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The Pulfrich Phenomenon:
Monocular Counterparts


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The classical Pulfrich phenomen refers to a peculiar distortion of binocular vision that might be labelled dynamic stereo dysmetropia. The phenomenon is most commonly elicited by means of a pendulum that is made to swing in the subject's frontal plane. When a light-attenuating filter is put in front of one eye, the pendulum appears to swing in and out of the plane, following a more or less ellipsoidal trajectory. The magnitude of the deviation in depth depends on both the density of the filter and the velocity of the swing.

The Pulfrich phenomenon is attributable to a relatively slower excitation of the photoreceptors in the eye with the dimmer image. This leads to a delayed cortical stimulation and sets the scene for stereo disparity, with resulting dysmetropia. Visit the Southern Illinois University Pulfrich Effect website [1] to see a detailed, animated explanation. Pulfrich's original papers from 1922 are available at the same location. For a modern review, see [2].

The Pulfrich phenomenon is not limited to pendulums, of course. All kinds of target trajectories will be affected in similar fashions.The phenomenon may also appear in unexpected situations, like viewing the "war-of-ants" pattern on a television screen lacking an input signal. Hold a light-attenuating filter in front of one eye (a sunglass lens usually does very well) to see the randomly flickering pattern transformed into a slowly rotating cylinder. Don't close the other eye! Lacking a television screen, try the random noise setting in the Filling-in panel.

An apparent dynamic stereo disparity may also arise from non-optical causes, viz, disorders that cause an asymmetry of neural conduction rates between the eyes. Optic neuropathies with bilaterally asymmetric demyelination are probably the most common causes of acquired dynamic stereo dysmetropia. It is not difficult to imagine how acquired Pulfrich phenomena may produce many kinds of problems in daily life, e g, in sports and in traffic situations. The obvious remedy, viz, to put a carefully titrated, tinted lens in front of the quicker eye, actually does work [3].


The Lazy Shadow phenomenon


The classical Pulfrich phenomenon has attracted much attention during the years but little notice has been given to the possible existence of monocular counterparts. Yet, there are good reasons to assume that such animals do exist. What should be required for a demonstration is an apparent dimming of a portion of the retinal image in one eye, plus a uniform movement of the image. When the image moves across the retina, the dimmer part should appear to lag behind the brighter part. Hence, instead of the three-dimensional, dynamic illusion of depth that occurs in the binocular situation, there should arise a two-dimensional, dynamic illusion of lag, or deformation, or both [4].

 Experimental induction

For an experimental induction of a monocular Pulfrich counterpart, a portion of the retinal image needs to be dimmed. Localized dimming cannot easily be produced by light-attenuating filters. A better approach is to present an external test target that contains different luminances. This can easily be done in computer graphics. Computer graphics also easily allows the generation of a variety of target movements. Here is an example of a display implementing these ideas:



(If you don't see a display in the space above, you need to
install the free Java JRE plug-in from Sun Microsystems.)

Use a dim room illumination when viewing the display. There are two bars of dissimilar luminances. Open the Action menu and click on Start to see the bars rotate around one and the same point. Use the Luminance menu to adjust the luminance of the dim bar so that it is barely visible. Now try to decide whether or not the two bars are exactly parallel. Most likely, they will seem to form an angle, as if the dim bar lags behind the bright bar. The lag can be compensated by pointing on the display with the cursor and repeatedly clicking the left and right mouse buttons. Once parallelism has been obtained, it is instructive to stop rotation (in the Action menu), to see how large the required lead angle is.

Experiment with various luminance and RPM settings to see how the lag of the dim bar depends on contrast and rate of rotation (note that the settings in the Luminance and RPM menus are nominal only: actual output depends on the computer's capacity). Also, try various geometric shapes to see if the clarity of lag depends on the target configuration.

The diagrams to the right show some quantitative results obtained with rotating, nesting squares. The vertical axes show the observed lag angles. In the upper diagram, rate of rotation increases from left to right and contrast increases with increasing depth. In the lower diagram, contrast is kept constant, and subtended angle increases with increasing depth. Each bar represents the average of three measurements in a normal subject. The full report was the Editor's Choice for the November 2007 issue of the British Journal of Ophthalmology [5].

Note: When done experimenting, be sure to stop rotation (in the Action menu). All links on this page are disabled whenever the display is active.

Loosely speaking, the dimmer, outer shape can be called a shadow of the brighter shape. Because the shadow lags behind, I have named the illusion the Lazy Shadow. To see another implementation of the Lazy Shadow phenomenon, visit Michael Bach's gold mine of illusions. Highly recommended.


 Are there acquired Lazy Shadows?

Can the monocular Lazy Shadow illusion arise spontaneously, precisely like the classical, binocular Pulfrich phenomenon? The prospects seem quite good. The primary requirement is the spontaneous presence of local variations in the apparent brightness of the retinal image. Such variations should occur within most kinds of relative, localized visual field defects. Obviously, absolute defects are disqualified as there is no vision within such defects. Likewise, overall, uniform depressions are disqualified: there must be local variation. Given local variation, the possibility exists that neural transmission may be locally delayed. What is required to unmask any local delays of transmission is a uniform movement of the retinal image.

