Have you ever stared out of a moving car and seen the world differently? Blurred. How ’bout conversely, when sitting in a standstill car and seeing the car beside you move…you’re moving?
That, dear friends, is a motion aftereffect.
Or perhaps, you’ve watched one of those trippy videos your psychedelic-using-friend has you stare at so you can trip out afterwards as your eyes melt the world around you for a second….
Let me explain how we got here :
Our tech guy, Cooper, (not saying he’s a hippy, but ya’know how bohemian-like tech guys are) suggested dissecting the science behind these videos…after spending an afternoon glued to the screen.
I watched black circles dwindling into smaller circles in the center for a minute, looked away and saw everything around me melting…rotating…then subtly the phenomenon vanishes and my view is back to normal.
Let me explain as simply as I can.
Repetitive eye movements are known to produce motion after-effects (MAE) when forced to track a moving stimulus/object.
Explanations typically center on the retinal motion created in the peripheral visual field by the eye movement.
After prolonged adaptation to a visual scene moving in a certain direction, observation of a stationary scene evokes an experience of motion in the opposite direction. In short, under certain conditions, a movement produces an aftereffect. This
ancient perceptual effect is easy to generate and very robust.
Mention of this phenomenon can be found as early as Aristotle, who in his treatise on Dreams (Parva Naturalia) writes as follows :
“Also, the senses are affected in this way when they turn quickly from objects in motion, e.g. from looking at a river and especially from looking at swiftly flowing streams. For objects at rest, then seem to be in motion.”
The motion after-effect is an illusion of visual motion resulting from exposure to a moving pattern. There is a widely accepted explanation of it in terms of changes in the response of direction-selective neurons.
Which is essentially the retina (eye) working with specific neurons (brain). However, the phenomenon has no definitive explanation.
The first scientific-case regarding this phenomenon is dated to 1825 by Purkinje after having looked for more than an hour at a cavalry procession, according to “The After-Effect of Seen Objects”, published in the British Journal of Psychology.
In attempting to explain the phenomenon, Johann Purkinje states that the eye, in endeavouring to fixate each individual soldier, moves unconsciously in the same direction.
This so often repeated movement becomes, for the time being, habitual and continued even after the procession has passed. The eye then wants to fixate the stationary objects in a similar manner to which it has learned to fixate the moving one; it unconsciously slides in the accustomed direction, which makes the objects appear to slip away in the opposite direction.
Research has distinguished several variants of the effect.
Three standard factors are variably agreed upon as hypotheses advance till this day, repeating the cause of the phenomenon, may be divided into processes:
(a) Physical (unconscious eye-movements), (b) Psychical (fixation), and (c) Physiological (temporary falsification of conclusions drawn in the central organ from correct sensations).
In a more schematic way, the result of these classifications may be given thus :
A. Early works had no attempt at explanation other than the phenomenon is central, ” between sense-organ and sensorium “.
With explanations ranging from “deeper than the retina” to hypotheses of summation-cells being most definite (method of signal transduction between neurons and action-potentials).
B. Explanation by physical processes.
C. Explanation by psychical processes.
D. Explanation by physiological processes.
(a) Passage of after-images across the retina (aided by association factors).
(b) Local retinal effects (analogous to negative after-images of light and colours).
(c) Principle of oscillation in the function of sense-organ.
(d) Displacement of retinal elements.
(e) Modified blood-flow in retina.
(f) Retinal fatigue plus association of contrast.
(g) Secondary nervous impulse.
(h) Feeling of innervation to antagonistic eye-muscles.
(i) Origin in central nervous system (Summation-cells).
A more recent article in the Journal of Vision, “The Extra-Retinal Motion Aftereffect”, dissects the post-MAE analysis more thoroughly.
Converging recent evidence from different experimental techniques (psychophysics, single-unit recording, brain imaging, transcranial magnetic stimulation, and evoked potentials) reveals that adaptation is not simply confined to one or even only two areas in the brain’s cortex, but involves up to five different sites, reflecting the multiple levels of processing involved in visual motion analysis.
A tentative motion-processing-framework is described, well, suggested, based on motion aftereffect research.
Recent ideas on the function of adaptation are seen as a form of control of the retina to maximize the efficiency of information transmitted, according to the authors of “The Motion Aftereffect Reloaded” in the US National Library of Medicine National Institutes of Health.
Whether or not extra-retinal MAE exhibits ‘storage’ refers to the remarkable finding that retinal MAE persists even if you delay the time between adaptation and test beyond the aftereffect duration.
In essence, storage is used synonymously for the remnants of aftereffects. According to “The After-Effect of Seen Objects”, the motion around the fixed stimulus must remain at a fixed frequency or the retina never adapts.
Some hypotheses believe if the velocity is too slow, the retina doesn’t have to work overtime to adjust, so no aftereffect is created.
“see if it works slowed down for you… – Cooper”
The motion aftereffect has a long and venerable history within vision science.
Less attention has been paid to extra-retinal contributions to MAE following eye-movement. Prolonged eye movement leads to after-nystagmus which must be suppressed in order to fixate the stationary test.
Nystagmus most commonly causes the eyes to look involuntarily from side to side in a rapid, swinging motion rather than staying fixed on an object or person. Some nystagmuses, however, cause the eyes to jerk sideways or up and down.
Afternystagmus, then, is the residual eye movement thought to result from a slowly-dissipating velocity-storage mechanism that aids image stabilization when eye and surroundings move relative to one another.
However, the nystagmus-suppression hypothesis states that extra-retinal MAE should not store, simply because afternystagmus eye movements fade in the dark and so, should cease to exist at time of test if the delay is made long enough.
Nystagmus-suppression gives rise to an extra-retinal motion signal that is incorrectly interpreted as movement of the target. We test this by covering (or adding flickers in this case) your eyes and readjusting your focal point to the same object.
“Do you still see the MAE? – Cooper”
Here are described conditions for newer theories : extra-retinal MAE follows more reflexive, nystagmus-like eye movement. Thus, the MAE is extra-retinal in origin because it occurs in part of the visual field that receives no retinal motion stimulation during adaptation…However, the physical motion of the dot almost certainly gives rise to pursuit-like eye movements, so it is not entirely clear what motion percept is being nulled, or how eye movement, retinal slip and aftereffect interact during tests.
The basis for these experiments is based around reminiscence (remembering) vs. obliviscence (forgetfulness) of the mind.
But as stated throughout, this phenomenon process is “almost certain”.
Several important issues remain to be resolved, including :
- How do the different adaptation variations/components combined and individually determine the kind of observed after-effect seen?
Let us know if our motion aftereffect videos tricked your eyes.