Transient Fever Response After ECT in a Patient with Catatonic Schizophrenia: A Case Report. / Katatonik Sizofreni Hastasinda EKT Sonrasi Ortaya Çikan Geçici Ates Yaniti: Olgu Sunumu.

Electroconvulsive therapy (ECT) is an effective and safe treatment method for many psychiatric disorders. In general medical practice, ECT may cause side effects as most other treatment methods do. Headache, myalgia, nausea, vomiting, confusion, anterograde amnesia are common side effects of electroconvulsive therapy. Fever; in addition to general medical conditions such as infection, malignancy, connective tissue diseases, drug treatments, malignant hyperthermia, convulsions, it can also occur due to conditions such as neuroleptic malignant syndrome (NMS), serotonin syndrome, catatonia, malignant catatonia, which are frequently encountered in psychiatry clinics. In the literature, transient fever response due to electroconvulsive therapy application have been described, albeit rarely. Although there are many proposed mechanisms for the emergence of a fever response, regardless of its cause, it is still not understood why some fever responses occur. In this article, we present the differential diagnosis of the fever response, possible causes, and the mechanisms that may reveal the secondary fever response to electroconvulsive therapy in a case with a diagnosis of catatonic schizophrenia, who developed a fever response during electroconvulsive therapy sessions and no fever response was observed at times other than electroconvulsive therapy sessions. In this case, postictal benign fever response associated with electroconvulsive therapy was considered after excluding other medical conditions that may cause a fever response after electroconvulsive therapy. Keywords: ECT, Fever, Catatonia, NMS.

A case report of a patient with Turner syndrome who develops catatonia secondary to psychotic symptoms.

RATIONALE: Turner syndrome (TS) is a genetic disorder associated with partial or complete monosomy X abnormalities; some patients may have a higher risk of psychiatric symptoms. Catatonia is associated with a wide range of life-threatening complications with complex pathogenesis; However, It very rare for patients with TS to develop psychotic symptoms and eventually progress to catatonia. This case report describes the diagnostic and therapeutic course of catatonia-associated TS. PATIENT CONCERNS: In this study, we report the case of a patient with TS who initially developed sudden hallucinations, delusions, and emotional instability, followed by catatonia. DIAGNOSES: The patient was diagnosed with: unspecified catatonia; TS. INTERVENTIONS: Treatment included administering a combination of esazolam injections and olanzapine tablets, placing a gastric tube and urinary catheter, and providing nutritional support. OUTCOMES: After treatment, the patient's hallucinations, delusions, and catatonia disappeared, with no residual sequelae, and social functioning returned to normal. LESSONS: For patients with TS who present with psychotic symptoms and catatonia, a comprehensive evaluation is necessary, and treatment with antipsychotics and benzodiazepines is effective.

Palliative psychiatry for a patient with treatment-refractory schizophrenia and severe chronic malignant catatonia: case report.

BACKGROUND: Palliative psychiatry is an emerging field that suggests a role for palliative interventions in the management of severe and persistent mental illness (SPMI). Current literature describes using a palliative approach for patients with severe anorexia nervosa. To our knowledge, this is the first case report describing end-of-life care in a patient with treatment-refractory catatonic schizophrenia. CASE DESCRIPTION: We describe the case of a 49-year-old man with schizophrenia and severe chronic agitated/malignant catatonia who was hospitalized for ten months. Multiple treatment trials including medication such as neuroleptics and benzodiazepines, electroconvulsive therapy, and empiric interventions such as intravenous immunoglobulins were either not tolerated or did not result in clinically significant improvement. The patient continued to intermittently require intubation and sedation to control intractable behavioral and psychiatric disturbances. Ultimately, with collaboration of psychiatry, neurology, ethics, intensive care, and palliative care teams, the patient's parents decided to forgo further diagnostic testing and life-sustaining treatments. The patient died weeks later of aspiration pneumonia with good symptom control. CONCLUSIONS: This case permits discussion of palliative interventions in patients with SPMI such as treatment-refractory psychotic disorders who likely cannot achieve a quality of life that is acceptable to them. Here, it can be justified to prioritize relief of suffering and prevention of further burdensome interventions over treatment of the SPMI symptoms such as catatonia and even over keeping the patient alive.

