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.

Hyperosmolar dextrose infused through peripheral venous access can extravasate into surrounding soft tissue and produce local injury. We present the case of a 44-year-old woman with a history of seizure disorder and hyperlipidemia who underwent anterior lumbar interbody fusion (ALIF). On the day of admission, she experienced a witnessed generalized seizure on the floor that terminated following administration of intravenous lorazepam. Point-of-care glucose obtained during the event was 39 mg/dL and corrected with intravenous dextrose. She was transferred to the intensive care unit (ICU), where hypoglycemia recurred despite continuous dextrose support. Computed tomography (CT) of the head showed no acute intracranial process, and electroencephalography (EEG) demonstrated diffuse slowing without epileptiform activity. Endocrinology was consulted, and the clinical picture was felt to be most consistent with endogenous hyperinsulinism from a suspected insulinoma. At a serum glucose of 55 mg/dL, insulin was 13 uIU/mL and C-peptide was 4.7 ng/mL, both inappropriately unsuppressed and consistent with endogenous hyperinsulinism. She was maintained on continuous 10% dextrose at 150-200 mL per hour with as-needed 50% dextrose boluses, glucagon, and subcutaneous octreotide 200 mcg every eight hours, with capillary glucose monitoring every two hours. On hospital day 4, the peripheral catheter site was found to be infiltrated, and the catheter was removed, with the infusion transferred to central access. On hospital day 6, nursing and physician staff identified multiple tense, fluid-filled bullae over the right anterior forearm with associated swelling and erythema at the site of a previously removed peripheral intravenous catheter. The patient reported that forearm tenderness had been present since admission and had progressively worsened. Examination demonstrated moderate asymmetric swelling of the right upper extremity with intact distal pulses and preserved sensation. Range of motion was limited by swelling and a sensation of heaviness rather than by pain. The findings were felt to be most consistent with hyperosmolar dextrose extravasation injury. This case demonstrates that sustained peripheral administration of concentrated dextrose can produce progressive bullous and soft tissue injury and that these changes may evolve insidiously over several days. Early changes may be subtle and difficult to distinguish from routine infusion site irritation. Patients with suspected endogenous hyperinsulinism often require a multiday dextrose bridge while localization and definitive treatment are arranged, which places them at particular risk. Early consideration of central venous access, structured infusion site surveillance, and prompt escalation when local changes are identified are important components of care in patients requiring prolonged high-concentration dextrose therapy.

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.

Periodic catatonia is a rare subtype of catatonia characterized by a variety of neuropsychiatric symptoms that follow a cyclical pattern. These episodes typically involve alternating phases of catatonic symptoms separated by periods of remission. Despite this condition being rare, it is still considered a medical emergency and usually requires inpatient care for assessment and treatment. Unfortunately, managing periodic catatonia can be challenging, largely because its underlying biological causes are not well understood and appear to be less clearly defined as compared to other forms of catatonia. This case report features a 54-year-old male U.S. veteran diagnosed with post-traumatic stress disorder (PTSD) and traumatic brain injury (TBI) after military service who has suffered multiple episodes of catatonia symptoms since being diagnosed with PTSD 21 years before presentation. He presented to the hospital for catatonic symptoms, where the patient was treated with IV lorazepam. Despite early clinical improvement after 24 hours, the patient became highly sedated. Chart review revealed similarities to prior catatonic episodes requiring hospitalization, including normal medical workups. This report is the first to describe a case of periodic catatonia in a patient with PTSD and TBI. Further, the ideological complexity of periodic catatonia is elucidated in order to provide clinical insights into its management.

Amphetamine overdose can cause severe cardiovascular toxicity, including rarely reversible cardiomyopathy. A 26-year-old man presented approximately 33 hours after intentionally ingesting 25 20-mg extended-release mixed amphetamine salt tablets with lorazepam. He developed chest pain, tachycardia, hypotension, hypoxemia, lactic acidosis, rhabdomyolysis, and markedly elevated cardiac biomarkers. Electrocardiography showed diffuse ST-segment depressions, and chest imaging demonstrated bilateral pulmonary edema and acute lung injury without pulmonary embolism. Echocardiography revealed severe global biventricular systolic dysfunction with a left ventricular ejection fraction below 20%. Progressive hypoxemic respiratory failure required intubation and mechanical ventilation. He improved with supportive intensive care, intravenous diuresis, and heart failure therapy. Although coronary angiography was recommended, he declined and left against medical advice. At two-month follow-up, echocardiography showed complete recovery of biventricular function, with an ejection fraction of 55-60%. This case highlights profound but reversible biventricular cardiomyopathy following massive extended-release amphetamine overdose.

