OBJECT:The purpose of this paper was to define the general efficacy of and morbidity associated with stereoelectroencephalography using modem methods of imaging and to particularize the risks related to specific lobes of the brain.METHODS:All patients admitted to the Montreal Neurological Institute who had undergone either computerized tomography- or magnetic resonance imaging-guided electrode implantation by one surgeon (A.O.) were reviewed. The procedure was considered efficient if the obtained information was sufficient to make a decision either in support of or against surgery. Two hundred seventeen patients underwent 224 implantations with 3022 electrodes. Complications related to each lobe were as follows: temporal lobe, two abscesses (0.54%); frontal lobe, one abscess and three hematomas (1.4%); and occipital lobe, one hypointense lesion found 1 week after electrode explantation (2.6%). Significant risk factors associated with hematomas were implantation in the frontal lobe (p < 0.05) and the use of four or more implanted electrodes (p < 0.025). General complications included the following: 26 patients, psychiatric symptoms during monitoring; one patient, meningitis; four patients, scalp cellulitis; and two patients, hemiparesis during angiography in the early 1980s. One of these latter patients maintained a mild hemiparesis and represents the only case of permanent neurological sequela in the entire series. Data obtained during recordings supported an indication for surgery in 178 patients (79.5%), excluded a surgical option in 37 patients (16.5%), and were unsatisfactory in nine patients (4%). Thus, the overall efficacy as defined previously was 96%.CONCLUSIONS:Stereoelectroencephalography is an efficient procedure with low associated morbidity. Bilateral exploration of the temporal lobes has a morbidity rate of approximately 1%. A higher risk of hematomas occurs with the implantation of four or more electrodes in the frontal lobes.

We report two cases of transient epileptic foci in humans associated with placement of intracranial electrodes. The abnormalities consisted of restricted areas of active, almost continuous, rhythmic spiking, intermittently evolving into electrographic seizure activity, which resolved spontaneously within 3–4 days. The first occurred after placement of a subdural electrode grid and the second following insertion of epidural peg electrodes. Neuroimaging demonstrated a small subdural hematoma overlying the grid and a focal intraparenchymal hemorrhage underlying the affected epidural electrodes. The insertion of intracranial electrodes may be complicated by the induction of transient epileptic foci unrelated to a patient's typical epileptic generator.

The prognostic significance of epileptiform activity (EA) recorded at electrocorticography (ECOG) was examined in a group of 60 consecutive non-tumoral patients with intractable frontal lobe epilepsy (FLE). Pre-excision EA was documented as absent, focal (one gyrus), regional (two gyri), lobar (3 gyri) or multilobar (frontal+temporal gyri). Post-excision EA was documented as absent, restricted to the resection border, or recorded distant to the resection border, and was quantitated by spike frequency. Pre-excision EA from ≤2 gyri and absence of post-resection EA correlated with Class I or II (Engel classification) outcome while pre-excision EA from ≥3 gyri and persistent post-resection EA, especially distant to the resection border, correlated with Class III or IV outcome (P<0.001). A significant correlation between poorer outcomes and increased abundance of distant post-resection EA was observed (P<0.001). EA restricted to the resection border was not significantly correlated with outcome. Presence of a circumscribed lesion correlated with Class I outcome (P<0.01) and absence of pathological abnormality correlated with Class IV outcome (P<0.05). Neither side nor extent of surgical excision correlated with outcome. EA recorded at ECOG is of prognostic significance in FLE. A lobar or multilobar distribution of pre-excision EA and persistent post-excision EA distant to the resection border, especially when abundant, are highly unfavorable prognostic indicators. In contrast, a restricted distribution of pre-excision EA and absence of post-resection EA both herald a favorable outcome.

Intracranial interictal epileptiform activity (EA) was recorded by chronic stereotactic depth electroencephalography (SDEEG) and acute electrocorticography (ECOG) in 22 patients with complex partial seizures of temporal lobe origin. Chronic SDEEG recordings defined two groups of patients with respect to the presence of absence of lateral temporal EA; 13 patients showed independent lateral temporal EA during chronic recordings and 9 patients did not. All patients had EA recorded from mesial temporal structures during SDEEG. The presence of lateral temporal EA was correlated with a higher pre-operative seizures frequency but not with ictal onset zones, structural pathology, age at onset of epilepsy, or duration of epilepsy. Results of acute ECOG recordings performed on the same patients 1–24 months after SDEEG accurately reproduced the mesial versus lateral distribution of EA within patients (P < 0.0003). Though ECOG was less sensitive than SDEEG in demonstrating EA confined to mesial structures, positive findings at ECOG were 100% specific with respect to SDEEG. These results suggest that, at least with respect to mesial temporal versus lateral temporal structures, there is a constancy within patients in the distribution of interictal EA recorded with chronic intracranial electrodes. In addition, acute ECOG provides an accurate representation of individual patients' interictal EA.

