Concurrent catatonia and COVID-19 infection - An experiential account of challenges and management of cases from a tertiary care psychiatric hospital in India.

Catatonia has been reported as one among many neuropsychiatric manifestations associated with COVID-19 infection. Catatonia and COVID-19 co-occurrence remain clinical concerns, often posing challenges pertaining to diagnosis, and especially management. Limited information is available regarding the appropriate approaches to the management of catatonia in COVID-19 infection, particularly with reference to the safety and efficacy of benzodiazepines and Electro-convulsive therapy (ECT). We present our experience of five patients with catatonia consequent to heterogeneous underlying causes and concurrent COVID-19 infection, who received care at the psychiatric COVID unit of our tertiary care psychiatric hospital. An interesting observation included varying underlying causes for catatonia and the potential role that COVID-19 infection may have played in the manifestation of catatonia. In our experience, new-onset catatonia with or without pre-existing psychiatric illness and concurrent COVID-19 can be safely and effectively managed with lorazepam and/or ECTs. However, critical to the same is the need to implement modified protocols that integrate pre-emptive evaluation for COVID-19 disease and proactive monitoring of its relevant clinical parameters, thereby permitting judicious and timely implementation of catatonia-specific treatment options.

Resting state functional connectivity and structural abnormalities of the brain in acute retarded catatonia: an exploratory MRI study.

In this first cross-sectional MRI study in acute catatonia, we compared the resting state whole-brain, within-network and seed (left precentral gyrus)-to-voxel connectivity, as well as cortical surface complexity between a sample of patients in acute retarded catatonic state (n = 15) diagnosed as per DSM-5 criteria and a demographically matched healthy control sample (n = 15). The patients had comorbid Axis-I psychiatric disorders including schizophrenia spectrum disorders and psychotic mood disorders, but did not have diagnosable neurological disorders. Acute retarded catatonia was characterized by reduced resting state functional connectivity, most robustly within the sensorimotor network; diffuse region of interest (ROI)-ROI hyperconnectivity; and seed-to-voxel hyperconnectivity in the frontoparietal and cerebellar regions. The seed (left precentral gyrus)-to-voxel connectivity was positively correlated to the catatonia motor ratings. The ROI-ROI as well as seed-to-voxel functional hyperconnectivity were noted to be higher in lorazepam responders (n = 9) in comparison to the non-responders (n = 6). The overall Hedges' g effect sizes for these analyses ranged between 0.82 and 3.53, indicating robustness of these results, while the average Dice coefficients from jackknife reliability analyses ranged between 0.6 and 1, indicating fair (inter-regional ROI-ROI connectivity) to perfect (within-sensorimotor network connectivity) reliability of the results. The catatonia sample showed reduced vertex-wise cortical complexity in the right insular cortex and contiguous areas. Thus, we have identified neuroimaging markers of the acute retarded catatonic state that may show an association with treatment response to benzodiazepines. We discuss how these novel findings have important translational implications for understanding the pathophysiology of catatonia as well as for the mechanistic understanding and prediction of treatment response to benzodiazepines.

Revisiting lorazepam challenge test: Clinical response with dose variations and utility for catatonia in a psychiatric emergency setting.

