Terrance M. Darcey

The magnetic and electric fields agree with intracranial localizations of somatosensory cortex

We measured the magnetoencephalogram (MEG), electroencephalogram (EEG), and electrocorticogram (ECoG) after stimulation of contralateral median nerve in four patients with partial epilepsy evaluated for surgery. Quantitative localization estimates from equivalent source modeling were compared with locations of central fissure in hand sensorimotor area determined by cortical stimulations, intraoperative photographs, and examination after excision in frontal lobe. We also measured MEG and EEG in nine control subjects. MEG and EEG localizations were within 2.5 cm of the estimated location of central fissure in all 13 subjects. In the three patients who had complete mapping of all three fields, the average distance of localizations from central fissure was approximately 4 mm in both MEG and EEG, 3 mm in ECoG, and 3 mm in combined MEG and EEG. MEG was simpler than EEG, which was simpler than ECoG. MEG resolved ambiguities in both EEG and ECoG. The combination of the three fields added information about the spatiotemporal activity of somatosensory cortex. Localization of central fissure was essential to surgical treatment.

Medial Temporal Objective Lobe Epilepsy: Videotape Analysis of Clinical Seizure Characteristics

Summary: Purpose: The syndrome of temporal lobe epilepsy has been described in great detail. Here we focus specifically on the clinical manifestations of seizures originating in the hippocampus and surrounding mesial temporal structures.

Localized Pain Associated with Seizures Originating in the Parietal Lobe

Summary: Purpose: Ictal pain is a rare symptom of seizures. Epileptic pain may be experienced unilaterally (lateral/peripheral), cephalically, or in the abdomen. Painful seizures have been associated with seizure origin in both the parietal and the temporal lobes. We report on the different types of epileptic pain and discuss its etiology and possible localizing value.

Interictal PET and ictal subtraction SPECT: Sensitivity in the detection of seizure foci in patients with medically intractable epilepsy

Purpose:  Interictal positron emission tomography (PET) and ictal subtraction single photon emission computed tomography (SPECT) of the brain have been shown to be valuable tests in the presurgical evaluation of epilepsy. To determine the relative utility of these methods in the localization of seizure foci, we compared interictal PET and ictal subtraction SPECT to subdural and depth electrode recordings in patients with medically intractable epilepsy.

Secondarily Generalized Seizures in Mesial Temporal Epilepsy: Clinical Characteristics, Lateralizing Signs, and Association With Sleep–Wake Cycle

Summary:  Purpose: Secondarily generalized seizures (SGSs) are often considered to be stereotyped, presumably sharing a common electrical pathway. We examined whether SGSs are uniform in a homogeneous group of patients with mesial temporal epilepsy, and whether certain clinical signs associated with generalization are lateralizing with regard to seizure origin.

SEP topographies elicited by innocuous and noxious sural nerve stimulation. III. Dipole source localization analysis

The dipole source localization method was used to determine which of the brain areas known to be involved in somatosensation are the best candidate generators of the somatosensory evoked potential evoked by sural nerve stimulation. The ipsilateral central negativity and contralateral frontal positivity which occurred between 58 and 90 msec post stimulus (stable period 1) were best represented by a single source located in the primary somatosensory cortex (SI). The symmetrical central negativity and bilateral frontal positivity which occurred between 92 and 120 msec post stimulus (stable period 2) was best represented by 3 sources. One of these sources was located in SI and the other 2 were located bilaterally in either the frontal operculum or near the second somatosensory cortex (SII). The widespread negativity whose minimum was located in the contralateral fronto-temporal region and which occurred between 135 and 157 msec post stimulus (stable period 3) was also best represented by 3 sources. Two of these sources may be located bilaterally in the hippocampus. We cannot, however, eliminate the possibility that multiple sources in the cortex overlying the hippocampus (e.g., SII and frontal cortex) are responsible for these potentials. At innocuous stimulus levels the third source for stable period 3 was located near the vertex, possibly involving the supplementary motor cortex, whereas at noxious levels this source appears to be located in the cingulate cortex. We were unable to achieve any convincing source localization for the widespread positivity which occurred between 178 and 339 msec post stimulus (stable periods 4-6). Available evidence suggests that more sources were active during this interval than the three we could reliably test under these conditions.

Intractable occipital lobe epilepsy: clinical characteristics and surgical treatment.

