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.



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