Electrocorticography (ECOG) compared the effects of methohexital (MTH) and selective amygdalo-hippocampectomy (selAH) upon lateral temporal neocortical epileptiform activity (EA) in 31 patients with mesial temporal epilepsy. Pre-excision ECOG showed independent neocortical EA before MTH in 12/31 and after MTH in 18/31. MTH (20-50 mg) activated neocortical EA in 12 cases and induced burst-suppression (BS) over temporal neocortex in 14/31. Post-excision ECOG showed neocortical EA in 21/31 and BS in 27/31: compared with pre-excision ECOG before MTH, selAH activated neocortical EA in 15 cases. Significant correlations were found between presence of pre-excisional neocortical EA and presence of post-excisional neocortical EA (P < 0.001) and between activation of pre-excisional neocortical EA by MTH and activation of (post-excisional) neocortical EA by selAH (P < 0.006). Presence or severity of BS in the post-excision ECOG was not correlated with presence, absence or activation of post-excisional EA. Presence of neocortical EA was significantly correlated with a higher pre-operative seizure frequency (P < 0.001) but not with duration of epilepsy nor surgical outcome. Both MTH and selAH can induce neocortical BS, likely through chemical and surgical disconnection of cortex, respectively. Unrelated to induction of BS, MTH and selAH appear to decrease threshold for expression of neocortical EA in a similar fashion.

Cortical dysplastic lesions (CDyLs) are often associated with severe partial epilepsies. We describe the electrographic counterpart of this high degree of epileptogenicity, manifested by continuous or frequent rhythmic epileptogenic discharges recorded directly from CDyLs during intraoperative electrocorticography (ECoG). These ictal or continuous epileptogenic discharges (I/CEDs) assumed one of the following three patterns: (1) repetitive electrographic seizures, (2) repetitive bursting discharges, or (3) continuous or quasicontinuous rhythmic spiking. One or more of these patterns were present in 23 of 34 patients (67%) with intractable partial epilepsy associated with CDyLs, and in only 1 of 40 patients (2.5%) with intractable partial epilepsy associated with other types of structural lesions. I/CEDs were usually spatially restricted, thus contrasting with the more widespread interictal ECoG epileptic activity, and tended to colocalize with the magnetic resonance imaging-defined lesion. Completeness of excision of cortical tissue displaying I/CEDs correlated positively with surgical outcome in patients with medically intractable seizures; i.e., three-fourths of the patients in whom it was entirely excised had favorable surgical outcome; in contrast, uniformly poor outcome was observed in those patients in whom areas containing I/CEDs remained in situ. We conclude that CDyLs are highly and intrinsically epileptogenic, and that intraoperative ECoG identification of this intrinsically epileptogenic dysplastic cortical tissue is crucial to decide the extent of excision for best seizure control.

A consecutive series of 170 patients who have been submitted to intracranial depth electrode recordings is reviewed to assess the overall morbidity of the technique. Most patients had bitemporal and frontal electrodes inserted and were monitored for an average period of 18 days. A surgically amenable focus was found in 85% of the cases. There were 4 cases of infection including 2 cerebral abscesses which required surgical evacuation. One patient with frontal lobe atrophy developed an acute subdural hematoma after electrode implantation. There was no death or neurological deficit in the entire series. Morbidity was encountered mainly in the neuropsychological sphere, several patients having developed transient postictal psychosis after repetitive seizures. Our recording technique has been associated with low surgical morbidity. Patients undergoing depth electrode recordings should be closely monitored to minimize the occurrence of psychotic episodes associated with drug withdrawal and increased seizure frequency.

We used intraoperative electrocorticography to identify and compare specimens from two groups of patients undergoing temporal lobectomy: (1) spiking cortex (12 patients)—epileptic activity recorded over much of the temporal convexity; and (2) nonspiking cortex (9 patients)—temporal convexity free of interictal spiking, epileptic activity confined to the hippocampus and/or amygdala. Comparative amino acid levels were (μmol/g protein, mean ±: SEM): glutamate—spiking 109.8 ±: 1.8, nonspiking 87.4 ±: 2.0 (p < 0.001); aspartate—spiking 15.2 ±: 0.9, nonspiking 12.2 ±: 0.5 (p < 0.05); GABA—spiking 15.0 ±: 1.0, nonspiking 13.9 ±: 1.4 (NS); taurine—spiking 14.5 ±: 0.8, nonspiking 12.2 ±: 0.8 (NS); and glycine—spiking 11.5 ±: 0.8, nonspiking 7.4 ±: 0.6 (p < 0.01). Cortical epileptic activity appears to be associated with elevated concentrations of glutamate, aspartate, and glycine, but not GABA and taurine, perhaps indicating a relative imbalance between putative excitatory and inhibitory amino acid neurotransmitters.