Correspondence

Neurocardiogenic Syncope

N Engl J Med 1998; 339:1857December 17, 1998

Article

To the Editor:

The Image in Clinical Medicine by Diehl and Linden (July 30 issue)1 shows the cardiovascular changes associated with neurocardiogenic syncope. Unfortunately, the syncope progressed to a generalized seizure. I question the ethics of observing and recording this episode without intervening. Allowing the patient's hypoxia to worsen concerns me because of the possibility of irreversible damage to the myocardium or brain. Such a seizure may induce a kindling process, which lowers the threshold for future seizures.2,3 Instead of allowing the syncope to progress to more severe cerebral hypoxia and seizure, the observing physician could have decreased brain hypoxia by elevating the patient's legs, lowering his head, or both.

Mary Hoyt May Bibb, M.D.
3409 Michigan Ave., Cincinnati, OH 45208

3 References

1. 1

   Diehl RR, Linden D. Neurocardiogenic syncope. N Engl J Med 1998;339:312-312
   Full Text | Web of Science | Medline

2. 2

   Samoriski GM, Applegate CD. Repeated generalized seizures induce time-dependent changes in the behavioral seizure response independent of continued seizure induction. J Neurosci 1997;17:5581-5590
   Web of Science | Medline

3. 3

   Scotti AL, Bollag O, Nitsch C. Seizure patterns of Mongolian gerbils subjected to a prolonged weekly test schedule: evidence for a kindling-like phenomenon in the adult population. Epilepsia 1998;39:567-576
   CrossRef | Web of Science | Medline

Author/Editor Response

The authors reply:

To the Editor: We thank Dr. Bibb for her comments. We agree that one should intervene immediately after signs of syncope are apparent in order to prevent the development of full syncope. Because of space limitations, it was not possible to report our assessment in detail. Shortly after the first presyncopal signs were apparent in the patient, we of course intervened by elevating his legs. Unfortunately, we were unable to interrupt the progress of his syncope.

Convulsions during syncope are a nonepileptic phenomenon. In the growing literature on patients with tilt-table–induced syncope (10 to 30 percent of whom have convulsive syncope even after postural treatment), we found no reports of a risk of hypoxic brain damage or reduced seizure threshold.

Our main intention in monitoring cerebral blood-flow velocity and blood pressure during a medically indicated venipuncture in a patient with a history of centrally induced neurocardiogenic syncope was to ensure the safety of the patient. Besides this, monitoring gave us the opportunity to study circulatory mechanisms in centrally induced syncope.

Induction of syncope by venipuncture should not be used routinely to confirm the diagnosis of neurocardiogenic syncope. In patients with a differential diagnosis of epilepsy of neurocardiogenic syncope, the test may help avoid the use of anticonvulsant drugs when they are not indicated.

Rolf R. Diehl, Ph.D.
Dieter Linden, M.D.
Alfried Krupp Krankenhaus, 45117 Essen-Rüttenscheid, Germany