Epilepsia
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Information regarding outcome in patients with psychogenic nonepileptic seizures (PNES) is limited. We attempted to contact 72 consecutive patients with PNES confirmed by video-EEG monitoring: 51 of 72 (71%) were reached a mean of 15 months (range 12-27 months) after diagnosis and agreed to answer a structured telephone questionnaire. The questionnaire assessed the number of PNES in the last 6 months, antiepileptic drug (AED) use, occupational status, global self-rating, and extent of psychotherapeutic treatments. ⋯ This did not affect the number of psychotherapy visits or outcome. We conclude that PNES cease or significantly decrease in most patients, but occupational status does not improve as often. Earlier diagnosis may improve outcome.
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Thirty-two neonates (26 term and 6 premature) having seizures were prospectively recruited and studied. Using prolonged video/EEG monitoring, we quantified seizure variables (electrographic and clinical seizure durations, interictal periods and electrographic seizure spread) for all 1,420 seizures recorded. The effects of time and antiepileptic drug (AED) therapy were analyzed statistically. ⋯ Among neonates with clear clinical correlates, clinical observations underestimated electrographic seizures in individual neonates by a mean of 54% (range 0-95%). Seizures generally had limited electrographic spread. Use of only four recording electrodes, characteristic of some portable EEG systems, underestimated seizures in 19 neonates, and missed all seizures in 2.
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Comparative Study
Intraoperative thermal inactivation of the hippocampus in an effort to prevent global amnesia after temporal lobectomy.
In an effort to assess the risk of amnesia after anterior temporal lobectomy (ATL), we conducted localized thermal inactivation (cooling) of the hippocampus with memory testing. Thirty-three ATL patients whose preoperative evaluation suggested risk for postoperative amnesia underwent hippocampal cooling. Cooling consisted of inserting a catheter in the temporal horn and irrigating it with an iced solution until a stable hippocampal temperature of approximately 20 degrees C was reached. ⋯ No patient became amnestic. These results suggest that intraoperative hippocampal cooling may be useful in selected cases. However, even among many patients who could cooperate with testing, discomfort, sedation, attentional deficits, confusion, and anxiety made test interpretation difficult.
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We performed a retrospective study of 30 patients with presumed intractable temporal lobe epilepsy (TLE) who underwent chronic intracranial EEG monitoring (CIEM). Multicontact depth electrodes were stereotactically implanted through the medial occipital lobe into amygdala and hippocampus. All patients had previously undergone extracranial ictal EEG monitoring that proved inadequate to localize the epileptogenic zone. ⋯ Nine patients (43%) had a class I outcome (seizure-free, auras only, or provoked seizures), 3 patients (14%) had a class II outcome (> or = 95% seizure reduction), 4 patients (19%) had a class III outcome (> or = 50% seizure reduction); and 5 patients (24%) had a class IV outcome (< 50% seizure reduction or no change). A prolonged interhemispheric propagation time (p < 0.01) and magnetic resonance imaging (MRI)-identified hippocampal atrophy (p < 0.01) correlated with a favorable surgical outcome. Results of this study may prove useful in counseling patients who undergo CIEM before temporal lobe surgery.
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Established antiepileptic drugs (AEDs) decrease membrane excitability by interacting with neurotransmitter receptors or ion channels. AEDs developed before 1980 appear to act on sodium channels, gamma-aminobutyric acid type A (GABAA) receptors, or calcium channels. Benzodiazepines and barbiturates enhance GABAA receptor-mediated inhibition. ⋯ The mechanism of action of oxcarbazepine (OCBZ) is not known; however, its similarity in structure and clinical efficacy to CBZ suggests that its mechanism of action may involve inhibition of sustained high-frequency repetitive firing of voltage-dependent sodium action potentials. Vigabatrin (VGB) irreversibly inhibits GABA transaminase, the enzyme that degrades GABA, thereby producing greater available pools of presynaptic GABA for release in central synapses. Increased activity of GABA at postsynaptic receptors may underline the clinical efficacy of VGB.