Catatonic Syndrome Research Articles

Catatonia and neurocognitive disorder in the context of schizophrenia spectrum disorders

Background. Currently, researchers are aiming to establish the relationship between neurocognitive disorder and other clinical manifestations of endogenous diseases and functional indicators of the patient’s adaptation to social life. According to some data, the development of cognitive disorders is associated with the severity of catatonic disorders in the clinical picture of various diseases, in particular the presence of catatonic symptoms determines the worst indicators of cognitive functioning in the case of schizophrenia.The aim. To study the clinical and psychopathological features of catatonic syndrome in connection with schizophrenia spectrum disorders, as well as its connection with neurocognitive disorder manifestations among patients with endogenous disorders.Methods. From September 2022 to March 2024, we conducted a prospective, multicenter study of patients (n = 69) suffering from paroxysmal schizophrenia with primary catatonic symptoms in the structure of attacks. Mental status, the severity of catatonic symptoms using Bush – Francis Catatonia Rating Scale, neurocognitive profile using a number of validated scales (Montreal Cognitive Scale, Brief Assessment of Cognition in Schizophrenia, Frontal Assessment Battery) were assessed.Results. Neurocognitive disorder was revealed in all cases studied. It has been noted that, depending on the presence/absence of affective symptoms, various domains of the neurocognitive profile are affected. Thus, in patients without severe affective symptoms, auditory and verbal memory, attention, processing speed, and motor skills are impaired. In patients with pronounced affective disorders, processing speed, motor skills, and problem-solving behavior are affected.Conclusion. Based on the results of processing the material, it was revealed that the most pronounced neurocognitive disorders were found in case of the manifestation of paroxysmal paranoid schizophrenia in male patients with a relatively early onset of the disease and hypokinetic catatonic disorders. In the future, we are planning to compare these results with the results of control group of patients with endogenous diseases and without catatonia.

Clinical and neuroimaging predictors of benzodiazepine response in catatonia: A machine learning approach

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.

Catatonic syndrome and seronegative encephalitis in children: Diagnostic and therapeutic difficulties, a case report

Catatonic syndrome and seronegative encephalitis in children: Diagnostic and therapeutic difficulties, a case report

Idiopathic catatonic syndrome in a young male with no prior psychiatric history: a case report

BackgroundCatatonia is a syndrome characterized by severe psychomotor disturbances such as hypomotility, bradykinesia, and unusual movements. The condition has been described in the context of a wide variety of primary disease processes, including psychotic and mood disorders and numerous general medical conditions. In the medical community, catatonia is misunderstood, under-recognized, and under-treated. There continues to be debate about whether catatonia is an independent syndrome or a secondary expression of other conditions. This is a unique case presentation, as there are few reports describing cases of isolated catatonic syndrome in the absence of any other psychiatric or medical condition.Case PresentationWe present the case of a 20-year-old previously healthy Caucasian male whose initial presentation to psychiatric care was in the form of an acute catatonic syndrome dominated by mutism, blank staring, and poverty of movement. As the nature of the patient’s symptoms precluded the collection of a complete psychiatric and medical history, we employed a broad differential diagnosis including catatonia due to another medical condition, catatonia as a specifier for a number of mental disorders, and catatonia not otherwise specified.ConclusionsThe presentation of an acute onset of psychomotor symptoms in the absence of a history of mental illness warrants extensive workup to rule out medical causes to ensure effective treatment of any underlying illness. Benzodiazepines are the first-line treatment for catatonic symptoms, and electroconvulsive therapy can be used to resolve symptoms in patients who do not respond to medical intervention.

A case of catalepsy after multiple cerebral infarctions

AbstractReports of stroke‐related catalepsy and other catatonia syndromes are rare. A 68‐year‐old man was admitted to a local hospital 10 days prior for heart failure. He subsequently developed multiple cerebral infarctions and was referred to our hospital for emergency care. He spontaneously opened his eyes but did not speak. He had hemiparesis on the right side. Diffusion‐weighted imaging revealed high‐intensity areas in the left frontal and parietal lobes and right cerebellar hemisphere. Rehabilitation therapy was initiated in the acute stage. When he was instructed to raise his left upper limb 90°, he maintained the posture for more than 5 min. We hypothesized that catatonia syndromes, including catalepsy, were caused by damage to the orbitofrontal, premotor, supplementary motor cortices, and basal forebrain. These abnormalities disappeared after 4 months. Catalepsy may also be observed in organic central nervous system diseases, such as stroke, and should be considered in stroke care.

