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Lithium may cause toxicity as it has a narrow therapeutic range. Lithium intoxication may manifest in the form of acute, acute on chronic and chronic intoxication. Neurotoxicity is a common component of chronic lithium intoxication and the symptoms include tremor, ataxia, dysarthria, extrapyramidal symptoms, hyperreflexia, seizures and status epilepticus. Although rare, catatonia could as a manifestation of lithium neurotoxicity. In this report, we present a patient with bipolar disorder presenting with catatonic symptoms secondary to lithium intoxication. We will discuss the risk factors, differential diagnosis and the treatment of catatonic symptoms. Lithium neurotoxicity may present with various clinical symptoms including catatonia, and differential diagnosis should be made well in such cases. If lithium neurotoxicity is suspected, rapid and appropriate intervention is required to prevent permanent neurological damage. Keywords: Lithium, Neurotoxicity, Catatonia.

Catatonia is characterized by psychomotor alterations and reduced contact with the environment. Initially linked to schizophrenia, it also occurs in mood disorders or organic conditions. In children, catatonia remains poorly delineated, despite dramatically increasing the risk of premature death. As data on pediatric drug-induced catatonia bears many uncertainties, we aimed to characterize its age-dependent patterns, using real-world data from the WHO safety database (VigiBase®).VigiBase® was queried for all reports of catatonia registered up to December 8th 2022. Reports involving patients <18 years were classified into 3 groups: ≤23 months, 2-11 years, and 12-17 years. Disproportionality analyses relied on the Reporting Odds Ratio (ROR), and the positivity of the lower end of the 95% confidence interval of the Information Component (IC) was required to suspect a signal. Catatonia was evoked in 421 pediatric reports. In infants, vaccines were leading. In children, the main signals involved haloperidol (ROR 104.3; 95% CI 45.6-238.5), ondansetron (ROR 40.5; 95% CI 16.5-99.5), and ciclosporin (ROR 27.4; 95% CI 13.8-54.1). In adolescents, chlorpromazine (ROR 199.1; 95% CI 134.8-294.1), benzatropine (ROR 193; 95% CI 104.1-361.6), and olanzapine (ROR 135.7; 95% CI 104.6-175.9) reached the highest RORs. In infants, catatonia was related to vaccines, it was ascribed to multiple drugs in children, and mainly to psychotropic drugs in adolescents. Less suspected drugs, such as ondansetron, were highlighted. Despite limitations inherent in spontaneous reporting systems, this study supports that a careful anamnesis is warranted to separate catatonia associated with medical conditions from drug-induced catatonia in pediatric patients., (© 2023. The Author(s).)

Background: Catatonia due to a general medical condition may result from a variety of causes, including substance intoxication and withdrawal. Stimulants are occasionally associated with catatonia, though there has been little investigation of methamphetamine's relationship to catatonia. Here we present 5 cases of catatonia associated with methamphetamine use and a systematic review of the associated literature from 1943 to 2020., Methods: We performed a systematic review of the literature and present 5 cases of catatonia evaluated using the Bush-Francis Catatonia Rating Scale and KANNER catatonia rating scale., Results: Methamphetamine use was associated with catatonia in a small number of cases in the literature. However, some of these reports included other possible etiologies. The patients in our case series met DSM-5 criteria for catatonia due to a general medical condition, with all reporting recent methamphetamine use and testing positive for amphetamines on urine drug screen., Conclusions: Given the ongoing rise in methamphetamine use in the United States, it is important that clinicians understand that methamphetamine use can be associated with catatonia. Patients with methamphetamine-associated catatonia may respond favorably to lorazepam and require shorter hospital stays than other catatonic patients. Lastly, methamphetamine-associated catatonia highlights how alteration in dopamine function and projections may be a critical neural mechanism underlying catatonia in general.

Opioid-induced catatonia is underrecognized and poorly understood in the literature. An 81-year-old woman with chronic kidney disease stage III taking sertraline underwent surgery with general anesthesia, receiving fentanyl, hydromorphone, and ketamine. Postoperatively, she was unresponsive, rigid, and cataleptic with pinpoint pupils. Symptoms resolved with a naloxone infusion suggesting opioid-induced catatonia as the leading diagnosis. Differential diagnoses and etiologies discussed reveal a possible multifactorial catatonia mechanism involving opioids, ketamine, and serotonin. Anesthesiologists should consider these potential interactions when using opioids for management of vulnerable patients., Competing Interests: The authors declare no conflicts of interest., (Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the International Anesthesia Research Society.)

