Catatonia was often complicated by pneumonia, and the development of severe pneumonia after admission posed significant challenges to its treatment. This study aimed to develop a Nomogram Model based on pre-admission characteristics of patients with catatonia to predict the risk of pneumonia after admission.

This retrospective observational study reviewed catatonia patients hospitalized at Hangzhou Seventh People's Hospital from September 2019 to November 2024. Data included demographic characteristics, medical history, maintenance medications, and pre-admission clinical presentations. Patients were divided into catatonia with and without pneumonia groups. The LASSO Algorithm was used for feature selection, and seven machine learning models: Decision Tree(DT), Logistic Regression(LR), Naive Bayes(NB), Random Forest(RF), K Nearest Neighbors(KNN), Gradient Boosting Machine(GBM), Support Vector Machine(SVM) were trained. Model performance was evaluated using AUC, Accuracy, Sensitivity, Specificity, Positive Predictive Value, Negative Predictive Value, F1 Score, Cohen's Kappa, and Brier Score, and Brier score. The best-performing model was selected for multivariable analysis to determine the variables included in the final Nomogram Model. The Nomogram Model was further validated through ROC Curves, Calibration Curves, Decision Curve Analysis (DCA), and Bootstrapping to ensure discrimination, calibration, and clinical applicability.

Among 156 patients, 79 had no pneumonia, and 77 had pneumonia. LASSO Algorithm identified 15 non-zero coefficient variables (LASSO 1-SEλ=0.076). The GBM showed the best performance (AUC = 0.954, 95% CI: 0.924-0.983, vs other models by DeLong's test: P < 0.05). Five key variables: Age, Clozapine, Diaphoresis, Intake Refusal, and Waxy Flexibility were used to construct the Nomogram Model. Validation showed good discrimination (AUC = 0.803, 95% CI: 0.735-0.870), calibration, and clinical applicability. Internal validation (Bootstrapping, n=500) confirmed model stability (AUC = 0.814, 95% CI: 0.743-0.878; Hosmer-Lemeshow P = 0.525).

This study developed a Nomogram Model based on five key factors, demonstrating significant clinical value in predicting the risk of pneumonia in hospitalized patients with catatonia.

Autoimmune encephalitis (AE) tends to manifest as a mixture of neuropsychiatric and somatic symptoms, either of which may predominate, and often shows a progressive clinical course sometimes leading to life-threatening conditions. Catatonic and psychotic syndromes, regardless of whether associated with dysautonomia, are common manifestations of AE, especially concerning the anti-NMDAR subtype. Several autoantibodies targeting different neuronal epitopes have been linked to specific clinical manifestations and their detection is embedded in some of the diagnostic criteria for AE. Therapeutical management of AE is challenged by limited diagnostic abilities and poor understanding of the underlying pathophysiology for most of its subtypes. Although the prompt delivery of disease-modifying therapies represents the cornerstone of treatment and primarily affects prognosis, less is known about the role of symptom specific supportive measures like electroconvulsive therapy (ECT). Based on a systematic review of 26 patient-level descriptions of individuals, each with a diagnosis of AE treated with ECT, a favorable clinical response was found in more than ¾ of the revised cases (76.9%). The most common indications for ECT administration were catatonic and psychotic syndromes, often nonresponsive to prior pharmacotherapy with benzodiazepines, antipsychotic, and other psychotropic drugs. Noteworthy side effects were only reported for 3 of 26 patients. Though the low number of cases and publication bias should be considered as major limitations, current available reports are in support of the inclusion of ECT in the integrated therapeutic algorithm of AE to address psychiatric conditions such as severe psychosis and catatonia.

Creatine kinase (CK) is an intracellular enzyme expressed most commonly in tissues such as skeletal muscle. CK can be used as an investigation to support the diagnosis of conditions such as neuroleptic malignant syndrome (NMS), a rare idiosyncratic drug reaction - classically to antipsychotic medications - which can be fatal. Routine screening of CK in psychiatric inpatients is a known practice, but its value is uncertain. We aimed to ascertain whether such screening resulted in new diagnoses of NMS or other conditions, and changes in clinical management.

Using an electronic case register, we conducted a descriptive retrospective cohort study, identifying all psychiatric inpatient admissions in a South London mental health trust over a four-year period where a CK test was conducted within 48 h of admission. We extracted the demographic and clinical characteristics (e.g., diagnosis) of those who met inclusion criteria. Free-text review was performed on all those with a CK potentially suggestive of NMS (CK ≥ 4x upper limit of normal reference range (ULN)) to determine the impact of this abnormal result on subsequent management and diagnosis (including NMS if identified).

Of 14,236 inpatient episodes in the specified window, 2358 (16.6%) had a CK test within 48 h of admission. This was ≥ 4x ULN in 327 (13.8%) cases (free-text successfully reviewed in 318). There were no cases of NMS identified. An abnormal CK result led to a new alternative diagnosis, such as dehydration or catatonia, in only 14 patients (4.4% raised CK sample, 0.6% total CK sample). Impact on subsequent management appeared limited, with the most common adjustment being an increase in frequency of physical observations in 47 instances (14.8%).

The clinical utility of untargeted screening using a serum CK for psychiatric inpatients appears limited, with poor specificity in detection of NMS and a minimal impact on subsequent clinical management.

N-methyl-D-aspartate receptor encephalitis (NMDARE) presents serious neurological manifestations such as reduced consciousness, seizures, and movement disorders, which can escalate to coma or severe autonomic dysfunction. Treatment typically involves immunotherapy and tumor removal to mitigate the autoimmune response. Timely diagnosis and treatment are critical to prevent severe neurological impairment or death. Memantine, an NMDA receptor antagonist, has shown variable effectiveness in treating NMDARE according to several case reports, yet comprehensive analyses remain scarce. This mini review draws on five literature sources and eight case studies from databases including PubMed, Embase, the Cochrane Library, and Web of Science, highlighting both the potential and risks of memantine as an adjunct therapy. We explore how memantine may reduce symptoms by blocking excessive NMDA receptor (NMDAR) antibody binding, while potentially worsening symptoms by reducing extracellular NMDAR availability, thus impairing neuronal communication. This dual effect calls for further investigation into the optimal use and duration of memantine treatment in NMDARE management.

