Catatonia

This study aims to investigate the neurophysiological and inflammatory changes associated with electroconvulsive therapy (ECT) in older age patients diagnosed with Major Depressive Episode, Major Depression, and Bipolar Disorder, using microstate analysis derived from resting-state electroencephalography (EEG) recordings. Within this scope, EEG recordings obtained before and after ECT will be compared to determine the relationships between changes in microstate parameters and inflammatory marker levels, clinical variables, and psychometric scale scores reflecting clinical improvement. Peripheral blood samples collected from the same patient group will be analyzed for complete blood count parameters as well as levels of interleukin-1 alpha (IL-1α), interleukin-1 beta (IL-1β), interleukin-2 (IL-2), interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-10 (IL-10), tumor necrosis factor-alpha (TNF-α), soluble glycoprotein 130 (sgp-130), soluble interleukin-6 receptor (sIL-6R), interferon gamma-induced protein 10 kDa (IP-10), and C-reactive protein (CRP). In addition, inflammatory indices, including the Neutrophil-to-Lymphocyte Ratio (NLR), Platelet-to-Lymphocyte Ratio (PLR), and Monocyte-to-Lymphocyte Ratio (MLR), will be calculated. The association between baseline levels of these biomarkers and treatment response will be evaluated. Moreover, changes in biomarker levels following ECT will be statistically examined in relation to clinical scale scores and EEG microstate parameters. Although microstate analysis and inflammatory biomarkers have each been extensively investigated in psychiatric disorders, studies evaluating these two biomarkers together, particularly with the inclusion of healthy control participants, in the older age population remain limited. In this regard, the present study aims to evaluate the effects of ECT on older age patients using objective neurophysiological indicators, contribute to the understanding of the pathophysiology of depression at the level of brain networks, and provide a scientific basis for the development of personalised treatment approaches in the future.

The disruption of immune system is a key candidate in the pathogenesis of psychiatric disorders, especially those resistant to traditional treatments. Involving complex processes within the brain and peripheral immune system, inflammation may lead to imbalance of neurotransmitter systems and synaptic plasticity and directly contribute to the psychiatric symptoms observed in conditions such as depression, bipolar disorder (BD) and schizophrenia (SCZ). Studies show that treatment-resistant depression (TRD) is associated with elevated levels of inflammatory markers in the blood, which are linked to a lower response to conventional antidepressants. Interventions that modulate this inflammatory response, such as immunomodulatory treatments or therapies targeting pro-inflammatory cytokines, have demonstrated beneficial effects by reducing symptoms and improving patients' quality of life. A thorough understanding of the links between inflammation and treatment resistance therefore paves the way for innovative therapeutic strategies. These approaches could transform current practices by offering more personalized and effective solutions for patients suffering from chronic and resistant psychiatric disorders.

Catatonia is a severe form of psychomotor disturbance with a heterogenous presentation. It affects approximately 10% of acute psychiatric inpatients. According to the fifth edition of DSM-5 the diagnosis of catatonia can be made when three or more symptoms from the twelve following are present : catalepsy, waxy flexibility, stupor, agitation, mutism, negativism, posturing, mannerisms, stereotypies, grimacing, echolalia, echopraxia. It can occur in various psychiatric diseases, including mood disorders or schizophrenia, but also in various non-psychiatric disorders \[metabolic disturbances, viral infections (including HIV), typhoid fever, heat stroke, and autoimmune disease\]. Benzodiazepines, especially LORAZEPAM, are the most common initial treatment, with a remission rate of approximately 70-80 %, regardless of the cause or the clinical manifestations. This first line treatment is titrated gradually according to the therapeutic response over a few days up to 20-25 mg per day. Electroconvulsive therapy (ECT) is initiated on patients with catatonia who do not respond to benzodiazepines. Interestingly, pharmacogenetic variants can alter the metabolism of lorazepam (e.g., the UGT2B15 \* 2 allele slows it down). The main objective of this study is to assess the link between clinical response to lorazepam, residual plasma concentrations of lorazepam after 72 hours of fixed dosage, and the existence of genetic polymorphisms modifying the metabolism of lorazepam. Our hypothesis is that non-responding patients have lowered blood concentrations of lorazepam associated to a genetic profile of rapid metabolism. Evaluating the predictive factors of the response to treatment would allow early and precise identification of non-responder patients in order to adapt their first-line treatment.

This study aims to assess the incidence, sociodemographic and clinical characteristics, treatment response, and short-term outcomes of adult patients with catatonic syndrome in the Bilbao area (Spain). Data will be collected from January 2024 to December 2025 from all patients aged 18 years or older diagnosed with catatonia of any etiology at Basurto University Hospital who provide informed consent to participate.

The goal of this clinical trial is to improve how electroconvulsive therapy (ECT) stimulation settings are chosen. Researchers will use real-time brain monitoring to measure both seizures and a recently identified brain event called cortical spreading depolarization (CSD). The main questions it aims to answer are: What is the best way to increase ECT stimulation settings? How do different pulse settings affect the brain's response? Can certain settings produce CSD without causing a seizure? Participants already receiving ECT as part of their care will take part. They will be assigned to one of two groups: Index ECT group: Participants starting ECT will receive different standard titration approaches. Maintenance ECT group: Participants receiving ongoing ECT will undergo a brief, low-dose stimulation test before treatment. All participants will be monitored using brain physiology (EEG and blood flow) and symptom scales during treatment.

Rady Children's Institute for Genomic Medicine seeks to understand the genomes and immune systems in 40 children and adolescents who are admitted to Rady Children's Hospital San Diego with a catatonia diagnosis. Cutting-edge genome and protein sequencing technology will be used to better understand how immunological and genetic assessments may improve the ability to identify the cause of catatonia and impact care. The investigator also hopes to identify new genetic and/or autoimmune causes of catatonia that may inform new treatment for future patients.