Electroconvulsive Therapy and Nonconvulsive Status Epilepticus - Response to Anticonvulsants Might Solve the Dilemma

We are grateful for the comments of Dr. M. Fink [2] on our paper [6], and greatly appreciate his outstanding expertise in both ECT and related electrophysiology [3] [4].

Dr. Fink noted that inter-seizure high amplitude slowing with or without spike activity is a quite usual response to repeated induced seizures under ECT. This is in line with our experience when we look at the EEG data of our large sample of patients undergoing ECT, who usually receive EEG recordings at baseline and upon completion of this treatment approach. We agree that the mere occurrence of repetitive high amplitude slow waves and 3 cps rhythms is a quite usual finding after a series of electroconvulsive therapy and does not per se warrant the diagnosis of epileptiform activity or non-convulsive status epilepticus (NCSE).

The correct diagnosis of NCSE, however, is difficult and challenging for both clinicians and neurophysiologists. As Kaplan made clear in his comprehensive review on NCSE in 2005 [5], neither clinical symptoms nor EEG alterations are pathognomonic, and a high degree of awareness and suspicion seems to be necessary for an accurate diagnosis. The detection of electroencephalographic alterations (i. e. evidence of seizures), however, is indispensable to validate the clinical suspicion [1] [5].

As pointed out by Dr. Fink, ECT makes the situation even more complex, since ECT leads to variable and sometimes sustained alterations of the EEG including rhythmic changes and spikes [2] [3] [4].

In our reported subject, we as well took into account post-ECT memory loss and cognitive changes in combination with common ECT-induced EEG alterations [6]. However, since the clinical picture was so fluctuating and even progressive during the days after completion of the ECT series, we were in favour of additional etiologies, and after we had seen such a pronounced effect of lorazepam on both clinical and EEG alterations we believed having identified NCSE in this subject.

NCSE following ECT has been described in other case series [7], but it certainly is a rare, not unequivocal event, and Dr. Fink is right with his recommendation to be very cautious in making this diagnosis [2].

Since our recent report [6], we have seen two other subjects who similarly presented with mental and behavioural alterations and abnormal EEG including high amplitude rhythmic slowing and small bitemporal spikes. In one of these patients there was again a good and rapid response to lorazepam (in combination with phenytoin) leading to both clinical and EEG normalization, but in the second case, presenting with similar signs and symptoms, there was no response to anticonvulsive therapy. In the first case, we made the diagnosis of NCSE based on clinical, EEG, and response criteria. In the latter subject, the clinical symptoms and EEG activity gradually improved during the subsequent weeks, so that the diagnosis of unspecific, ECT-related alterations was more likely here.

We therefore would propose and recommend a trial with benzodiazepines and/or other anticonvulsants in any case suspicious of NCSE, especially after ECT, not only for diagnostic but also for therapeutic reasons. A rapid improvement of both clinical symptoms and EEG under this medication can help to establish the correct diagnosis. Moreover this might be indicated since it is known that also NCSE is associated with significant morbidity and should be adequately treated without too much delay [8].

References

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• 2 Fink M. Interseizure EEG slowing after ECT is not NCSE.  Pharmacopsychiatry. 2006;  39 115
• 3 Fink M. Nonconvulsive status epilepticus and electroconvulsive therapy.  J ECT. 2004;  20 131-132
• 4 Fink M. Convulsive Therapy: Theory and Practice. New York; Raven Press 1979
• 5 Kaplan P W. The clinical features, diagnosis, and prognosis of nonconvulsive status epilepticus.  Neurologist. 2005;  11 348-361
• 6 Pogarell O, Ehrentraut S, Rüther T, Mulert C, Hegerl U, Möller H J, Henkel V. Prolonged confusional state following electroconvulsive therapy - diagnostic clues from serial electroencephalography.  Pharmacopsychiatry. 2005;  38 316-320
• 7 Povlsen U J, Wildschiodtz G, Hogenhaven H, Bolwig T G. Nonconvulsive status epilepticus after electroconvulsive therapy.  J ECT. 2003;  19 164-169
• 8 Shneker B F, Fountain N B. Assessment of acute morbidity and mortality in nonconvulsive status epilepticus.  Neurology. 2003;  61 1066-1073