ABSTRACT: The term catatonia was first introduced in 1874 and several etiologies, both organic and psychiatric have been attributed to the clinical phenotype of catatonia. The interesting feature is their response to lorazepam irrespective of their etiology.Four patients admitted with verbal and motor unresponsiveness following febrile illness were evaluated for infective and metabolic causes. Those who qualified for catatonia as per Diagnostic and Statistical Manual of Mental Disorders-Fifth Edition criteria and Bush-Francis Catatonia Screening Instrument screening tool and rating scale were evaluated in detail and reported.Catatonia occurs in clusters, females are more affected than males. Electroencephalogram can be abnormal based on the precipitating symptom. Minor changes in serum total iron and transferrin saturation and nonspecific elevation of viral antibody titers are seen in some patients. Lorazepam challenge always gives the diagnosis.All patients where females and had preceeding systemic or CNS infection. Three out of the Four patients where independent at the end of one month.Catatonia should be considered as a differential diagnosis in all children with verbal and motor unresponsiveness, which have no other explanation. Early initiation of treatment is very rewarding at least during short term follow-up.
Project description:Nodding syndrome (NS) is a severe neuropsychiatric syndrome of an unknown etiology affecting children and adolescents mostly in Eastern Africa. Symptoms of NS and catatonia seem to overlap. We investigated the presence and types of catatonic symptoms in NS and their response to one or two doses of lorazepam, the first-line treatment for catatonia.A cross-sectional descriptive study with systematic assessment of catatonia in 33 patients with NS using a modified version of the Bush Francis Catatonia Rating Scale. Sixteen patients met criteria for catatonia and were observed in an open and uncontrolled study to examine the effects of one or two doses of lorazepam in them.Sixteen of 33 patients with NS had an average of 5 catatonia symptoms and met criteria for catatonia. The highest scores were found for mutism, staring, poor eating/drinking, stupor, and grimacing. Excitement, rigidity, negativism and impulsivity had lower scores. None of the children had echolalia or echopraxia. In 6 children, there was a reduction of more than 50% in catatonia ratings, representing a positive response to lorazepam. Three out of six children whose catatonia ratings did not change after the first dose, responded after administration of a second double dose. There were no unusual or critical side-effects.About half of a selected sample of children with NS met criteria for catatonia. Catatonia scores decreased in most patients after one or two doses of lorazepam. Larger, longer, and controlled studies are warranted to assess the prevalence of catatonia in NS and to assess the use of lorazepam in NS through its effects on catatonia.ClinicalTrials.gov NCT02462109 Date of formal registration: June 2, 2015.
Project description:OBJECTIVES:Catatonia, a condition characterized by motor, behavioral, and emotional changes, can occur during critical illness and appear as clinically similar to delirium, yet its management differs from delirium. Traditional criteria for medical catatonia preclude its diagnosis in delirium. Our objective in this investigation was to understand the overlap and relationship between delirium and catatonia in ICU patients and determine diagnostic thresholds for catatonia. DESIGN:Convenience cohort, nested within two ongoing randomized trials. SETTING:Single academic medical center in Nashville, TN. PATIENTS:We enrolled 136 critically ill patients on mechanical ventilation and/or vasopressors, randomized to two usual care sedation regimens. MEASUREMENTS AND MAIN RESULTS:Patients were assessed for delirium and catatonia by independent and masked personnel using Confusion Assessment Method for the ICU and the Bush Francis Catatonia Rating Scale mapped to Diagnostic Statistical Manual 5 criterion A for catatonia. Of 136 patients, 58 patients (43%) had only delirium, four (3%) had only catatonia, 42 (31%) had both, and 32 (24%) had neither. In a logistic regression model, more catatonia signs were associated with greater odds of having delirium. For example, patient assessments with greater than or equal to three Diagnostic Statistical Manual 5 symptoms (75th percentile) had, on average, 27.8 times the odds (interquartile range, 12.7-60.6) of having delirium compared with patient assessments with zero Diagnostic Statistical Manual 5 criteria (25th percentile) present (p < 0.001). A cut-off of greater than or equal to 4 Bush Francis Catatonia Screening Instrument items was both sensitive (91%; 95% CI, 82.9-95.3) and specific (91%; 95% CI, 87.6-92.9) for Diagnostic Statistical Manual 5 catatonia. CONCLUSIONS:Given that about one in three patients had both catatonia and delirium, these data prompt reconsideration of Diagnostic Statistical Manual 5 criteria for "Catatonic Disorder Due to Another Medical Condition" that preclude diagnosing catatonia in the presence of delirium.