Intractable occipital lobe epilepsy remains a surgical challenge. Clinical characteristics of 14 patients were analyzed. Twelve patients had surgery, seven patients had visual auras (50%) and only eight patients (57%) had posterior scalp EEG changes. Ictal single‐proton emission computed tomography (SPECT) incorrectly localized in 7 of 10 patients. Six patients (50%) had Engel’s class I outcome. Patients with inferior occipital seizure onset appeared to fare better (three of four class I) than patients with lateral or medial occipital seizure onset (three of eight class I). Patients who had all three occipital surfaces covered with electrodes had a better outcome (four of five class I) than patients who had limited electroencephalography (EEG) coverage (two of seven class I). Magnetic resonance imaging (MRI) lesions did not guarantee a seizure free outcome. In conclusion, visual auras, scalp EEG, and imaging findings are not reliable for correct identification of occipital onset. Occipital seizure onset can be easily missed in nonlesional epilepsy. Comprehensive intracranial EEG coverage of all three occipital surfaces leads to better outcomes.

Brain stimulation for the treatment of epilepsy

Direct brain stimulation is an emerging treatment of epilepsy. Scheduled or responsive stimulation has been applied. The most explored targets for scheduled stimulation are the anterior nucleus of the thalamus and the hippocampus. The anterior nucleus of the thalamus was studied in a large multicenter trial. There was a significant seizure reduction with the stimulator “on” versus “off” during several months after stimulator implantation. The hippocampus as stimulation target has not yet been studied in a large randomized trial. Responsive stimulation applies a stimulus whenever epileptiform activity occurs. It requires on‐line detection of epileptiform activity. This concept is based on the observation that epileptiform activity during functional mapping can be aborted by brief pulses of cortical stimulation. Current technology is able to detect seizure activity intracranially on‐line and delivers a high frequency stimulus if epileptiform activity is detected. A large randomized multicenter trial has been conducted testing this system for focal epilepsy.

Chronic focal epilepsy induced by microinjection of tetanus toxin into the cat motor cortex

The tetanus toxin model of epilepsy, involving direct microinjection of toxin into the mammalian brain, has a number of advantages relative to other chronic models. However, chronic seizure foci have been confined primarily to the hippocampus. In the present study, 5 cats received total doses of 7.5-22.5 ng of tetanus toxin applied to the left primary motor cortex through an epidural cannula. After 2-18 days, all 5 cats exhibited similar persistent epileptiform syndromes. Three distinct types of spontaneous seizures were noted: focal motor seizures of variable complexity, focal motor seizures with secondary generalization, and epilepsia partialis continua. All cats required anticonvulsant therapy. Simple focal motor seizures, which predominated, were electrographically characterized by 3-5 Hz spike-sharp wave activity, originating in the left motor cortex, associated with contralateral shoulder and forepaw clonus and jacksonian spread. Electrographic activity quickly spread to ipsilateral neocortical structures, and in longer episodes to the cingulate gyri. Seizure foci were still active as long as 37 days after toxin injection. Light microscopic damage attributable to the toxin was absent. These experiments further generalized the tetanus toxin model and confirmed its advantages.

Human intracranially-recorded cortical responses evoked by painful electrical stimulation of the sural nerve.

Intracranial recordings were obtained from 5 epilepsy patients to help identify the generators of the scalp somatosensory evoked potential (SEP) components that appear to be involved in orienting attention towards a potentially threatening, painful sural nerve electrical stimulus. The intracranial recording data support, for the most part, the generators suggested by our scalp SEP studies. The generators of the central negativity at 70-110 ms post-stimulus and the contralateral temporal negativity at 100-180 ms are located in the somatosensory association areas in the medial wall of the parietal cortex and in the parietal operculum and insula, respectively. The negative potential at 130-200 ms recorded from over the fronto-central scalp appears to be generated in the medial prefrontal cortex and primary somatosensory cortex foot area. The intracranial recording data suggest that the positive scalp potential at 280-320 ms, which corresponds to the pain-related P2, has multiple generators, including the anterior cingulate cortex, inferior parietal cortex, and possibly the somatosensory association areas in the medial wall of the parietal cortex. Finally, the positive scalp potential at 320-400 ms has generators in brain areas that others have shown to generate the P3a, including the dorsolateral and medial prefrontal cortices, temporal parietal junction, and the posterior hippocampus, which supports our hypothesis that this potential is a pain-evoked P3a. The putative functional roles of the brain areas generating these components and the response properties of the intracranial peaks recorded from these brain areas are in most cases consistent with the attention- and pain-related properties of their corresponding scalp SEP components. The intracranial recordings also demonstrate that the source configuration underlying the SEP components are often more complex than was suggested from the scalp studies. This complexity implies that the dipole source localization analysis of these components will at best provide only a very crude estimate of source location and activity, and that caution must be used when interpreting a change in the scalp component amplitude.