Autoimmune encephalitis, primary psychiatric illness, seizure disorders, and catatonia can produce overlapping neuropsychiatric manifestations that complicate diagnosis and management, particularly when autoimmune encephalitis is suspected without detectable neuronal autoantibodies. We describe a woman in her early 20s with prior resection of a mature cystic ovarian teratoma and a reported clinical diagnosis of possible seronegative autoimmune encephalitis without documented serologic confirmation who experienced recurrent mania, psychosis, reduced oral intake, withdrawal, psychomotor slowing, and catatonic features across several hospitalizations in the context of a co-occurring seizure disorder. Her evaluations included neuroimaging, lumbar puncture, electroencephalography, evaluation for recurrent ovarian teratoma, and repeated neurologic consultation. Intravenous immunoglobulin was administered during one hospitalization because an autoimmune encephalitis relapse remained under consideration. Subsequent magnetic resonance imaging, pelvic imaging, and electroencephalography did not demonstrate objective evidence supporting active inflammatory recurrence. Catatonia became increasingly clinically actionable because symptoms repeatedly improved after lorazepam administration, prior malignant catatonia had responded to an extended course of electroconvulsive therapy, and lorazepam tapering was followed by recurrent psychiatric and catatonic deterioration with improvement after treatment was resumed. Although benzodiazepine responsiveness supported the clinical diagnosis of catatonia, it was interpreted within the broader clinical context and was not considered diagnostic in isolation. This case illustrates the value of longitudinal syndromic reassessment when etiologic certainty remains limited. Recognition and treatment of episodes clinically concerning for catatonia should not be delayed while autoimmune, seizure-related, medication-related, and primary psychiatric contributors continue to be evaluated.

Electroconvulsive therapy (ECT) remains among the most effective interventions in psychiatry for severe depression, catatonia, and treatment-resistant psychosis. Despite its well-established efficacy and safety profile, particularly in medically complex and older patients, its use continues to evoke controversy due to the required medical clearance. Ethical dilemmas arise when patients lack insight or capacity to consent, creating tension between respect for autonomy and the duty of beneficence. We present the case of a 62-year-old woman with a longstanding history of paranoid schizophrenia, general anxiety disorder, hypertension, and hyperlipidemia who was admitted for acute psychosis following medication nonadherence and the recent death of her mother. Her presentation was notable for bizarre delusions, a disorganized thought process, and poor self-care. She was partially compliant with psychotropic therapy, including haloperidol, lorazepam, and lurasidone, but demonstrated limited improvement. Although ECT was considered given the severity and chronicity of her illness, the patient refused treatment. Her family emphasized the gradual deterioration they had observed and advocated strongly for pursuing ECT as the necessary intervention to prevent further decline, given her improvement with past ECT sessions. Over the course of hospitalization, her symptoms improved only mildly with pharmacotherapy alone, and she remained unable to maintain activities of daily living. This case highlights the enduring clinical and ethical complexities surrounding the use of ECT. It underscores the importance of evaluating capacity, engaging families in shared decision-making, and balancing the principles of autonomy and beneficence in the treatment of severe psychiatric illness.

Catatonia is often underrecognized and underdiagnosed, particularly in young children. Catatonia occurs secondary to a medical and/or psychiatric etiology. The diagnosis can be supported by validated rating scales, including the Pediatric Catatonia Rating Scale and/or response to a dose of a benzodiazepine, often lorazepam. We present the case of a 6-year-old boy with acute behavioral changes in speech, affect, awareness, and new odd behaviors, admitted to a quaternary care pediatric hospital for further assessment and work-up of symptoms consistent with catatonia. Laboratory testing was notable for previously undiagnosed Becker muscular dystrophy (BMD), although otherwise unremarkable. He received many medication treatments for catatonia, including escalating doses of lorazepam and augmentation with memantine, zolpidem, quetiapine, and ultimately clozapine, without adequate symptom improvement and with side effects including significant weight gain. Neither behavioral interventions nor empirical treatment of presumed seronegative autoimmune encephalitis with intravenous immunoglobulin and methylprednisolone conferred benefit. He ultimately received electroconvulsive therapy, with significant and relatively rapid improvement occurring over 2 weeks after a 4-month hospitalization. This case highlights the importance of the identification of catatonia to guide evidence-based treatment and the value of timely access to electroconvulsive therapy for pediatric patients. While the etiology of his catatonia remains undetermined, his diagnosis of BMD could play a role and further supports the importance of a comprehensive medical work-up.

Inadequate and poorly documented data on psychotropic drug utilization in schizophrenia in India necessitates systematic evaluation of prescribing patterns and associated adverse drug reactions. This prospective observational study assessed drug utilization, prescription rationality and adverse drug reactions among schizophrenia patients attending a tertiary care psychiatric outpatient department using WHO prescribing indicators. A total of 112 prescriptions comprising 285 drugs were analyzed, with atypical antipsychotics prescribed in 87% of first-visit cases, while combination therapies and polypharmacy were frequently observed. Significant dose variations were noted in commonly used antipsychotics such as risperidone, olanzapine and aripiprazole, as well as benzodiazepines like clonazepam and lorazepam (p<0.001). Atypical antipsychotics predominated due to better tolerability and lower extrapyramidal side effects, highlighting evolving prescribing trends. Thus, structured evidence on drug utilization patterns and variability in dosing, help in optimizing rational prescribing practices in schizophrenia management.