History Of Catatonia Research Articles

Acute Hyperactive Delirium followed by Excited Catatonia: A case study

Acute Hyperactive Delirium followed by Excited Catatonia: A case studyOluwole A Babatunde, MD, Frank Clark, MD, Jessica Hill, DO, Belynda Veser, MD, Anu Nagar, MDDepartment of Psychiatry, Prisma Health,109 Physicians Drive, Greer, SC 29650.Ms. A. is an 84-year-old Hispanic female with a past psychiatric history of Mild Neurocognitive Disorder due to Frontotemporal lobar degeneration, major depressive disorder (MDD), and one episode of catatonia about six years prior to current presentation. She first presented to the emergency department (ED) for a motor vehicle collision that led to bruising and generalized tenderness. She had four ED visits over the next four weeks. At the fifth visit, she was hospitalized because of concerns of altered mental status (AMS), agitation, and hallucinations. She was noted to have a urinary tract infection (UTI) and bacteremia with positive blood cultures for Escherichia Coli. She was subsequently admitted to the inpatient medical service and the working diagnosis was delirium secondary to UTI/bacteremia, exacerbated by sleep deprivation. Imaging was performed to rule out intracranial abnormalities (e.g., subdural hematoma) following MVC.Psychiatry was consulted for the recent onset of altered mental status (AMS), increasing confusion, and hallucinations. Patient was assessed by consult liaison psychiatry service on day one of admission. Mental status exam was remarkable for the following pertinent positives: oriented to self only, tangential with loose associations, perseveration on her deceased husband, religiously preoccupied and responding to internal stimuli. She was able to recall 0 out of 3 objects in both immediate and delayed recall and having auditory and visual hallucinations. Patient consistently denied suicidal ideation and homicidal ideation. CT scan and MRI were negative and helped rule out acute intracranial abnormalities (e.g., subdural hematoma).Working diagnosis of acute hyperactive delirium secondary to UTI/bacteremia was managed with quetiapine, improving gradually over the subsequent eight days. Medical team managed UTI/bacteremia with 10 days of antibiotics as recommended by the Infectious Disease team and there was clinical evidence of resolved bacteremia and UTI. Quetiapine was titrated to maximum dosage of 100mg QAM, 100mg QPM and 200mg QHS with ongoing gradual improvement. However, she decompensated on day eight with new symptoms of catatonic-like stereotypical hand movements, repetition of words, and general sustained hyperactivity. The Bush Francis score (BFS) was 12. It was at this point that the daughter (a nurse) provided additional collateral history that there was a history of a similar episode of catatonia six years ago. A trial dosage of lorazepam 2mg IV was administered with subsequent improvement of BFS to 6. Over the next four days, lorazepam 1 mg IV was administered daily, and patient continued to improve. During this time, the dosage of Quetiapine was reduced, considering that delirium had improved, and Quetiapine could have been exacerbating the catatonia. However, titrating down of Quetiapine was done slowly to avoid abrupt discontinuation which could cause delirium to re-emerge. After receiving second dose of lorazepam, Montreal Cognitive Assessment (MoCA) score also dramatically improved from 6/30 to 22/30. She was subsequently discharged on day 13 to a nursing home where she was managed for 20 days and discharged home.Two learning objectives.• There is need to ask about history of catatonia in elderly patients as this may help heighten clinical suspicion especially in patients with delirium.• It is possible for a patient who presented with hyperactive delirium with clinical improvement and resolution of delirium to develop excited catatonia in a short time, so clinicians need to have a high index of suspicion especially among patients who have a history of catatonia. Given that hyperactive delirium alone responds excellent to antipsychotics while excited catatonia responds excellent to lorazepam IV, early diagnosis is of utmost important to adjust medications at the earliest time of noticing symptoms of excited catatonia.

Clozapine as a treatment for catatonia: A systematic review

Catatonia is a neuropsychiatric disorder characterised by altered movement, speech, and behaviour. Clozapine is an established therapy for treatment-resistant schizophrenia, but its role in catatonia has not been systematically examined. In this systematic review, we aimed to assess the evidence for clozapine as a treatment for catatonia.Full text original research articles in English where at least one patient with catatonia was treated with clozapine were included, provided catatonia did not occur solely in the context of neuroleptic malignant syndrome. Results were tabulated with calculations of summary statistics presented. Risk of bias was assessed with the Tool for Evaluating the Methodological Quality of Case Reports and Case Series.182 patients were included, 81 from cohort studies and 101 from case reports or case series. 119/182 patients (65 %) had a specified underlying diagnosis of schizophrenia. Over 80 % of reported patients with catatonia had at least partial remission following treatment with clozapine across both cohort studies and case reports and case series. Among the case reports and series, 24/101 patients (23.8 %) followed clozapine withdrawal. Overall, 25 studies were of low quality, 60 of moderate quality and 8 of high quality.Our findings should be interpreted with caution, as the reliance on case reports, case series and small cohort studies is susceptible to reporting biases, regression to the mean and confounding by other treatments. Future research could use large healthcare databases to ascertain outcomes in those on clozapine with a history of catatonia given the difficulty and expense of conducting randomised controlled trials.

Catatonia: looking back and moving forward.

Catatonia is a complex neuropsychiatric syndrome with motor, cognitive-behavioural and affective manifestations. Hirjak et al. look back at the history of catatonia, but also provide a modern perspective on what the condition can tell us both clinically and scientifically, and how we can best understand it.

