Electroconvulsive therapy (ECT) can provoke a brief parasympathetic surge, commonly causing transient sinus bradycardia or a short sinus pause. Most events last only seconds and resolve without intervention. Rarely, however, bradyarrhythmia or asystole may persist long enough to threaten cerebral perfusion, requiring anesthesia teams to respond immediately. We report the case of a male patient with treatment-resistant major depressive disorder who underwent bilateral ECT under methohexital and succinylcholine. Baseline sinus bradycardia was present at 47 beats per minute. Immediately after the ECT stimulus, the monitor demonstrated high-grade atrioventricular block that progressed to ventricular asystole with a flat plethysmographic waveform. Within 10 to 15 seconds, while glycopyrrolate and epinephrine were being prepared, percussion pacing was delivered using the ulnar aspect of a closed fist over the left lower sternal edge at ∼ the fourth-to-fifth intercostal space. Each blow produced a QRS complex on electrocardiography and a pulsatile deflection on the plethysmogram. An organized intrinsic rhythm returned after 3 impulses. The patient recovered uneventfully, and subsequent ECT sessions were preceded by prophylactic intravenous glycopyrrolate without recurrence. This case describes percussion pacing as an immediately deployable, equipment-free bridge within the cardiovascular rescue strategy for ECT services, with a low threshold to escalate to chest compressions and advanced cardiac life support.
Somatic Symptom Disorder (SSD) is characterized by persistent, distressing somatic symptoms accompanied by disproportionate health-related cognitions and behaviors. Electroconvulsive therapy (ECT) has no established indication in SSD; however, isolated case reports have suggested po\tential benefit in severe, refractory presentations. We report a 46-year-old postmenopausal woman with severe, refractory SSD who failed to respond to 4 months of combined pharmacotherapy and cognitive-behavioral therapy. Three sessions of bifrontotemporal ECT produced a striking symptomatic response, with her Somatic Symptom Scale-8 (SSS-8) score declining from 18 (severe) to 3 (minimal), a reduction sustained at follow-up. ECT was well tolerated. We discuss putative neurobiological mechanisms, including ECT-mediated changes in limbic and prefrontal circuits implicated in SSD pathophysiology. This case supports consideration of ECT in treatment-refractory SSD and highlights the need for systematic investigation of its efficacy and optimal parameters in this population.
Background: Electroconvulsive therapy (ECT) is effective for severe psychiatric disorders, but relapse after a successful acute course of ECT remains common. Identification of biological predictors of relapse is therefore clinically important. In this exploratory prospective study, we investigated changes in inflammatory and neurogenesis-related biomarkers following an acute course of ECT, and examined their association with relapse during 1-year follow-up. Methods: Enrolled were 30 patients with major depressive disorder, bipolar disorder, or schizophrenia spectrum disorders who received their first acute course of bitemporal ECT. Clinical assessments and venous blood sampling were conducted before and after the ECT course. We measured serum inflammatory markers, anti-inflammatory factors, and brain-derived neurotrophic factor (BDNF). Relapse was prospectively evaluated using monthly Clinical Global Impression-Severity assessments over 1 year. Repeated-measures analyses were performed to examine biomarker changes and their interaction with relapse status. Results: Following the acute ECT course, 48.1% of patients achieved remission, and 37.0% experienced relapse during 1-year follow-up. ECT was associated with a significant decrease in serum soluble interleukin-2 receptor levels and significant increases in eicosapentaenoic acid and docosahexaenoic acid, indicating an anti-inflammatory effect. Notably, serum BDNF levels increased in the nonrelapse group but decreased in the relapse group, with a significant time-by-relapse interaction. Conclusion: An acute course of ECT is associated with anti-inflammatory biological changes and differential modulation of serum BDNF. Increases in BDNF after ECT may be linked to a reduced risk of relapse, suggesting that serum BDNF could be a potential prognostic biomarker for long-term outcomes following ECT.
