EEG telemetry with closely spaced electrodes in frontal lobe epilepsy.

The use of additional electrodes (other than standard 10-20 electrodes) has proved to be extremely useful in the investigation of patients with temporal lobe epilepsy. The development of 32- and 64-channel EEG machines, along with the reformatting capabilities of digital EEG has greatly increased the possibilities in the number of electrodes and recording montages. The authors wanted to determine whether the use of closely spaced electrodes designed to increase the coverage of frontocentral regions is of benefit in the investigation of patients with frontocentral epilepsy. Patients investigated for frontocentral epilepsy underwent EEG telemetry with closely spaced electrodes based on the 10-10 nomenclature. Twenty-three patients were studied. An additional 30 minutes was required by technicians to create the montage. Unilateral frontal or frontocentral epileptic abnormalities were observed in 10 patients, independent bifrontal in 5 patients, synchronous bifrontal in 4 patients, and no EEG changes in 4 patients. In no patient did the addition of closely spaced electrodes lead to a change in the classification of the EEG. Closely spaced electrodes did not reveal focal abnormalities, which were not already apparent with 10-20 electrodes, nor did they demonstrate evidence of laterality in bilaterally synchronous discharges.

Intracranial EEG with very low frequency activity fails to demonstrate an advantage over conventional recordings.

PURPOSE: Conventional scalp and intracranial EEG is recorded within a limited band of frequencies (0.3-70 Hz) based on the premise that clinically relevant cerebral activity occurs within this frequency range. Ikeda et al. recently demonstrated focal very low frequency activity (VLFA), <0.3 Hz, at seizure onset for both intra- and extracranial recordings. The purpose of this investigation was prospectively to study VLFA during seizures in intracranial recordings to determine whether activity in this frequency range provides useful information regarding localization of seizure onset and spread. METHODS: Patients undergoing intracranial electrode implantation were studied by using a high-pass filter of 0.01 Hz. The timing, location, and pattern of seizure onset were first determined by using a digital high-pass filter of 0.3 Hz (conventional seizure onset). Seizures were then reviewed without digital filters and the presence of VLFA recorded, along with its timing and location. RESULTS: Forty-seven seizures were recorded in four patients. VLFA was not observed in 29 seizures and, in one other case, VLFA occurred simultaneous with movement. Of seizures with VLFA (n = 17), the timing and location of VLFA were not consistent with those of conventional seizure onset or propagation. CONCLUSIONS: Our study failed to demonstrate any clinical advantage of intracranial telemetry recordings with a high-pass filter of 0.01 Hz over conventional recordings with regard to determining the timing and location of seizure onset and propagation.

Role of electrocorticography at surgery for lesion-related frontal lobe epilepsy.

BACKGROUND: The prognostic significance of epileptiform activity (EA) recorded intraoperatively at electrocorticography (ECOG) in patients with lesion-related frontal lobe epilepsy (FLE) is unknown. METHODS: The results of ECOG performed in 22 patients with intractable FLE and a circumscribed frontal lobe structural lesion were compared with postoperative seizure control. Three patients underwent re-operation for a total of 25 cases, 23/25 with post-resection ECOG. Lesions were neoplasms (12), hamartomas (6) and arteriovenous malformations (4). RESULTS: Outcomes were 15/25 Class I, 5/25 Class III and 5/25 Class IV (Engel classification). Class I outcome was associated with pre-excision EA recorded from < or = 2 gyri (p < 0.05) and absence of EA, or EA limited to the resection border, at post-excision ECOG (p < 0.01). Complete lesion excision was highly correlated with Class I outcome (p < 0.001). The most significant correlations were seen when ECOG and lesionectomy variables were considered together: all 12 cases with complete lesionectomy and absent post-excision EA distant to the resection border had Class I outcome (p < 0.00015) and all 13 cases with complete lesionectomy and pre-excision EA recorded from < or = 2 gyri had Class I outcome (p < 0.00005). CONCLUSIONS: Postoperative seizure control in lesion-related FLE is assured in the setting of complete lesion resection with pre-excision EA recorded from < or 2 gyri and no post-excision EA distant to the resection border; complete lesion excision is of paramount importance.

Chronic periodic lateralized epileptiform discharges during sleep in a patient with caudate nucleus atrophy: insights into the anatomical circuitry of PLEDs.

