Review of Newsome, Wurtz, Dursteler & Mikami, (1985), "Deficits in visual motion processing following ibotenic acid lesions of the middle temporal visual area of the macaque monkey", J. Neurosci 5: 825-840.

visual cortical area MT "contains a preponderance of neurons which encode the direction of motion of visual stimuli."

Does MT have something to do with smooth pursuit? What happens to smooth pursuit if MT is lesioned?

Ibotenic acid is "a neurotoxin which appears to affect cell bodies selectively, leaving fibers of passage unharmed."

Methods
3 macaques were trained to follow a small target moving on a screen 86 cm in front of them.
target speed, 16 deg/sec
Search coils implanted under eye muscles of one eye.
Smooth pursuit monitored and recorded.
Single cells in MT recorded, and classified for location w.r.t. fovea, and for Direc Selec.
   then 1 micro liter of ibotenic acid was injected, under ketamine anesthesia (see p.827, 3rd para)
1 mL = 1 mm^3.

Results
Fig 3A upper: note that a saccade is the first movement made for the step-ramp stimulus.
saccade size is greater than step, implies target speed taken into account.
ibotenic acid injected in a region monitoring 6 deg into periphery.
notice the step is about 6 deg
Fig 3A lower: recorded 24 hr later, after ketamine wore off...
reduced speed of pursuit initiation: due to lack of DS info 6 deg out where step lands?
normal SP speed is possible once the target is "acquired".
init saccade size is about equal to size of step stimulus: no acct of stim speed?
Fig 6: no saccade deficits when made to stationary targets.
Saline injection control.
Fig 7: step in opposite direction of ramp, no saccade needed
now init saccade is too large, headed for step only, not step - velocity vector
and again, pursuit init speed is lower than target speed.

SP before saccade: "The target light came on at the same time that the fixation light came on, but the target did not move until the fixation light went out". How is that different from the paradigm of Fig. 1?
Fig 9: no pre SP after ibotenic.

Conclusion: In the zone of MT lesioned by ibo, the speed signal is reduced, and this reduced speed signal is an error used both by the initial tracking and the saccade generator for a moving target. Once the SP is "on target, the foveal speed detectors take over and SP proceeds normally.

Recovery "Each monkey recovered from its deficits in the first week after the injection."

Where were the lesions? p. 833. Histology: Fig's 11, 12, 13 (poor quality in copies)
neuron "survival rate is less than 5%"
myelin appears to stain normally. White matter not affected.

Qualifications
"Since the speed of our target was always 16 deg/sec, a major predictive element
was present in our experiments which may have abetted the recovery process." Huh?
see p. 833, 2nd column.

Speed reduced, but not eliminated. as if fewer neurons responding represents lower speed...

Review of surgical ablation studies consistent with these results, but more severe:
effects on SP were permanent and also included effects on saccades to stationary targets.
not as selective as ibotenic acid.

p. 837: clinical data on cortical damage and SP deficits. parietal-occipital lesions result in deficits when target motion is TOWARD the side fo the lesion.

In general, lesions of visual cortex affect SP more than saccades.

What about the quick recovery? Point image of McIlwain not entirely eliminated from MT. Other cells in MT may compensate. Likely the recovery is routed through striate cortex, where permanent damage is possible. Could some cells be temporarily inactivated, then recover?

"Alternatively, behavioral recovery may be mediated by striate-fugal pathways parallel to MT." (dorsolateral pontine nuclei)

Hey! what else? What about David Robinson? Why not mention the possibility of plasticity, perhaps from the cerebellum, "repairing" the deficit: Turning up the gain on the remaining motion signal from MT?