Invasive EEG Investigation of the Insula

Invasive EEG investigation of the insular cortex is performed in various forms of focal drug-resistant epilepsies, including patients with a clear-cut intra-insular epileptogenic lesion, such as focal cortical dysplasia, as well as patients whose non-invasive presurgical evaluation suggests perisylvian epilepsy, temporal plus epilepsy, sleep hypermotor epilepsy, or MRI-negative frontal or parietal lobe epilepsy. Stereo-EEG (SEEG) is currently the preferred method for investigating the insula, using orthogonal or oblique trajectories, or a combination, with no evidence of higher risk of intracranial bleeding than in other brain regions. Intra-insular ictal EEG patterns are often characterized by a prolonged focal discharge restricted to one of the five insular gyri, requiring dense sampling of the insular cortex in suspected insular epilepsies. SEEG also offers the potential to perform thermolesion of insular epileptogenic zones, which, together with MRI-guided laser ablation, represents a possibly safer alternative to open-skull surgical resection of the insula.

Pediatric EEG

Electroencephalography (EEG) is an important part of the evaluation of many disorders in infants and children, including seizures and spells. This chapter identifies abnormal epileptiform patterns seen in infants and children and correlates these patterns to specific seizure types and electroclinical syndromes. Generalized discharge (associated with genetic generalized epilepsies as well as epileptic encephalopathies), focal discharge (associated with benign focal epilepsies as well as lesional epilepsies), and hypsarrhythmia are discussed. Additionally, abnormal, but non-epileptiform patterns—including periodic patterns, triphasic waves, intermittent rhythmic delta activity, suppression, asymmetry, and slowing—are reviewed. Specific etiologies associated with various abnormalities on pediatric EEG are identified.

Abstract 17189: Superior Vena Cava as the Substrate of Various Forms of Atrial Tachycarrhythmias: Consideration into the Mechanism and Tachycardia Circuit

Background: The superior vena cava (SVC) is known to possess the myocardial sleeves extending from the right atrium which has been shown to be a substrate for various atrial tachyarrhythmias. However, the precise mechanisms and electrophysiologic feature of these atrial tachyarrhythmias, originating from the SVC has not been elucidated well. Objective: The purpose of this study was to define the mechanisms and electrophysiologic characteristics of atrial tachyarrhythmias originating from the SVC. Methods: In 21 patients with atrail tachycarrhythmias originating from the SVC, the mechanism and tachycardia circuit were examined by the contact or non-contact mapping system (EnSite NavX or 3000). Results: There were 5 reentrant atrial tachycardia (AT), 4 focal ATs and 12 atrial fibrillation (AF). Three reentrant ATs showed a macro-reentrant activation around the SVC sleeve with critical slow conduction zone (SCZ) in the SVC and the remaining 2 showed a localized reentry within the SVC. Four focal AT showed a focal discharge source in the SVC. In 8 of 9 ATs, SCZ or focal discharge source was observed at the area extending from the anterior to lateral portions of the SVC. All 12 AF were initiated by the repetitive discharge from SVC and was maintained by the meandering reentrant activation within the SVC involving the junction between the SVC and right atrium during AF. All 9 ATs were terminated by the radiofrequency energy delivery to the SCZ (n=4) and the focal discharge source (n=3) or isolation of SVC (n=2). All 12 AF were terminated by the circular application of radiofrequency energy delivery around the junction between SVC and right atrium, resulting in the SVC isolation in 9 patients. Conclusions: SVC provides the focal discharge source and the substrate of SCZ of AT. These critical area for maintaining AT mostly located at the antero-lateral portions of the SVC. Focal discharge source and substrate for meandering reentry within the SVC also maintained the SVC origin AF. These unique electrophysiologic characteristics of SVC provide the substrate of various forms of atrial tachycarrhythmias.

High-density mapping of pulmonary veins and left atrium during ibutilide administration in a canine model of sustained atrial fibrillation

Ibutilide can prolong refractory period and terminate reentry. Whether ibutilide has the same effects on pulmonary vein (PV) focal discharge (FD) is unclear. We induced sustained atrial fibrillation (AF) in seven dogs by rapid left atrial (LA) pacing for 74 ± 46 days. Ibutilide was repeatedly infused until it terminated AF (0.02 ± 0.01 mg/kg) or when a cumulative dose was reached (0.04 mg/kg). High-resolution computerized epicardial mapping was performed. We found intermittent FD at the PVs and reentry at the PV-LA junction during AF. Ibutilide increased the cycle length of consecutive reentry from 97 ± 13 to 112 ± 18 ms and increased FD from 96 ± 7 to 113 ± 9 ms. In four dogs with both FD and reentry at the PVs, the incidence of reentry decreased from 3.5 ± 1.9/s at baseline to 2.2 ± 1.8/s after ibutilide administration. However, the incidence of FD remained unchanged. The conducted wave fronts between PV and LA were significantly reduced by ibutilide (10.4 ± 2.0/s vs. 8.0 ± 1.6/s). The ibutilide dose needed to terminate AF correlated negatively with the baseline effective refractory period of PV and LA. We conclude that ibutilide reduces reentrant wave fronts but not PV FD in a canine model of pacing-induced sustained AF. These findings suggest that the PV FD during AF is due to nonreentrant mechanisms. High doses of ibutilide may completely terminate all reentrant activity, converting AF to PV tachycardia before the resumption of sinus rhythm.