Callosal Mechanisms in Epileptogenesis

TLDR: This chapter will focus upon the role of the corpus callosum in secondary epileptogenesis, the process by means of which an initially normal neural network, as a consequence of its chronic exposure to the activity of a primary (1°) epileptic lesion, develops epileptogenic properties of its own.

Abstract: This chapter will focus upon the role of the corpus callosum in secondary epileptogenesis. Secondary (2°) epileptogenesis may be defined as the sum total of that series of events by means of which an initially normal neural network, as a consequence of its chronic exposure to the activity of a primary (1°) epileptic lesion, develops epileptogenic properties of its own. This transformation of the satellite or target network involves passage through several stages of development, as will be described on pp. 17 and 18 below. The primary epileptic lesion may be produced by any of a wide variety of locally acting metals or drugs [see Purpura et al. (1972) for details] or by chronic, recurrent electrical stimulation (kindling), or may arise as a consequence of some injury, as in the naturally occurring epilepsies in man. No matter what the causative agent of the primary lesion, there is a substantial likelihood that the latter will ultimately give rise to satellite foci in distant, but synaptically related, cerebral regions. These secondary foci eventually develop all the properties of the primary focus, including that of giving rise to clinical seizures, of establishing their own secondaries (tertiary epileptogenesis) and of maintaining the newly acquired epileptogenic behavior even after removal of the orginal or 1° focus. The process therefore represents a true spread of epileptogenicity to originally uninvolved regions of the brain. It is a kind of spread, however, that must be sharply distinguished from that which occurs when a formerly quiescent focus begins to spread into surrounding normal tissue and to give rise to clinical convulsive behavior.