No abstract

Ictal hypoxemia has been reported in small series of cases and may contribute to sudden unexpected death in epilepsy (SUDEP). We sought to determine the incidence and severity of ictal hypoxemia in patients with localization-related epilepsy undergoing in-patient video-EEG telemetry. We examined whether seizure-associated oxygen desaturation was a consequence of hypoventilation and whether factors such as seizure localization and lateralization, seizure duration, contralateral spread of seizures, patient position at seizure onset and body mass index influenced ictal-related hypoxemia. A total of 304 seizures with accompanying oxygen saturation data were recorded in 56 consecutive patients with intractable localization-related epilepsy; 51 of 304 seizures progressed to generalized convulsions. Pulse oximetry showed oxygen desaturations below 90% in 101 (33.2%) of all seizures with or without secondary generalization, with 31 (10.2%) seizures accompanied by desaturations below 80% and 11 (3.6%) seizures below 70%. The mean duration of desaturation below 90% was 69.2 +/- 65.2 s (47; 6-327). The mean oxygen saturation nadir following secondary generalization was 75.4% +/- 11.4% (77%; 42-100%). Desaturations below 90% were significantly correlated with seizure localization [P = 0.005; odds ratio (OR) of temporal versus extratemporal = 5.202; 95% CI = (1.665, 16.257)], seizure lateralization [P = 0.001; OR of right versus left = 2.098; 95% CI = (1.078, 4.085)], contralateral spread of seizures [P = 0.028; OR of contralateral spread versus no spread = 2.591; 95% CI = (1.112, 6.039)] and gender [P = 0.048; OR of female versus male = 0.422; 95% CI = (0.179, 0.994)]. In the subset of 253 partial seizures without secondary generalized convulsions, 34.8% of seizures had desaturations below 90%, 31.8% had desaturations below 80% and 12.5% had desaturations below 70%. The degree of desaturation was significantly correlated with seizure duration (P = 0.001) and with electrographic evidence of seizure spread to the contralateral hemisphere (P = 0.003). Central apnoeas or hypopnoeas occurred with 50% of 100 seizures. Mixed or obstructive apnoeas occurred with 9% of these seizures. End-tidal carbon dioxide (ETCO2) was recorded in seven patients (19 seizures). The mean increase in ETCO2 from preictal baseline was 18.6 +/- 17.7 mm Hg (13.2; 2.8-77.8). In these 19 seizures, all oxygen desaturations below 85% were accompanied by an increase in ETCO2. Ictal hypoxemia occurs often in patients with localization-related epilepsy and may be pronounced and prolonged; even with seizures that do not progress to generalized convulsions. Oxygen desaturations are accompanied by increases in ETCO2, supporting the assumption that ictal oxygen desaturation is a consequence of hypoventilation. Ictal hypoxemia and hypercapnia may contribute to SUDEP.

The extensive distribution and simultaneous termination of seizures across cortical areas has led to the hypothesis that seizures are caused by large-scale coordinated networks spanning these areas. This view, however, is difficult to reconcile with most proposed mechanisms of seizure spread and termination, which operate on a cellular scale. We hypothesize that seizures evolve into self-organized structures wherein a small seizing territory projects high-intensity electrical signals over a broad cortical area. Here we investigate human seizures on both small and large electrophysiological scales. We show that the migrating edge of the seizing territory is the source of travelling waves of synaptic activity into adjacent cortical areas. As the seizure progresses, slow dynamics in induced activity from these waves indicate a weakening and eventual failure of their source. These observations support a parsimonious theory for how large-scale evolution and termination of seizures are driven from a small, migrating cortical area.

ICA is a frequent, self-limiting semiological feature of focal epilepsy, often starting before surface EEG onset, and may be the only clinical manifestation of focal seizures. However, prolonged ICA (≥60 s) is associated with severe hypoxemia and may be a potential SUDEP biomarker. ICA is more frequently seen in temporal than extratemporal seizures, and in typical temporal seizure semiologies. ICA rarely persists after seizure end. ICA agnosia is typical, and thus it may remain unrecognized without polygraphic measurements that include breathing parameters.

Purpose Sudden unexpected death in epilepsy (SUDEP) is the leading cause of epilepsy-related mortality. Seizure-related respiratory dysfunction (RD), the duration of post-ictal generalized EEG suppression (PGES) and duration of postictal immobility (PI) may be important in the pathophysiology of SUDEP. Peri-ictal interventions may reduce the risk of SUDEP. Methods We assessed the impact of peri-ictal nursing interventions on RD, PGES and PI duration in patients with localization-related epilepsy and secondarily generalized convulsions (GC) recorded during video-EEG telemetry in the epilepsy monitoring unit. Video-EEG data were retrospectively reviewed. Interventions including administration of supplemental oxygen, oropharyngeal suction, and patient repositioning were evaluated. Interventions were performed based on nursing clinical judgment at the bedside and were not randomized. The two-sided Wilcoxon rank-sum test was used to compare GC with and those without intervention. Robust simple linear regression was used to assess the association between timing of intervention and duration of hypoxemia (SaO2 <90%), PGES and PI using data from only the first GC for each patient. Key Findings Data from 39 patients with 105 GC were analyzed. PGES >2 seconds occurred following 31 GC in 16 patients. There were 21 GC with no intervention (NOINT) and 84 GC with interventions (INT). In the INT group, the duration of hypoxemia was shorter (P=0.0014) when intervention occurred before hypoxemia onset (mean duration 53.1 sec) than when intervention was delayed (mean duration 132.42 sec). Linear regression indicated that in GC with nursing interventions, earlier intervention was associated with shorter duration of hypoxemia (p<0.0001) and shorter duration of PGES (p=0.0012). Seizure duration (p <0.0001) and convulsion duration (p=0.0457) were shorter with earlier intervention. PI duration was longer for GC with PGES than GC without PGES (p<0.0001). The mean delay to first active non-respiratory movement following GC with PGES was 251.96 sec and for GC without PGES was 66.06 sec. The duration of PI was positively associated with lower SaO2 nadir (p=0.003) and longer duration of oxygen desaturation (p=0.0026). There was no association of between PI duration and seizure duration (p=0.773), between PI duration and PGES duration (p=0.758), or between PI duration and the timing of first intervention relative to seizure onset (p=0.823). PGES did not occur in the NOINT group. The mean duration of desaturation was longer (110.9 seconds versus 49.9 seconds) (P<0.0001), mean SaO2 nadir was lower (72.8% v 79.7%) (p=0.0086) and mean end-tidal CO2 was higher (58.6 mmHg v 50.3 mmHg) (p=0.0359) in the INT group compared with the NOINT group. The duration of the seizure or of the convulsive component was not significantly different between the INT and NOINT groups. Significance Early peri-ictal nursing intervention was associated with reduced duration of RD, and reduced duration of PGES. These findings suggest the possibility that such inte...