Project description:The lorazepam-diazepam protocol had been proved to rapidly and effectively relieve catatonia in patients with schizophrenia or mood disorder. This study aims to investigate the efficacy of lorazepam-diazepam protocol in catatonia due to general medical conditions (GMC) and substance.Patients with catatonia that required psychiatric intervention in various settings of a medical center were included. The lorazepam-diazepam protocol had been used to treat the catatonia due to GMC or substance according to DSM-IV criteria. The treatment response had been assessed by two psychiatrists.Eighteen (85.7%) of 21 catatonic patients due to GMC or substance became free of catatonia after the lorazepam-diazepam protocol. Five (23.8%) of the 21 patients had passed away with various causes of death and wide range of time periods after catatonia.Our results showed that the lorazepam-diazepam protocol could rapidly and effectively relieve catatonia due to GMC and substance.
Project description:Catatonia is a psychomotor syndrome that not only frequently occurs in the context of schizophrenia but also in other conditions. The neural correlates of catatonia remain unclear due to small-sized studies. We therefore compared resting-state cerebral blood flow (rCBF) and gray matter (GM) density between schizophrenia patients with current catatonia and without catatonia and healthy controls. We included 42 schizophrenia patients and 41 controls. Catatonia was currently present in 15 patients (scoring >2 items on the Bush Francis Catatonia Rating Scale screening). Patients did not differ in antipsychotic medication or positive symptoms. We acquired whole-brain rCBF using arterial spin labeling and GM density. We compared whole-brain perfusion and GM density over all and between the groups using 1-way ANCOVAs (F and T tests). We found a group effect (F test) of rCBF within bilateral supplementary motor area (SMA), anterior cingulate cortex, dorsolateral prefrontal cortex, left interior parietal lobe, and cerebellum. T tests indicated 1 cluster (SMA) to be specific to catatonia. Moreover, catatonia of excited and retarded types differed in SMA perfusion. Furthermore, increased catatonia severity was associated with higher perfusion in SMA. Finally, catatonia patients had a distinct pattern of GM density reduction compared to controls with prominent GM loss in frontal and insular cortices. SMA resting-state hyperperfusion is a marker of current catatonia in schizophrenia. This is highly compatible with a dysregulated motor system in catatonia, particularly affecting premotor areas. Moreover, SMA perfusion was differentially altered in retarded and excited catatonia subtypes, arguing for distinct pathobiology.
Project description:Catatonia, originally described by Karl Kahlbaum in 1874, may be regarded as a set of clinical features found in a subtype of schizophrenia, but the syndrome may also stem from organic causes including vascular parkinsonism, brain masses, globus pallidus lesions, metabolic derangements, and pharmacologic agents, especially first generation antipsychotics. Catatonia may include paratonia, waxy flexibility (cerea flexibilitas), stupor, mutism, echolalia, and catalepsy (abnormal posturing). A case of catatonia as a result of acute renal failure in a patient with dementia with Lewy bodies is described. This patient recovered after intravenous fluid administration and reinstitution of the atypical dopamine receptor blocking agent quetiapine, but benzodiazepines and amantadine are additional possible treatments. Recognition of organic causes of catatonia leads to timely treatment and resolution of the syndrome.
Project description:There is growing interest in understanding the behavioral and neural mechanisms of catatonia. Here, we examine cognition and brain structure in schizophrenia spectrum disorder (SSD) patients with a history of catatonia. A total of 172 subjects were selected from a data repository; these included SSD patients with (n = 43) and without (n = 43) a history of catatonia and healthy control subjects (n = 86). Cognitive functioning was assessed using the Screen for Cognitive Impairment in Psychiatry (SCIP) and brain structure was assessed using voxel-based morphometry (VBM) in the CAT12 toolbox. SSD patients with a history of catatonia showed worse performance on tests of verbal fluency and processing speed compared to SSD patients without such a history, even after controlling for current antipsychotic and benzodiazepine use. No differences were found between patients with and without a history of catatonia in terms of brain structure. Both patient groups combined showed significantly smaller grey matter volumes compared to healthy control subjects in brain regions consistent with prior studies, including the anterior cingulate, insular, temporal, and medial frontal cortices. The results highlight a cognitive-motor impairment in SSD patients with a history of catatonia. Challenges and limitations of examining brain structure in patients with a history of catatonia are discussed.
