We report 31 episodes of ictal vomiting in nine patients, documented by simultaneous video and EEG recordings. In four patients, chronically implanted subdural electrode arrays recorded the event. Only one patient showed "projectile" vomiting. Amnesia for the episode occurred in eight of the nine patients. Interictal epileptiform abnormalities were maxmal in the right temporal region in seven patients and bitemporal in two. Ictal epileptiform abnormalities were lateralized to the right hemisphere and involved temporal lobe structures in all patients. Three of four patients recorded with subdural electrode arrays were seizure-free following right temporal lobectomy, and the fourth continues to have ictus emeticus at a reduced rate. The consistent right hemisphere lateralization of seizures in this series corroborates with earlier reports documenting right-sided lateralization in four of five previous cases. Two features that help delineate paroxysmal vomiting as an ictal event are (1) patient unawareness of vomiting and (2) its association with other ictal phenomena.
Characteristic of the intimate relationship between sleep and epilepsy are an increase in IEA in nonREM sleep and a decrease in REM sleep, in both generalized and partial epilepsies. The morphology of epileptiform discharges may also be affected by sleep, with a change or breakdown of the generalized pattern in generalized epilepsy, but a better definition of sharp waves in partial epilepsy, during nonREM sleep. One notes a predilection for certain types of epilepsy to occur in sleep, such as benign focal epilepsy of childhood, or to occur shortly after awakening (juvenile myoclonic epilepsy). Epilepsy may disrupt the sleep architecture with an increase in light sleep and a decrease in deep sleep, and an increase in awake time after sleep onset. Sleep is an important activator of IEA and is of value both in the routine EEG evaluation of epilepsy as well as in more prolonged studies used in epilepsy monitoring units.
We observed unilateral dystonic posturing of an arm or leg in 41 complex partial seizures (CPS) from 18 patients. In all cases this was contralateral to the ictal discharge. Unilateral automatisms occurred in 39 of 41 seizures on the side opposite the dystonic limb. Version occurred in 11 of the 41 CPS to the same side as the dystonic posturing and always followed the posturing. Subdural recordings of seven seizures showed ictal onset from the mesial basal temporal lobe. At the onset of dystonic posturing, maximum ictal activity was in the basal temporal lobe with minimal involvement of the cerebral convexity. Unilateral dystonic posturing occurs frequently in CPS of temporal lobe onset and is a lateralizing sign with a high degree of specificity. It probably reflects spread of the ictal discharge to basal ganglia structures.
Twelve patients with medically intractable epilepsy had plates of chronic subdural electrodes placed over the lateral and basal cortical hemispheres during evaluations for surgical therapy. During cortical stimulation, ipsilateral sensations involving any of the branches of the trigeminal nerve were noted in the eye, face, and mouth. Some responses could have been due to dural or direct trigeminal nerve trunk stimulation, but others were probably due to electrical stimulation of trigeminal fibers accompanying the pial-arachnoidal vessels. These fibers had been demonstrated in animals, but not in humans.
Supplementary motor seizures (SMS) are among the group of frontal lobe seizures that may often be misdiagnosed as pseudoseizures (PS). We designed this study to determine the value of clinical phenomena in distinguishing between the two. In a series of patients with SMS, we identified those with symptoms mimicking PS and compared the clinical phenomena with those of clinically similar PS. We found that SMS are short in duration, stereotypic, tend to occur in sleep, and often present with a tonic contraction of the upper extremities in abduction. This sign was specific for SMS, particularly when occurring at the onset. Conversely, PS are long in duration, nonstereotypic, and occur in the awake state. We conclude that clinical phenomena may be useful in distinguishing PS from SMS, although the final diagnosis must be documented by neurophysiologic means.
With the aid of chronic subdural electrodes we have been able to record from the posterior banks of the sylvian fissure, auditory evoked potentials (AEPs) that had morphologies and peak latencies compatible with the primary AEPs described by Celesia and Puletti (1969). These AEPs had amplitudes that were not only affected by the side of stimulus presentation but were maximal in an area close to the primary auditory cortex. The AEPs also displayed an extremely steep spatial gradient and were not altered by pentobarbitone sodium and nitrous oxide anaesthesia. Together, these properties suggest that these subdurally recorded potentials are near-field evoked potentials from the primary auditory cortex. The focal nature of these potentials also allows them to be used as effective electrophysiological tools for localization of the primary auditory cortex in patients.
