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.

Electroconvulsive therapy (ECT) is a well-established treatment for severe or treatment-resistant major depressive disorder and schizophrenia, often leading to rapid symptom improvement. However, ECT can rarely cause adverse psychological effects, including new-onset auditory hallucinations. We present the case of a 71-year-old woman with major depressive disorder who showed rapid clinical improvement following ECT, along with restoration of cerebral blood flow in the frontotemporal and parietal regions as shown by neuroimaging. Despite remission of depressive symptoms, she developed de novo auditory hallucinations with a running commentary, classified as Schneiderian first-rank symptoms, which persisted for several months despite continued treatment with olanzapine. Unlike previously reported cases in which hallucinations resolved shortly after completion of ECT, this case highlights a rare instance of persistent hallucinations that emerged during the same period as cerebral perfusion changes but cannot be interpreted as causally or associatively related based on the available data. Although perfusion improvement was observed, these imaging findings should be regarded solely as descriptive observations rather than indicators of a mechanistic link. To our knowledge, this is the first report to describe the coexistence of ECT-induced cerebral blood flow changes and new-onset auditory hallucinations; however, no meaningful clinical-biological connection can be inferred from this single case. This finding underscores the need for further investigation into the neurobiological mechanisms underlying rare ECT-related side effects to improve patient management and safety.

Autoimmune encephalitis frequently presents with prominent psychiatric symptoms and may mimic primary psychiatric disorders, particularly in the early stages. We report the case of a 38-year-old man who presented with a 2-week history of behavioral disturbance, persecutory ideation, auditory hallucinations, and fluctuating disorganization of thought and behavior, without prior psychiatric history. During hospitalization, the clinical picture evolved to include psychomotor retardation and prominent catatonic features. Given the subacute onset and atypical presentation, autoimmune encephalitis was suspected. Cancer screening identified a mixed testicular germ cell tumor, and right orchiectomy was performed. Despite tumor removal and immunotherapy, the patient showed no meaningful clinical improvement and progressed to severe catatonia. Pharmacological treatment with benzodiazepines and antipsychotic medications was ineffective. Electroconvulsive therapy was therefore initiated. After 12 bitemporal electroconvulsive therapy sessions, a marked and sustained clinical improvement was observed, with progressive resolution of catatonic, psychotic, and behavioral symptoms. This case highlights that severe catatonia may represent the dominant psychiatric manifestation of seronegative paraneoplastic encephalitis and suggests that electroconvulsive therapy may be an effective therapeutic option for refractory catatonia in this context.

We report a diagnostically challenging case of treatment-resistant depression (TRD) in a 52-year-old woman with multiple factors potentially increasing susceptibility to central nervous system (CNS) adverse effects, including global cortical atrophy, concomitant lithium and antipsychotic treatment, and ongoing programmed cell death protein 1 (PD-1) inhibitor therapy. After failing multiple pharmacological and neuromodulatory treatments, electroconvulsive therapy (ECT) was initiated. While ECT led to marked clinical improvement, the patient developed a prolonged delirium after the 12th session, lasting 7 to 10 days, initially raising concern for autoimmune encephalitis under immunotherapy. A comprehensive diagnostic work-up including electroencephalography (EEG), contrast-enhanced magnetic resonance imaging (MRI), and lumbar puncture (LP) found no evidence of nonconvulsive status epilepticus (NCSE), acute structural pathology, or florid autoimmune encephalitis, despite borderline SOX1 antibody reactivity in CSF. Cognition returned to baseline without specific therapy, and follow-up paired serum/CSF testing was negative for SOX1 antibodies. The episode was considered a multifactorial delirium, with ECT as one likely contributing factor alongside concomitant medication, structural brain changes, and PD-1 inhibitor therapy. Following relapse, maintenance ECT was resumed using a modified protocol without recurrence of prolonged delirium. This case highlights that ECT may remain an option in carefully selected complex patients when accompanied by structured diagnostic work-up and interdisciplinary monitoring.

Peripartum depression is a significant cause of maternal and neonatal morbidity and mortality. Electroconvulsive therapy (ECT) is often used in the treatment of severe peripartum depression, but its use may increase the risks of obstetric complications. Accelerated transcranial magnetic stimulation (TMS) protocols, such as the Stanford Accelerated Intelligent Neuromodulation Therapy (SNT), may confer efficacy that rivals ECT with less potential risks. Here, we present a case of severe, treatment-resistant depression in a 38-year-old pregnant female. The patient was referred for ECT; however, she was subsequently diagnosed with placenta previa. To minimize potential complications, the patient was instead treated with SNT TMS. The patient demonstrated a robust response, resulting in remission of her depressive symptoms. The treatment was administered at eighteen weeks' gestation and did not cause any obstetric complications. Accelerated TMS may represent a viable treatment strategy for peripartum depression in patients vulnerable to the increased risks associated with ECT.

Parkinsonian syndromes with comorbid psychiatric illness present a therapeutic paradox wherein antipsychotics may worsen motor symptoms while dopaminergic agents may exacerbate psychosis. Maintenance electroconvulsive therapy (mECT) has emerged as a critical relapse-prevention strategy, reducing 6-month relapse risk by 43% compared to pharmacotherapy alone. We present 2 cases demonstrating mECT efficacy in sustaining both psychiatric and motor improvements. First, a 70-year-old woman with Parkinson's disease and treatment-resistant schizophrenia improved after acute ECT; motor symptoms relapsed 2 months post-discontinuation but recovered with mECT, allowing medication de-escalation without cognitive decline. Next, a 47-year-old man with multiple system atrophy and severe depression with psychosis showed marked improvement after acute ECT; motor relapse at 1 month was prevented by mECT. Both cases demonstrate that motor improvement cannot be sustained without continued ECT intervention. mECT represents an underutilized strategy deserving wider adoption in neurodegenerative-psychiatric comorbidity, warranting larger prospective trials to establish standardized protocols.