4.7 Article

Enhanced QT shortening and persistent tachycardia after generalized seizures

Journal

NEUROLOGY
Volume 74, Issue 5, Pages 421-426

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1212/WNL.0b013e3181ccc706

Keywords

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Funding

  1. Department of Health
  2. Deutsche Forschungsgemeinschaft
  3. Medical Research Council [G0400136, G0802158, G0701050, G069336]
  4. European Community
  5. Wellcome Trust
  6. Epilepsy Research UK
  7. Medical Research Council [G0802158, G0801316, G0400136, G0701050] Funding Source: researchfish
  8. MRC [G0802158, G0801316] Funding Source: UKRI

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Objective: Generalized tonic-clonic seizures (GTCS) are a major risk factor for sudden unexpected death in epilepsy (SUDEP). We investigated whether ictal/postictal cardiac features were dependent on seizure type within individual patients. Methods: ECG data from patients with medically refractory temporal lobe epilepsy (TLE) undergoing presurgical investigation who had both complex partial seizures and secondarily GTCS during video-EEG telemetry were retrospectively reviewed. Peri-ictal heart rate (HR), corrected QT interval (QTc), HR variability, and cardiac rhythm were assessed. Results: Twenty-five patients were included in this study. Secondarily GTCS led to higher ictal HR, persistent postictal tachycardia, and decreased postictal HR variability. Moreover, abnormal shortening of QTc occurred in 17 patients mainly during the early postictal phase and significantly more often in secondarily GTCS. Abnormal QTc prolongation occurred in 3 patients with no significant association with GTCS. Benign cardiac arrhythmias occurred in 14 patients and were independent of seizure type. Conclusions: Our data suggest a substantial disturbance of autonomic function following secondarily generalized tonic-clonic seizures (GTCS) in patients with medically refractory temporal lobe epilepsy. The observed alterations could potentially facilitate sudden cardiac death and might contribute to the association of sudden unexpected death in epilepsy with GTCS. Neurology(R) 2010;74:421-426

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