Psychiatric illness is thought to be a brain somatic crosstalk disorder. However, the existing phenomenology-based Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) diagnostic framework overlooks various dimensions other than symptoms. In this study, we investigated the associations between peripheral blood test indexes with various symptom levels of major depressive disorder (MDD), bipolar disorder (BD), and schizophrenia (SCZ) to explore the availability of peripheral blood test indexes.

We extracted cases diagnosed with MDD, BD, and SCZ at West China Hospital from 2009 to 2021, translated their main complaints into Research Domain Criteria (RDoC) symptom severity scores using nature language processing (NLP), and collected their detailed psychiatric symptoms and peripheral blood test results. Then, generalized linear models were performed between seven types of peripheral blood test values with their transformed RDoC scores and detailed symptom information adjusted for age, gender, smoking, and alcohol history.

Several inflammatory-related indexes were strongly associated with the negative valence system (NVS) domain (basophil percentage adjusted β = 0.275, lymphocyte percentage adjusted β = 0.271, monocyte percentage adjusted β = 0.223, neutrophil percentage adjusted β = -0.310, neutrophil count adjusted β = -0.301, glucose adjusted β = -0.287, leukocyte count adjusted β = -0.244, NLR adjusted β = -0.229, and total protein adjusted β = -0.170), the positive valence system (PVS) domain (monocyte percentage adjusted β = 0.228, basophil count adjusted β = 0.176, and glutamyl transpeptidase adjusted β = 0.171), and a wide range of mood, reward, and psychomotor symptoms. In addition, glucose, urea, urate, cystatin C, and albumin showed considerable associations with multiple symptoms. In addition, based on the direction of associations and the similarity of symptoms in terms of RDoC thinking, it is suggested that "positive" mood symptoms like mania and irritability and "negative" mood symptoms like depression and anxiety might be on a continuum considering their opposite relationships with similar blood indexes.

The cross-sectional design, limited symptoms record, and high proportion of missing values in some other peripheral blood indexes limited our findings.

The proportion of high inflammatory indexes in SCZ was relatively high, but in terms of mean values, SCZ, BD, and MDD did not differ significantly. Inflammatory response showed a strong correlation with NVS, PVS, and a range of psychiatric symptoms especially mood symptoms, psychomotor symptoms, and cognitive abilities.

Catatonia, characterized by motor, affective, and speech disturbances, is a prevalent yet frequently misdiagnosed syndrome in the psychiatric domain, with reported prevalence ranging from 5% to 18%. This study aimed to ascertain the incidence of catatonia diagnoses and the quality of care provided within the psychiatric emergency room (ER), while also evaluating psychiatrists' general awareness of the syndrome through a survey.

A retrospective analysis of psychiatric ER records spanning June 18th to August 20th, 2022, was conducted to assess catatonia diagnosis frequency and treatment approaches. A Google Survey was distributed to full-time psychiatrists in the ER, querying their knowledge about catatonia prevalence, diagnostic modalities, and treatment strategies.

Analysis of 1118 patient records revealed a catatonia diagnosis rate of 0.36% (four cases) in the psychiatric ER. Remarkably, 75% of diagnosed patients were assessed by a single psychiatrist among nine available. Survey responses from all nine ER psychiatrists highlighted that 44% considered encountering catatonia as infrequent, while 33% regarded it as generally rare. Furthermore, 33% expressed willingness to employ potent antipsychotic interventions.

The study revealed a markedly low catatonia detection rate in the psychiatric ER, coupled with inconsistent treatment approaches. Survey findings reflected a considerable proportion of psychiatrists holding outdated perceptions of catatonia.

This is a case report of a previously healthy 26-year-old female with unexplained neurological symptoms that eventually developed malignant catatonia. Because malignant catatonia has a range of clinical manifestations, making prompt diagnosis a challenging task. Due to her relapsing symptoms, the patient was admitted to the inpatient psychiatric unit three times in less than 2 months, and eventually recovered with high doses of lorazepam and several electroconvulsive therapy (ECT) treatments after a stay in the intensive care unit (ICU). This case highlights the importance of avoiding of antipsychotics with dopamine blockade prior to administering a standardized catatonia rating scale in patients with negative symptoms, especially those who have unexplained neurological symptoms or vital sign abnormalities. It also emphasizes the importance of definitive decision-making in pursuing ECT treatment for patients with suspected malignant catatonia, as our patient showed remarkable improvement after ECT. Ultimately, more research is needed to study this rare illness to standardize procedures for treatment of malignant catatonia.

Encephalitis lethargica, an epidemic neurological illness, typically involved a severe sleep disorder and progressive parkinsonism. A century later, our understanding relies on seminal descriptions, more recent historical research and the study of small numbers of possible sporadic cases. Theories around infection, environmental toxins, catatonia and autoimmune encephalitis have been proposed. We aimed to describe the presentation of encephalitis lethargica and test these diagnostic and aetiological theories. Subjects with encephalitis lethargica were identified in the archives of the National Hospital for Neurology and Neurosurgery, UK between 1918 and 1946. Case notes were examined to establish illness temporality, clinical features and cerebrospinal fluid results. Controls from the archives were identified for 10% of cases, matching on discharge year, sex and neurologist. Clinical presentation was compared to modern diagnostic criteria for encephalitis lethargica, catatonia and autoimmune encephalitis. In a case-control design, a multilevel logistic regression was conducted to ascertain whether cases of encephalitis lethargica were associated with febrile illnesses and with environmental exposures. Six hundred and fourteen cases of encephalitis lethargica and 65 controls were identified. Cases had a median age of 29 years (interquartile range 18) and a median time since symptomatic onset of 3.00 years (interquartile range 3.52). Motor features were present in 97.6%, cranial nerve findings in 91.0%, ophthalmological features in 77.4%, sleep disorders in 66.1%, gastrointestinal or nutritional features in 62.1%, speech disorders in 60.8% and psychiatric features in 53.9%. Of the 167 cases who underwent lumbar puncture, 20 (12.0%) had a pleocytosis. The Howard and Lees criteria for encephalitis lethargica had a sensitivity of 28.5% and specificity of 96.9%. Among the cases, 195 (31.8%, 95% confidence interval 28.1-35.6%) had a history of febrile illness within one calendar year prior to illness onset, which was more common than among the controls (odds ratio 2.70, 95% confidence interval 1.02-7.20, P = 0.05), but there was substantial reporting bias. There was no evidence that occupational exposure to solvents or heavy metals was associated with encephalitis lethargica. Two hundred and seventy-six (45.0%) of the cases might meet criteria for possible autoimmune encephalitis, but only 3 (0.5%) might meet criteria for probable NMDA receptor encephalitis. Only 11 cases (1.8%) met criteria for catatonia. Encephalitis lethargica has a distinct identity as a neuropsychiatric condition with a wide range of clinical features. Evidence for a relationship with infectious or occupational exposures was weak. Autoimmune encephalitis may be an explanation, but typical cases were inconsistent with NMDA receptor encephalitis.