Objective: Clozapine is a potent antipsychotic medication with a complex receptor profile. It is reserved for treatment-resistant schizophrenia. We systematically reviewed studies of non-psychosis symptoms of clozapine withdrawal., Methods: CINAHL, Medline, PsycINFO, PubMed, and the Cochrane Database of Systematic Reviews were searched using the keywords 'clozapine,' and 'withdrawal,' or 'supersensitivity,' 'cessation,' 'rebound,' or 'discontinuation'. Studies related to non-psychosis symptoms after clozapine withdrawal were included., Results: Five original studies and 63 case reports / series were included in analysis. In 195 patients included in the five original studies, approximately 20% experienced non-psychosis symptoms following discontinuation of clozapine. In 89 patients in four of the studies, 27 experienced cholinergic rebound, 13 exhibited extrapyramidal symptoms (including tardive dyskinesia), and three had catatonia. In 63 case reports / series included, 72 patients with non-psychosis symptoms were reported, which were catatonia (n=30), dystonia or dyskinesia (n=17), cholinergic rebound (n=11), serotonin syndrome (n=4), mania (n=3), insomnia (n=3), neuroleptic malignant syndrome (NMS) [n=3, one of them had both catatonia and NMS], and de novo obsessive compulsive symptoms (n=2). Restarting clozapine appeared to be the most effective treatment., Conclusions: Non-psychosis symptoms following clozapine withdrawal have important clinical implications. Clinicians should be aware of the possible presentations of symptoms to ensure early recognition and management. Further research is warranted to better characterise the prevalence, risk factors, prognosis, and optimal drug dosing for each withdrawal symptom., Competing Interests: As an editor of the journal, SKW Chan was not involved in the peer review process. Other authors have disclosed no conflicts of interest.

Objective: Catatonia is a life-threatening psychomotor syndrome that occurs in approximately 10% of patients with acute psychiatric illnesses. Although some case reports have argued that first generation antipsychotics (FGAs) are more likely to induce catatonia than second generation antipsychotics (SGAs), no large observational study has confirmed this hypothesis. We investigated whether FGAs were associated with an increased risk of reporting catatonia when compared with SGAs., Methods: A pharmacovigilance study was performed within VigiBase to compare the cases of catatonia syndromes reported in patients exposed to FGAs with those reported in patients exposed to SGAs. This approach is similar in concept to case-control study, but adapted to a pharmacovigilance database, and allows the estimation of reporting odds ratios (RORs) with 95% confidence intervals., Results: We identified 60,443 adverse effects reported in patients who received FGAs and 253,067 adverse effects reported in patients treated with SGAs. Compared with SGAs, the use of FGAs was associated with an increased risk of reporting catatonia syndromes (ROR = 2.2; 95% CI, 2.0-2.3). Consistent results were observed when the analysis was restricted to reports generated from physicians, reports from the US, and reports with the highest completeness score. The highest RORs were found for molindone (6.0; 95% CI, 3.1-10.4) and haloperidol (3.8; 95% CI, 3.5-4.0)., Conclusions: In this large pharmacovigilance study of patients exposed to antipsychotics, the use of FGAs was associated with an increased risk of reporting catatonia syndromes compared to the use of SGAs. This increased risk is consistent with the pharmacodynamic hypothesis of antipsychotic-induced catatonia. Our results warrant replication in population-based studies., (© Copyright 2022 Physicians Postgraduate Press, Inc.)

Competing Interests: The authors declare no conflict of interest.

