Purpose: As part of a presurgical extracranial study, we performed intracranial electroencephalographic (EEG) recording by using micro‐guidewires as active intravascular electrodes in two patients with temporal lobe epilepsy in combination with the Wada test. In one case, there was good agreement among information derived from the non‐invasive assessments, such as ictal semiology, interictal and ictal data from long‐term EEG and video monitoring, magnetic resonance imaging (MRI) findings, single photon emission computed tomography (SPECT) findings, and neuropsychological studies, that consistently pointed to one temporal lobe as the epileptogenic region. The other case showed no definite information about the laterality of the epileptogenic region. The interictal scalp EEG for the two cases showed independent, bilateral, anterior to midtemporal spike foci. The ictal EEGs with sphenoidal electrodes showed no apparent changes initially and during simple partial seizures. Methods: After giving informed consent, the patients underwent intracranial EEG recording from intravascular guidewires in combination with the Wada test. With the routine transfemoral catheter technique, two guiding catheters were manipulated into the common carotid arteries via bilateral femoral punctures. These catheters were used not only for the introduction of microcatheters and microguidewires by a “roadmap” technique, but also for the injection of sodium amobarbital for the Wada test. The guidewire tips were advanced 10 mm from the tips of the micro‐catheters, which were placed in the middle meningeal arteries at the level of the foramen spinosum. This distance placed the guidewire tips superficial to the inferior surfaces of the temporal lobes. The proximal end of the steel wire shaft was connected to the recording unit, and the guidewires were used as active intracranial recording electrodes: 10 scalp EEG electrodes were also used to record for ∼1 h, without a sleep tracing. We evaluated the usefulness of this technique by comparison with a simultaneously recorded scalp EEG, and, in addition, with the results of long‐term intracranial EEG recordings. Results: In both cases, intracranial EEG recording from intravascular electrodes revealed frequent spikes and sharp waves from one electrode interictally, but at that time, the scalp EEG revealed no definite paroxysmal discharges except infrequently at the active reference electrode. The laterality of these frequent epileptic discharges was in complete agreement with that of the origin of the ictal discharges recorded from long‐term intracranial EEG electrodes. Conclusions: Currently, the protocol for resections for patients with intractable temporal lobe epilepsy consists of three phases: extracranial studies, long‐term intracranial recording when necessary, and finally surgical resection. Although long‐term intracranial recording is recommended for many patients, the temporal lobectomy may be performed without further invasive EEG studies if there is good agreement among information derived from the noninvasive assessments. For such straightforward cases, if this recording shows interictal discharges on the same side as the noninvasive studies, the outcome of temporal lobectomy may also be improved without further invasive testing and, at least, the reliability of determining the laterality of the epileptogenic focus can be increased. In the cases that have conflicting results from the extracranial studies, it is useful for deciding the side on which the subdural electrodes will be mainly placed. Although the duration of the recording was limited, this technique appears to be very useful because it can be performed easily in the course of angiography without additional invasive steps.
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