The term "catatonia" was introduced by German psychiatrist Karl Kahlbaum in 1874. Although historically tied to schizophrenia, catatonia exhibits a diverse range of phenotypes and has been observed in various medical and neuropsychiatric conditions. Its intrinsic movement characteristics and association with hypokinetic and hyperkinetic phenomenologies place catatonia within the purview of movement disorders. Despite the presence of catatonia in psychiatry literature for over 150 years, many gaps and controversies persist regarding its etiopathogenesis, phenomenology, diagnostic criteria, and treatment. The current versions of the International Classification of Diseases (ICD-11) and the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) require clinicians to identify any three signs of 15 (ICD-11) or 12 (DSM-5) for the diagnosis of catatonia. Catalepsy and waxy flexibility are the only motor features with high specificity for the diagnosis. We highlight the gaps and controversies in catatonia as a movement disorder, emphasize the lack of a clear definition, and discuss the inconsistencies in the description of various catatonic signs. We propose the exploration of a bi-axial classification framework similar to that used for dystonia and tremor to encourage the evaluation of underlying etiologies and to guide therapeutic decisions to improve the outcome of these patients. © 2024 International Parkinson and Movement Disorder Society.

Abrus cantoniensis Polysaccharides (ACP) exhibit antioxidant activity and immune-regulatory functions. Abrus cantoniensis Hance widely distributed in the Guangdong and Guangxi regions of China. In this study, this research investigated the impact of phosphorylation modification on the biological activity of ACP, aiming to provide theoretical insights for its development. This research modified ACP through phosphorylation and evaluated changes in its in vitro antioxidant capacity, including free radical scavenging and resistance to cellular oxidative damage. Additionally, this research administered both native ACP and phosphorylated ACP (P-ACP) to mice to assess their protective effects against acute ethanol-induced oxidative injury. This research explored whether these effects were mediated through the Keap1-Nrf2 signaling pathway and their influence on gut microbiota. Results revealed that phosphorylation significantly enhanced ACP's antioxidant capacity and protective effects (p < 0.05). P-ACP improved mice resistance to acute oxidative injury, mitigating the adverse effects of 50 % ethanol (p < 0.05). Moreover, both ACP and P-ACP are involved in modulating the expression of the Keap1-Nrf2 signaling pathway and, to some extent, alter the composition of the gut microbiota in mice. In summary, phosphorylation modification effectively enhances ACP's antioxidant capacity and provides better protection against acute oxidative injury in mice.

Catatonia is currently conceived in the major diagnostic manuals as a syndrome with a range of possible psychiatric and general medical underlying conditions. It features diverse clinical signs, spanning motor, verbal and behavioural domains and including stupor, catalepsy, mutism, echolalia, negativism and withdrawal. The existing literature suggests that seizure activity may underlie catatonia in approximately 2% of cases. There are three possible temporal relationships between catatonia and seizure activity: (1) ictal catatonia, in which catatonia is a presentation of non-convulsive status epilepticus; (2) postictal catatonia, in which catatonia follows a seizure, and (3) interictal catatonia, in which catatonia and seizures occur in the same individual without any clear temporal relationship between them. Electroencephalographic (EEG) abnormalities are common in catatonia, even in those cases with a presumed primary psychiatric origin, and often consist of generalised background slowing. Paradoxically, electroconvulsive therapy is an effective treatment for catatonia. There are several converging pieces of evidence suggesting that there may be underlying seizure activity in more cases of catatonia than has hitherto been recognised, though identification of these seizures may require intracranial EEG recording.

Catatonia is a neuropsychiatric disorder characterized by motor, affective and cognitive-behavioural signs, which lasts from hours to days. Intensive research over the past two decades has led to catatonia being recognized as an independent diagnosis in the International Classification of Diseases, 11th Revision (ICD-11) since 2022. Catatonia is found in 5-18% of inpatients on psychiatric units and 3.3% of inpatients on medical units. However, in an unknown number of patients, catatonia remains unrecognized and these patients are at risk of life-threatening complications. Hence, recognizing the symptoms of catatonia early is crucial to initiate appropriate treatment to achieve a favourable outcome. Benzodiazepines such as lorazepam and diazepam, electroconvulsive therapy, and N-methyl-D-aspartate antagonists such as amantadine and memantine, are the cornerstones of catatonia therapy. In addition, dopamine-modulating second-generation antipsychotics (for example, clozapine and aripiprazole) are effective in some patient populations. Early and appropriate treatment combined with new screening assessments has the potential to reduce the high morbidity and mortality associated with catatonia in psychiatric and non-psychiatric settings.

Catatonia, a psychomotor disorder characterized by diverse clinical signs, including stupor and mutism, remains elusive in its causes and a challenge to diagnose. Moreover, it is often underrecognized due to its resemblance to disorders of consciousness. However, when diagnosing catatonia, an antipsychotic medication may exacerbate the condition. The first-line treatment typically includes benzodiazepines and/or electroconvulsive therapy (ECT).

A 60-year-old woman with systemic lupus erythematosus (SLE) and epilepsy presented with catatonic stupor. Despite stable treatment, she experienced an acute deterioration in consciousness, requiring hospitalization. Her condition improved markedly following a benzodiazepine challenge, as documented on EEG. This improvement was short-lived, but a second benzodiazepine challenge restored her from E1V1M1 (stupor) to E4V5M6 within minutes, as documented by a video recording. The patient was treated with lorazepam 1.5 mg/day orally and did not experience further relapses.

