ICE can provide high-fidelity intracranial EEG in an intensive care unit setting, can detect ictal discharges not readily apparent on scalp EEG, and can identify early changes in brain activity caused by secondary neurological complications. We predict that ICE will facilitate the development of EEG-based alarm systems and lead to prevention of secondary neuronal injury.

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SUMMARYPurpose: Centrotemporal sharp (CTS) waves, the electroencephalogram (EEG) hallmark of rolandic epilepsy, are found in approximately 4% of the childhood population. The inheritance of CTS is presumed autosomal dominant but this is controversial. Previous studies have varied considerably in methodology, especially in the control of bias and confounding. We aimed to test the hypothesis of autosomal dominant inheritance of CTS in a well-designed family segregation analysis study. Methods:Probands with rolandic epilepsy were collected through unambiguous single ascertainment. Siblings in the age range 4-16 years underwent sleep-deprived EEG; observations from those who remained awake were omitted. CTS were rated as present or absent by two independent observers blinded to the study hypothesis and subject identities. We computed the segregation ratio of CTS, corrected for ascertainment. We tested the segregation ratio estimate for consistency with dominant and recessive modes of inheritance, and compared the observed sex ratio of those affected with CTS for consistency with sex linkage.Results: Thirty siblings from 23 families under-went EEG examination. Twenty-three showed evidence of sleep in their EEG recordings. Eleven of 23 recordings demonstrated CTS, yielding a corrected segregation ratio of 0.48 (95% CI: 0.27-0.69). The male to female ratio of CTS affectedness was approximately equal. Conclusions:The segregation ratio of CTS in rolandic epilepsy families is consistent with a highly penetrant autosomal dominant inheritance, with equal sex ratio. Autosomal recessive and X-linked inheritance are rejected. The CTS locus might act in combination with one or more loci to produce the phenotype of rolandic epilepsy. KeywordsCentrotemporal; Rolandic; Focal sharp wave; Epilepsy; Genetic; Family; EEG; Segregation Address correspondence and reprint requests to Dr. Deb K. Pal, Mailman School of Public Health, Columbia University, 722 West 168th Street, Sixth floor, New York, NY 10032. E-mail: dkp28@columbia.edu. DECLARATIONS The authors declare that they have no competing financial interests. The study was conceived and designed by DKP. Data collection and processing was performed by BB, TC, LLK, and CIA. BB, LS, TC, DKP conducted the analysis. BB wrote the first draft. All authors took part in revising the manuscript for the final draft. Focal sharp waves (FSWs) on the surface electroencephalogram (EEG) are a common (1.6-3.5%) finding in early to mid-childhood (Eeg-Olofsson et al., 1971;Okubo et al., 1994). Although they can be found in asymptomatic children, they are particularly associated with idiopathic focal epilepsy syndromes and have been noted in other epileptic encephalopathies including Landau-Kleffner syndrome (Doose et al., 1996). FSWs are inconstant: they may disappear from one location or other in serial EEGs, and appear to migrate from posterior to anterior regions with maturation (Gibbs et al., 1954). They may occur only in non-rapid eye movement (NREM) sleep, not in a waking state or in rapid eye m...

Propofol has been proposed as a sedative agent during awake craniotomies. However, there are reports of propofol suppressing spontaneous epileptiform electrocorticography (ECoG) activity during seizure surgery, while others describe propofol-induced epileptiform activity. The purpose of this study was to determine if propofol interferes with ECoG and direct cortical stimulation during awake craniotomies in children. Children scheduled for awake craniotomies for resection of epileptic foci or tumours were studied. An intravenous bolus of 1-2 mg.kg-1 followed by infusion of 100-200 microgram.kg-1.min-1 of propofol was administered to induce unconsciousness. Fentanyl (0.5 microgram.kg-1) was administered incrementally to provide analgesia. After the cortex was exposed, the propofol infusion was stopped and the patient permitted to awaken. Cortical electrodes were applied. ECoG was recorded continuously on a Grass polygraph. Motor, sensory, language, and memory testing were done throughout the procedure. The cortex was stimulated with a hand-held electrode using sequential increases in voltage to map the relevant speech and motor areas. We studied 12 children (aged 11-15 years) with intractable seizures. The raw ECoG did not reveal any prolonged beta-waves associated with propofol effect. Electroencephalogram spikes due to spontaneous activity or cortical stimulation were easily detected. Cognitive, memory and speech testing was also successful. We conclude that propofol did not interfere with intraoperative ECoG during awake craniotomies. Using this technique, we were able to fully assess motor, sensory, cognitive, speech and memory function and simultaneously avoid routine airway manipulation.