The human retina has two classes of light receptor cells: Rods, of which there are about 120 million, and Cones of which there are roughly 6 million. Rod cells are responsible for night vision and contain the pigment rhodopsin, which is sensitive to levels of light about a thousand times weaker than that needed to activate the cone system. The images obtained from the rod system are very coarse and blurred. The cone cells on the other hand, are responsible for the very finely detailed images we obtain from the fovea. FIG 1: shows the structure of cells within the retina which is strangely set up since the light receptors are actually at the back of the retina and not facing the incoming light as one might suppose. They are divided into three groups, each of which has a slightly different spectral response roughly corresponding to the three primary colours of light. (See fig.3) The cone cells congregate exclusively in the foveal region at the centre of vision while the rod cells occupy the peripheral zone. Some cone cells, however, are scattered in the peripheral regions of the fovea allowing for some colour outside of the centre of vision. The positioning of the rods outside of the fovea accounts for our inability to focus on objects that are dimly lit. Most people have noticed that in order to observe a nocturnal object, they have to look away from it a little and catch it using their peripheral vision.

FIG 1:

FIG 2: Retinal Surface.

FIG 3:

Setting aside the vagaries of light adaptation, the eye has to inform the visual cortex of the average illumination of the whole field the fact that the, image surface contains both black and white sub fields. One of those sub fields has a hard, contrasting edge and a soft edge which disappears into the white background at a certain rate (Fourier Series). It would appear that the retina does most of the processing work prior to passing signals to the cortex. In the diagram of the cellular structure of the retina we observe six different types of cell: Rods and cones gather light input and then output their information to the ganglion cells via the bipolar cells. This is the main input-output pathway to the optic nerve. The horizontal and amacrine cells mediate information, using the 1-DE as an example, a receptor cell receiving input from about the middle of this plane sends information down the bipolar cell to the ganglion cell whilst simultaneously sending signals about local conditions laterally across the retina to adjacent cells, thus modifying the output of the ganglia to the optic nerve. Signals are sent back and forth, laterally, about the intensity of incoming light. One imagines that if the neighbouring intensities, as registered by each cell, fall within some 'difference' parameter they will not be registered as an edge, they are merely part of a continuing surface whose hue or tone happens to be changing. However if they turn out to be greater than the difference parameter then an edge will be indicated. Obviously under the former condition, with a gradual fading of black through many greys to white there will be no edge detected but under the second condition, at the 1-DE edge, the sharp difference in colour and tone will result in the detection of an edge. A process called lateral inhibition has been proffered to account for the inhibition of signals across the retina where edges are detected t is not known whether this lateral inhibition actually takes place but it is not implausible to suppose that an amacrine or horizontal cell might switch itself off or into neutral when confronted with opposing strong signals, from two or more of its dendrites.
This is known to be true of the ganglions. There are two distinct types which both can be shown to have circular response fields that are either excitatory or inhibitory (Fig.4).

In the centre of each ganglion response field there is a concentric field that is opposite in activity to the main surrounding field. Thus there are the 'On centre-off periphery' and 'Off-centre-on periphery' types.

FIG 4:
Concentric fields typical of retinal ganglion and lateral geniculate cells elicit an on response if a spot of light hits their 'on' fields and conversely an off response if a spot of light hits the 'off field. These cells normally fire signals without stimulus so an 'on' signal elicits increased firing rates while an 'off signal is inhibitory. If equal spots of light, hit one in the centre and one in the periphery, the response is neutralized to normal firing.

FIG 5:

The 1-DE is the basis of the illusion and experiments have shown that the higher the contrast between the 1-DE and the background, the stronger is the illusory movement. Given that a 1-DE is black at its edge and gradually fades into the background, on a scale of 20 evenly rising grades of grey from white to dark-grey there is a corresponding decrease in the activity of the illusion. The graph in Fig.? shows a response curve for a field composed of black 1-DEs superimposed onto backgrounds of varying shades of grey.
In this test, subjects determined grades of activity for each grey field by allotting a number between 0 and 9. An allotment of 0 was given to fields on a black background and then ranging to 9 for fields on a white background. This assumed a value of 0 for no activity and 9 for maximum activity. Illuminance of the test fields was constant. A basic problem with any measurements of response for the visual system is that responses are very much subject to the light and dark adaptation
of the eye to the illuminance of peripheral objects and surfaces as distinct from the actual object or surface under scrutiny. This means that it is difficult to get truly accurate results to apply generally to all manner of circumstances and environments.

The graph of relative activity to illuminance (Fig.5) is an extrapolation from data collected in 1988 in
a non-standardised environment and using an image different from the one used at present ie Fig.l. It
is included here because it shows an interesting peak activity and fall off both in the dim, near
twilight conditions around Log 0 to -1 of illuminance and a corresponding fall off when the light
became very bright at around Log 2 to Log 3. A test (test 'A') is at present being set up using a
standard test image in standardised conditions to verify these results. Another test (test 'B') using the
twenty backgrounds of evenly graded shades of grey is also being prepared. The different
backgrounds will have the effect of varying the reflected illumination and therefore the illuminance
of the field, the test is to determine whether the relative activity of the illusion, under constant
ambient lighting, corresponds with the results found in test'A'. Still another test (test'C') will
combine relative activity with the variable illuminance of twenty shades of grey and a lighting source
which casts a variable light over the range log -3 to log +3. A 3-dimensional graph will map the test.
Results will be available on completion.


FIG 6:

Processing of the 1-DE Field.

Inspite of the incompleteness of the tests, there is enough information to make conjectures that can direct preparations for future experiments to determine possible reasons for this illusion of movement. Initial thoughts point to two separate processes that initiate the illusion. The first involves the retinal cells. There are a few reasons for this: Firstly, the illusion doesn't work at the centre of vision, in the fovea where there are no rod cells. The properties of movement diminish at the lower
end of the cone receptor threshold and also at the upper end of the rod receptor threshold. This is evident on the one hand as the illuminance gets so low that the activity of the cone system is minimised ie. when colours are only slightly discernible. On the other hand, as the illuminance increases close to the rod saturation threshold the illusory movement slows down and even stops. Colours are still plainly discernible so the cone system is still active indicating that both rod and cone signals are required to filter down to the ganglions in order for the illusion to work. No single receptor type can accommodate the illusion. From the receptors signals pass along interconnections across the retina where edges and continuous surfaces are defined. These are then processed by the ganglia into relative on, off and neutral signals. Logically, the 'on off signals would herald an edge and the 'neutral' signals indicate a continuing surface, the strength of the signals having something to do with hue and illuminosity. I would suggest at this stage that the ganglions representing the 'dissipation plane' of the 1-DE tend to manufacture their own information since they are interconnected via the amacrine cells. If the firing rate from ganglion to ganglion is changing as one travels from the hard edge of a 1-DE across the dissipation plane, interconnecting signals would tend to smooth them out by actually carrying the signals further along thus putting in information that doesn't exist in that region. All this, as long as the change in signal strength doesn't exceed a threshold that signals the presence of an edge. Such an action might be called a 'Continuance Effect'. Secondly, in the visual cortex, the association between simple cells and complex cells is such that a single complex cell can receive input from a large number of simple cells that all have matching orientation sensitivities and matching 'on off areas. The transference of input into the complex cell, from one simple cell to the next, requires a movement down a cortical column or across to another column with cells of the same orientation sensitivity. If the simple cells in a column are interconnected a similar continuance effect, this time for edges, may enhance the illusory movement initiated by the ganglia.


Projexts  Index

Last Revised: 30/12/99