Perception of Visual Motion
25 important questions on Perception of Visual Motion
Who is the classic Akintopsia patient?
- 43 year old patient
- vascular abnormality (superior sagittal sinus thrombosis)
---> felt like she was moving even when she was stationary
What is cerebral akinetopsia?
- you see broken up movement, like a series of snapshots (i.e. not a continuous flow of movement)
- for these patients, all activity must be extremely slow & cautious
What intact functions does LM still have?
Her visual fields are not impaired. She has normal visual acuity, depth perception and spatial contrast sensitivity.
---> she can see the visual field, she just can't see movement
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What sort of problems might someone with akinetopsia experience in everyday life?
- sports
- crossing the street
- watching TV
- socialising (people suddenly appear & disappear)
- interacting with other moving objects - they can't judge the speed (e.g. stepping on an escalator)
What does VEP demonstrate with regards to cerebral akinetopsia?
- shows signals from light stimuli are still coming through - pathways (e.g. retina and optic raditaions) are still intact
= not a problem with the early processing (V1 is still intact)
Patient LM can draw; however, what can she not see when she is drawing?
Who tested the motion perception ability of akinetopsia patients? What did they find?
Examined patient LM
Results:
- No perception of motion above 14 degrees/second
- Impaired discrimination of the direction or speed of moving objects (LM's aspect of movement is impaired)
- Most apparent for high speeds (> 20 deg/s) but also hesitant to report lower speed movement
- Above 7 deg/s her performance declines (she is okay with slower moving objects) ---> to LM, things above 7 deg/s still look like they are around 7/10 deg/s
(see slides 5 & 6 p. 2 for graph)
Who demonstrated that akinetopsia patients have impaired interaction with moving objects?
Akinetopsia patients fail almost every time after 0.6m/s
Interaction with moving objects = you always need updates of info to adjust your movements accordingly
LM cannot interact well with moving objects; however, what 2 things can she detect?
- Distinguish biological from non-biological motion but cannot detect the overall direction of movement (McLeod et al., 1996) - slide 3 p. 3 of notes
What is the doppler effect?
---> Source moves towards receiver = frequency compression
---> Source moves away from receiver = frequency expansion
LM was the 1st case to show what?
Where is the deficit in cerebral akinetopsia?
- Large bilateral lesions: posterior and lateral portions of middle temporal gyrus
- MT = V5 (Temporo-occipito-parietal-junction)
Apart from V5 what other areas are also involved in motion perception?
(Zeki, 1980; Maunsell and Van Essen, 1983; Desimone and Ungerleider, 1986)
What did Gilaie-Dotan et al. (2013) test?
overlapped with V5.
---> Patients with right ventral visual lesions had impaired motion perception
= additional cortical regions are required to support motion perception
Motion perception deficits have also been associated with what part of the brain? (not associated with V5)
What 3 things could underlie LM's preserved minimal motion perception?
- Intact V1
- Some functional sparing of V5 (though this seems unlikely)
- Intact higher-order visual cortical areas
---> other sites in the cortex which are interconnected with V5 compensate deficit of V5 = LM's brain has managed to rearrange itself - example of neural plasticity
What are 3 principal regions of the cortex activated by motion in LM?
- precuneus
- cuneus
In contrast to normal subjects, there was no significant activation of area VI or V2 i.e. LM's visual processing is not in the same areas as the neural typcial population
What did Vaina et al. (2000) measure and what did they find?
Results:
- Increased threshold for motion detection in Group II patients
- Normal motion detection thresholds for patients with only occipito-temporal or anterior frontal lesions
What did Zeki (1974) study?
Results: Cells found in V5/MT that were specialised for visual motion.
(specialised = the preferred movement in one direction)
What is a benefit and a limitation of Zeki's (1974) study?
- single cell recording = good spatial resolution & specificity
Limitation:
- monkeys not humans
What did Newsome et al., 1985; Newsome and Pare, 1988 study?
Results:
After lesion, 100% coherence in order to detect movement
- details of a similar exp (Stevens et al. 2009) p. 204 neuropsychology textbook
Unlike patients such as LM whose akinetopsia is chronic, the monkeys recovered normal motion detection thresholds after a few days - why is this?
---> LM's lesion was also in other areas
What did Tootell et al. (1999) find?
Results: increased activation in V5 (also increased activation in V2) with moving visual images
Benefits of imaging evidence
- neurotypical population processes info in this way
- purely correlational - says what the brain is doing
What did Beckers & Zeki (1995) study and what did they find?
TMS over V5 induced transient deficits in motion perception if applied -10 to + 10 ms after onset
What are the benefits of using TMS?
- investigators can vary the timing of the magnetic pulses ---> knowing when a disruption occurs can help locate where it is occurring
- temporary (allows repetition on the same participant to see if there is the same results in different conditions) = good exp. control
(more info p. 206 neuropsychology)
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