AJMONE-MARSAN 165The experimental aspect of the Electroencephalography Branch in
cluded some interesting studies on the physiology of the visual system,
on callosal interactions, and on thalamocortical mechanisms, but the
main investigative goals were focused, from the very beginning, on the
basic neuronal mechanisms underlying the electrographic changes that
are considered the expression of epileptic activity. Through the years,
starting in 1954, and in collaboration with many of the Research Asso
ciates whose names are listed in Table 1, various experiments were
designed using models to mimic acute seizure disorders in the cat and
the monkey, with emphasis on: (a) models that would reproduce the
interictal and ictal manifestations of focal cortical epileptogenic pro
cesses; (b) models that might throw some light on possible subcortical
mechanisms for primary generalized seizure disorders; and c) models to
analyze patterns of electrographic seizure activity and those at the basis
of seizure onset, or transition from interictal phenomena. Most of these
investigations utilized extra- and intracellular microelectrodes for record
ing cortical and subcortical structures. In addition, several chemical
substances were either systemically administered, topically applied, or
iontophoresed to reproduce epileptiform phenomena. Repetitive electri
cal stimulation leading to after discharges was also utilized.
The results from these various studies were published between 1955
and 1980. Studies by T. Francis Enamoto and I^22 and Hideo Matsumoto
and I,^23 dealing with analysis of the neuronal events underlying the
occurrence of the so-called “EEG spike,” demonstrated that in an acute
epileptogenic focus produced by topical application of strychnine or
penicillin, there is a high degree of synchronization in the firing of
most neurons within the local population affected by the epileptogenic
agent, in correspondence with, and obviously resulting in, the surface cor
tical EEG spike. This confirmed Jasper’s “hypersynchronization” theory.
However, this “spike,” is not a simple “envelope” of action potentials, but
rather the summation of large, and relatively long-duration shifts of de-
polarization undergone paroxysmally by the membrane of the individual
neurons (see fig. 2), often followed by considerable hyperpolarizing shifts.
This was the first systematic analysis and description of these charac
teristic membrane modifications and cellular events within the (acute)
epileptogenic process. Some of these phenomena had been described by