A single-health system retrospective case series of electroconvulsive therapy for catatonic syndrome associated with anti-NMDAR encephalitis and new-onset psychosis of suspected immune origin

A single-health system retrospective case series of electroconvulsive therapy for catatonic syndrome associated with anti-NMDAR encephalitis and new-onset psychosis of suspected immune origin

Catatonia: Development of a neuropsychiatric entanglement through a clinical case

IntroductionCatatonia is a transnosographic and potentially fatal syndrome, most often associated with mood disorders or schizophrenia, but can also develop in autistic disorders, dementia, as well as in general medical conditions such as epilepsy, autoimmune encephalitis, hypercalcemia, hepatic encephalopathy, or diabetic ketoacidosis.Objectivesthe objective is to understand the semiology and treatment of catatonic syndrome in a clinical caseMethodsClinical caseResultsThe work we present is based on a clinical case of a patient with schizophrenia presenting a catatonic syndrome, of which a neurological cause was first evoked but after clinical investigations the diagnosis of schizophrenia was retained and currently the patient is stabilized on Clozapine. It is imperative to recognize a catatonic syndrome in order to treat it quickly, as some of the etiologies that cause this syndrome and the consequences of the syndrome itself can be life-threatening.ConclusionsCatatonia remains a subject of research for centuries, the diagnosis is clinical, based on a set of criteria grouped in the DSM5, its etiologies are psychiatric and organic including neurological. Rapid diagnostic and therapeutic management is essential to avoid life-threatening complications.Disclosure of InterestNone Declared

Brain evolution and the meaning of catatonia - An update

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 Due to General Medical Conditions in Psychiatric Patients: Implications for Clinical Practice

Catatonic syndrome is frequently observed over the course of severe mental disorders and general medical conditions, but when catatonia occurs in psychiatric patients with co-morbid medical or neurologic conditions, diagnosis and management may be challenging. Several medical conditions may cause catatonia in psychiatric patients, but some, such as brain injury, infections, hyponatremia and critical illness, may be most relevant in this population. Alongside appropriate etiologic treatment, benzodiazepines and electroconvulsive therapy in refractory cases are effective and safe, and may resolve catatonic syndrome rapidly. When newly-onset psychotic symptoms in catatonic patients with established psychotic disorders occur, delirium should be suspected and appropriately managed. An extensive clinical and laboratory diagnostic workup to determine the underlying etiology of catatonic syndrome should be carried out. In cases of acute multi-morbidity, the exact cause of catatonic syndrome in psychiatric patients may be unclear. It is recommended to avoid antipsychotic drugs in acutely catatonic patients, because they may exacerbate the catatonic symptoms. The akinetic type of catatonia should be differentiated from hypoactive delirium, as treatments for these syndromes differ substantially. When a psychiatric patient presents with symptomatology of both catatonia and delirium, treatment is particularly challenging.

A Case Series of Noncatatonic Mutism with Poor Response to Conventional Treatment Approach

Abstract Mutism is the absence or marked paucity of verbal output due to functional or organic causes. Selective mutism is commonly seen in children with anxiety disorder. In psychiatric literature, long-standing mutism is most commonly associated with catatonic syndrome in adults. Although less commonly reported, long-standing mutism has also been associated with noncatatonic schizophrenia and posits a treatment challenge. Here, we describe two cases of long-standing noncatatonic mutism secondary to Schneiderian first rank symptoms, which were poorly responsive to conventional antipsychotic treatment and had good response to the combination of antipsychotics and electroconvulsive therapy (ECT). ECT is an underutilized treatment modality in patients with schizophrenia and is usually limited to catatonic states. The case series, thus, highlights the need for the development of an evidence base for the use of ECT in patients with noncatatonic mutism.

Comparison of psychometric and pathopsychological approaches in the assessment of intellectual activity in children and adolescents with progressive forms of schizophrenia

To study the intellectual activity of children and adolescents with progressive forms of schizophrenia using quantitative and qualitative diagnostic methods. An experimental group consisted of 67 children and adolescents (mean age 11.1±2.8 years) with mental pathology of schizophrenia spectrum with varying severity of the disease (malignant, progressive, and low progressive course) and leading clinical syndromes (catatonic, psychopathic, neurosis-like, and hyperkinetic). A control group included 63 children and adolescents (mean age 11.1±3.0 years) without a verified psychiatric diagnosis, secondary schools' students. The Wechsler Intelligence Scale for Children (WISC) was used for assessing intelligence, the Design of objects method was used for assessing the characteristics of thinking. The relationship between thinking disorders and the parameters of verbal intelligence in patients with schizophrenia was shown (the Information subtest is related to all Object Construction parameters, r=0.401 to r=0.634; verbal IQ score is associated with some Object Construction scores, r=0.541 to r=0.537). In the control group, such a relationship was not noted. A decrease in the level of intelligence and severe thinking disorders is associated with such clinical factors as the malignant course of the disease (mean Full IQ score is 60.1, z-value of the coefficient of standardization in relation to the age norm is -2.1) and catatonic syndrome (mean Full IQ score is 68.1, coefficient of standardization is 60%). The use of psychometric and pathopsychological approaches in the diagnosis of intellectual activity complements each other.