The diagnosis of catatonia had been based on her scores on the Bush-Francis Catatonia Rating Scale (BFCRS; Screening, 6/14; Severity, 19), despite meeting only two DSM-5 criteria for catatonia (stupor and mutism). The diagnosis was supported by EEG and video documentation, excluding other potential differential diagnoses such as nonconvulsive status epilepticus and encephalopathy. Additional quantitative EEG analyses indicated that benzodiazepine administration increased brainwide alpha and beta band power significantly, suggesting that the benzodiazepine normalized attention, consciousness, and long-range synchronization. This report additionally emphasizes the significance of video recordings in managing catatonia, and it helps in accurately tracking symptoms, documenting comprehensively, and improving patient understanding, which is crucial for treatment adherence.

Catatonia is a complex neuropsychiatric syndrome involving a constellation of psychomotor disturbances including catalepsy, waxy flexibility, stupor, mutism, negativism, agitation, posturing, stereotypes, mannerisms, grimacing, echolalia, and echopraxia. Catatonia occurs in several conditions including psychotic, affective and neurodevelopmental disorders such as autism spectrum disorder (ASD). ASD is a neurodevelopmental disorder characterized by persistent deficits in communication, social interaction, restricted interests, repetitive behaviours and sensory sensitivities. Catatonia can occur in response to life stressors such as extreme fear or threat, interpersonal conflict, tragic events or following significant loss. Those with ASD may be particularly vulnerable to the negative impact of stressors and the link between catatonia and ASD is being increasingly recognized. The overlapping features of catatonia and ASD make it difficult to differentiate often resulting in delayed or missed diagnosis. Catatonia in ASD remains a significant clinical challenge; it is difficult to diagnose and can pose debilitating difficulties for those affected. Catatonia is a treatable condition and prompt recognition is vital in securing the best possible outcome. We report a complex and unique case of a 15-year-old boy who presented with severe cognitive and functional decline with a background history of significant bullying and deterioration in his mental state. This case posed a diagnostic conundrum leading to a diagnosis of underlying ASD, anxiety and trauma.

Karl Ludwig Kahlbaum (1828-1899) was the first to conceptualize and describe the main clinical features of a novel psychiatric illness, which he termed catatonia in his groundbreaking monograph published 150 years ago. Although Kahlbaum postulated catatonia as a separate disease entity characterized by psychomotor symptoms and a cyclical course, a close examination of his 26 cases reveals that most of them presented with motor symptom complexes or syndromes associated with various psychiatric and medical conditions. In his classification system, Kraepelin categorized catatonic motor symptoms that occur in combination with psychotic symptoms and typically have a poor prognosis within his dementia praecox (schizophrenia) disease entity. Because of the substantial influence of Kraepelin's classification, catatonia was predominantly perceived as a component of schizophrenia for most of the 20th century. However, with the advent of the psychopharmacotherapy era starting from the early 1950s, interest in catatonia in both clinical practice and research subsided until the early 2000s. The past two decades have witnessed a resurgence of interest in catatonia. The Diagnostic and Statistical Manual of Mental Disorders Fifth Edition, marked a paradigmatic shift by acknowledging that catatonia can occur secondary to various psychiatric and medical conditions. The introduction of an independent diagnostic category termed "Catatonia Not Otherwise Specified" significantly stimulated research in this field. The authors briefly review the history and findings of recent catatonia research and highlight promising directions for future exploration.

Primary Sjögren's syndrome (pSS) is recognized for its autoimmune origin. Its hallmark symptoms, dry eyes and mouth, result from glandular inflammation. Prior literature indicates that pSS not only affects the peripheral system but also involves the central nervous system (CNS), giving rise to various neuropsychiatric symptoms. However, there is limited published research on the psychiatric comorbidities in individuals with pSS.

A comprehensive search was conducted on PubMed and Google Scholar for this narrative review. The search spanned from inception until August 2023. Its aim was to locate studies focusing on the psychiatric manifestations of pSS and the potential underlying mechanisms.

The most commonly reported psychiatric complications among these individuals are depression and cognitive dysfunction. Other psychiatric manifestations that have been reported in pSS individuals include anxiety, sleep disorders, psychosis, catatonia, bipolar disorder, and obsessive-compulsive disorder.

In conclusion, patients with pSS often display multiple psychiatric symptoms. These symptoms can significantly impair functioning and reduce quality of life. Hence, prompt diagnosis and management are crucial.

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.

Certain clinical features, like changes in presentation, the presence of neurological signs, and a poor response to treatment, mandate an organic evaluation of psychiatric illnesses. In this case series, four cases with established mental illnesses who presented with psychiatric symptoms, on evaluation by neuroimaging, were found to have neurological disorders like neurocysticercosis, sub-arachnoid hemorrhage, sub-dural hemorrhage, and lacunar infarction. They were managed with a combination of medical and surgical treatment and psychotropics, and no relapse of symptoms was noted at follow-up. The formulation of clinical practice guidelines can be a way forward in holistic management for such patients.

Catatonia is a well characterized psychomotor syndrome combining motor, behavioural and neurovegetative signs. Benzodiazepines are the first-choice treatment, effective in 70 % of cases. Currently, the factors associated with benzodiazepine resistance remain unknown. We aimed to develop machine learning models using clinical and neuroimaging data to predict benzodiazepine response in catatonic patients. This study examined a cohort of catatonic patients who underwent standardized clinical evaluation, 3 T brain MRI, and benzodiazepine trial. Based on clinical response, patients were classified as benzodiazepine responders or non-responders. Cortical thickness and regional brain volumes were measured. Two machine learning models (linear model and gradient boosting tree model) were developed to identify predictors of treatment response using clinical, demographic, and neuroimaging data. The cohort included 65 catatonic patients, comprising 30 benzodiazepine responders and 35 non-responders. Using clinical data alone, the linear model achieved 63% precision, 51% recall, a specificity of 61%, and 58% AUC, while the gradient boosting tree (GBT) model attained 46% precision, 60% recall, a specificity of 62% and 64% AUC. Incorporating neuroimaging data improved model performance, with the linear model achieving 66% precision, 57% recall, a specificity of 67%, and 70% AUC, and the GBT model attaining 50% precision, 50% recall, a specificity of 62% and 70% AUC. The integration of imaging data with demographic and clinical information significantly enhanced the predictive performance of the models. The duration of the catatonic syndrome, along with the presence of mitgehen (passive obedience) and immobility/stupor, and the volume of the right medial orbito-frontal cortex emerged as important factors in predicting non-response to benzodiazepines.