Neurodevelopmental Disorders Including Autism Spectrum Disorder and Intellectual Disability as a Risk Factor for Delayed Diagnosis of Catatonia.

OBJECTIVE: Catatonia is a distinct and severe medical syndrome comprising motor, somatic, and psychiatric symptoms that is reported in upwards of 17% of young patients with autism spectrum disorders. Clinical experience indicates catatonia is often under-recognized in this clinical population. Here we characterize the clinical presentation of catatonia in patients with and without neurodevelopmental disorders (NDDs) including autism, including the time from symptom onset to diagnosis of catatonia. METHOD: Retrospective chart review of electronic medical records at a large, academic pediatric medical center identified 113 pediatric and young adult patients with a charted history of catatonia, as identified by an encounter diagnosis or problem list entry between September 2017 and September 2021. Workup, treatments, and diagnoses (psychiatric, neurodevelopmental, and genetic) were identified. RESULTS: We observed a clear and substantial delay in identification of catatonia in those with NDDs (diagnosis after 330 days for those without psychosis) compared with neurotypical patients (∼16 days). Psychiatry involvement was associated with shorter delays. CONCLUSION: Intellectual disability and autism are risk factors for significantly delayed diagnosis of catatonia. It is unknown whether delayed diagnosis contributes to the difficulty in treating catatonia in this patient population or whether the treatment difficulties relate instead to differential and ongoing biological mechanisms and underlying encephalopathy. Overall, these findings highlight the importance of increased recognition of catatonia symptoms in patients with NDDs and suggest early referral to psychiatric specialists may shorten the delay to diagnosis.

How to manage catatonia, Parkinson and dementia in ICU.

PURPOSE OF REVIEW: The rising prevalence of neurodegenerative and mental disorders, combined with the challenges posed by their frailty, has presented intensivists with complex issues in the intensive care unit (ICU). This review article explores specific aspects of care for patients with catatonia, Parkinson's disease (PD), and dementia within the context of the ICU, shedding light on recent developments in these fields. RECENT FINDINGS: Catatonia, a neuropsychiatric syndrome with potentially life-threatening forms, remains underdiagnosed, and its etiologies are diverse. PD patients in the ICU present unique challenges related to admission criteria, dopaminergic treatment, and respiratory care. Dementia increases the risk of delirium. Delirium is associated with long-term cognitive impairment and dementia. SUMMARY: While evidence is lacking, further research is needed to guide treatment for ICU patients with these comorbidities.

[Catatonia in youth with developmental disabilities: challenges in recognition and management]. / Katatonie bij jongeren met een ontwikkelingsstoornis: uitdagingen in herkenning en aanpak.

Catatonia in children and adolescents is not rare and, as in adults, has a favorable outcome, provided it is recognized and treated promptly. Nevertheless, in clinical practice we encounter several obstacles in terms of diagnosis and treatment in this population of patients. We describe a 14-year-old boy with an intellectually disability and autism spectrum disorder (ASD) in which clinicians did not diagnose catatonia until 1 year after the development of symptoms. Moreover, hesitations surrounding the correct treatment led to its delayed initiation. With this case report we aim to contribute to reduced reluctance and increased alertness in the treatment of catatonia in adolescents with developmental disorders.

Evaluation of catatonia in autism and severe depression revealing Phelan-McDermid syndrome and tetrahydrobiopterin deficiency.

