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INTRODUCTION: Catatonia, documented since the 19th century, remains a significant challenge in terms of recognition and treatment. Over the last two decades, ketamine has brought new perspectives to psychiatry, sparking widespread interest. Concurrently, catatonia has attracted heightened scientific attention. Preliminary evidence suggests the therapeutic potential of ketamine for catatonia. METHODS: We systematically searched Medline/PubMed, Embase, PsycINFO, Lilacs, and Cochrane Library databases, as well as Google Scholar, for studies with ketamine or its enantiomers as intervention for catatonia, with no restrictions to underlying diagnosis, date, language, or study design. RESULTS: Twenty articles were included, encompassing a total of 25 catatonic patients receiving ketamine or esketamine. Predominantly female (61.9 %), with a mean age of 44.4 years, patients mostly exhibited manifestations compatible with the retarded subtype of catatonia. Mood disorders were the most prevalent underlying diagnoses. Ketamine was primarily administered intravenously over a 40-minute period and in multiple-dosing schemes. Mean response and remission rates of catatonic manifestations for the whole sample were 80 % and 44 %, respectively, with no reports of worsening catatonic features or psychotic symptoms. Only one patient discontinued treatment due to intolerable dissociative effects. CONCLUSION: Challenging the conventional contraindication of ketamine in psychotic disorders, current evidence highlights its potential efficacy, particularly in treating catatonia. Pending further research, we advocate reevaluating this contraindication, as it may offer a promising therapeutic option, especially for challenging cases. Preliminary evidence suggests potentially greater benefits for catatonic patients with underlying mood disorders compared to primary psychotic disorders.

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La catatonía es un síndrome neuropsiquiátrico que se presenta con una serie heterogénea de signos y síntomas psicomotores, afectivos, conductuales y autonómicos. Es una manifestación inespecífica de ciertos trastornos mentales, metabólicos, inmunológicos, endocrinológicos, infecciosos y neurológicos, y es fundamental establecer estrategias de diagnóstico precoz para implementar medidas terapéuticas eficaces y oportunas. El objetivo de esta revisión sistematizada es evaluar la utilidad de la prueba de lorazepam como estrategia diagnóstica en individuos con catatonía. Se utilizó los buscadores Cochrane, Lilacs, Scielo, Pubmed y Scopus. Los artículos seleccionados son ensayos clínicos y cohortes prospectivos, en los cuales se analizó la forma de diagnóstico de catatonía, la utilización y protocolo de la prueba de lorazepam y las medidas de respuesta. La búsqueda inicial determinó 87 artículos; aplicando los criterios de inclusión y exclusión se culminó en la elección de 8 artículos. La identificación de la catatonía presenta dificultades y su diagnóstico es variable, lo cual genera limitaciones en cuanto a intervenciones precoces. Existe una heterogeneidad de evaluaciones y de estrategias, pero la bibliografía es sugerente en cuanto a la utilización de lorazepam como evaluación confirmatoria y tratamiento inicial de la catatonía. La prueba de lorazepam forma parte de un protocolo de manejo, y puede ser un paso en la toma de decisiones para que individuos con catatonía reciban una intervención oportuna. Se concluye que la prueba de lorazepam es una técnica accesible y replicable, con resultados prometedores para su eventual implementación, pero se necesita nuevos estudios que involucren su aplicación estandarizada.

Catatonia is a neuropsychiatric syndrome characterized by a heterogeneous range of psychomotor, affective, behavioral, and autonomic signs and symptoms. It is a nonspecific manifestation of certain mental, metabolic, immunological, endocrinological, infectious, and neurological disorders. Therefore, it is essential to establish early diagnostic strategies to implement effective and timely therapeutic measures. This review aims to evaluate the utility of the Lorazepam Challenge Test as a diagnostic strategy in individuals with catatonia. A review was conducted using search engines such as Cochrane, Lilacs, Scielo, Pubmed, and Scopus. The initial search yielded 87 articles, and after applying inclusion and exclusion criteria, 8 articles were selected. The selected articles are clinical trials and prospective cohorts, where catatonia diagnosis, the use and protocol of the Lorazepam Challenge Test, and response measures were analyzed. Identifying catatonia is challenging, and its diagnosis varies, leading to limitations in early interventions. There is a heterogeneity of evaluations and strategies, but the literature suggests the use of lorazepam as a confirmatory evaluation and initial treatment for catatonia. The Lorazepam Challenge Test is part of a management protocol and can be a decision-making step for individuals with catatonia to receive timely intervention. It is concluded that The Lorazepam Challenge Test is an accessible and replicable technique with promising results for potential implementation, requiring further studies involving its standardized application.