A clinical practice guideline (CPG) was created to standardize evaluation and treatment for patients with suspected anti-methyl-d-aspartate receptor (NMDAR) autoimmune encephalitis (AE), the most common AE in children. The objective of this study was to evaluate the CPG effect on time to diagnosis, treatment, and hospital length of stay (LOS).

Patients with an inpatient consult to pediatric rheumatology for AE during a 4-year period (period 2) after CPG implementation were identified. Data were extracted and compared with data over the preceding 4-year period (period 1).

During period 1, fewer patients underwent diagnostic testing than during period 2 (34 vs 80). Number of patients diagnosed with AE did not differ from period 1 to that from period 2 (NMDAR AE 9 vs 8; seronegative AE 4 vs 5). The average time to diagnostic evaluation with lumbar puncture decreased from 5.4 to 1.5 days (p = 0.0082), and time to treatment decreased from 7.6 to 3.9 days (p = 0.018). LOS showed a trend toward improvement (40.4-29.2 days (p = 0.23)).

Creation of a CPG for patients with suspected AE was associated with an improved time to diagnostic evaluation and treatment. With the CPG, more patients underwent AE testing, though total diagnoses remained the same.

Crush syndrome (CS), alternatively termed traumatic rhabdomyolysis, is a paramount posttraumatic complication. Given the infeasibility of conducting direct simulation research in humans, the role of animal models is pivotal. Regrettably, the dearth of standardized animal models persists. The objective of this study was to construct a repeatable standardized rat CS models and, based on this, simulate specific clinical scenarios. Methods: Using a self-developed multichannel intelligent small-animal crush injury platform, we applied a force of 5 kg to the hind limbs of 8-week-old rats (280-300 g), subjecting them to a continuous 12 h compression to establish the CS model. Continuous monitoring was conducted for both the lower limbs and the overall body status. After decompression, biochemical samples were collected at 3, 6, 12, and 24 h. In addition, we created a CS model after resection of the left kidney (UNx-CS), which was conceptualized to simulate a more challenging clinical scenario to investigate the physiological and pathological responses rats with renal insufficiency combined with crush injury. The results were compared with those of the normal CS model group. Results : Our experiments confirm the stability of the crush injury platform. We defined the standardized conditions for modeling and successfully established rats CS model in bulk. After 12 h of compression, only 40% of the rats in the CS group survived for 24 h. Systemically, there was clear evidence of insufficient perfusion, reflecting the progression of CS from localized to generalized. The injured limbs displayed swelling, localized perfusion deficits, and severe pathological alterations. Significant changes were observed in blood biochemical markers: aspartate transaminase, lactate dehydrogenase, K+, creatine kinase, creatinine, and blood urea nitrogen levels rose rapidly after decompression and were significantly higher than the sham group. The kidney demonstrated characteristic pathological changes consistent with established CS diagnostic criteria. Although the UNx-CS rat model did not exhibit significant biochemical differences and pathological scores when compared with the standard CS model, it did yield intriguing results with regard to kidney morphology. The UNx-CS group manifested a higher incidence of cortical and medullary protein casts compared with the NC-CS group. Conclusion: We developed and iteratively refined a novel digital platform, addressing the multiple uncontrollable variables that plagued prior models. This study validated the stability of the platform, defined the standardized conditions for modeling and successfully established the CS model with good repeatability in bulk. In addition, our innovative approach to model a clinically challenging scenario, the UNx-CS rat model. This offers an opportunity to delve deeper into understanding the combined effects of preexisting renal compromise and traumatic injury. In summary, the development of a standardized, reproducible CS model in rats represents a significant milestone in the study of Crush syndrome. This study is of paramount significance as it advances the standardization of the CS model, laying a solid foundation for subsequent studies in related domains, especially in CS-AKI.

Anti-NMDAR encephalitis is the most common cause of immune-mediated catatonia.

Three females presented with neuropsychiatric symptoms and were empirically treated with first-line immunotherapy and ovarian teratoma resection for suspected autoimmune encephalitis, preceding diagnostic confirmation via NMDAR antibody positivity. They required escalating large doses of benzodiazepines for refractory malignant catatonia resulting in ICU level care. ECT treatments were initiated, and patients were gradually noted to have clinical improvement as was measured by the Bush-Francis Catatonia Rating Scale.

Clinicians should recognize catatonia among patients with suspected anti-NMDAR encephalitis and consider the early implementation of ECT into treatment algorithms.

At present, current diagnostic criteria and systems neglect affective symptom expression in catatonia. This potentially serious omission could explain why putative contributions of limbic system structures, such as amygdala, hippocampus or hypothalamus, to catatonia in schizophrenia spectrum disorders (SSD) have been scarcely investigated so far. To determine whether topographical alterations of the amygdala, hippocampus and hypothalamus contribute to catatonia in SSD patients, we conducted structural magnetic resonance imaging (MRI) of SSD patients with (SSD-Cat, n = 30) and without (SSD-nonCat, n = 28) catatonia as defined by a Northoff Catatonia Rating Scale (NCRS) total score of ≥3 and =0, respectively, in comparison with healthy controls (n = 20). FreeSurfer v7.2 was used for automated segmentation of the amygdala and its 9 nuclei, hippocampus and its 21 subfields and hypothalamus and its associated 5 subunits. SSD-Cat had significantly smaller anterior inferior hypothalamus, cortical nucleus of amygdala, and hippocampal fimbria volumes when compared to SSD-nonCat. SSD-Cat had significantly smaller amygdala, hippocampus and hypothalamus whole and subunit volumes when compared to healthy controls. In SSD-Cat according to DSM-IV-TR (n = 44), we identified positive correlations between Brief Psychiatric Rating Scale (BPRS) item #2 (reflecting anxiety) and respective amygdala nuclei as well as negative correlation between NCRS behavioral score and hippocampus subiculum head. The lower volumes of respective limbic structures involved in affect regulation may point towards central affective pathomechanisms in catatonia.