The authors describe a female in her late twenties, presenting with catatonia and diagnosed with epilepsy, autism spectrum disorder, mild intellectual disability, psychosis, dysthymia, anxiety and bipolar disorder, receiving weekly electroconvulsive therapy (ECT). After testing, findings indicated an interstitial deletion in the 22q13.33 region associated with Phelan-McDermid syndrome. In addition, the patient had low cerebral spinal fluid tetrahydrobiopterin (BH4) levels, suggesting dysfunction in the pterin biosynthetic pathway. As a result, the patient started on sapropterin, a BH4 replacement small molecule. After sapropterin treatment, catatonia improved, and the need for ECT decreased. There was an improvement in her cognitive ability, attention and independence. However, there has been no improvement in seizure frequency.

Historical postmortem studies on catatonia: Close reading and analysis of Kahlbaum's cases and scientific texts between 1800 and 1900.

In the 19th century, postmortem brain examination played a central role in the search for the neurobiological origin of psychiatric and neurological disorders. During that time, psychiatrists, neurologists, and neuropathologists examined autopsied brains from catatonic patients and postulated that catatonia is an organic brain disease. In line with this development, human postmortem studies of the 19th century became increasingly important in the conception of catatonia and might be seen as precursors of modern neuroscience. In this report, we closely examined autopsy reports of eleven catatonia patients of Karl Ludwig Kahlbaum. Further, we performed a close reading and analysis of previously (systematically) identified historical German and English texts between 1800 and 1900 for autopsy reports of catatonia patients. Two main findings emerged: (i) Kahlbaum's most important finding in catatonia patients was the opacity of the arachnoid; (ii) historical human postmortem studies of catatonia patients postulated a number of neuroanatomical abnormalities such as cerebral enlargement or atrophy, anemia, inflammation, suppuration, serous effusion, or dropsy as well as alterations of brain blood vessels such as rupture, distension or ossification in the pathogenesis of catatonia. However, the exact localization has often been missing or inaccurate, probably due to the lack of standardized subdivision/nomenclature of the respective brain areas. Nevertheless, Kahlbaum's 11 autopsy reports and the identified neuropathological studies between 1800 and 1900 made important discoveries, which still have the potential to inform and bolster modern neuroscientific research in catatonia.

Lorazepam in catatonia - Past, present and future of a clinical success story.

The effect of lorazepam in the treatment of catatonia is outstanding and almost immediate. Clinicians are familiar with its effects: mute patients can speak again, akinetic patients can move again and patients with negativism can eat and drink again within usually a short duration of about 10 min to 1-2 h. Fear is often gone after lorazepam administration. While not always effective, the introduction of lorazepam into clinical practice represented a breakthrough and was often life-saving for many patients suffering from catatonia. It is rare to observe such rapid therapeutic effects in other domains of psychiatry. In this narrative review we will briefly look at the past, present and future of lorazepam in the treatment of catatonia. It is gratifying to reflect on the fact that clinicians using the age-old medical practice of observation and empirical treatment succeeded in advancing the management of catatonia 40 years ago. The present evidence shows that the clinical effect of lorazepam in catatonia treatment is excellent and more or less immediate although it remains to be explicitly tested against other substances such as diazepam, zolpidem, clozapine, quetiapine, amantadine, memantine, valproate and dantrolene in randomized clinical trials. In addition, future studies need to answer the question how long lorazepam should be given to patients with catatonia, months or even years? This narrative review promotes the rapid use of lorazepam in the treatment of acute catatonic patients and stipulates further scientific examination of its often impressive clinical effects.

Catatonia in the peripartum: A cohort study using electronic health records.

BACKGROUND: Due to limited existing literature available on the presentation and treatment of catatonia in the peripartum, this retrospective descriptive cohort study aimed to examine demographic data, catatonic features, diagnoses pre- and post-catatonic episodes, treatment and the presence of obstetric complications. METHODS: Individuals with catatonia were identified in a previous study using anonymised electronic healthcare records from a large mental health trust in South-East London. The presence of features from the Bush-Francis Catatonia Screening Instrument was coded by the investigators and longitudinal data were extracted from structured fields and free text. RESULTS: 21 individuals were identified from the larger cohort, each of whom experienced one episode of catatonia in the postpartum period, and all had had an inpatient psychiatric admission. 13 patients (62 %) presented after their first pregnancy and 12 (57 %) experienced obstetric complications. 11 (53 %) attempted breastfeeding and 10 (48 %) received a diagnosis of a depressive disorder following the episode of catatonia. The majority presented with immobility or stupor, mutism, staring and withdrawal. All were treated with antipsychotics and 19 (90 %) received benzodiazepines. CONCLUSIONS: This study suggests that signs and symptoms of catatonia during the peripartum are similar to other catatonic presentations. However, the postpartum may be a period of high risk for catatonia and obstetric factors, such as birth complications, may be relevant.

