Respiratory changes with seizures in localization-related epilepsy: Analysis of periictal hypercapnia and airflow patterns

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Seyal M, Bateman LM, Albertson TE, Lin TC, and Li CS (2010) Respiratory changes with seizures in localization-related epilepsy: Analysis of periictal hypercapnia and airflow patterns.

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Abstract: PURPOSE: The rate of sudden unexpected death in epilepsy (SUDEP) approaches 9 per 1,000 patient-years in patients with refractory epilepsy. Respiratory causes are implicated in SUDEP. We reported that ictal hypoxemia occurs in one-third of seizures in localization-related epilepsy. We now report on respiratory changes in the ictal/postictal period including changes in end-tidal CO₂ (ETCO₂) that correlate directly with alveolar CO(2) , allowing a precise evaluation of seizure-related respiratory disturbances. METHODS: One hundred eighty-seven seizures were recorded in 33 patients with localization-related epilepsy, with or without secondarily generalized convulsions, undergoing video-electroencephalography (EEG) telemetry with recording of respiratory data. RESULTS: The ictal/postictal ETCO₂ increase from baseline was 14 ± 11 mm Hg (11, -1 to 50) [mean ± standard deviation (SD) (median, range)]. ETCO₂ peak was at or above 50 mm Hg with 35 of 94 seizures, 60 mm Hg with 15, and 70 mm Hg with five seizures. Eleven of the 33 patients had seizures with ETCO₂ elevation above 50 mm Hg. The duration of ictal/postictal ETCO(2) increase above baseline was 424 ± 807 s (154, 4 to 6225). The duration of ictal apnea was 49 ± 46 s (31, 6-222); most ictal apneic events were central. Oxygen desaturation to 60% or less occurred with 10 seizures, including five that did not progress to generalized convulsions. Respiratory rate and amplitude increased postictally. The peak ictal ETCO₂ change and duration of change were not associated with apnea duration or seizure duration. Peak ETCO₂ change was significantly associated with contralateral seizure spread. CONCLUSIONS: Severe and prolonged increases in ETCO₂ occur with seizures. Postictally, respiratory effort is not impaired. Ictally triggered ventilation-perfusion inequality from pulmonary shunting or transient neurogenic pulmonary edema may account for these findings.

Keywords: Sudden unexpected death in epilepsy, Hypercapnia, Hypoxemia, Seizure, Localization-related epilepsy


  • Study of 33 patients (187 seizures) undergoing video EEG. End-tidal CO2 increased in a large proportion of seizures. Spread of the seizure to the contralateral hemisphere (Bateman et al.) was associated with higher end-tidal CO2. Carbon dioxide elevations took 1,000 seconds to return to baseline, on average, in partial seizures that secondarily generalized, and, interestingly, longer than 1,400 on average in partial seizures that did not generalize. By measuring respiratory parameters, the authors were able to demonstrate that apnea occurring in association with seizures is generally central. However, as increased respiratory rate and tidal volume were frequently observed, and CO2 measurements did not correlate with apnea duration, the authors infer that a primary pulmonary defect, such as increased shunting or impaired gas exchange due to pulmonary edema is the primary cause of the increased CO2. This view contrasts with that taken by So. Potential mechanisms of such shunting are discussed at length. The potential for hypercapnic acidosis to terminate seizures is also touched on in the discussion. There was no evidence of lateralization of central control of respiration.


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