(This was an essay for my cognitive neuroscience class to review a paper on a neurological disorder. I’m on break this week, so I should get a chance to write something for real soon. In the meantime, you can amuse yourself with the first graphic I have put together. I’m a little proud of it)
In 1983, Zihl, Von Carmon, and Mai published about a patient that had developed motion blindness after brain lesions. Although she was capable of seeing stationary objects, her perception of moving objects was impaired, a disorder known as akinetopsia. In this report, I will discuss some of the original findings in the Zihl et al. (1983) paper, then address more recent findings on akinetopsia.
Although previous patients with akinetopsia are mentioned, a review (Zeki, 1991) found that there were very few cases. The case study in Zihl et al. (1983) focuses on patient L.M. with bilateral lesions in the lateral temporo-occipital cortex and associated white matter. Other than minor difficulties with naming objects (anomic aphasia), her impairment was limited to an inability to perceive motion. Instead of perceiving fluid motion, she saw objects appear at various locations along their trajectories. An example of her impairment was that “she could not stop pouring at the right time since she was unable to perceive the movement in the cup (or a pot) when the fluid rose.” The authors ran several experiments to determine the extent of the impairment.
First, they established normal visual function on stationary targets. Visual acuity (sharpness), binocular vision, stereopsis (depth perception), foveal color discrimination, and recognition of shape stimuli and words were near normal and did not indicate any deficit. Potentials recorded from checkboard pattern stimuli, and various tests of visual fields, flickering, localization, and reaction time were all also normal.
Next, they tested various moving stimuli. With a moving spot of light in the fovea, L.M. had slightly better perception when allowed to track the stimulus instead of fixating at a central point. Generally, she could see slow movement ( <14 deg/s for horizontal and <10 deg/s for vertical movement), but could not for faster speeds. In her peripheral vision, L.M. was unable to distinguish either direction or speed of motion. She was unable to notice any motion in depth of a cube moved towards and away from her. L.M. under-predicted “motion time” as to how far an object should move along a trajectory. She also did not perceive motion affect effects or apparent motion. Tactile and acoustic motion perception, however, were normal.
With visual pursuit eye movements, L.M. could smoothly track at lower speeds (< 8 deg/s) but could not at higher speeds without her eyes jumping. When blindfolded, she performed as well as a normal subject with finger tracing, but she was not able to benefit and speed up from visual information as the normal subject was able.
From L.M., the authors conclude that movement vision is processed separately from primary vision because there was no impairment with stationary or non-visual stimuli. The region responsible for motion perception has been identified as V5 (or MT, middle temporal), and temporary motion blindness can be induced by TMS over V5 (Beckers & Homberg 1992). Currently, there are no known treatments for the problem, though L.M. reported development of other senses to compensate for the impairment. A follow-up study also found that L.M. was able to distinguish human movements when lights are attached to joints of a person in the dark.
Given the few cases of akinetopsia, these findings are largely specific to L.M., though the exact nature of the impairment has been studied in monkeys recently as well.
Beckers, G., Homberg, V. (1992). Cerebral Visual Motion Blindness: Transitory Akinetopsia Induced by Transcranial Magnetic Stimulation of Human Area V5. Proceedings: Biological Sciences, 249 (1325), 173-178.
Zeki, S. (1991). Cerebral Akinetopsia. Brain, 114, 811-824.
Zihl, J., Von Carmon, D., Mai, N. (1983). Selective disturbance of movement vision after bilateral brain damage. Brain, 106, 313-340.