Extension, translation and preliminary validation of the Northoff Scale for Subjective Experience in Catatonia (NSSC).

BACKGROUND: In the last two decades, much neuroscientific research has been done on the pathomechanisms of catatonia. However, catatonic symptoms have mainly been assessed with clinical rating scales based on observer ratings. Although catatonia is often associated with strong affective reactions, the subjective domain of catatonia has simply been neglected in scientific research. METHODS: The main objective of this study was to modify, extend and translate the original German version of the Northoff Scale for Subjective Experience in Catatonia (NSSC) and to examine its preliminary validity and reliability. Data were collected from 28 patients diagnosed with catatonia associated with another mental disorder (6A40) according to ICD-11. Descriptive statistics, correlation coefficients, internal consistency and principal component analysis were employed to address preliminary validity and reliability of the NSSC. RESULTS: NSSC showed high internal consistency (Cronbach's alpha = 0.92). NSSC total scores were significantly associated with Northoff Catatonia Rating Scale (r = 0.50, p < .01) and Bush Francis Catatonia Rating Scale (r = 0.41, p < .05) thus supporting its concurrent validity. There was no significant association between NSSC total score and Positive and Negative Symptoms Scale total (r = 0.26, p = .09), Brief Psychiatric Rating Scale (r = 0.29, p = .07) and GAF (r = 0.03, p = .43) scores. CONCLUSION: The extended version of the NSSC consists of 26 items and was developed to assess the subjective experience of catatonia patients. Preliminary validation of the NSSC revealed good psychometric properties. NSSC is a useful tool for everyday clinical work to assess the subjective experience of catatonia patients.

A systematic scoping review of rodent models of catatonia: Clinical correlations, translation and future approaches.

Catatonia is a psychiatric disorder, which subsumes a plethora of affective, motor and behavioral symptoms. In the last two decades, the number of behavioral and neuroimaging studies on catatonia has steadily increased. The majority of behavioral and neuroimaging studies in psychiatric patients suggested aberrant higher-order frontoparietal networks which, on the biochemical level, are insufficiently modulated by gamma-aminobutyric acid (GABA)-ergic and glutamatergic transmission. However, the pathomechanisms of catatonic symptoms have rarely been studied using rodent models. Here, we performed a scoping review of literature available on PubMed for studies on rodent models of catatonia. We sought to identify what we could learn from pre-clinical animal models of catatonia-like symptoms, their underlying neuronal correlates, and the complex molecular (i.e. genes and neurotransmitter) mechanisms by which its modulation exerts its effects. What becomes evident is that although many transgenic models present catatonia-like symptoms, they have not been used to better understand the pathophysiological mechanisms underlying catatonia so far. However, the identified neuronal correlates of catatonia-like symptoms correlate to a great extent with findings from neuroscience research in psychiatric patients. This points us towards fundamental cortical-striatal-thalamocortical and associated networks modulated by white matter inflammation as well as aberrant dopaminergic, GABAergic, and glutamatergic neurotransmission that is involved in catatonia. Therefore, this scoping review opens up the possibility of finally using transgenic models to help with identifying novel target mechanisms for the development of new drugs for the treatment of catatonia.

Distribution and frequency of clinical criteria and rating scales for diagnosis and assessment of catatonia in different study types.

