Catatonia, a complex syndrome characterized by immobility and communication impairment, presents with varying responses to lorazepam treatment among individuals with different cognitive impairments and underlying dementias. This study examines a case series involving four distinct catatonic patients to elucidate the factors contributing to the variable lorazepam response. Although lorazepam, a GABAergic modulator, can effectively alleviate symptoms in some cases, its limited impact in others highlights the intricate interplay between the underlying pathophysiology of diverse dementias and treatment mechanisms. This abstract provides insights into the intricate relationship between neurochemical pathways, catatonic symptoms, and treatment approaches, shedding light on the complexities of managing catatonia in the context of cognitive impairments and dementias.

Catatonia is a psychomotor syndrome associated with neurotransmitter disturbances, common in both psychiatric and medical settings. Hypoactivity of the GABAA receptor is one of the predominant theories behind the pathophysiology of catatonia, affecting both motor functioning and emotional regulation. Benzodiazepines such as lorazepam are considered the first-line treatment for catatonia. However, up to 27% of catatonia cases fail to respond to benzodiazepines alone. Zolpidem, which can be used as a challenge, monotherapy, or augmentation agent, serves as a promising pharmacological agent for catatonia due to its unique pharmacodynamic and pharmacokinetic profile.

We sought to systematically examine the evidence behind zolpidem's use among adult patients to understand its clinical utility in the management of catatonia against prevailing treatments such as lorazepam and electroconvulsive therapy.

We conducted a systematic review using search terms related to zolpidem and catatonia in PubMed, EMBASE, and Web of Science. We followed Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines and identified 29 studies, including case studies and case series that met inclusion criteria.

We reviewed 35 cases in which zolpidem was used for catatonia management (age: mean = 51.5 ± 21.0 standard deviation years; 68.6% female; Bush Francis Catatonia Rating Scale: mean = 22.2 ± 9.0 standard deviation). Proportions of positive responses for zolpidem on catatonia varied by treatment approach: 91% as a challenge agent (n = 10), 100% as a first-line monotherapy agent (n = 3), 57% as a first-line combination therapy agent (n = 4), 70% as a second-line monotherapy agent (n = 7), and 100% as a second-line augmentation agent (n = 4). In total, 28 out of the 35 reported cases of catatonia (80%) responded positively to zolpidem.

An 80% positive response rate for zolpidem in lysing catatonia is encouraging but may be an overestimate due to reporting bias of case-level data. Results may be explained by zolpidem's selectivity for the α1 subunit of the GABAA receptor. Thus, zolpidem may be an underutilized catatonia treatment and prove useful in situations when benzodiazepines fail or when electroconvulsive therapy access is limited. Given that current literature on the use of zolpidem for catatonia is limited to case reports, more robust research in this area is warranted.

Catatonia is a neuropsychiatric syndrome characterized by motor, behavioral, and autonomic abnormalities. It is often underdiagnosed in geriatric patients with dementia despite established diagnostic criteria and treatment options.

This systematic review investigates catatonia in the elderly, particularly those with dementia, to examine their clinical presentation, treatment response, and prognosis compared to elderly patients without dementia.

We comprehensively searched MEDLINE and EMBASE, including case reports and series on catatonia in elderly patients. Reviewers independently performed data extraction and quality assessments. Statistical significance was set at a p value ≤0.05, and a multivariate logistic regression model was used to analyze differences between patients with and without dementia.

Our review included 182 articles with 225 cases. We found no significant differences in the clinical presentation of catatonia between patients with and without dementia, with both groups commonly exhibiting the hypokinetic variant. However, patients with dementia were more frequently treated with NMDA receptor antagonists (OR: 3.27; CI: 1.05-10.11; p = 0.040) and had a lower complete response rate to treatment (OR: 0.37; CI: 0.19-0.75; p = 0.006). Patients with dementia also exhibited fewer acute medical conditions (OR: 0.17; CI: 0.05-0.65; p = 0.009).

Catatonia in dementia does not have a different syndromic presentation. However, the diagnosis of dementia leads to varying preferences regarding the choice of symptomatic therapy and seems to be a predictor of a poorer therapeutic response. Actively treating catatonia, particularly in patients with dementia, addressing the characteristics of these patients is of paramount importance.

