Interseizure EEG Slowing after ECT is not NCSE

In a report describing a confusional state after the course of electroconvulsive therapy in a 55-year-old depressed woman, Pogarell and co-workers present an inter-seizure EEG recording with continuing 3 cps rhythms that were blocked by the oral administration of 1 mg lorazepam. Prescription of lorazepam resulted in resolution of the patient’s confusional state within a few days [10]. The authors’ interpret their experience as an ECT-induced non-convulsive status epilepticus (NCSE), an untoward side-effect of the treatment. The authors may wish to consider an alternative explanation for the experience, that inter-seizure EEG high amplitude slowing with spike activity is a physiologic response to repeated induced seizures and not NCSE [3].

When EEG recording was part of the monitoring of psychiatric patients, such epileptic-like rhythms were commonly reported in inter-seizure recordings, especially when high voltage alternating electric currents and bilateral electrode placement were used to induce seizures [1] [4] [5] [14]. The presence of EEG slowing in the inter-seizure EEG was considered necessary for behavioral clinical improvement and the absence of such patterns was associated with a poor clinical outcome [5].

High voltage slow wave and spike EEG frequencies were replaced by rhythms of much lower amplitude and higher frequency after the administration of the anticholinergic chemicals, atropine, scopolamine, diethazine, ditran and imipramine, and the hallucinogens lysergic acid and mescaline [6]. The rhythms were further slowed and voltages increased by chlorpromazine, other antipsychotic agents, and barbiturates [5] [12].

These findings were interpreted that induced seizures in ECT stimulated an increase in CNS acetylcholine and became the basis for the cholinergic theory of the mode of action of convulsive therapy [7].

Finally, induced seizures raise seizure thresholds and reduce the likelihood of seizures [13]. This physiologic effect is the basis for the recommendation of ECT in the interruption of status epilepticus and NCSE [2] [8]. The rarity of persistent clinical seizure activity after ECT and the difficulty that electrotherapists have in inducing effective seizures late in the course of ECT in some patients, especially the elderly, attest to the physiologic consequence of repeated seizures as raising seizure thresholds and not to an occasional toxic effect.

Others have reported similar post-ECT EEG findings associated with confusion and disorientation and interpreted the events as evidence of ECT induced NCSE [11]. But such reports are rare and offer no more compelling evidence than the clinician’s interpretation.

In the face of the known physiology of seizures and the frequency of inter-seizure EEG slowing and spike activity after a course of ECT, is it not better to interpret these events as physiologic expressions of the ECT process itself and not as ”abnormal”? If the recordings are considered ”abnormal,” the patient is logically considered to be suffering from a seizure disorder, a conclusion that is followed by extensive neurological assessment, prescription of anticonvulsant medications, and labeling the patient as suffering from a seizure disorder, a label that carries an unfortunate stigma [9].

While there is little reason not to follow the prescription of benzodiazepines advocated by these authors in patients who are confused immediately after a course of ECT, it is equally efficient, and considerably safer and less expensive, to let time resolve the cognitive and EEG effects of ECT, as these are typical findings when the treatment is successful.

References

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