Recovery of motion perception after surgery

For a while now I’ve been revisiting an article by Nawrot, Rizzo, Rockland and Howard III in Vision Research (“A transient deficit of motion perception in human“). I’m fascinated because it is a very well-documented case of functional recovery after surgery for epilepsy. I’m also intrigued by what the authors don’t ask about or comment on (how was the recovery mediated?), and by the implications of this case for understanding neural modularity (or equipotentiality, the complementary idea). These latter two discussions will be held over for another post.

The authors describe patient SF, a 19 year old female with intractable epilepsy in the posterior portion of the temporal lobe, at the occipital lobe junction, in the right hemisphere. They discuss the difficulty in finding a human homologue to motion area MT in the macaque, which takes part in many kinds of motion computation and which provides input to and receives input from other areas, even ones not particularly associated with motion processing. For example, there is connectivity between area V4, commonly associated with the processing of color, and MT in the macaque. Fans of the binding problem understand why connections between MT and V4 are potentially important.

SF was tested extensively prior to topectomy (the removal of tissue corresponding to epileptic foci). The area removed was the lightly-shaded area in the below figure – the small, numbered darker areas were removed for microscopic examination. White matter and surrounding vasculature was generally spared in the operation.


Nawrot et al. tested SF on first-order motion tasks, second-order motion tasks, and mental rotation. The authors describe the types of motion in this way:

First-order motion refers to a change in luminance over both space and time that would arise, for instance, when a dark object translates over a light background. The perception of first-order motion relies on neural mechanisms that correlate luminance displacements over time (spatiotemporal energy). In contrast, second-order motion is characterized by a complex movement for which the simple first-order mechanism is insensitive.

…a second-order motion is created in a region filled with black and white random dots by reversing the luminance of the dots first at one side of the region and continuing this transformation successively across this region over time.

Excellent demos of these types of motion stimuli (though not using dots) can be found here.

Nawrot et al. used dot stimuli popularized by Newsome and Pare (1988). Here’s what they look like…


In stimuli like these, the threshold for accurately detecting the global motion of the dots (the amount of correlated movement required) for observers of SF’s age is about 12%. Higher threshold percentages mean that you are having trouble detecting coherent motion.

If you look at SF’s presurgery data on the left of the figure below, she was in (or very near) the normal range for detecting dot motion for dot patterns presented to each visual field in the first-order motion task. Note also that her right hemisphere is responsive to the left visual field and vice versa. The hatched area delineates normal performance.


At Day 4 she showed a dramatic rise in her motion threshold only in the left visual field, but shows complete recovery by Day 18.

Nawrot et al. demonstrate this recovery, utilizing the same type of graphs, for SF’s second-order motion thresholds and for mental rotation performance. She exhibited nearly perfect functional recovery by between 18 and 32 days post-surgery, depending on the task. The $64,000 question is how does this happen?

5 responses to “Recovery of motion perception after surgery

  1. Here’s your answer in a nutshell: plasticity

    In the experiments with monkey done by Newsome and so many others ( refs here, monkeys trained to respond these motion stimuli will show severe deficits immediately after surgical ablation of MT, but then recover most of their ability very rapidly. As I recall, recovery in these subjects is usually attributed to the rewiring of other motion areas not usually doing the job of global motion integration, so that now they do.

    See, for example, that large literature and the many papers on cortical plasticity generated by John Kaas and his students, particularly Ken Catania and Leah Krubitzer ( an example)

  2. boojie,
    Of course plasticity is what is responsible (it wasn’t the ether!). It sounds like you read the same stuff I read.
    My plan was indeed to write about the lesioning work with ibotenic acid in the next post. I was also planning on writing more specifically about recruitment of nearby areas and the possibility of homologous MT being responsible, and about functional reorganization as a result of this patient’s epilepsy.
    More comments are certainly welcome.

  3. Excellent post. Really enjoyed the analysis. Look forward to more like this….

  4. this is excellent…

  5. Pingback: Are “big ideas” taught in grad school now? An appreciation of John Hughlings Jackson. | Peripersonal Space

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