OBJECTIVE: Periodic lateralized epileptiform discharges have been recognized for 33 years; however, little is known about the underlying mechanism causing periodic discharges. The following case provides an opportunity to study PLEDs in a patient with precisely localized subcortical grey matter lesions. METHODS: Routine EEGs and overnight polysomnography were performed on the study patient. Standard 10-20 electrode positions were used, as well as EOG and chin EMG for polysomnography. RESULTS: The study patient was a 39-year-old woman with severe left caudate nucleus atrophy and right hemi-dystonia. She had left ventral-lateral (VL) thalamotomies in 1989 and 1991, pallidotomy in 1992, and centromedian thalamic stimulator implantation in 1997. EEGs prior to surgical intervention demonstrated left hemisphere PLEDs during sleep. Following CM nucleus stimulatory implantation, the patient had overnight polsomnography. EEG during wakefulness and REM sleep was normal. With stages I-IV sleep left hemisphere PLEDs at 1-2 Hz were seen with fronto-temporal predominance. Sleep spindles were present bilaterally. There was no history of seizures, before or after surgery. CONCLUSIONS: The finding of PLEDs confined to synchronized sleep which were not affected by surgical manipulation of the motor basal ganglia circuit suggests a role of the associative basal ganglia circuit in the generation of periodic phenomenon.

Epileptiform and non-epileptiform paroxysmal activity from isolated cortex after functional hemispherectomy.

The relationship of acute complete cortical isolation to paroxysmal cerebral activity was examined in 16 patients with electrocorticography (ECOG) before and after functional hemispherectomy (FH). Burst-suppression activity appeared over isolated cortex in all cases, the severity of which could be increased by systemic administration of propofol or methohexital. Interictal epileptiform activity (EA) recorded from frontal or parietal-occipital cortex before FH invariably persisted after FH (11 cases). No EA was recorded before or after FH in 3 cases while in 2 cases EA appeared following FH which had not been present before FH. The intensity of burst-suppression activity was not related to the presence or absence of post-excision EA. In total, 30 disconnected cortices were recorded from; relative abundance of EA was increased in 10, unchanged in 17, and decreased in 3 cases. Unrelated to the induction of burst-suppression activity, cortical isolation may decrease the threshold for expression of interictal EA.

Significance of mesial temporal atrophy in relation to intracranial ictal and interictal stereo EEG abnormalities.

We studied 31 consecutive patients with temporal and extratemporal epilepsy who underwent presurgical evaluation with stereotaxic depth EEG (SEEG) to assess the relationships between amygdalo-hippocampal (AM-HF) atrophy and the location of SEEG seizure onset and SEEG interictal abnormalities. Scalp EEG recordings with sphenoidal electrodes had shown bitemporal ictal or interictal epileptic abnormalities in all. Patients underwent high quality MRI scans, including MRI volumetric measurements of mesial temporal structures. None had foreign tissue lesions. The final conclusions of the SEEG investigation coincided with the lateralization obtained by MRI volumetric measurements in the eight patients who had significant unilateral atrophy of the amygdala, hippocampus or both (> 2 SD below the mean of controls). In these patients with unilateral atrophy, all or > 75% of clinical seizures originated from the atrophic side. The seven patients with bilateral, but significantly asymmetrical, mesial atrophy had bilateral seizure onsets with > 70% originating from the more atrophic side in four, from the less atrophic side in two, and without predominance in one. The one patient with severe bilateral symmetrical atrophy had seizures originating equally from both sides. Five patients had no atrophy on MRI, but depth electrodes revealed predominant unilateral ictal temporal onsets in four of them. There was no significant correlation between the frequency of SEEG interictal spikes and the amount of AM-HF atrophy. However, we found a significant correlation between the severity of SEEG background disturbance in AM and HF and the degree of atrophy of these structures. Patients with unilateral atrophy were more frequently free of seizures after surgery than those with bilateral or no atrophy (P < 0.05). We conclude that unilateral mesial atrophy predicts ipsilateral mesial SEEG seizure onset despite bitemporal extracranial EEG foci. However, in patients with significant bilateral mesial atrophy, SEEG seizures may originate from either side, even in the presence of significant asymmetry. Finally, the identification of unilateral mesial atrophy has prognostic importance.

Usefulness of focal rhythmic discharges on scalp EEG of patients with focal cortical dysplasia and intractable epilepsy.

We examined the significance and frequency of occurrence of rhythmic epileptiform discharges (REDs) on the scalp EEGs of 74 patients with intractable partial epilepsy. We also analyzed the relationship of this abnormality to the continuous epileptiform discharges (CEDs) recorded on ECoG. Both REDs and CEDs had been found to be highly specific and sensitive indicators of focal cortical dysplastic lesions. Thirty-four patients (group I) had focal cortical dysplastic lesions (FCDLs) and 40 (group II) had non-dysplastic structural lesions. REDs were observed in 15 (44%) of the 34 patients of group I and in none of group II. REDs did not occur in isolation, were associated with more intermittent interictal spikes involving other regions, but had a greater (P < 0.05) significance for the localization of the epileptogenic area. A strong relationship was observed between the presence of REDs on scalp EEG and the occurrence of CEDs on ECoG recordings. Twelve (80%) of 15 patients with REDs had CEDs. Focal cortical dysplastic lesions are likely to be present when rhythmic epileptiform discharges are found.

