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.

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.

Electroconvulsive therapy (ECT) is typically performed under general anesthesia without a secured airway, placing patients with retained gastric contents at increased risk of aspiration. As more patients present for ECT while taking GLP-1 receptor agonists, standard fasting requirements pose unique safety and patient-experience challenges. A 24-hour clear-liquid diet every other day is burdensome, while frequent rapid sequence intubations may prolong treatment and recovery. To address this, ECT and anesthesia leadership developed a novel pre-ECT fasting protocol for patients on GLP-1 RAs. We report a patient with refractory major depressive disorder on tirzepatide who successfully completed 17 ECT treatments without complications.

Catatonia is a neuropsychiatric syndrome that may complicate medical and surgical conditions but is often underrecognized, particularly in patients with intellectual disability. Electroconvulsive therapy (ECT) is an established treatment for benzodiazepine-resistant catatonia, although seizure induction can be difficult in some cases. We report a 52-year-old man with intellectual disability who developed postoperative catatonia after laparoscopic pancreaticoduodenectomy for insulinoma. Despite prolonged agitation, echolalia, mutism, rigidity, and catalepsy, catatonia was not recognized at multiple hospitals, and he was repeatedly discharged without appropriate treatment. After transfer to our facility, catatonia was confirmed. Because of recurrent aspiration pneumonia and oversedation with lorazepam, ECT was initiated promptly. Seizure induction was exceptionally difficult. Bilateral electrode placement with standard pulse width required escalation to the maximum charge output (200%, 1008 mC), and adequate seizures remained inconsistent. Sequential modifications included right unilateral electrode placement, ultrabrief pulse width, and later extension of pulse width to 1.50 ms at 50 Hz. Even then, consistent seizure induction was not achieved until the anesthetic was changed from propofol to thiamylal and flumazenil pretreatment was added, which suggests a synergistic effect of extended pulse width with right unilateral electrode placement, together with thiamylal and flumazenil. This case underscores that catatonia in patients with acute medical illness or intellectual disability is easily overlooked and that delayed recognition can result in serious medical complications; early diagnosis and prompt treatment are therefore essential. It further suggests that multimodal optimization of ECT parameters and anesthetic management may be required for reliable seizure induction in refractory cases.

An 18-year-old female patient with a history of autism spectrum disorder and SCN2A loss-of-function variant received a course of electroconvulsive therapy (ECT) for catatonia, which had been present and disabling for 1 year. After a partial lorazepam taper, bitemporal ECT was initiated. The patient had a rapid and robust response to ECT with improvement in the Bush-Francis Catatonia Rating Scale to 0 after 4 treatments and sustained catatonia remission even after lorazepam cessation. After the patient's family opted to discontinue ECT after the index course, she suffered a recurrence of her catatonia 2 months later, which remitted after a second index ECT course. The patient's brain physiology was highly stereotyped across treatments, with prominent EEG postictal suppression coinciding with cortical spreading depolarization (CSD). This case represents the fourth-ever reported case of SCN2A-associated catatonia and the oldest onset of catatonia in this population. In addition, it provides support for the emerging evidence for CSD as a potential contributor to both ECT postictal suppression and clinical response.

Major depressive disorder (MDD) is characterized in a substantial proportion of patients by an inadequate response to standard pharmacological and psychotherapeutic interventions, thereby increasing the need for more rapid and potent biological treatments. In this context, convulsive neuromodulation therapies play a central clinical role, particularly in severe, psychotic, treatment-resistant, or life-threatening depressive states. Electroconvulsive therapy (ECT) is regarded as one of the most effective biological interventions for the treatment of MDD, supported by decades of clinical experience and high-level evidence. Magnetic seizure therapy (MST), by contrast, aims to exert antidepressant effects through convulsive mechanisms similar to those of ECT and has attracted increasing interest due to its more focal cortical stimulation and its potential to offer a more favorable cognitive adverse-effect profile. In this review, ECT and MST in MDD are examined comparatively in light of the current evidence, with acute efficacy, cognitive safety, and use in special patient populations evaluated within an integrated framework. While the acute antidepressant efficacy and clinical predictability of ECT are supported at the highest level, MST appears to be a promising yet still experimental option, particularly in selected cases in which cognitive safety is prioritized. This review aims to clarify the position of ECT and MST within treatment algorithms for MDD and to support clinical decision-making.