Abstract: In our brief literature review, we discuss the changes in the concept of catatonia as well as its various types and symptoms. We also succinctly review the possible symptoms of clozapine withdrawal. In addition, we analyze the main features of the very few published cases of clozapine withdrawal-induced catatonia and the relationship between neuroleptic malignant syndrome and the malignant subtype of catatonia. Furthermore, we present the case of a 29-year-old male patient with schizophrenia in whom a malignant catatonic episode/neuroleptic malignant syndrome (with negativism, stupor, mutism, autonomic signs [eg, fever, hyperhidrosis], and elevated creatine kinase levels) began 5 days after the patient decided arbitrarily to cease his clozapine treatment. His catatonic symptoms quickly (ie, within a few days) resolved after the reinstitution of clozapine. Finally, we attempt to provide a theoretical explanation for the surprising finding in the literature that the withdrawal of clozapine, unlike the withdrawal of any other antipsychotics, may be associated with catatonia (frequently its malignant subtype). The take-home message of our case is that clinicians should bear in mind the risk of catatonia (especially the malignant subtype of it) after the prompt withdrawal of clozapine therapy., Competing Interests: Conflicts of Interest and Source of Funding: The authors have no conflicts of interest to declare., (Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.)

A 13-year-old girl with moderate intellectual disability and autism spectrum disorder (ASD) was admitted to the paediatric high-dependency unit following an 8-week history of altered mental status and motor behaviour. Her symptoms emerged followed shortly after discontinuation of risperidone, an atypical antipsychotic previously commenced to manage disruptive behaviour associated with ASD. On physical examination, the patient presented with negativism, grimacing, automatic obedience, waxy flexibility and ambitendency. Blood tests, neuroimaging and lumbar puncture failed to reveal an acute infectious or neurological precipitant. She responded immediately to a trial of intramuscular lorazepam titrated to a total daily dose of 12 mg. This case presents challenges of accurately diagnosing and managing catatonic symptoms in adolescent patients with ASD. We also discuss the potential risk of precipitating catatonia following the discontinuation of antipsychotic treatment that has been prescribed for a prolonged duration., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2021. No commercial re-use. See rights and permissions. Published by BMJ.)

Objective: Cannabis and synthetic cannabinoids (SC) are related to several neuropsychiatric symptoms and disorders, especially psychotic symptoms and disorders. Interestingly, catatonia-like symptoms associated with cannabis and SC have been generally neglected in research and scarcely described despite the clinical repercussions. Hence, this review aims to analyze current clinical publications on catatonia induced by cannabis or SC in a systematized way. Methods: A search using PRISMA guidelines was performed on three databases based on a specific inclusion and exclusion criteria. Results: 11 publications describing 14 patients (10 males; mean age 22.50 ± 6.67 years old) with catatonia apparently precipitated by the use of cannabis ( n  = 6) or SC ( n  = 8) were found. Clinical features and treatment are described and discussed. Conclusion: From a clinical perspective, cannabis and SC use may be related to catatonia-like symptoms and catatonia syndrome in the same way these substances (cannabis and SC) are related to induced-psychotic episodes. However, further research will be required to understand the exact nature of that relationship. Additionally, investigations focused on the clinical significance (i.e., prognosis, evolution, and outcomes) of catatonia-like symptoms induced by cannabis and SC use in patients are also needed.

The article describes a clinical case of catatonic syndrome. We describe the manifestations of the syndrome, its diagnostic criteria and associated scales. The modalities of the challenge test, constituting a diagnostic test, and first line treatment are detailed. Clinical and paraclinical investigations are proposed to determine the etiology. The benzodiazepine withdrawal as an etiology of catatonic syndrome is detailed.

Catatonia can be described structurally as a motor dysregulation syndrome with a concomitant behavioral component. However, despite its initial recognition nearly 150 years ago, the exact pathophysiological causes underlying this syndrome are still somewhat unknown and are potentially variable. This report reviews a case of a patient with multiple catatonic episodes precipitated by the use of an immunomodulator medication, and in doing so suggests a possible mechanism speaking to the immune system's role in the etiology of some cases of catatonia.

Malignant catatonia is a life-threatening syndrome, associated mostly with psychiatric diseases but also with neurological and neurodegenerative syndromes. We report the case of a 72-year-old patient, hospitalized for a major depressive episode with delusional symptoms, who presented a malignant catatonia. The patient had been transferred to an intensive care unit and treated with electroconvulsive therapy (ECT) leading to a rapid disappearance of the catatonic syndrome associated with a remission of the depressive symptoms. Complementary investigations helped us to secondarily diagnose a Lewy Body Dementia, which probably caused, associated with a treatment by haloperidol, the onset of catatonia. This case illustrates the need of an early diagnosis of neurodegenerative diseases in psychiatric outpatients and the importance of a quick management of catatonia, including ECT., (Copyright © 2019 L'Encéphale, Paris. Published by Elsevier Masson SAS. All rights reserved.)

