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LETTER TO THE EDITORS
Seizure, syncope, or both: cardiac pacemaker reveals temporal
lobe epilepsy
Jan Re
´mi •Soheyl Noachtar
Received: 7 April 2011 / Revised: 9 May 2011 / Accepted: 10 May 2011 / Published online: 27 May 2011
ÓSpringer-Verlag 2011
Dear Sirs,
Sudden loss of consciousness is a common presenting
symptom in clinical neurology. Differential diagnoses
include syncope and epilepsy. Distinguishing the two may
be difficult when syncopes are followed by convulsions [1]
or when epileptic seizures have vegetative symptoms like
ictal asystole [2].
A 55-year-old woman presented to our epilepsy center
with persistent spells of loss of consciousness after
implantation of a cardiac pacemaker in the previous year.
She had had three episodes of sudden loss of consciousness
and subsequent falls. After routine cardiological work up,
including 24 h ECG, did not reveal any abnormalities, a
cardiac event monitor was implanted and documented 12
asystoles of up to 9 s duration, some of them associated
with syncope. She was diagnosed with a sick-sinus syn-
drome, and had a cardiac DDDR-pacemaker implanted. No
more falls occurred after that, but the patient had episodes
where she would perform inadequate manual automatisms
and wander about aimlessly. The patient herself was
amnesic for these events. Her past medical history was non
contributory. A cranial MRI and a routine EEG had been
without abnormal findings.
We admitted the patient to our epilepsy monitoring unit
for differential diagnosis of her spells. We recorded one
seizure, beginning with an unspecific aura followed by loss
of responsiveness and manual automatisms. Within 4 s
after clinical onset, she was tachycardic at 120 beats/min
(bpm). We recorded a right temporal seizure pattern 12 s
after clinical onset, which evolved into a left temporal
seizure pattern 25 s later. Coinciding with the beginning of
the left temporal seizure pattern, the heart rate slowed
down to below the pacemaker’s sensing frequency of
60 bpm and the pacemaker started stimulation. Twenty-
five seconds after the end of the seizure pattern, the heart
regained full sinus node activity (Fig. 1).
A high resolution MRI did not reveal any pathology. We
diagnosed right temporal lobe epilepsy, and started lev-
etiracetam (2,500 mg daily). She has been seizure free for
12 months now. The cardiac pacemaker was read out and it
had not been active during that time.
Our patient illustrates the difficulties that may be
encountered in the differential diagnosis of syncope and
epilepsy. Our patient’s leading symptom was sudden loss of
consciousness and falls, which eventually led to the implan-
tation of a cardiac pacemaker. Only then were her epileptic
seizures—characterized by loss of responsiveness and mild
automatisms—unmasked, because the ictal asystole was
averted by the pacemaker, preventing the syncopal fall. Even
though the patient has been seizure free for 12 months, and
the pacemaker has not been active in that time, we believe that
the pacemaker was necessary in any case, because asystoles
may not revert on their own and may be associated with
sudden unexpected deaths in epilepsy patients [3].
Ictal asystole is mostly associated with left hemispheric
seizure activity [4], which was the case in our patient, when
the seizure pattern propagated from right to left. She would
have become asystolic, which was prevented only by the
pacemaker. Ictal tachycardia, when not due to physical
exertion or emotional distress, lateralizes to the right
hemisphere [5], which was the case in our patient as well.
Our patient demonstrates that vegetative symptoms of
temporal lobe epilepsy such as syncopal falls due to ictal
J. Re
´mi S. Noachtar (&)
Epilepsy Center, Department of Neurology,
University of Munich, Marchioninistr 15,
81377 Munich, Germany
e-mail: noa@med.uni-muenchen.de
123
J Neurol (2011) 258:2291–2292
DOI 10.1007/s00415-011-6103-0
asystole may obscure the underlying epilepsy until treated
adequately.
Conflict of interest The authors declare that they have no conflict
of interest.
References
1. Lempert T, Bauer M, Schmidt D (1994) Syncope: a videometric
analysis of 56 episodes of transient cerebral hypoxia. Ann Neurol
36:233–237
2. Schuele SU, Bermeo AC, Alexopoulos AV, Locatelli ER, Burgess
RC, Dinner DS et al (2007) Video-electrographic and clinical
features in patients with ictal asystole. Neurology 69:434–441
3. So EL, King DW, Murvin AJ (1984) Misdiagnosis of complex
absence seizures. Arch Neurol 41:640–641
4. Rocamora R, Kurthen M, Lickfett L, Von Oertzen J, Elger CE
(2003) Cardiac asystole in epilepsy: clinical and neurophysiologic
features. Epilepsia 44:179–185
5. Weil S, Arnold S, Eisensehr I, Noachtar S (2005) Heart rate
increase in otherwise subclinical seizures is different in temporal
versus extratemporal seizure onset: support for temporal lobe
autonomic influence. Epileptic Disord 7:199–204
Fig. 1 EEG and ECG tracing. A referential EEG montage (vs. CPZ)
shows first a right temporal seizure pattern (a) with tachycardia, then
the propagation from right to left temporal and bradycardia/
pacemaker action (b) and lastly reversion to normal sinus rhythm
after the seizure (c). Scale amplitude for EEG only
2292 J Neurol (2011) 258:2291–2292
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