Catatonia is a highly prevalent syndrome in patients presenting with major neurocognitive disorders (dementia). In this study, we aim to provide a comprehensive description of the clinical and therapeutic aspects of catatonia in patients with dementia.

This descriptive study, conducted between September 2015 and June 2022, collected data from 25 patients diagnosed with dementia, out of 143 patients treated for catatonia in our specialized psychiatry department. We collected sociodemographic, clinical and treatment data for each patient.

Dementia patients constituted 17% of the catatonic cases. Predominantly female, the cohort had a mean age of 65. Diagnoses included Alzheimer's (4 patients, 17%) and Parkinson's (1 patient, 4%) diseases, Lewy body dementia (5 patients, 21%), vascular dementia (4 patients, 17%) and frontotemporal lobar degeneration (10 patients, 41%). The mean Bush-Francis Catatonia Rating Scale score upon admission was 20/69. Overall, complete remission of catatonia was achieved in 75% of patients (n=18), with only 13% (n=3) responding to lorazepam alone, while others required additional interventions such as electroconvulsive therapy (ECT) and/or amantadine. Vascular dementia was predominantly observed in cases resistant to treatment.

The findings indicate a frequent co-occurrence of catatonia and dementia, highlighting treatability yet suggesting a potential for resistance to lorazepam, which varies by dementia diagnosis. Investigating the mechanisms underlying this resistance and the variability in treatment response is crucial for developing more precise therapeutic strategies.

This editorial addresses catatonia, a complex neuropsychiatric syndrome characterised by a spectrum of psychomotor disturbances. The editorial seeks to clarify the ambiguous aspects of catatonia, integrating recent research findings, including global studies and diagnostic advancements. It discusses catatonia's clinical manifestations, prevalence, and associated psychiatric and medical conditions, with particular emphasis on its frequent co-occurrence with schizophrenia and mood disorders. The prevalence of catatonia, which varies across psychiatric populations, is illustrated by a significant study conducted in Nelson Mandela Bay, South Africa. This study provides valuable insights into the effectiveness of the Bush-Francis Screening Instrument compared to the Diagnostic and Statistical Manual 5 criteria in diagnosing catatonia. The editorial evaluates treatment approaches, primarily focusing on benzodiazepines and electroconvulsive therapy, and discusses emerging therapeutic strategies. It underscores the importance of robust diagnostic frameworks and early intervention in managing catatonia, as recommended by the latest evidence-based consensus guideline. Furthermore, it suggests future research directions, particularly in exploring the neurobiological and genetic factors of catatonia, to enhance our understanding and improve treatment outcomes. This editorial succinctly aims to demystify catatonia and provide valuable insights for clinicians and researchers in mental health care.

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 has been defined by ICD-11 as a nosologically unspecific syndrome. Previous neuropsychiatric conceptions of catatonia such as Wernicke-Kleist-Leonhard's (WKL) one, have isolated chronic catatonic entities, such as progressive periodic catatonia (PPC) and chronic system catatonias (CSC). This study aimed at comparing the clinical and neuropsychological features of PPC, CSC and non-catatonic patients, all diagnosed with a schizophrenia spectrum disorder (SSD). The clinical and cognitive measures were compared among 53 SSD patients, first by separating catatonic (C-SSD, n = 27) and non-catatonic patients (NC-SSD, n = 26), and second, by separating PPC (n = 20), CSC (n = 6) and NC-SSD patients. Bayes factors were used to compare the model with 1 or 2 catatonic groups. We found that PPC had a more frequent schizo-affective presentation, higher levels of depression and less positive psychotic symptoms than both CSC and NC-SSD. CSC patients had an earlier illness onset, a poorer cognitive functioning, and higher antipsychotics doses than both PPC and NC-SSD. Most differences between C- and NC-SSD were accounted by characteristics of either PPC or CSC. The model with 2 catatonic groups clearly outperformed that with 1 catatonic group. Our results point to a substantial clinical heterogeneity of 'catatonia' within the SSD population and suggest that distinguishing (at least) 2 chronic catatonic phenotypes (PPC and CSC) may represent a relevant step to apprehend this heterogeneity. It is also a more parsimonious attempt than considering the around 32.000 distinct catatonic presentations resulting from the combinations of 3 out of 15 polythetic criteria for ICD-11 catatonia.