BACKGROUND: A comprehensive assessment of catatonic symptoms is decisive for diagnosis, neuronal correlates, and evaluation of treatment response and prognosis of catatonia. Studies conducted so far used different cut-off criteria and clinical rating scales to assess catatonia. Therefore, the main aim of this study was to examine the frequency and distribution of diagnostic criteria and clinical rating scales for assessing catatonia that were used in scientific studies so far. METHODS: We conducted a systematic review using PubMed searching for articles using catatonia rating scales/criteria published from January 1st 1952 (introduction of catatonic schizophrenia to first edition of the Diagnostic and Statistical Manual of Mental Disorders [DSM]) up to December 5th, 2022. RESULTS: 1928 articles were considered for analysis. 1762 (91,39 %) studies used one and 166 (8,61 %) used ≥2 definitions of catatonia. However, 979 (50,7 %) articles did not report any systematic assessment of catatonia. As for clinical criteria, DSM criteria were used by the majority of studies (n = 290; 14.0 %), followed by International Classification of Diseases (ICD) criteria (n = 61; 2.9 %). The Bush-Francis Catatonia Rating Scale (BFCRS) was found to be by far the most frequently utilized scale (n = 464; 22.4 % in the respective years), followed by Northoff Catatonia Rating Scale (NCRS) (n = 31; 1.5 % in the respective years). CONCLUSION: DSM and ICD criteria as well as BFCRS and NCRS were most frequently utilized and can therefore be recommended as valid instruments for the assessment of catatonia symptomatology.

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.

Molecular and immunological origins of catatonia.

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.

Amoxicillin Induced Fever, Rash, and Catatonia - A Case Study.

INTRODUCTION: Adverse drug reactions (ADR) are defined as any harmful or unpleasant events or injuries resulting from the use of any particular drug. Among those antibiotics that cause adverse reactions, amoxicillin is one of them. Catatonia and vasculitic rash are its rare adverse effects. CASE PRESENTATION: A 23-year-old postpartum female, with a history of taking empirical Amoxiclav (amoxicillin-clavulanic acid 625 mg) injection and oral tablets for episiotomy wound, presented with altered sensorium and fever followed by maculopapular rash. On examination, she had generalized rigidity with waxy flexibility that improved by lorazepam challenge and was diagnosed as catatonia. On evaluation, amoxicillin was found to be precipitating catatonia in this patient. CONCLUSION: Since the diagnosis of catatonia is often missed, any cases with clinical presentation of fever, rash, altered sensorium, and generalized rigidity should also be suspected for druginduced ADR and the precipitating factor should be searched for.

Microstructural white matter biomarkers of symptom severity and therapy outcome in catatonia: Rationale, study design and preliminary clinical data of the whiteCAT study.

The number of magnetic resonance imaging (MRI) studies on neuronal correlates of catatonia has dramatically increased in the last 10 years, but conclusive findings on white matter (WM) tracts alterations underlying catatonic symptoms are still lacking. Therefore, we conduct an interdisciplinary longitudinal MRI study (whiteCAT) with two main objectives: First, we aim to enroll 100 psychiatric patients with and 50 psychiatric patients without catatonia according to ICD-11 who will undergo a deep phenotyping approach with an extensive battery of demographic, psychopathological, psychometric, neuropsychological, instrumental and diffusion MRI assessments at baseline and 12 weeks follow-up. So far, 28 catatonia patients and 40 patients with schizophrenia or other primary psychotic disorders or mood disorders without catatonia have been studied cross-sectionally. 49 out of 68 patients have completed longitudinal assessment, so far. Second, we seek to develop and implement a new method for semi-automatic fiber tract delineation using active learning. By training supportive machine learning algorithms on the fly that are custom tailored to the respective analysis pipeline used to obtain the tractogram as well as the WM tract of interest, we plan to streamline and speed up this tedious and error-prone task while at the same time increasing reproducibility and robustness of the extraction process. The goal is to develop robust neuroimaging biomarkers of symptom severity and therapy outcome based on WM tracts underlying catatonia. If our MRI study is successful, it will be the largest longitudinal study to date that has investigated WM tracts in catatonia patients.