Consider, for example, a mid-chiasmal syndrome, with temporal hemifield depressions and normal nasal hemifields. Conceivably, a lagging percept within a temporal hemifield might be unmasked by sliding a horizontal, bar-shaped test target along the vertical meridian. The "temporal" part of the bar should then appear to lag behind the "nasal" part, as if the bar had a vertical offset in the middle. The test would have to be done monocularly, of course. However, the offset effect would presumably be quite small and easily obscured by extraneous factors like variations in target speed and fixation stability.

For a credible demonstration of an acquired Lazy Shadow illusion, a more formal approach is required. It should include a nulling feature. A display like the one presented above might prove useful, although the test task would need to be changed. Instead of trying for alignment of the dim and bright bars, the observer should watch the center of the bright bar and signal any apparent changes of its shape. Conceivably, whenever one half of the rotating bar enters the depressed temporal hemifield, it should appear to be darker and to lag behind the bar in the nasal hemifield, as if the whole bar was slightly bent in the middle. Further, the whole bar should appear to stutter slightly when crossing the vertical meridian. These effects should be nullable by introducing an adjustable lead angle within the temporal hemifield. Here is a dynamic demonstration:



The display aims to demonstrate the possible appearance of a luminous rotating bar to a subject with a right hemifield depression who fixates on the red dot. The lag of the apparently dimmed temporal bar part has been exaggerated for clarity.

The above display should allow quantitative testing in subjects with hemifield depressions. Select the field area to be tested in the Hemifield menu and deselect dimming. Set the lead angle to zero by repeatedly tapping the left or right mouse buttons. Begin with a rotation rate of 20 or 30 RPM. Ask the subject to fixate on the center dot and to try to decide whether the rotating bar is perfectly straight. If the bar appears to be bent, try to compensate the apparent bending by adding a lead angle, by clicking the mouse buttons.

Note: When done experimenting, be sure to stop rotation (in the Action menu). All links on this page are disabled whenever the display is active.

To present the displays on a uniform background, click here.


Clinical implications

The above discussion used the simple example of a hemifield depression but the reasoning about localized delays of neural transmission should be applicable to most types of monocular, relative, localized visual field defects. A clinical corollary, i e, a perception of a spontaneous, dynamic, two-dimensional dysmetropia, also requires movement of the retinal image. Movement of natural retinal images occurs more or less continuously in daily life, e g, during pursuit eye movements, and when moving through the environment. Hence, there is certainly a potential for a frequent occurrence of spontaneous Lazy Shadow phenomena.

Prediction of the nature of acquired Lazy Shadows is fairly easy for localized field defects with simple shapes and uniform depths. However, defects with complex shapes and non-uniform depths, e g, arcuate scotomata, are presumably associated with quite complex varieties of Lazy Shadows. Actually, the conceivable complexities of Lazy Shadow phenomena within localized, relative visual field defects boggle the mind, and particularly so when considering the frequent co-existence of bilateral and asymmetric visual field defects. These complexities make it unlikely that patients might provide spontaneous, verbal descriptions. Nevertheless, knowledge of Lazy Shadow phenomena should prove helpful when attempting to understand the grand picture of life with abnormal vision.

As mentioned above, an acquired, binocular Pulfrich phenomenon may be compensated by putting a light-attenuating filter in front of the quicker eye. Unfortunately, there seems to be no comparable remedy for monocular Lazy Shadows.

Finally, a curio note. Carl Pulfrich had suffered a unilateral eye injury and was effectively monocular. Hence, he was unable to see the phenomenon that carries his name. However, Dr Pulfrich should have been able to see the monocular counterpart described here, 80+ years later.


 The Lazy Shadow may race ahead!


The results presented above from the rotating square study showed that the lag angle of the dimmer, outer square decreased monotonically with decreasing contrast, approaching zero at a luminance level approximating one-half of the luminance of the brighter, inner square, as exemplified in the diagram to the right. With this kind of behavior there seemed to be little point in trying higher outer square luminances in the original study [5]. However, extended measurements have shown that this was an unfortunate decision. Indeed, these new measurements have revealed a completely unexpected phenomenon, namely, that the dimmer square will race ahead at higher luminances (click on the diagram to see the results from the higher luminance range).

The diagram shows lag angles as a function of outer square luminance, for two normal subjects. The inner square luminance was kept constant at 140 cd/m². Each datum point represents the average of three measurements; for clarity, standard deviations are shown for one subject only. Rate of rotation, 39 RPM; subtended visual angles, 4.3° for the inner square and 5.9° for the outer one. Data collected in October, 2007.

While the original results remain compatible with the contention that neural signals from dimly illuminated areas of the retina may be delayed relative to those from more brightly illuminated areas, the new results obviously must have another type of explanation. Presently, none can be offered. These new observations indicate that clinical corollaries of disturbed neural transmission may be truly baffling.


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