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• Unapparent seizures as cause of recurrent asystole
  Adam Strzelczyk
  Published on: 13 April 2016

• Published on: 13 April 2016

  Unapparent seizures as cause of recurrent asystole

  • Adam Strzelczyk, MD
  • Other Contributors:
    • Felix Rosenow

  Dear Editor

  The authors present a very interesting case of recurrent asystole in the acute phase of ischemic stroke. However, the pathophysiology of this rare event remains speculative. We agree that a Cushing reflex due to intracranial hypertension is very unlikely to be the culprit as the asystole occurred well before the mass effect developed. An interruption of sympathetic cardiac tone as proposed by the aut...

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  Dear Editor

  The authors present a very interesting case of recurrent asystole in the acute phase of ischemic stroke. However, the pathophysiology of this rare event remains speculative. We agree that a Cushing reflex due to intracranial hypertension is very unlikely to be the culprit as the asystole occurred well before the mass effect developed. An interruption of sympathetic cardiac tone as proposed by the authors is a possible mechanism, but the occurrence in the first 20 hours may also point towards focal seizures in the acute phase of stroke as underlying cause for asystole.

  Seizures are frequently associated with hemorrhagic as well as ischemic stroke with cortical involvement. Up to 9% of patients will suffer from seizures after stroke with only about one quarter of them to develop epilepsy afterwards. 40% of all the seizures will occur within 24 hours after stroke onset (1). These early-onset seizures are possibly due to regional metabolic dysfunction and excitotoxic neurotransmitter release secondary to hypoxia. We propose that clinically unapparent focal seizures might be the cause for recurrent ictal asystole in this patient.

  Ictal bradycardia and asystole are rare, but well documented autonomic symptoms during epileptic seizures and may lead to life-threatening cardiac arrest, syncope and trauma. Electrical brain stimulation studies in humans show that variation in heart rate, mostly bradycardia, can be obtained by stimulation of the anterior cingulus, frontal, temporal and insular cortex as well as the right uncus. Intracranial and scalp EEG data points towards EEG seizure origin in the temporal, insular as well as frontal cortex before the onset of ictal asystole or bradycardia (2). Current hypotheses state that seizures may lead to stimulation of insula, cingulated cortex, amygdala or hypothalamus which regulate cardiac function through connections to brainstem and spinal cord nuclei (3).

  Case series usually show auras or partial seizures preceding the ictal bradycardia and asystole, however ictal asystole with loss of consciousness can be the exclusive ictal semiology (4).

  As post-stroke seizures can present in a variety of atypical forms including acute confusional state, slowing, behavioural change, and syncope of unknown origin a high index of suspicion is required for the correct and early diagnosis (5). We conclude that in this case during the acute phase of a right temporo-insular stroke unapparent seizures may have been the cause for recurrent asystole. However the cause will remain elusive as the diagnosis of ictal asystole would have required the recording of a representative clinical event during simultaneous EEG/ECG monitoring.

  A. Strzelczyk and F. Rosenow

  The authors report no competing interests.

  References

  1. Bladin CF, Alexandrov AV, Bellavance A, Bornstein N, Chambers B, Cote R, et al. Seizures after stroke: a prospective multicenter study. Arch Neurol 2000;57(11):1617-22.

  2. Leung H, Kwan P, Elger CE. Finding the missing link between ictal bradyarrhythmia, ictal asystole, and sudden unexpected death in epilepsy. Epilepsy Behav 2006;9(1):19-30.

  3. Oppenheimer S. Cortical control of the heart. Cleve Clin J Med 2007;74 Suppl 1:S27-9.

  4. Strzelczyk A, Bauer S, Knake S, Oertel WH, Hamer HM, Rosenow F. Ictal asystole in temporal lobe epilepsy before and after pacemaker implantation. Epileptic Disord 2008;10(1):39-44.

  5. Myint PK, Staufenberg EF, Sabanathan K. Post-stroke seizure and post-stroke epilepsy. Postgrad Med J 2006;82(971):568-72.

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  Conflict of Interest:
  None declared.

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