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Catatonia was initially a clinical presentation of certain types of schizophrenia, but basic and epidemiological evidence has demonstrated its association with multiple somatic and psychiatric conditions. We describe and discuss current clinical, etiological, pathophysiological, and therapeutic concepts regarding catatonia. We conducted a broad narrative review of articles published in MEDLINE/PubMed. The diagnosis is clinical and can be supported by additional tests, but there are psychometric instruments with different clinical focus. The most validated subtypes are inhibited and excited catatonia. It is mostly associated with somatic, neurological, affective, psychotic, and autistic spectrum disorders. Genetic factors related to oligodendrocytes have been studied in its pathophysiology. Some findings point to an imbalance in neurotransmission and density of GABA and dopamine receptors, consistent with their function in motor pathways and therapeutic response with benzodiazepines. Likewise, glutamatergic activity has been analyzed from the pathophysiological model of autoimmune encephalitis. The cortico-cortical and cortico-subcortical pathways would have a central role, including structures such as the orbitofrontal and temporal cortex, basal nuclei, and brainstem, involved in decision-making, emotion regulation, storage, planning, and motor processing. The main therapeutic lines are benzodiazepines and electroconvulsive therapy. Other interventions studied are zolpidem, antipsychotics, mood stabilizers, glutamatergic modulators, and transcranial magnetic stimulation. New neurobiological findings challenge nosological and therapeutic precepts, renewing the cycle in the conceptualization of catatonia. We highlight the affective component of the psychomotor syndrome and the role of interventions aimed at its modulation.

Inicialmente la catatonía fue un componente clínico de algunas formas de esquizofrenia, pero la evidencia básica y epidemiológica demuestra su vinculación con múltiples cuadros somáticos y psiquiátricos. Se describen y analizan conceptos clínicos, etiológicos, fisiopatológicos y terapéuticos actuales respecto a la catatonía. Se realizó una revisión narrativa amplia de artículos publicados en MEDLINE/PubMed. El diagnóstico es clínico y puede apoyarse en exámenes complementarios, pero existen instrumentos psicométricos con distinto énfasis clínico. Los subtipos más validados son el inhibido y el excitado. Se asocia mayormente a patologías somáticas, neurológicas, afectivas, psicóticas y del espectro autista. En su fisiopatología se han estudiado factores genéticos relacionados con los oligodendrocitos. Algunos hallazgos señalan un desbalance en la neurotransmisión y densidad de receptores de GABA y dopamina, hecho concordante con su función en las vías motoras y la respuesta terapéutica con benzodiacepinas. Asimismo, se ha analizado la actividad glutamatérgica, desde el modelo fisiopatológico de la encefalitis autoinmune. Las vías córtico-corticales y córtico-subcorticales tendrían un rol central, incluyendo estructuras como las cortezas orbitofrontal y temporal, núcleos basales y tronco encefálico, involucradas en la toma de decisiones, regulación emocional, almacenamiento, planificación y elaboración motora. Las principales líneas terapéuticas son las benzodiacepinas y la terapia electroconvulsiva. Otras intervenciones estudiadas son el zolpidem, antipsicóticos, estabilizadores del ánimo, moduladores glutamatérgicos y estimulación magnética transcraneal. Los nuevos hallazgos neurobiológicos discuten los preceptos nosológicos y terapéuticos, renovando el ciclo en la conceptualización de la catatonía. Se destaca el componente afectivo del síndrome psicomotor y el rol de las intervenciones que apunten a su modulación.

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RESUMEN El tratamiento de la catatonía considera habitualmente el uso de benzodiacepinas y, de fallar estas, se procede a la terapia electroconvulsiva. Sin embargo, las hipotéticas vías neurobiológicas implicadas en la catatonía postulan un efecto benéfico de fármacos gabaérgicos y bloqueadores de glutamato. Se presenta el caso clínico de una paciente mujer de 45 años de edad, con diagnóstico de esquizofrenia paranoide, que desarrolló un cuadro de estupor catatónico (sin respuesta a las benzodiacepinas) y varias complicaciones médicas; sin embargo, el cuadro mejoró rápidamente con la combinación de zolpidem, memantina y aripiprazol. De este modo, se registró un desenlace no logrado con la terapia estándar de benzodiacepinas. Se concluye que la combinación de medicamentos gabaérgicos y bloqueadores de glutamato puede ser utilizada beneficiosamente en casos de estupor catatónico que no logran responder al manejo usual con benzodiacepinas.

ABSTRACT Objective: The treatment of catatonia usually involves the use of benzodiazepines and, if these fail, electroconvulsive therapy is applied. Nevertheless, hypothetical neurobiological pathways involved in catatonia postulate beneficial effects of GABAergic drugs and glutamate blockers. Clinical case: A 45-year-old female patient, diagnosed with paranoid schizophrenia who developed a catatonic stupor (with no response to benzodiazepines) and various medical complications; however, the condition improved rapidly with the combination of zolpidem, memantine and aripiprazole. Result: A favorable outcome was obtained in this case, not achieved with the previous use of standard benzodiazepine therapy. Conclusions: The combination of GABAergic drugs and glutamate blockers can be beneficially implemented in cases of catatonic stupor that fail to respond to the usual management with benzodiazepines.

