Response to comment on: Residual neuromuscular blockade following electroconvulsive therapy

We thank Kellner and Bryson for their interest in our paper and their comments. ¹ We appreciate the opportunity to clarify aspects of our study and address the concerns raised.

Firstly, we would like to clarify what a T1 value is, as it is not derived from train-of-four data as they have written in their letter. T1 is a measure of thumb acceleration in response to discrete single-twitch supramaximal stimuli. One discrete twitch is done prior to the administration of suxamethonium which acts as a reference value. Subsequent single discrete twitches are then done following the administration of suxamethonium and compared with the magnitude of thumb acceleration obtained from the initial pre-suxamethonium discrete twitch. This ratio is the T1 (%) value. This is in contrast to train-of-four measurements, which deliver four stimuli in quick succession with the train-of-four ratio calculated from the first and fourth twitch of that current train-of-four.

We wholeheartedly agree that measuring outcomes in the post-procedural area is an important part of studying the significance of residual neuromuscular blockade. Indeed, this would be the next step for future studies on this topic. This was not done in this case as this was an exploratory study which aimed to see if there was firstly any degree of post-procedural residual neuromuscular blockade. Furthermore, as this study was an exploratory study, only a small number of patients were recruited which made detecting potentially infrequent respiratory complications in the recovery area difficult. For this reason, we did not examine this outcome.

We disagree with the assertion that ‘. . .one can observe the length of time that the paralysis lasts’ with suxamethonium. To make a comparison with non-depolarising neuromuscular blocking drugs, in the past a patients’ ability to take adequate tidal volumes or protrude their tongue was taken as evidence that they had recovered adequately from neuromuscular paralysis. As we now know, patients can still have clinically significant residual neuromuscular paralysis despite being able to do these actions.^2,3 We wonder if this is the case with depolarising neuromuscular paralysis during electroconvulsive therapy (ECT) as well, something which further studies measuring outcomes in the post-procedural areas will be able to elucidate.

Finally, we maintain that the ideal dose of neuromuscular blocking drug to give prior to ECT is unknown. From the literature there is a range of starting suxamethonium doses which we provided in our original paper, as was also included in the comment on our paper. However, there have been limited studies done on why these starting doses are appropriate and what the ideal degree of neuromuscular paralysis is for patients undergoing ECT. ⁴ This is further complicated by patient-specific considerations as we discussed in our paper, such as the risk of skeletal fractures in elderly patients undergoing ECT. Overall, the published starting doses of neuromuscular blocking drugs do allow ECT to be carried out. We believe the next step is objectively to study, measure and refine the end point for neuromuscular paralysis during ECT and titrate the dose of neuromuscular blocking drug based on this.

We appreciate the opportunity to engage in this scholarly discussion and hope this response clarifies some aspects of our study and discussion points. We look forward to further discourse on this topic.