Convulsive syncope: a Stokes-Adams caseA 26-year-old male with two-days prior cocaine consumption, presented with a 5-day history of new-onset focal nonmotor dyscognitive epileptic events. After three days of treatment with oral phenytoin (PHT) 100 mg t.i.d., a convulsive status epilepticus developed at the same time a third-degree atrioventricular block was registered (Figures 1 and 2).
Figure 1.
6 consecutive epochs (11:02:28 to 11:03:28) are shown. Montage: Bipolar, longitudinal, double-banana. HF: 70 Hz, LF: 1 Hz, NF: 60 Hz, Sens: 70 μV/cm; 13 seconds after a 10-second ventricular pause, 2‒3 Hz generalized polymorphous slow waves are registered with greater expression in the anterior regions. Following this, a new ventricular pause of 9 seconds appears, which will continue in the following figure.
6 consecutive epochs (11:02:28 to 11:03:28) are shown. Montage: Bipolar, longitudinal, double-banana. HF: 70 Hz, LF: 1 Hz, NF: 60 Hz, Sens: 70 μV/cm; 13 seconds after a 10-second ventricular pause, 2‒3 Hz generalized polymorphous slow waves are registered with greater expression in the anterior regions. Following this, a new ventricular pause of 9 seconds appears, which will continue in the following figure.
Figure 2.
The last ventricular pause described in Fig. 1 continues for 17 more seconds (26 in total). Synchronous generalized slow waves are again registered. On the 24th second, generalized electrodecrement with muscle artifact due to a generalized tonic seizure of 4 seconds of duration. This event ends with the recovery of the heart rhythm and subsequent slow waves in delta range before recovering its alpha rhythm.
The last ventricular pause described in Fig. 1 continues for 17 more seconds (26 in total). Synchronous generalized slow waves are again registered. On the 24th second, generalized electrodecrement with muscle artifact due to a generalized tonic seizure of 4 seconds of duration. This event ends with the recovery of the heart rhythm and subsequent slow waves in delta range before recovering its alpha rhythm.
As we know, cocaine consumption and PHT (specially in infusions >50 mg/min or previous heart disease) are both related with adverse cardiovascular effects, specially arrhythmias1,2. Our case exemplifies the lethal combination of both, and the narrow neurological and cardiologic assessment of syncope versus epilepsy in patients with stereotypic paroxysmal episodes3,4.
References
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1 Phillips K, Luk A, Soor GS, Abraham JR, Leong S, Butany J. Cocaine cardiotoxicity: a review of the pathophysiology, pathology, and treatment options. Am J Cardiovasc Drugs. 2009;9(3):177-96. https://doi.org/10.2165/00129784-200909030-00005
» https://doi.org/https://doi.org/10.2165/00129784-200909030-00005 -
2 Guldiken B, Rémi J, Noachtar S. Cardiovascular adverse effects of phenytoin. J Neurol. 2016;263:861-70. https://doi.org/10.1007/s00415-015-7967-1
» https://doi.org/https://doi.org/10.1007/s00415-015-7967-1 -
3 Ozkara C, Metin B, Kucukoglu S. Convulsive syncope: a condition to be differentiated from epilepsy. Epileptic Disord. 2009 Dec;11(4):315-9. https://doi.org/10.1684/epd.2009.0281
» https://doi.org/https://doi.org/10.1684/epd.2009.0281 -
4 Díaz-Castro O, Orizaola P, Vázquez S, Gonzáles-Rios C, Pardo M, Fernández-López JÁ, et al. “Stokes-Adams Epilepsy” Sometimes We Need the Electroencephalogram. Circulation. 2005;112(8):e101-2. https://doi.org/10.1161/CIRCULATIONAHA.104.503144
» https://doi.org/https://doi.org/10.1161/CIRCULATIONAHA.104.503144