Project description:INTRODUCTION:Catatonia arises from serious mental, medical, neurological or toxic conditions. The prevalence range depends on the setting and the range is anything from 7% to 63%?in other countries. South African prevalence rates are currently unknown. The proposed study is a quantitative descriptive study using the Bush Francis Catatonia Screening Instrument as a screening tool with a data capturing information sheet to extract clinical information from patient folders. The study will investigate: (1) prevalence of catatonia, (2) clinical and demographic correlates associated with catatonia, (3) predictors of catatonia, (4) response to treatment and (5) subjective experience of catatonia. METHODS AND ANALYSIS:The setting is an acute mental health unit (MHU) within a regional, general medical hospital in Nelson Mandela Bay, South Africa, which accepts referrals from within the hospital and from outlying clinics. Participants will be recruited from inpatients in the MHU from beginning of September 2020 to end of August 2021. Most admissions are involuntarily, under the Mental Health Care Act of 2002 with an age range of 13 to over 65 years. Participants who screen positive for catatonia will be followed up after discharge for 3?months to measure outcomes. Primary outcomes will include the 12-month prevalence rate of catatonia, descriptive and other data on presentation and assessment of catatonia in the MHU. Secondary outcomes will include data on treatment response, participants' report of their subjective experience of catatonia and predictors of catatonia. Descriptive statistics, multivariate binomial logistic regression and univariate analyses will be conducted to evaluate associations between catatonia and clinical or demographic data which could be predictors of catatonia. Survival analysis will be used to examine the time to recovery after diagnosis and initiation of treatment. The 95% CI will be used to demonstrate the precision of estimates. The level of significance will be p?0.05. ETHICS AND DISSEMINATION:The study has received ethical approval from the Research and Ethics Committees of the Eastern Cape Department of Health, Walter Sisulu University and Nelson Mandela University. The results will be disseminated as follows: at various presentations and feedback sessions; as part of a PhD thesis in Psychology at Nelson Mandela University; and in a manuscript that will be submitted to a peer-reviewed journal.
Project description:Catatonia is a psychomotor syndrome associated with several psychiatric and medical conditions. Psychomotor signs range from stupor to agitation, and include pathognomonic features such as verbigeration and waxy flexibility. Disturbances of volition led to the classification of catatonia as a subtype of schizophrenia, but changes in nosology now recognise the high prevalence in mood disorders, overlap with delirium, and comorbidity with medical conditions. Initial psychometric studies have revealed three behavioural factors, but the structure of catatonia is still unknown. Evidence from brain imaging studies of patients with psychotic disorders indicates increased neural activity in premotor areas in patients with hypokinetic catatonia. However, whether this localised hyperactivity is due to corticocortical inhibition or excess activity of inhibitory corticobasal ganglia loops is unclear. Current treatment of catatonia relies on benzodiazepines and electroconvulsive therapy-both effective, yet unspecific in their modes of action. Longitudinal research and treatment studies, with neuroimaging and brain stimulation techniques, are needed to advance our understanding of catatonia.
Project description:Abstract Catatonia is a serious, common syndrome of motoric and behavioral dysfunction, which carries high morbidity and mortality. Electroconvulsive therapy (ECT) is the definitive treatment for catatonia, but access to ECT for the treatment of catatonia remains inappropriately limited. Catatonia is observable, detectable, and relevant to various medical specialties, but underdiagnosis impedes the delivery of appropriate treatment and heightens risk of serious complications including iatrogenesis. Current understanding of catatonia’s pathophysiology links it to the current understanding of ECT’s mechanism of action. Definitive catatonia care requires recognition of the syndrome, workup to identify and treat the underlying cause, and effective management including appropriate referral for ECT. Even when all of these conditions are met, and despite well-established data on the safety and efficacy of ECT, stigma surrounding ECT and legal restrictions for its use in catatonia are additional critical barriers. Addressing the underdiagnosis of catatonia and barriers to its treatment with ECT is vital to improving outcomes for patients. While no standardized protocols for treatment of catatonia with ECT exist, a large body of research guides evidence-based care and reveals where additional research is warranted. The authors conducted a review of the literature on ECT as a treatment for catatonia. Based on the review, the authors offer strategies and future directions for improving access to ECT for patients with catatonia, and propose an algorithm for the treatment of catatonia with ECT.
Project description:Catatonia is a central aspect of schizophrenia spectrum disorders (SSD) and most likely associated with abnormalities in affective, motor, and sensorimotor brain regions. However, contributions of different cortical features to the pathophysiology of catatonia in SSD are poorly understood. Here, T1-weighted structural magnetic resonance imaging data at 3 T were obtained from 56 right-handed patients with SSD. Using FreeSurfer version 6.0, we calculated cortical thickness, area, and local gyrification index (LGI). Catatonic symptoms were examined on the Northoff catatonia rating scale (NCRS). Patients with catatonia (NCRS total score ?3; n = 25) showed reduced surface area in the parietal and medial orbitofrontal gyrus and LGI in the temporal gyrus (P < .05, corrected for cluster-wise probability [CWP]) as well as hypergyrification in rostral cingulate and medial orbitofrontal gyrus when compared with patients without catatonia (n = 22; P < .05, corrected for CWP). Following a dimensional approach, a negative association between NCRS motor and behavior scores and cortical thickness in superior frontal, insular, and precentral cortex was found (34 patients with at least 1 motor and at least 1 other affective or behavioral symptom; P < .05, corrected for CWP). Positive associations were found between NCRS motor and behavior scores and surface area and LGI in superior frontal, posterior cingulate, precentral, and pericalcarine gyrus (P < .05, corrected for CWP). The data support the notion that cortical features of distinct evolutionary and genetic origin differently contribute to catatonia in SSD. Catatonia in SSD may be essentially driven by cortex variations in frontoparietal regions including regions implicated in the coordination and goal-orientation of behavior.