Abstracts

The strong association between epilepsy and psychiatric disorders is probably related to a common neurobiological mechanism , which so far remains elusive. During the evaluation of patients with OCD and bipolar disease we found focal or regional MEG epileptiform activity ( MEA ) in the limbic system. We compared the source localization of this activity with the source localization of generalized spike-wave activity (G SWA) recorded in patients with generalized epilepsy. Simultaneous MEG ( Magnes 148 channels ) and EEG ( 20 channels ) were performed in 5 patients with medically refractory generalized epilepsy ( mean age : 39 year) , in 12 OCD patients ( mean age: 33 years) and in 19 patients with bipolar disease (mean age: 39 years). Dipole source localization was performed for all epileptiform potentials ( OCD and bipolar disorder ) and for 84 generalized and bilaterally synchronous spike-waves ( generalized epilepsy group ), which generated 2.853 dipoles. Minimum requirements for dipole selection criteria included : correlation [gt] 0.90, GOF [gt] 0.90, volume [lt] 15 cm3 and Q [lt] 400 nAm. MEG was also performed in 12 normal subjects for control purpose. 1) Generalized epilepsy: Most GSWA bursts had a frequency of 2 to 2 1/2 Hz. The anatomical distribution of dipole source localization for SWA was as follows: cingular cortex= 1768 / 2853 ( 62%), frontal-mesial= 304 / 2853 (10%) and frontal-lateral= 781 / 2853 ( 28%).
2) OCD : MEA consisting of spikes or polyspikes not followed by slow wave activity was seen in 11 / 12 patients ( 92%) involving the cingular cortex ( 11 /12 paients ), insula ( 7 /12 patients ) and orbito-frontal area ( 4 / 12 patients ).
3) Bipolar disease : MEA was documented in 12 / 18 patients ( 68%) and the corresponding dipole source involved the following regions : posterior cingular cortex (7 /12 patients) and posterior insular area ( 10/12 patients ).
4) MEG recordings in control subjects was normal. Our findings show that MEA can be recorded in patients with OCD and bipolar disorder with a predominant distribution in anterior and posterior cingular cortex respectively. Similarly , 62 % of the dipole sources for GSWA in patients with generalized epilepsy, were localized in the cingular cortex . This implies that generalized epilepsy , OCD and bipolar disease share a common neurobiological substrate . We postulate a pathophysiological linkage involving a deficit in serotoninergic neurotransmission.