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Updated: Jul 12, 2026

Pupillary Response as Assessment of Effective Seizure Induction by Electroconvulsive Therapy
04:51

Pupillary Response as Assessment of Effective Seizure Induction by Electroconvulsive Therapy

Published on: April 11, 2019

Pseudocholinesterase deficiency and electroconvulsive therapy.

Joseph Williams1, Peter Rosenquist, Lorraine Arias

  • 1Department of Psychiatry and Behavioral Medicine, Wake Forest University School of Medicine, Winston-Salem, NC 27157, USA. joswilli@wfubmc.edu

The Journal of ECT
|September 7, 2007
PubMed
Summary

Pseudocholinesterase deficiency poses challenges in electroconvulsive therapy (ECT) by limiting muscle relaxant options. This case highlights managing ECT with alternative agents when succinylcholine is contraindicated due to this deficiency.

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Area of Science:

  • Anesthesiology
  • Pharmacology
  • Neurology

Background:

  • Pseudocholinesterase deficiency is a rare genetic disorder affecting muscle relaxant metabolism.
  • Electroconvulsive therapy (ECT) often utilizes muscle relaxants like succinylcholine.
  • Succinylcholine's action is prolonged by pseudocholinesterase deficiency, posing risks.

Observation:

  • A patient undergoing ECT for depression was administered succinylcholine.
  • The patient experienced prolonged neuromuscular blockade, necessitating mechanical ventilation.
  • This indicated an unsuspected pseudocholinesterase deficiency.

Findings:

  • Succinylcholine, a common ECT muscle relaxant, is metabolized by pseudocholinesterase.
  • The patient's deficiency led to an inability to metabolize succinylcholine, causing extended paralysis.
  • Diagnosis was confirmed by the prolonged response to succinylcholine.

Implications:

  • Clinicians must consider pseudocholinesterase deficiency in patients undergoing ECT.
  • Alternative muscle relaxants, not dependent on pseudocholinesterase, are crucial for safe ECT in deficient patients.
  • Proper patient selection and alternative anesthetic management are vital for ECT safety.