We compared the findings of scalp electroencephalogram with subdural electrode array (SEA) recordings in 19 patients with refractory frontal lobe epilepsy. Prolonged scalp interictal recordings localized the epileptogenic zone in 12 patients; seven had no interictal sharp waves. The SEAs showed multifocal interictal sharp waves in all patients. Seven patients with localized seizure onset on scalp recording showed extensive ictal onset on the SEA recording. Five patients with lateralized seizure onset to one hemisphere on scalp recording were found to have ictal onset on SEA restricted to a smaller area. Because of the large epileptogenic zone found on SEA recordings, a complete resection was possible in only five (33%) of the 15 patients who had resections. Eight (53%) of the 15 patients benefited from surgery (mean follow-up, 4.6 years). The SEAs also allowed functional localization in most patients. From these data, we suggest that a localizing scalp electroencephalogram in patients with frontal lobe epilepsy may be misleading because SEA recordings show larger epileptogenic zones than anticipated. Furthermore, we postulate that the larger extensive epileptogenic zone may account for the poorer surgical outcome in patients with frontal lobe epilepsy compared with patients with temporal lobe epilepsy.
Summary: We have evaluated the afterdischarge thresholds and functional response thresholds in 21 patients with chronically implanted arrays of subdural electrodes. Afterdischarge thresholds varied from 2 to > 15 mA over the tested cortex, by as much as 12 mA in individual patients, and by as much as 12 mA between adjacent electrodes. Thresholds for functional alteration varied from 2 to 15 mA in tested cortex, by as much as 9.5 mA in individually tested patients, and by as much as 6.5 mA between adjacent electrodes. We conclude that the optimal localization of functional cortical areas requires different stimulation intensities at different points. The use of too high an intensity would produce afterdischarges at some positions. The use of too low an intensity would falsely make others appear functionally “silent.” RESUMEN Hemos evaluado los umbrales post‐descarga y los umbrales de respuesta funcional en 21 pacientes con series de electrodos subdurales implantados crónicamente. Los umbrales post‐descarga variaron entre 2 y más de 15 miliamperios en la corteza investigada, variaron tan to como 12 miliamperios en pacientes individuales y tanto como 12 miliamperios entre electrodos contíguos. El umbral de la alteración funcional varió de 2 a 15 miliamperios en la corteza explorada, tanto como 9.5 miliamperios en un mismo enfermo y tanto como 6.5 miliamperios entre electrodos contíguos. Hemos concluido que para localizar las áreas funcionales corticales óptimas se requieren diferentes estímulos eléctricos en puntos diversos. La utilización de intensidades demasiado elevadas podría producir post‐descargas en algunas posiciones. El uso de intensidades demasiado bajas haría que otras áreas aparecieran como falsas silentes, funcionalmente. ZUSAMMENFASSUNG Wir haben bei 21 Patienten mit chronisch implantierten subduralen Elektroden, die Schwelle der Nachentladung und der funktionellen Antwort geprüft. Über dem untersuchten Cortex variierten die Schwellen für die Nachentladung von 2 bis iiber 15 Milliampere; sie variierten innerhalb einzelner Patienten um mehr als 12 Milliampere und zwischen benachbarten Elektroden um etwa 12 Milliampere. Die Schwellenwerte für die funktionellen Veränderungen variierten von 2 bis 15 Milliampere im getesteten Cortex, um 9,5 Milliampere bei einzelnen Individuen und um 6,5 Milliampere zwischen benachbarten Elektroden. Wir folgern daraus, daß die optimale Lokalisation funktioneller kortikaler Areale unterschiedliche Reizintensitäten an unterschiedlichen Punkten erfordert. Die Verwendung zu hoher Intensitäten würde an einzelnen Stellen Nachentladungen hervorrufen. Die Benutzung zu schwacher Intensitäten würde andere Areale fälschlich erweise als stumm ausweisen.
