Authors :
Presenting Author: Deidre Dragon, BS – University of Iowa
Rup Sainju, MBBS – University of Iowa; Justin Kuhn, RRT – University of Iowa; Jeni Michelson, BS – University of Iowa; Linder Wendt, MS – University of Iowa; Patrick Ten Eyck, PhD – University of Iowa; George Richerson, MD – University of Iowa; Brian Gehlbach, MD – University of Iowa
Rationale: There are two sources of tonic respiratory drive: "wakefulness drive” from descending forebrain projections and “chemoreceptor drive” from central CO
2 chemoreceptors (Figure 1). The hyperoxic hypercapnic ventilatory response (HCVR) is a direct measure of central CO
2 chemoreception. Low interictal HCVR is associated with severe postictal hypoventilation after generalized convulsive seizures (GCS).
1 HCVR may also be attenuated by focal impaired aware seizures.
2 Thus, an attenuated HCVR is a potential biomarker for SUDEP risk. Here, we report a case of complete abolition of “chemoreceptor drive” measured immediately after a focal aware temporal lobe seizure.
Methods: Our subject was admitted to the epilepsy monitoring unit for video-EEG study at the University of Iowa Hospitals and Clinics. She was prospectively enrolled in an ongoing research study evaluating the effect of seizures on HCVR. In this protocol, HCVR is measured using a modified hyperoxic CO
2 rebreathing technique.
1 Simple linear regression is performed on data points above the ventilatory recruitment threshold to calculate HCVR slope (∆VE/∆ETCO
2). HCVR is measured during the interictal and early postictal periods and at least 12 hours after the last seizure to assess recovery.
Results: The subject is a woman in her forties with drug resistant epilepsy for six years
. Semiology consisted of impaired awareness, repetitive clicking noises, or swallowing, with or without preceding aura (experiences of familiar taste, smell, or vision from her childhood), occurring one to two times per month. She had a mild concussion due to a fall seven years prior to seizure onset. Epilepsy protocol 3T MRI brain did not reveal a potential etiology for epilepsy, and outpatient EEG showed independent sharp waves in bilateral temporal regions. She underwent interictal measurement of HCVR on day one of admission. On day three, she had a subclinical seizure at 08:24 AM. At 09:07 AM she experienced a brief aura while her baseline minute ventilation was being measured, immediately prior to performing the planned postictal HCVR. Subsequent review of her EEG revealed a second seizure that ended immediately prior to the onset of CO2 inhalation. Both seizures were of left temporal onset. The HCVR was repeated on day 4 prior to discharge. Analysis of HCVR slopes revealed complete abolition of the chemoreceptor drive to breathe by the focal aware seizure with restoration of this drive when retested a day later (Figure 2).
Conclusions: This case illustrates that focal aware temporal lobe seizures can transiently abolish central CO2 chemoreceptor drive for breathing. Chemoreceptor drive is not required when the patient is awake but becomes the major drive for breathing when wakefulness drive is compromised, as in the postictal state after GCS. The absence or attenuation of chemoreceptor drive may lead to severe postictal respiratory depression, and possibly an increased risk of SUDEP.
Funding: NIH-R01 NS113764-01 George Richerson and Brian Gehlbach (co-PIs)