OBJECTIVE: Catatonia can be life-threatening unless timely identified and treated. Lorazepam's ubiquitous response has led to its universal acceptance as being the first-line management of catatonia and alludes to catatonia's neurobiological underpinnings. Lorazepam challenge test (LCT) is widely used to either confirm a catatonia diagnosis or determine lorazepam sensitivity. It has a proposed schedule for administering lorazepam. However, efficacy of recommended LCT doses lack systematic evidence, resulting in variable LCT doses used in clinical and research settings contributing to findings that are challenging to generalize or assist with developing standardized lorazepam treatment protocols for catatonia. Given the same, this study aimed to objectively compare the response between two groups receiving different LCT doses and factors influencing the same. METHODS: The 6-month study in a psychiatric emergency setting at a tertiary neuropsychiatric center in India evaluated 57 catatonia patients, before and after administration of single 2 mg (n = 37; LCT-2) or 4 mg (n = 20; LCT-4) lorazepam dose, applying Bush Francis Catatonia Rating Scale (BFCRS), Mini International Neuropsychiatric Interview (MINI 5.0) and obtaining sociodemographic, clinical data. RESULTS: No between-group differences (LCT-2 vs LCT-4) for sociodemographic, clinical profiles or BFCRS severity score changes to lorazepam on Mann-Whitney U test were noted. Applying Wilcoxon signed rank test comparing individual sign severity demonstrated response variability, with significant response noted to both doses (stupor, mutism, staring, posturing, withdrawal, ambitendency, automatic obedience) and others selectively to 2 mg (echolalia, rigidity, negativism, mitgehen). Notably, sign resolution (present/absent) only to 2 mg was significant for stupor, mutism, staring, posturing, echolalia, rigidity, negativism and mitgehen. CONCLUSION: This study suggests 2 mg lorazepam may be an optimal LCT dose, given significant response to most catatonic signs thereby ensuring accurate detection and preventing misinterpretation of response. It offers future studies direction for standardizing lorazepam dosing schedules for catatonia management and exploring neurobiological underpinnings for individual catatonic signs that may be potentially different, given these findings.

Diagnosing catatonia and its dimensions: Cluster analysis and factor solution using the Bush Francis Catatonia Rating Scale (BFCRS).

Advances in research into catatonia in the preceding two decades has offered increasing clarity and an improved understanding of various aspects of this complex syndrome. Despite the above, there are several aspects that hinder a broader interpretation of these findings, the most common being a lack of consensus on the criteria required for diagnosing catatonia. Whilst being the most frequently used tool for diagnosis, the number of signs from Bush-Francis Catatonia Rating Scale (BFCRS) needed to diagnose catatonia remain unclear. This study aimed to determine the number of signs required to accurately diagnose catatonia using BFCRS and delineate its dimensions in an acute inpatient unit in the Indian setting. A random sample of 300 patients were evaluated for catatonia within 24 h of admission. Cluster Analysis followed by discriminant analysis and receiver operating curve analysis (ROC) provided cut-off values for diagnosing catatonia syndrome. Principle Component Analysis (PCA) with varimax rotation was used to identify factors in those with catatonia. Findings revealed that a cut off of two signs from both Bush-Francis Catatonia Screening Instrument or BFCSI (sensitivity of 100 %, specificity of 96.2 % as well as a positive predictive value [PPV] of 79.6 % and negative predictive value [NPV] 100 % with ROC AUC value of 0.98) and complete BFCRS (sensitivity of 100 % and specificity of 90.7 %, PPV of 80.7 and NPV of 100 % with ROC AUC for at least two items cut-off being 0.95) accurately detected catatonia. However, the prevalence of catatonia in the same population increased by 4% from 16.3% to 20.3% using the BFCRS rather than the BFCSI. The BFCRS generated a 3-factor model accounting for 65.48 % variance offering the best fit, indicating three discrete dimensions to catatonia, namely retarded, excited and what we named as "aberrant volitional". Interestingly, the aberrant volitional dimension comprises of signs that need to be elicited rather than passively observed and excluding one, none of them are part of the BFCSI. Findings of this study suggest that the BFCRS more accurately detects catatonia rather than the BFCSI. Additionally, three dimensions of catatonia more coherently explain the catatonic syndrome given that 55.7 % of the sample had signs from more than one factor concurrently. We propose that the BFCRS rather than BFCSI be routinely administered for evaluating all suspected cases of catatonia to ensure more accurate detection as well as identifying the aberrant volitional dimensional signs more consistently. The three-dimensional model also offers great opportunities to further unravel the pathophysiological basis of catatonic signs more systematically.