G. Alarcon et al., INTRACEREBRAL PROPAGATION OF INTERICTAL ACTIVITY IN PARTIAL EPILEPSY - IMPLICATIONS FOR SOURCE LOCALIZATION, Journal of Neurology, Neurosurgery and Psychiatry, 57(4), 1994, pp. 435-449
The hypothesis MEG interictal epileptiform activity can be modelled by
single dipoles or by a limited number of dipoles was examined. The ti
me course and spatial distribution of interictal activity recorded sim
ultaneously by surface electrodes and by electrodes next to mesial tem
poral structures in 12 patients being assessed for epilepsy surgery ha
ve been studied to estimate the degree of confinement of neural activi
ty present during interictal paroxysms, and the degree to which volume
conduction and neural propagation take part in the diffusion of inter
ictal activity. Also, intrapatient topographical correlations of ictal
onset zone and deep interictal activity have been studied. Correlatio
ns between the amplitudes of deep and surface recordings, together wit
h previous reports on the amplitude of scalp signals produced by;artif
icially implanted dipoles suggest that the ratio of deep to surface ac
tivity recorded during interictal epileptiform activity on the scalp i
s around 1:2000. This implies that most such activity recorded on the
scalp does not arise from volume conduction from deep structures but i
s generated in the underlying neocortex. Also, time delays of up to 22
0 ms recorded between interictal paroxysms at different recording site
s show that interictal epileptiform activity can propagate neuronally
within cortex. Large areas of archicortex and neocortex can then be si
multaneously or sequentially active via three possible mechanisms: (1)
by fast association fibres directly, (2) by fast association fibres t
hat trigger rise to sharp/slow along the neocortex. The low ratio of t
he simultaneous activation of large neocortical areas can yield spurio
us equivalent dipoles localised in deeper structures. Frequent interic
tal spike activities can also take place independently in areas other
than the ictal onset zone and their interictal propagation to the surf
ace is independent of their capacity to trigger seizures. It is conclu
ded that: (1) the deep-to-surface ratios of electromagnetic fields fro
m deep sources are extremely low on the scalp; (2) single dipoles or a
limited number of dipoles are not adequate models for interictal acti
vity for surgical assessment; (3) the correct localisation of the onse
t of interictal activity does not necessarily imply the onset of seizu
res in the region or in the same hemisphere. It is suggested that, unt
il volume conduction and neurophysiological propagation can be disting
uished, semiempirical correlations between symptomatology, surgical ou
tcome, and detailed presurgical modelling of the neocortical projectio
n patterns by combined MEG, EEG, and MRI could be more fruitful than s
ource localisation with unrealistic source models.