interpolation task by eliminatingirrelevant information.
Chung and Levi (1997) conducted a further study that in additioncompares amblyopic vision to normal peripheral vision. Chung and Levistate that vernier acuity in both amblyopic and normal peripheralvision is degraded. Vernier acuity is dependent on stimulus contrastwhen stationary stimuli is produced (Levi, Klein, & Wang, 1994),which for amblyopes would result in low visual acuity. However, inaccordance with the previously mentioned study by Fahle and Bachmann(1996), Chung and Levi found that in amblyopic eyes vernierthresholds are lower with regard to image motion. This isunderstandable, they say, because in amblyopic (and normalperipheral) vision the spatial scale for vernier discrimination isalready larger compared to normal foveal vision, therefor imagemotion does not exert any detrimental effect on the vernierthreshold. The increased tolerance to image motion in amblyopic eyesmay be beneficial to amblyopes, because they show higher eye driftvelocities when fixating with their amblyopic eyes than do normalobservers (Ciuffreda et al., 1980 as cited in Chung and Levi,1997).
Even though several studies support the hypothesis that themotion pathway remains unimpaired in amblyopia, other researchcontinues to show deficits in motion perception. Hess, Demanins, andBex (1997) conducted research using motion aftereffects (MAEs) todetermine whether motion processing is impaired. The researchersfound that amblyopes experienced reduced MAEs for both stationary andmoving stimuli. It was reported that no interocular transfer wasexhibited in amblyopes. The researchers considered the possibilitythat the reduced MAEs resulted from spatial scrambling and testedthis possibility also. Even when spatial scrambling was accountedfor, there was a reduction in duration of MAE. Also considered wasthe effect of naso-temporal asymmetry. This too was accounted forproviding similar results. Unstable fixation of amblyopes was alsotaken into account; however the method used incorporated individualswith normal vision who were instructed to voluntarily make rapid eyemovements in an attempt to simulate the unstable fixation ofamblyopia. Hess and his colleagues suggest that stationary and movingstimuli reflect activity of different aspects or sites of motionprocessing.
One study using drifting sine-wave gratings showed that at highand low frequencies, amblyopes could discriminate direction of motionat detection threshold (Hess & Anderson, 1993). However, Hess andAnderson did not attribute the ability to discriminate motiondirection to the motion pathway. This is, in part, a conclusion basedon the lack of evidence for significant spatial undersampling in thecentral field of amblyopes. Hess and Anderson propose that themotion-sensitive pathway of the amblyopic visual system is aspatially scaled version of the normal visual system. The researchersdo acknowledge that the possibility exists that a motion deficit mayresult from a spatio-temporal deficit that does not include themotion pathway.
Even though it is still controversial as to whether the motionpathway is unaffected in humans with amblyopia, treatments have beenimplicated and though they may not be the potentially most effective,they do help moderate amblyopia or allow dealing with amblyopia lessdifficult for people who exhibit symptoms. Various forms of treatmentof amblyopia include occlusion, penalisation (institution of fog inthe "good" eye), use of drugs, and in some cases surgery. Accordingto Campos, (1997) of these methods occlusion is the ideal treatmentbecause it has more positive results with fewer side effects.
Despite lack of consensus in certain areas, research of amblyopiahas made significant headway. For example, Levi and Polat (1996)argue that even as adults, the effects of amblyopia can be somewhatcorrected. In an experiment measuring acuity, adults were found toimprove after practice entailing a Vernier acuity test. Theyconcluded that the involved type of learning indicated alterations inearly neural processes.
As researchers continue to isolate the areas of the brain involvedin image motion, amblyopia and its causes and effects will becomemore easily evaluated. One of the primary causes for conflict is thatresearchers in this field seem to only loosely categorize types ofmotion. Perhaps the motion pathway is segregated with regard to thetypes of motion allowing amblyopes to exhibit deficits in specificareas while others remain unimpaired. Another area for conflict isvariation in attribution of the causative factors involved in motionimpairment. Researchers are unsure as to whether the deficits inmotion-related tasks are a result of impairment of the motion pathwayor are a result of deficits, such as contrast sensitivity, earlier inthe visual pathway that affect subsequent motion analysis.
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