Benzodiazepine withdrawal symptoms vary from mild anxiety to life-threatening delirium or seizures. In susceptible individuals, such as those with mood disorders, benzodiazepine withdrawal may also precipitate catatonia. A 26-year-old man with schizoaffective disorder (depressed type with catatonia) ran out of lorazepam and presented with catatonia, delirium, and seizures. He was taking olanzapine, venlafaxine, and trazodone for schizoaffective disorder. Lorazepam 2 mg twice daily kept him free of catatonia for 6 months. Besides catatonia and delirium, lorazepam withdrawal also triggered convulsive seizures and nonconvulsive status epilepticus. He was admitted to the intensive care unit where he underwent continuous video-EEG monitoring. Catatonia resolved with lorazepam on day 2. Seizures stopped with levetiracetam, lacosamide, and propofol on day 4. His mental status was normal when he was discharged on day 6. If not immediately recognized and treated, catatonia and delirium can lead to significant morbidity or mortality. Unfortunately, physicians tend to overlook catatonia and delirium, especially if both syndromes are present. At first, we suspected that our patient had ictal catatonia, but video-EEG showed no clear-cut correlation between catatonia, seizures, and epileptiform activity. As with prior observations, the patient's catatonia was more sensitive to benzodiazepine withdrawal and treatment than his seizures. The efficacy of benzodiazepines in aborting catatonia, seizures, and mixed delirium-catatonia syndromes suggests a key pathogenetic role of abnormal GABA neurotransmission in these brain disorders.

Tacrolimus, a potent posttransplant immunosuppressant, has been associated with major neuropsychiatric complications, including catatonia and psychosis. We report a novel case of tacrolimus-induced encephalopathy that developed 16 years after renal transplantation while the drug was at a therapeutic level. Discontinuation of tacrolimus and switching to an alternative immunosuppressant resulted in significant clinical improvement over 1 week. Our experience illustrates the possibility of acute neurotoxicity from tacrolimus even when the patient has tolerated the drug for 16 years and drug levels are within the therapeutic range. This case also highlights the importance of collaboration between psychiatry and transplant clinicians.

Background: Catatonia is a neuropsychiatric syndrome characterized by diverse psychomotor abnormalities, including motor dysregulation and behavioral and affective disturbances. Once thought to occur primarily in the context of schizophrenia, recent data suggest most cases of catatonia develop in individuals with depressive or bipolar disorders. Moreover, catatonia may ensue in general medical and neurological conditions, as well as due to a variety of pharmaceuticals, drugs of abuse, and toxic agents. At one time considered rare in pediatric patients, evidence now suggests catatonia is both underrecognized and undertreated in this population, where it carries an elevated risk of morbidity and mortality. Here we present the case of a child with steroid-resistant nephrotic syndrome who developed catatonia due to cyclosporine A-related neurotoxicity., Case Presentation: A 9-year-old African-American boy with no psychiatric history and a 9-month history of nephrotic syndrome due to focal segmental glomerulosclerosis was admitted to the local children's hospital for management of mutism, posturing, insomnia, gait abnormalities, and somatic delusions. Seven days prior to admission, his cyclosporine plasma concentration was elevated at 1224 ng/mL (therapeutic range: 100-200 ng/mL). Upon admission, cyclosporine was discontinued and psychiatry was consulted, diagnosing catatonia. The patient subsequently received propofol 80 mg IV resulting in a transient lysis of catatonia. Over a lengthy hospitalization, the patient's catatonia was initially treated with lorazepam, quetiapine being added later to target psychosis. All signs and symptoms of catatonia resolved, and the patient was eventually tapered off both lorazepam and quetiapine with no return of symptoms more than 6 months later., Conclusions: To our knowledge, this case represents the first reported instance of cyclosporine A-induced catatonia in a patient with steroid-resistant nephrotic syndrome. It illustrates the importance of maintaining vigilance for signs and symptoms of cyclosporine A-related neurotoxicity (including catatonia) in patients with steroid-resistant nephrotic syndrome. In addition, it highlights the challenges faced by clinicians in jurisdictions that prohibit the use of electroconvulsive therapy in pediatric patients.