Tumoural parietal lobe epilepsy. Clinical manifestations and outcome in 34 patients treated between 1934 and 1988.

Between 1934 and 1988, 34 patients with tumoural parietal lobe epilepsy were treated surgically at the Montreal Neurological Institute (MNI). Fifteen had right-sided and 16 left-sided resections. The remaining three patients had biopsies only. Follow-up ranging from 1 to 40 years (mean 12.3 years) was available for 28 patients. Seventy-five percent (21 out of 28) became seizure free or had rare seizures. Permanent post-operative sensory deficits were described in 12% of patients. An aura was described by 79%. 62% had somatosensory symptoms, contralateral to the epileptogenic region in all but one. Visual illusions (12%), aphasia (9%) and disturbances of body image (6%), were much less common at the beginning of the attacks. Intra-operative cortical stimulation reproduced the habitual aurae in 10 out of 25 (40%) of the patients. The clinical manifestations suggested different spread patterns: 21% had tonic posturing of the extremities, 82% focal clonic activity, 15% head deviation, 9% automatisms and 6% difficulty speaking. Eleven (32%) had Todd's paralysis and 18% postictal dysphasia. Almost half the patients had impaired two-point discrimination in contralateral fingers; two of these also had impaired stereognosis, but only one had astereognosis without coexisting primary cortical sensory deficit. Review of this, now historical, series shows that parietal lobe tumours can be resected with good control of previously intractable seizures. Such an approach is preferable to postponing resection until the lesion is shown to increase in volume.

Parietal lobe epilepsy. Clinical manifestations and outcome in 82 patients treated surgically between 1929 and 1988.

We report the clinical manifestations and outcome of 82 patients with nontumoural parietal lobe epilepsy treated surgically at the Montreal Neurological Institute between 1929 and 1988. Patients with extensive resections extending outside the parietal lobe were excluded. Ninety-four percent exhibited aurae: the most common were somatosensory, described by 52 patients; 13 of these also described pain. Other aurae included disturbances of body image, visual illusions, vertiginous sensations and aphasia or dysphasia. A few patients exhibited complex visual or auditory hallucinations and elementary visual hallucinations. Intraoperative cortical stimulation reproduced the habitual aurae in 44 patients. Often the clinical manifestations indicated ictal spread to the frontal, supplementary motor area, or temporo-limbic areas: 28% of patients exhibited tonic posturing of the extremities, 57% unilateral clonic activity, 17% oral or gestural automatisms and 4% complex automatisms. Sixty-one percent of patients with tonic posturing had epileptogenic zones which included the superior parietal lobe, and in 79% of patients with automatisms the epileptogenic zones extended to the inferior parietal lobe, suggesting different spread patterns. Forty-three patients underwent right, and 39 left parietal corticectomies. Postoperative sensory deficits were seen only when the corticectomy extended into the post-central gyrus. Early in the series extensive nondominant inferior parietal resections led to disturbances of body image in a few patients. Follow-up ranging from 2 to 50 years was available for 79 patients. Sixty-five percent had a complete or nearly complete cessation of seizures. Those patients with no post-resection electrocorticographic epileptiform discharges had a more favourable outcome.

Seizures with onset in the sensorimotor face area: clinical patterns and results of surgical treatment in 20 patients.

It is not generally appreciated that intractable seizures involving the face area are amenable to surgical treatment. Twenty patients with onset of sensorimotor seizures in the face area of the pre- and postcentral gyri have been studied and surgically treated since 1948. Seizures started in the face, tongue, or throat, followed by diverse patterns depending on spread of seizure activity. Two patients had epilepsia partialis continua; 6 had either tonic or atonic drop attacks. All patients had pre- and postcentral face area resections, 12 in the dominant hemisphere. In addition, 3 had more extensive postcentral removal, 7 had temporal lobe, and 4 had small separate or contiguous frontal or parietal resection. Because the seizures were not sufficiently reduced by the first operation, 6 required reoperation; 4 of these patients had residual epileptiform activity on electrocorticogram (ECoG) after the first resection. Three patients had new neurologic signs that did not return to the preoperative level, but in 2 of them the deficit related mainly to higher resection in the central area. All but 2 of these 20 patients had at least moderate seizure reduction. Corticectomy can be performed for treatment of seizures arising in the lower central area and usually does not lead to significant permanent neurologic deficit.