Catatonia is a neuropsychiatric syndrome associated with both psychiatric disorders and medical conditions. Understanding of the pathophysiology of catatonia remains limited, and the role of the environment is unclear. Although seasonal variations have been shown for many of the disorders underlying catatonia, the seasonality of this syndrome has not yet been adequately explored.

Clinical records were screened to identify a cohort of patients suffering from catatonia and a control group of psychiatric inpatients, from 2007 to 2016 in South London. In a cohort study, the seasonality of presentation was explored fitting regression models with harmonic terms, while the effect of season of birth on subsequent development of catatonia was analyzed using regression models for count data. In a case-control study, the association between month of birth and catatonia was studied fitting logistic regression models.

In total, 955 patients suffering from catatonia and 23,409 controls were included. The number of catatonic episodes increased during winter, with a peak in February. Similarly, an increasing number of cases was observed during summer, with a second peak in August. However, no evidence for an association between month of birth and catatonia was found.

The presentation of catatonia showed seasonal variation in accordance with patterns described for many of the disorders underlying catatonia, such as mood disorders and infections. We found no evidence for an association between season of birth and risk of developing catatonia. This may imply that recent triggers may underpin catatonia, rather than distal events.

Catatonia occurs secondary to both primary psychiatric and neuromedical etiologies. Emerging evidence suggests possible linkages between causes of catatonia and neuroinflammation. These include obvious infectious and inflammatory etiologies, common neuromedical illnesses such as delirium, and psychiatric entities such as depression and autism-spectrum disorders. Symptoms of sickness behavior, thought to be a downstream effect of the cytokine response, are common in many of these etiologies and overlap significantly with symptoms of catatonia. Furthermore, there are syndromes that overlap with catatonia that some would consider variants, including neuroleptic malignant syndrome (NMS) and akinetic mutism, which may also have neuroinflammatory underpinnings. Low serum iron, a common finding in NMS and malignant catatonia, may be caused by the acute phase response. Cellular hits involving either pathogen-associated molecular patterns (PAMP) danger signals or the damage-associated molecular patterns (DAMP) danger signals of severe psychosocial stress may set the stage for a common pathway immunoactivation state that could lower the threshold for a catatonic state in susceptible individuals. Immunoactivation leading to dysfunction in the anterior cingulate cortex (ACC)/mid-cingulate cortex (MCC)/medial prefrontal cortex (mPFC)/paralimbic cortico-striato-thalamo-cortical (CSTC) circuit, involved in motivation and movement, may be particularly important in generating the motor and behavioral symptoms of catatonia.

Back in 2004, in a chapter titled "Brain Evolution and the Meaning of Catatonia", a case was made that the syndrome's core meaning is embedded in millions of years of vertebrate brain evolution. (Fricchione, 2004) In this update, advances over the last almost 20 years, in catatonia theory and research in particular, and pertinent neuropsychiatry in general, will be applied to this question of meaning. The approach will rely heavily on a number of thought leaders, including Nicos Tinbergen, Paul MacLean, John Bowlby, M. Marsel Mesulam, Bruce McEwen and Karl Friston. Their guidance will be supplemented with a selected survey of 21sty century neuropsychiatry, neurophysiology, molecular biology, neuroimaging and neurotherapeutics as applied to the catatonic syndrome. In an attempt to address the question of the meaning of the catatonic syndrome in human life, we will employ two conceptual networks representing the intersubjectivity of the quantitative conceptual network of physical terms and the subjectivity of the qualitative conceptual network of mental and spiritual terms. In the process, a common referent providing extensional identity may emerge (Goodman, 1991). The goal of this exercise is to enhance our attunement with the experience of patients suffering with catatonia. A deeper understanding of catatonia's origins in brain evolution and of the challenges of individual epigenetic development in the setting of environmental events coupled with appreciation of what has been described as the most painful mammalian condition, that of separation, has the potential to foster greater efforts on the part of clinicians to diagnose and treat patients who present with catatonia. In addition, in this ancient and extreme tactic, evolved to provide safety from extreme survival threat, one can speculate what is at the core of human fear and the challenge it presents to all of us. And when the biology, psychology and sociology of catatonia are examined, the nature of solutions to the challenge may emerge.

Catatonia is a severe psychomotor syndrome mainly associated with psychiatric disorders, such as mood disorders and schizophrenia. Seasonal patterns have been described for these psychiatric disorders, and a previous study conducted in South London showed for the first time a seasonal pattern in the onset of catatonia. In this study, we aim to extend those findings to a larger national sample of patients admitted to French metropolitan hospitals, between 2015 and 2022, and to perform subgroup analyses by the main associated psychiatric disorder. A total of 6225 patients diagnosed with catatonia were included. A seasonal pattern for catatonia diagnosis was described, using cosinor models. Two peaks of diagnoses for catatonic cases were described in March and around September-October. Depending on the associated psychiatric disorder, the seasonality of catatonia diagnosis differed. In patients suffering with mood disorders, peaks of catatonia diagnosis were found in March and July. For patients suffering with schizophrenia, no seasonal pattern was found.

Catatonia is a complex psychomotor disorder characterized by motor, affective, and behavioral symptoms. Despite being known for almost 150 years, its pathomechanisms are still largely unknown.

A systematic research on PubMed, Web of Science, and Scopus was conducted to identify neuroimaging studies conducted on group or single individuals with catatonia. Overall, 33 studies employing structural magnetic resonance imaging (sMRI, n = 11), functional magnetic resonance imaging (fMRI, n = 10), sMRI and fMRI (n = 2), functional near-infrared spectroscopy (fNIRS, n = 1), single positron emission computer tomography (SPECT, n = 4), positron emission tomography (PET, n = 4), and magnetic resonance spectroscopy (MRS, n = 1), and 171 case reports were retrieved.

Observational sMRI studies showed numerous brain changes in catatonia, including diffuse atrophy and signal hyperintensities, while case-control studies reported alterations in fronto-parietal and limbic regions, the thalamus, and the striatum. Task-based and resting-state fMRI studies found abnormalities located primarily in the orbitofrontal, medial prefrontal, motor cortices, cerebellum, and brainstem. Lastly, metabolic and perfusion changes were observed in the basal ganglia, prefrontal, and motor areas. Most of the case-report studies described widespread white matter lesions and frontal, temporal, or basal ganglia hypoperfusion.

