Catatonia is a potentially life-threatening condition that is characterized by psychiatric and motor disturbances, such as negativism, hypomotility, bradykinesia, and unusual movements. The diagnosis is based on clinical examination and occurs in both pediatric and adult patients and is associated with an increased mortality. Catatonia is associated with psychiatric illnesses such as schizophrenia, major depression, encephalitis, and bipolar disorder. The physiopathology of catatonia is complex and not fully understood. There is an ongoing debate in the medical community whether catatonia is an independent syndrome, or secondary to other mental illnesses. This case presentation is unique, as there are few reports describing cases of isolated catatonic syndrome in the absence of any other psychiatric or medical condition with a delayed onset caused by recreational drug abuse.

We present the case of a 17-year-old Caucasian athletic girl with no previous contact with child and adolescent psychiatry, nor any previous drug abuse. After recreational intake of drugs, there was a delay of approximately 7 days, before the patient searched care with symptoms that were at a later stage recognized as catatonia. Treatment with a high dose of lorazepam in combination with memantine and lithium resulted in a regression of the symptoms. After 6 weeks the patient could be discharged from the hospital almost fully recovered.

An acute onset of psychomotor symptoms without any previous history of mental illnesses must be addressed early as a potential catatonic syndrome. Delayed onset of catatonic symptoms after intake of drugs should not be overlooked, and we here suggest that mephedrone might be capable of inducing delayed catatonia. It is feasible to use memantine as an adjuvant to the treatment of catatonia in adolescents.

Catatonia is a neuropsychiatric syndrome that is an increasingly recognized cause of acute behavioural changes in children and adolescents with neurodevelopmental disorders (NDD). Literature suggests that catatonia can present differently in this population and can be missed due to diagnostic overshadowing. Catatonia is a treatable condition, and management strategies in children with NDD include benzodiazepines and electroconvulsive therapy (ECT). Untreated, it can cause significant morbidity including severe medical complications, and therefore timely recognition and management of catatonia in children and adolescents with NDD is essential. In this case series, we present three cases of children ages 7, 14, and 10, with diagnoses of autism spectrum disorder, Down syndrome, and Prader-Willi syndrome, respectively. All were admitted to a pediatric inpatient unit for acute behavioural regression. Each had symptoms consistent with catatonia, resulting in trials of benzodiazepine therapy with inadequate response, and were then treated with bilateral ECT. In all cases, marked improvement was noted after ECT, with no apparent adverse effects. The cases are used to highlight the nuances of diagnosis and management of catatonia in children and adolescents with NDD. This includes insights on how presentations of catatonia may differ in this population, challenges with the use of available diagnostic tools, and how these patients may respond differently to recommended treatments such as benzodiazepines. The case series aims to increase clinicians' awareness of pediatric catatonia when children and adolescents with NDD present with acute behavioural changes, and to encourage consideration of the full spectrum of treatments, including bilateral ECT.

The current study aimed to evaluate subtle catatonia behaviors and functionality in adolescents with autism spectrum disorders (ASD). The sample consisted of 48 patients (11 female, 37 male) aged 12-18 (13.77 ± 2.01). DSM-5 catatonia criteria and Bush-Francis Catatonia Rating Scale (BCRS) was utilized to assess catatonia, while the impairment in functionality was appraised using the Global Assessment Scale. Parents fulfilled the Revised Child Anxiety and Depression Scale-Parent version (RCADS-PV) and Repetitive Behavior Scale-Revised (RBS-R). The presence of catatonia was detected in 18 out of 48 (37.5 %) participants according to BCRS, and in 16 cases (35.4 %) according to DSM-5 criteria. A significant association between two diagnostic tools was observed (p < 0.001). In the group with mild impairment in functionality, 2 cases had catatonia (12.5 %), while in the group with more impaired functionality, 16 cases (50 %) had catatonia (p = 0.011) according to BCRS. Major depressive disorder subscale scores of RCADS-PV and stereotypic movements (RBS-R) were correlated with the presence of catatonia (p < 0.05). The findings suggest a higher prevalence of catatonia in ASD, and a potential correlation between the presence of catatonia and functionality. More research is warranted to highlight the presence and course of catatonia beginning from the early years of ASD.

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.

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 complex syndrome with prominent psychomotor, cognitive, and affective manifestations. Among the commonly described manifestations of catatonia are mannerisms and stereotypies. Kahlbaum, who coined the term catatonia, described several presentations of mannerisms and stereotypies as complex behaviors in his monograph. However, most of the subsequent psychiatric literature has described both phenomena in the context of simple motor movements or actions.

We identified complex behavioral presentations of mannerisms and stereotypies described by Kahlbaum in his monograph. We summarize the development and use of mannerisms and stereotypies as psychiatric terminology since Kahlbaum, emphasizing the spectrum of behavior captured early in this usage. We list the inconsistent and interchangeable use of these terms in subsequent literature and describe recent examples of complex behavioral manifestations of mannerisms and stereotypies in the context of catatonia.

We propose a new framework for mannerisms and stereotypies that utilizes descriptive psychopathology factors in various normative references, the context of the behavior examined, and critical pathological processes identified in mannerisms and stereotypies to identify and describe complex manifestations of these phenomena.

Catatonia continues to remain under-recognized and under-treated. Our current diagnostic tools can make mannerisms and stereotypies complex and challenging to recognize. We suggest defining stereotypies as non-contextual repetitive activities while mannerisms as non-contextual peculiarities of activities. Utilizing our proposed framework and definitions can improve the description, recognition, and treatment of catatonia.

Catatonia is a highly morbid psychomotor and affective disorder which can affect autistic individuals with and without profound impairment. Catatonic symptoms are treatable with pharmacotherapy and electroconvulsive therapy, but the longitudinal effectiveness of these treatments has not been described.

We conducted a prospective observational cohort study of patients with autism and co-morbid catatonia who received outpatient care in a specialized outpatient clinic from July 1st, 2021 to May 31st, 2024. Data investigating pharmacologic interventions, and clinical measures including the Bush Francis Catatonia Rating Scale (BFCRS), Kanner Catatonia Severity Scale (KCS), Kanner Catatonia Examination (KCE), and Clinical Global Impression - Improvement (CGI-I) were collected.

Forty-five patients were identified with 39 (86.7%) meeting criteria for profound autism. All patients received pharmacotherapy. 44 (97.8%) were treated with benzodiazepines with a mean maximal daily dose of 17.4 mg (SD=15.8) lorazepam equivalents. Thirty-five patients (77.8%) required more than one medication class for treatment. Fourteen patients (31.1%) attempted to taper off benzodiazepines during the study period; of these, 5 patients (11.1%) were successfully tapered off, and the remaining 9 (17.8%) discontinued the taper due to a return of catatonic symptoms. Statistically significant improvement was observed across all clinical domains except the KCS. However, the majority remained symptomatic over the study period.

Despite clinical improvements while receiving the gold standard for psychopharmacologic management of catatonia, chronic symptoms remained for the majority of catatonia patients over the study period, and few were able to taper and discontinue benzodiazepine treatment.

This is the first report of pediatric catatonia syndrome in MED13L haploinsufficiency syndrome. This report describes unique challenges in diagnosis and management of catatonia in rare genetic conditions. The case also illustrates the use of electroconvulsive therapy in patients with epilepsy, epileptic encephalopathy, or other epileptic diathesis and the clinical conundrum in determining the course of maintenance electroconvulsive therapy.

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.

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.