FRANK MORRELL 379 



cortex and the animal was again tested 7 days after development ot the 

 lesion (second column of tracings). The marked augmentation of the 

 directly evoked response limited to the contralateral visual cortex is 

 clearly apparent. A similar augmentation of the direct cortical response in 

 areas contralateral to a cortical circumscction has been noted by Eidelberg 

 Konigsmark and French (1959). These authors also attribute such aug- 

 mentation to increased epileptogenic properties. 



These data suggest that the secondary area of discharge may be described 

 as a ganglionic network in which spontaneous and evoked activity have 

 been chronically altered as a result of experimental alteration of its 

 environmental input in the form of continuous epileptiform bombard- 

 ment. 



The sequence just described may be altered and the development of the 

 mirror focus prevented by section of the corpus callosum either before 

 production of the primary lesion or within 24 hours afterwards. A similar 

 observation has been made by Erickson (1940) with respect to electrically 

 induced after-discharges. Interestingly enough, the development ot 

 independent contralateral secondary discharge may also be prevented if 

 the callosal connections remain intact but a subpial partial isolation of the 

 contralateral cortex is carried out within the same time interval. Such an 

 isolation deprives the cortex of all of its subcortical connections as well as 

 those relating it to other cortical areas of the same hemisphere (Fig. 5 A 

 and B). This would suggest that the enduring changes in synaptic function 

 which form the basis of the independent mirror focus require that at least 

 two forms of input be available to the cortical region concerned. 



We may now proceed to ask whether the change in excitability or 

 irritability is dependent upon impulses circulating in closed chains oi 

 neurones or whether it is based upon structural alterations of cells within 

 the network. As a first step, neuronal isolation of the region of primary 

 discharge was carried out according to the technique of Kristians'en and 

 Courtois (1949). Fig. 6A illustrates persistent, perhaps even augmented, 

 activity in the mirror focus after isolation of the primary lesion. Note that 

 the paroxysmal discharge in the primary lesion had ceased: (Compare 

 with Fig. 3 on the same ammal.) The mirror region may then be similarh' 

 isolated (Fig. 6B and C). Some residual spiking sometimes persists for 

 several minutes in the isolated mirror region (Fig. 6B) but soon disappears 

 to be replaced by electrical silence (Fig. 6C). After these isolations were 

 performed, the calvarium was replaced and the animal returned to its cage 

 for several months. Surface recording during that period indicated no 

 return of paroxysmal discharge. At the time for the definitive experiment, 