Catatonia is characterized by structural, functional, perfusion, and metabolic cortico-subcortical abnormalities. However, the majority of studies and case reports included in this systematic review are affected by considerable heterogeneity, both in terms of populations and neuroimaging techniques, which calls for a cautious interpretation. Further elucidation, through future neuroimaging research, could have great potential to improve the description of the neural motor and psychomotor mechanisms underlying catatonia.

Catatonia is a severe and potentially life-threatening neuropsychiatric condition. Electroconvulsive therapy (ECT) is the gold standard second-line intervention for catatonia after benzodiazepine failure. However, the access to ECT can be particularly challenging, especially during periods of increased strain on medical facilities, such as the COVID-19 pandemic. Several case reports have suggested the potential efficacy of transcranial direct current stimulation (tDCS) in addressing catatonia. In our case, we present the successful application of intensive tDCS, delivering five sessions per day, each lasting 20 min, with an intensity of 2 mA. The tDCS montage involved placing the anode on the left dorsolateral prefrontal cortex (DLPFC) and the cathode on the left temporoparietal junction (TPJ). This approach was well-tolerated and resulted in a significant improvement in a 70-year-old patient with catatonia, for whom ECT was deemed necessary. While these results are promising, it is crucial to confirm them through a randomized controlled study.

Catatonia, a psychomotor disorder, can have underlying psychiatric and medical etiologies. Around 29% of the catatonias with medical etiologies are related to either infectious or immune causes. Benzodiazepines like lorazepam and electroconvulsive therapy are the conventional treatment modalities for catatonia. In this case series, three cases of catatonia secondary to pulmonary tuberculosis, pneumococcal pneumonia, and neurocysticercosis have been described, in which conventional treatment modalities like lorazepam or electroconvulsive therapy either failed or were disadvantageous and were successfully treated with memantine (20-30 mg).

Catatonia is a psychomotor syndrome frequently observed in disorders with neurodevelopmental impairments, including psychiatric disorders such as schizophrenia. The orbitofrontal cortex (OFC) has been repeatedly associated with catatonia. It presents with an important interindividual morphological variability, with three distinct H-shaped sulcal patterns, types I, II, and III, based on the continuity of the medial and lateral orbital sulci. Types II and III have been identified as neurodevelopmental risk factors for schizophrenia. The sulcal pattern of the OFC has never been investigated in catatonia despite the role of the OFC in the pathophysiology and the neurodevelopmental component of catatonia.

In this context, we performed a retrospective analysis of the OFC sulcal pattern in carefully selected homogeneous and matched subgroups of schizophrenia patients with catatonia (N = 58) or without catatonia (N = 65), and healthy controls (N = 82).

Logistic regression analyses revealed a group effect on OFC sulcal pattern in the left (χ2 = 18.1; p < .001) and right (χ2 = 28.3; p < .001) hemispheres. Catatonia patients were found to have more type III and less type I in both hemispheres compared to healthy controls and more type III on the left hemisphere compared to schizophrenia patients without catatonia.

Because the sulcal patterns are indirect markers of early brain development, our findings support a neurodevelopmental origin of catatonia and may shed light on the pathophysiology of this syndrome.

Venous thromboembolism (VTE) comprises pulmonary embolism (PE) and deep vein thrombosis (DVT). PE, as the most severe manifestation of VTE, can cause increased mortality in patients with mental disorders. Here we describe two cases of young male patients with catatonia who developed PE and DVT during their hospital stay. We also discuss the possible pathogenesis, with a focus on immune and inflammatory mechanisms.

In some patients, neuroleptic malignant syndrome is accompanied significant high levels of erythrocyte sedimentation rate (ESR), C-reactive protein (CRP).

Neuroleptic malignant syndrome (NMS) is an idiosyncratic life-threatening adverse reaction and usually triggered in response to antipsychotic drugs. In addition, leukocytosis and increased muscle enzymes levels (especially creatine phosphokinase) are observed in NMS. In addition, a transient increase in different types of acute phase reactants in NMS has been mentioned. This article describes a woman treated with haloperidol, perphenazine, escitalopram, and alprazolam because she developed catatonic symptoms after psychological stress. She suffered from NMS symptoms and had elevated CRP and ESR levels, among other signs and symptoms. Given the COVID-19 pandemic and reports of co-occurrence of catatonia and NMS and COVID-19 and elevated erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), this patient was a diagnostic dilemma. After consultation with the consultation-liaison psychiatry units, she was managed adequately with electroconvulsive therapy and lorazepam.

Catatonia, a neuropsychiatric syndrome characterized by psychomotor and behavioral symptoms, can be associated with various underlying conditions, including demyelinating diseases such as multiple sclerosis. This paper presents a case study of a 47-year-old female with recurrent catatonic relapses and an underlying demyelinating disease. The patient exhibited symptoms of confusion, decreased oral intake, and difficulty with movement and speech. Neurological examinations, brain imaging, and laboratory tests were conducted to evaluate the etiology and guide treatment. The patient showed improvement with lorazepam and electroconvulsive therapy (ECT). However, relapses occurred after the abrupt withdrawal of medication. The case study highlights the potential connection between demyelinating diseases and catatonia and emphasizes the importance of considering demyelinating diseases in the workup, treatment, and relapse prevention of catatonia. Further research is needed to explore the mechanisms underlying the relationship between demyelination and catatonia and to investigate how different etiologies may impact the recurrence rates of catatonic episodes.

Based on the neuroinflammation hypothesis in schizophrenia and known anti-inflammatory effects of berberine, the aim of the present study is to investigate the efficacy of berberine in treating negative symptoms and cognitive deficits in adult patients with chronic schizophrenia.

Enrolled participants were randomized to receive berberine or placebo for 3 months. The Scale for the Assessment of Negative Symptoms (SANS), Trail-making Test A (TMT-A), Trail-making Test B (TMT-B), and Hopkins Verbal Learning Test (HVLT) were used to evaluate the negative symptoms and cognitive function at four-time points (baseline, 1st, 2nd, and 3rd month). Serum levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) were used as inflammatory markers. 106 patients with per-protocol were analyzed, 56 in the experimental (berberine) group and 50 in the control (placebo) group.