COVID-19 Catatonia—Would We Even Know?

COVID-19 Catatonia—Would We Even Know?

Cognitive motor impairments and brain structure in schizophrenia spectrum disorder patients with a history of catatonia

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.

Book Review: Edward Shorter and Max Fink, The Madness of Fear: A History of Catatonia

Book Review: Edward Shorter and Max Fink, <i>The Madness of Fear: A History of Catatonia</i>

Pragmatic Guidance for EEG Interpretation

Professor of Psychiatry and Neurology Emeritus Stony Brook University School of Medicine Long Island, NY Co-author: The Madness of Fear: A History of Catatonia. NY: Oxford University Press, 2018 The author has no conflict of interest or financial disclosures to report.

The Madness of Fear—A History of Catatonia

The Madness of Fear—A History of Catatonia

A ROCK AND A HARD PLACE: A CASE OF CLOZAPINE-INDUCED NEUROLEPTIC MALIGNANT SYNDROME

SESSION TITLE: Critical Care 4 SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: Neuroleptic malignant syndrome (NMS) is a rare life-threatening neurologic emergency characterized by mental status changes, rigidity, fever, and dysautonomia. The incidence rate of NMS is 0.02-3% among patients taking typical or atypical neuroleptic agents; however, clozapine-induced NMS is a rarely-reported and unique entity as it doesn’t present with the four cardinal clinical features of NMS. We present a rare case of clozapine-induced NMS with the four cardinal features of NMS. CASE PRESENTATION: A 45-year-old man with history of schizoaffective disorder and catatonia was transferred from a local psychiatric hospital to the emergency department (ED) for evaluation of fever and altered mental status. Two days prior to the transfer, he was started on clozapine. In the ED, he had a temperature of 39.1° Celsius, blood pressure of 100/57 mmHg, respiratory rate of 24 breaths-per-minute, and heart rate of 118 beats-per-minute. The patient was diaphoretic, drooling, and shivering. He was lethargic with Glasgow Coma Scale of 8 and was therefore intubated. At that point, the rest of the examination was non-significant. Initial laboratory work-up including creatinine phosphokinase (CPK) was non-significant. Computed tomography (CT) scan of the head was normal. Lumbar puncture was performed and cerebrospinal fluid analysis was unremarkable. The patient was admitted to the intensive care unit (ICU) where he continued to develop fevers despite the use of antipyretics, cooling blankets, an d aggressive intravenous hydration. The fever spikes were associated with intermittent episodes of sinus tachycardia and fluctuations of his blood pressure. On day two, he developed rigidity, and blood work-up was significant for CPK level of 4419 U/L. He was started on benzodiazepines and dantrolene for a presumed diagnosis of NMS. However, his rigidity and fever didn’t improve. On day four, he developed ventilator-associated pneumonia. After a week in the ICU with no success in liberation of mechanical ventilation, family decided to shift care to comfort measures only. The patient perished a few hours later. DISCUSSION: Clozapine is considered among the most potent neuroleptic agents, with use reserved for treatment-resistant cases. Although it has many side effects, there are very few case reports about clozapine-induced-NMS. Risk factors for developing clozapine-induced NMS include young age, male gender, and history of catatonia. CONCLUSIONS: It is important to be aware of these risk factors for early recognition and treatment of NMS, given its high mortality rate of 10-30%. Reference #1: Clozapine-induced neuroleptic malignant syndrome: review and report of new cases.P. Sachdev, J. Kruk, M. Kneebone, D. KissaneJ Clin Psychopharmacol. 1995 Oct; 15(5): 365–371. DISCLOSURES: No relevant relationships by Abdullah Chahin, source=Web Response No relevant relationships by Faeq Kukhon, source=Web Response No relevant relationships by Mahmoud Mowafy, source=Web Response No relevant relationships by Magaly Sazani, source=Web Response No relevant relationships by Abraham Walusimbi, source=Web Response

571 A Successful Treatment of Aripiprazole in Catatonic Schizophrenia with Paroxysmal Perceptual Alteration

Catatonia is a neuropsychiatric disorder characterised by altered movement, speech, and behaviour. Clozapine is an established therapy for treatment-resistant schizophrenia, but its role in catatonia has not been systematically examined. In this systematic review, we aimed to assess the evidence for clozapine as a treatment for catatonia.Full text original research articles in English where at least one patient with catatonia was treated with clozapine were included, provided catatonia did not occur solely in the context of neuroleptic malignant syndrome. Results were tabulated with calculations of summary statistics presented. Risk of bias was assessed with the Tool for Evaluating the Methodological Quality of Case Reports and Case Series.182 patients were included, 81 from cohort studies and 101 from case reports or case series. 119/182 patients (65 %) had a specified underlying diagnosis of schizophrenia. Over 80 % of reported patients with catatonia had at least partial remission following treatment with clozapine across both cohort studies and case reports and case series. Among the case reports and series, 24/101 patients (23.8 %) followed clozapine withdrawal. Overall, 25 studies were of low quality, 60 of moderate quality and 8 of high quality.Our findings should be interpreted with caution, as the reliance on case reports, case series and small cohort studies is susceptible to reporting biases, regression to the mean and confounding by other treatments. Future research could use large healthcare databases to ascertain outcomes in those on clozapine with a history of catatonia given the difficulty and expense of conducting randomised controlled trials.