216 Information Storage and Neural Control 



It appears then 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. 



It seemed appropriate to inquire whether the change in excita- 

 bility or irritability of the mirror focus was dependent upon 

 impulses circulating in closed chains of neurones or whether it 

 was 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 Kristiansen and 

 Courtois (33). Figure 21 A illustrates persistent, perhaps even 

 augmented activity, in the mirror focus after isolation of the pri- 

 mary lesion. There was cessation of paroxysmal discharge in the 

 isolated primary lesion. The mirror region was then similarly 

 isolated (Fig. 21 B and C). Some residual spiking sometimes 

 persisted for several minutes in the isolated mirror region (Fig. 2 IB) 

 but soon disappeared to be replaced by electrical silence (Fig. 21C). 

 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. The lack of grossly recordable spontaneous paroxysmal 

 activity was associated with a corresponding absence of spon- 

 taneous unit discharge when at a later date, single cells of the 

 isolated epileptic zone were probed with microelectrodes. The 

 last two observations afford reasonably compelling proof that self- 

 re-exciting impulse chains do not persist after the isolation pro- 

 cedure. If the increased excitability characteristic of the epileptic 

 focus is dependent upon continuous self re-excitation, the isolation 

 procedure should abolish the abnormal excitability. A direct test of 

 this prediction was then undertaken. 



The animals which had been subjected to complete neuronal 

 isolation of both primary and secondary epileptogenic regions 

 were prepared for an acute experiment. Several non-epileptic 

 animals had had a comparable isolated cortical slab prepared 

 at the same time as those in the epileptic group. In a third group 

 of animals neuronal isolation of normal cortical tissue in one 

 hemisphere was accomplished prior to the introduction of an 

 epileptogenic lesion in the opposite hemisphere at a point exactly 