From baseline to month 3, patients receiving berberine demonstrated a decrease in total scores on clinical scales SANS, TMT-A and TMT-B and showed a serum level reduction of IL-1β, IL-6 and TNF-α comparing with patients in the control group (P < 0.05). There were positive correlations between the change of serum IL-1β level and the change of SANS (r = 0.210, P = 0.039), TMT-A (r = 0.522, P < 0.001), and TMT-B (r = 0.811, P < 0.001); between the change of serum IL-6 level and the change of TMT-A (r = 0.562, P < 0.001), and TMT-B (r = 0.664, P < 0.001); between the change of serum TNF-α level and the change of TMT-B (r = 0.472, P < 0.001) after berberine treatment.

Berberine is an anti-inflammatory agent that can potentially mitigate the negative symptoms and cognitive deficits in patients with schizophrenia.

The following paper described two cases of patients with catatonic depression in bipolar disorder (BD) referred to our electroconvulsive therapy (ECT) service. Both were deemed not medically fit for ECT, and were, instead, treated with intravenous (IV) ketamine. Both responded with a resolution of symptoms, returning to baseline level of functioning. During the COVID-19 pandemic, given the risks associated with providing ECT (an aerosol generating procedure) and, in the context of limited resources, ketamine therapy for catatonia is a potentially beneficial alternative or supportive treatment to ECT that merits additional research.

The British Association for Psychopharmacology developed an evidence-based consensus guideline on the management of catatonia. A group of international experts from a wide range of disciplines was assembled. Evidence was gathered from existing systematic reviews and the primary literature. Recommendations were made on the basis of this evidence and were graded in terms of their strength. The guideline initially covers the diagnosis, aetiology, clinical features and descriptive epidemiology of catatonia. Clinical assessments, including history, physical examination and investigations are then considered. Treatment with benzodiazepines, electroconvulsive therapy and other pharmacological and neuromodulatory therapies is covered. Special regard is given to periodic catatonia, malignant catatonia, neuroleptic malignant syndrome and antipsychotic-induced catatonia. There is attention to the needs of particular groups, namely children and adolescents, older adults, women in the perinatal period, people with autism spectrum disorder and those with certain medical conditions. Clinical trials were uncommon, and the recommendations in this guideline are mainly informed by small observational studies, case series and case reports, which highlights the need for randomised controlled trials and prospective cohort studies in this area.

Catatonia, a severe neuropsychiatric syndrome, has few studies of sufficient scale to clarify its epidemiology or pathophysiology. We aimed to characterise demographic associations, peripheral inflammatory markers and outcome of catatonia.

Electronic healthcare records were searched for validated clinical diagnoses of catatonia. In a case-control study, demographics and inflammatory markers were compared in psychiatric inpatients with and without catatonia. In a cohort study, the two groups were compared in terms of their duration of admission and mortality.

We identified 1456 patients with catatonia (of whom 25.1% had two or more episodes) and 24 956 psychiatric inpatients without catatonia. Incidence was 10.6 episodes of catatonia per 100 000 person-years. Patients with and without catatonia were similar in sex, younger and more likely to be of Black ethnicity. Serum iron was reduced in patients with catatonia [11.6 v. 14.2 μmol/L, odds ratio (OR) 0.65 (95% confidence interval (CI) 0.45-0.95), p = 0.03] and creatine kinase was raised [2545 v. 459 IU/L, OR 1.53 (95% CI 1.29-1.81), p < 0.001], but there was no difference in C-reactive protein or white cell count. N-Methyl-d-aspartate receptor antibodies were significantly associated with catatonia, but there were small numbers of positive results. Duration of hospitalisation was greater in the catatonia group (median: 43 v. 25 days), but there was no difference in mortality after adjustment.

In the largest clinical study of catatonia, we found catatonia occurred in approximately 1 per 10 000 person-years. Evidence for a proinflammatory state was mixed. Catatonia was associated with prolonged inpatient admission but not with increased mortality.

We present the case of a 65-year-old female with a past psychiatric history of obsessive-compulsive disorder and anxiety who recently underwent diagnostic laparoscopy in the setting of a recent computerized tomography scan revealing a peritoneal mass. Postoperatively, she was delirious and soon found to be malignantly catatonic. This patient's treatment was complicated by an acute stroke, which was a relative contraindication for electroconvulsive therapy. Top experts in the consultation-liaison psychiatry and electroconvulsive therapy fields provide guidance for this clinical scenario based on their experience and a review of the available literature. Key teaching points include a review of diagnosing and treating catatonia, a review of electroconvulsive therapy for the treatment of catatonia, as well as a review of the role of the consultation-liaison psychiatrist in medically complex cases. Specifically, we offer guidance in treating patients that have malignant catatonia when electroconvulsive therapy is unavailable.

Catatonia is a complex neuropsychiatric syndrome that can be associated with several underlying etiologies including primary psychiatric and autoimmune disorders. Anti-N-methyl-D-aspartate receptor encephalitis is an autoimmune disorder typically characterized by seizures, movement abnormalities, and behavioral changes. Anti-N-methyl-D-aspartate can present with complex neuropsychiatric symptoms including catatonia which can be challenging for clinicians to identify as excited catatonia can mimic delirium and psychiatric disorders such as psychosis and mania.

To identify and present cases of anti-N-methyl-D-aspartate receptor encephalitis where excited catatonia is the presenting symptom.

We present 2 case studies of agitation and disinhibition in an adolescent and young adult that were ultimately found to be secondary to autoimmune receptor encephalitis, in both cases, confirmed by cerebrospinal fluid analysis to be due to anti-N-methyl-D-aspartate receptor antibodies.

Excited catatonia was suspected and initially treated with immunological therapy and high doses of lorazepam. As the severity of catatonia progressed with limited improvement with lorazepam, both cases were ultimately effectively treated with electroconvulsive therapy.

Excited catatonia should be considered with presentations of bizarre behavior, agitation, disinhibition, and other psychotic symptoms in patients with no prior psychiatric history. Although the primary treatment for catatonia associated with anti-N-methyl-D-aspartate receptor encephalitis is immunomodulatory therapy paired with benzodiazepines, electroconvulsive therapy has been shown to be an effective and safe adjuvant treatment that is especially useful for management of excited catatonia.