Anoxic-epileptic seizures: observational study of epileptic seizures induced by syncopes

Abstract

Aims: To describe a large series of children with anoxic-epileptic seizures (AES)--that is, epileptic seizures induced by syncopes.

Methods: Retrospective case-note review in a tertiary paediatric neurology unit. For all 27 children seen with a definite diagnosis of AES between 1972 and 2002, a review of clinical histories, videotapes, and EEG/ECG studies was undertaken. Main outcome measures were: age of onset, frequency and type of syncopes; age of onset and frequency of AES; type and duration of induced epileptic seizures; effect of treatment of syncopal and epileptic components.

Results: Median age of onset of syncopes was 8 months (range 0.2-120), frequency 2 in total to 40/day, median total approximately 200. Syncopes were predominantly reflex asystolic (RAS), prolonged expiratory apnoea (cyanotic breath-holding spells), or of mixed or uncertain origin; there was one each of ear piercing and hair grooming vasovagal syncope and one of compulsive Valsalva. Median age of onset of AES was 17 months (range 7-120), frequency from total 1 to 3/day, median total 3. The epileptic component was almost always bilateral clonic; three had additional epilepsy, one each with complex partial seizures, myoclonic absences, and febrile seizures plus. Median duration of epileptic component was 5 minutes (range 0.5-40, mean 11). Cardiac pacing prevented RAS in two patients: most other anti-syncope therapies were ineffective. Diazepam terminated the epileptic component in 6/8. Valproate or carbamazepine abolished AES in 5/7 without influencing syncope frequency.

Conclusions: Although uncommon compared with simple syncopes, syncope triggered epileptic seizures (AES) are an important treatable basis of status epilepticus.

Figure 1

EEG/ECG recording showing AES induced by ocular compression (OC). Each panel lasts about 20 s. In the upper panel OC induces instant asystole and the EEG becomes isoelectric within 12 s (the fast deflections in the 9th and 11th channels correspond to down-beat nystagmus). In the centre panel the tonic phase of the anoxic seizure is shown on the ECG line as black "fuzz" due to tonic EMG activity. Midway across the centre panel while the EEG is still isoelectric, rhythmic 2–3/s jerk artefacts are seen on EEG and ECG channels. By the time of the lower panel, rhythmic EEG spike wave is visible, slowing towards the conclusion. Jerking lasted 28 s but the child was unresponsive for a further 8 minutes (reproduced with permission from Stephenson,¹ Mac Keith Press, fig. 11.4).