Some references

Brain 2009: 132; 3072–3086

Data from intracranial EEG including SEEG and electrocorticography (ECoG) in human patients have confirmed that FCDs are intrinsically epileptogenic (Palmini et al., 1995; Gambardella et al., 1996; Chassoux et al., 2000; Ferrier et al., 2001; Tassi et al., 2001). However, in many cases, it is established that the epileptogenic zone extends beyond the structural lesion seen on MRI (Chassoux et al., 2000; Colombo et al., 2003).

Brain 2011: 134; 1015–1032

The HMGB1-mediated proconvulsant mechanism, described in temporal lobe epilepsy models, and concordant with data in temporal lobe epilepsy human tissue, … is likely to be operative in MCD epileptogenic areas.

Epilepsia. 2013 Sep;54 Suppl 6:33-6

The data highlight the mechanistic relevance of glutamate/NMDA hyperactivation in FCD epileptogenesis and suggest that epilepsy is a pathologic process capable of affecting structure and function of both neurons and glia.

While the presence of unresectable areas within the lesion or the epileptogenic zone limited the utility of surgical resection, the poor outcomes in some of our patients, particularly in the AD group, require comment. One possible explanation is that the anatomical or functional alteration extended beyond the lesion revealed by MRI or SEEG and was not removed. Another possibility is that, following surgical ablation of the leading or at least electroclinically evident epileptogenic zone, another zone that previously was silent or covered by the leading one could become evident or ‘switched on.’

http://brain.oxfordjournals.org/content/125/8/1719.full

I think you will find these articles interesting

http://www.ncbi.nlm.nih.gov/pubmed/24999693

http://www.ncbi.nlm.nih.gov/pubmed/24001068

http://www.ncbi.nlm.nih.gov/pubmed/19679496

http://www.ncbi.nlm.nih.gov/pubmed/19506069

http://www.ncbi.nlm.nih.gov/pubmed/16411966

http://www.ncbi.nlm.nih.gov/pubmed/25296550