Catatonia Through the Ages - from Kahlbaum to the ICD-11

For decades, the psychomotor syndrome of catatonia was considered exclusively a subtype of schizophrenia. The use of antipsychotics and changes in the teaching content in the further training of psychiatrists led to the fact that catatonia was hardly recognized anymore. Yet catatonia is in principle well treatable. The new status in ICD-11 will probably allow to better teach, recognize, and treat catatonia in the future.

Catatonia during COVID-19 pandemic - diagnostic and therapeutic approach.

Catatonia can be defined as an etiologically heterogeneous syndrome, with predominant psychomotor disturbances. Historically, the concept of catatonia has been associated with mental disorders, especially schizophrenia. However, nowadays our understanding of catatonia has evolved to recognize it as neuropsychiatric syndrome that can arise from diverse etiological factors ranging from neurological to systemic diseases. Furthermore, there is now a recognized association between catatonia and a broader spectrum of mental disorders. Catatonia as a secondary neuropsychiatric syndrome may be a clinical manifestation of COVID-19 also due to the known neuroinvasive potential of the SARS-CoV-2 virus or in connection with the overall somatic alteration of the patient. In clinical practice, co-infection with SARS-CoV-2 could impede the process of diagnosing and treating catatonia as the primary psychopathological syndrome. The administration of benzodiazepines and electroconvulsive therapy could endanger the patient's physical health with active COVID-19 infection. Management of catatonic syndrome associated with COVID-19 is a challenge and requires a comprehensive therapeutic approach. The article demonstrates the above-mentioned difficulties of treatment through two case presentations (Tab. 2, Ref. 29). Text in PDF www.elis.sk Keywords: catatonia, COVID-19, SARS-CoV-2, neuropsychiatry, diagnosis, differential.

Comparative Effects of 30 Antipsychotics on Risk of Catatonia

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.

Acute catatonia

Catatonia is an underdiagnosed psychomotor syndrome that can occur in the context of various mental and somatic diseases. Malignant catatonia is particularly relevant in the context of intensive medical care. Clear recommendations in guidelines are missing. To present the current state of the diagnosis and treatment of catatonia, especially malignant catatonia. The literature was evaluated with respect to acute catatonic conditions, with aspecial focus on the differential diagnosis, relevance to intensive medical care and treatment of catatonia. In psychiatric inpatients, catatonic syndromes are relatively frequent with aprevalence between 9% and 17%, and in neurological patients somewhat less frequent with aprevalence of 3.3%. There is aclear recommendation for pharmacological treatment with lorazepam. Additional electroconvulsive therapy (ECT) should be considered as early as possible, especially in cases not responding to benzodiazepines. Response rates to ECT have been shown to be 80-100%. In malignant catatonia, ECT should be performed immediately as an emergency indication. Several factors lead to the underdiagnosis of catatonia. It is problematic that even life-threatening malignant catatonia is often not recognized as such, although there is a mortality of about 50% if untreated. The best treatment outcome is achieved with acombination of benzodiazepines and ECT. The treatment of severe malignant catatonia represents an emergency indication for ECT.

Catatonia: Development of a Neuropsychiatric Entanglement through a Clinical Case

Catatonia is a transnosographic and potentially fatal syndrome, most often associated with mood disorders or schizophrenia, but can also develop in autistic disorders, dementia, as well as in general medical conditions such as epilepsy, autoimmune encephalitis, hypercalcemia, hepatic encephalopathy, or diabetic ketoacidosis. The work we present is based on a clinical case of a patient with schizophrenia presenting a catatonic syndrome, of which a neurological cause was first evoked but after clinical investigations the diagnosis of schizophrenia was retained and currently the patient is stabilized on Clozapine. It is imperative to recognize a catatonic syndrome in order to treat it quickly, as some of the etiologies that cause this syndrome and the consequences of the syndrome itself can be life- threatening.

Catatonic syndrome and Baraitser Winter syndrome: Case report and review of the literature

Catatonic syndrome and Baraitser Winter syndrome: Case report and review of the literature

Postpartum Depression, Catatonia and Covid-19 Infection: One Case, Different Clinical Presentations

IntroductionPost-partum depression may occur in the first year after childbirth in approximately 25% of women, at times presenting with psychotic symptoms and catatonic states. Catatonia is a psychomotor syndrome that occurs in association with various neuropsychiatric disorders and can be described according to the characteristics of its manifestation in types such as retarded or agitated.ObjectivesWe report the case of a patient with postpartum depression and catatonic syndrome who, after a session of electroconvulsive therapy, was infected with Sars-COV-2, suspended treatment, and had her condition aggravated with distinct clinical manifestations.MethodsClinical case report and non-systematic review of articles consulted in the PubMed platform.ResultsA 24-year-old patient develops depressive symptoms and obsessive behaviour 6 months after delivery and deteriorates with mutism, stupor and motor immobility. She was hospitalised and medicated with lorazepam, with no improvement. One session of electroconvulsive therapy was carried out with improvement of the symptoms. Due to an inpatient Covid-19 outbreak, in which the patient was infected, treatment was suspended. During isolation, deterioration of the patient’s condition was observed with psychomotor agitation, bizarre behaviour, and perseverative speech. The patient resumed treatment with ECT, with total remission of the catatonic syndrome and improvement of the affective symptoms.ConclusionsCatatonic syndromes are relatively rare, but its association with post-partum depression is not so uncommon. The occurrence of different presentations of catatonia, although described as possible in the same episode in the literature, were not found in any clinical studies reviewed, which leads us to conclude that it is an uncommon situation.DisclosureNo significant relationships.

Malignant catatonia due to clozapine withdrawal: A case report and a brief review of the literature

IntroductionWithdrawal symptoms are common upon discontinuation of many psychotropic drugs. Catatonia, a neuropsychiatric condition characterized by a number of motor, behavioral, emotional, and autonomic abnormalities, has been described as a withdrawal syndrome in a growing number of case reports, but it is not well recognized. Treatment of catatonia usually includes benzodiazepines and electroconvulsive therapy. Standard consensus states that the use of neuroleptics should be avoided, as they are thought to worsen catatonia.ObjectivesWith this case report, we attempt to contribute to the finding in literature that the withdrawal of clozapine may be associated with catatonia, and how reintroduction of clozapine could be indicated for its treatment.MethodsA clinical case is presented of a 37-year-old female with a history of schizophrenia, presenting with altered mental status and new onset of catatonic signs and symptoms in the setting of a 7-day emetic syndrome. The possibility that vomiting prevented proper absorption of clozapine is postulated, causing the patient to present clinical features compatible with malignant catatonia.ResultsThe patient required treatment with benzodiazepines, electroconvulsive therapy and clozapine re-initiation, leading to improvement of catatonic symptoms within a few days.ConclusionsThis case serves as a reminder to consider alternative diagnostic hypotheses in cases of catatonic syndrome unresponsive to standard treatments. When the clinical suspicion of drug withdrawal is high, restarting the discontinued medication, even an antipsychotic agent, may be indicated.DisclosureNo significant relationships.

On the problem of the catatonic disorders taxonomy

IntroductionIn accordance with the systematics of modern international clinical guidelines (DSM-V, ICD-11), catatonia is qualified as a transnosological formation, which boundaries expandes by including non-psychotic movement disorders (hysterical, affective, negative, etc.). This study presents the psychopathological systematics of movement disorders, based on a new dimensional model of catatonia.Objectives60 patients with an established diagnosis of schizophrenia or SSD (F20, F21, F25.01, F25.11, F25.21, F25.22), catatonic disorders in the structure of which persist throughout the course of the disease or determine the clinical picture of phases.MethodsClinical, psychometric (BFCRS, SANS, SAPS, HADS), statistic.ResultsThree catatonic syndromes (S.) have been identified. 1. S. of stereotypical catatonia - presented by the mechanism of affiliation with negative symptoms (R between BFCRS Total Score (TS) and Avolition-Apathy SANS – 0,875): tendency to stereotypical activity; general, increasing slowness (SANS avolition-apathy -2,9±0,5; BFCRS TS – 11,1±0,2). 2. S. of parakinetic catatonia - includes paroxysms formes by the mechanism of mental automatism (with the loss of motor acts voluntary effect ) (R BFCRS TS/Persecutory Delusions SAPS– 0,764): irregular polymorphic movement disorders of hyperkinetic and akinetic types, impulsive actions, akinesias (Persecutory Delusions - 2,3±0,4; BFCRS – 19,5±2,3). 3. Affective - catatonic S. - including both the lightest (at the level of recurrent depression) variants of affective-catatonic phases (R BFCRS TS/HADS – 0,732; BFCRS – 5,1±0,4; HADS -15,1±2,4), and more severe affective-catatonic states based on schizoaffective psychoses (R BFCRS TS/SAPS TS– 0,783; BFCRS – 15,3±2,1; SAPS – 3,1±0,2).ConclusionsCatatonia is not a single dimension, represented by heterogeneous movement disorders, differing both in the mechanism of formation and in the psychopathological structure.DisclosureNo significant relationships.