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Inicialmente la catatonía fue un componente clínico de algunas formas de esquizofrenia, pero la evidencia básica y epidemiológica demuestra su vinculación con múltiples cuadros somáticos y psiquiátricos. Se describen y analizan conceptos clínicos, etiológicos, fisiopatológicos y terapéuticos actuales respecto a la catatonía. Se realizó una revisión narrativa amplia de artículos publicados en MEDLINE/PubMed. El diagnóstico es clínico y puede apoyarse en exámenes complementarios, pero existen instrumentos psicométricos con distinto énfasis clínico. Los subtipos más validados son el inhibido y el excitado. Se asocia mayormente a patologías somáticas, neurológicas, afectivas, psicóticas y del espectro autista. En su fisiopatología se han estudiado factores genéticos relacionados con los oligodendrocitos. Algunos hallazgos señalan un desbalance en la neurotransmisión y densidad de receptores de GABA y dopamina, hecho concordante con su función en las vías motoras y la respuesta terapéutica con benzodiacepinas. Asimismo, se ha analizado la actividad glutamatérgica, desde el modelo fisiopatológico de la encefalitis autoinmune. Las vías córtico-corticales y córtico-subcorticales tendrían un rol central, incluyendo estructuras como las cortezas orbitofrontal y temporal, núcleos basales y tronco encefálico, involucradas en la toma de decisiones, regulación emocional, almacenamiento, planificación y elaboración motora. Las principales líneas terapéuticas son las benzodiacepinas y la terapia electroconvulsiva. Otras intervenciones estudiadas son el zolpidem, antipsicóticos, estabilizadores del ánimo, moduladores glutamatérgicos y estimulación magnética transcraneal. Los nuevos hallazgos neurobiológicos discuten los preceptos nosológicos y terapéuticos, renovando el ciclo en la conceptualización de la catatonía. Se destaca el componente afectivo del síndrome psicomotor y el rol de las intervenciones que apunten a su modulación.

Catatonia was initially a clinical presentation of certain types of schizophrenia, but basic and epidemiological evidence has demonstrated its association with multiple somatic and psychiatric conditions. We describe and discuss current clinical, etiological, pathophysiological, and therapeutic concepts regarding catatonia. We conducted a broad narrative review of articles published in MEDLINE/PubMed. The diagnosis is clinical and can be supported by additional tests, but there are psychometric instruments with different clinical focus. The most validated subtypes are inhibited and excited catatonia. It is mostly associated with somatic, neurological, affective, psychotic, and autistic spectrum disorders. Genetic factors related to oligodendrocytes have been studied in its pathophysiology. Some findings point to an imbalance in neurotransmission and density of GABA and dopamine receptors, consistent with their function in motor pathways and therapeutic response with benzodiazepines. Likewise, glutamatergic activity has been analyzed from the pathophysiological model of autoimmune encephalitis. The cortico-cortical and cortico-subcortical pathways would have a central role, including structures such as the orbitofrontal and temporal cortex, basal nuclei, and brainstem, involved in decision-making, emotion regulation, storage, planning, and motor processing. The main therapeutic lines are benzodiazepines and electroconvulsive therapy. Other interventions studied are zolpidem, antipsychotics, mood stabilizers, glutamatergic modulators, and transcranial magnetic stimulation. New neurobiological findings challenge nosological and therapeutic precepts, renewing the cycle in the conceptualization of catatonia. We highlight the affective component of the psychomotor syndrome and the role of interventions aimed at its modulation.

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Resumen El autismo es un desorden del neurodesarrollo caracterizado por una alteración cualitativa en la interacción social y la comunicación, asociada a intereses restringidos y conductas estereotipadas. Puede asociarse a problemas médicos como epilepsia, disfunciones gastrointestinales, trastornos de sueño, otros trastornos del neurodesarrollo como deterioro del lenguaje, discapacidad intelectual, disfunciones sensoriales, TDA/H, torpeza motriz y/o trastornos neuropsiquiátricos como ansiedad, depresión, catatonia, esquizofrenia, trastornos obsesivo-compulsivo, trastornos de conducta e impulsividad, entre otros. La catatonía es reconocida como un síndrome neuropsiquiátrico identificado en todos los trastornos psicóticos y del estado de ánimo mayor, debido a condiciones médicas generales o como un síndrome no especificado de otra manera; esto permite codificar la catatonia en el contexto de otros trastornos psiquiátricos o del neurodesarrollo, como el trastorno obsesivo compulsivo o el autismo. Se caracteriza por síntomas motores, vocales y conductuales anormales, con alteración de la volición y la función vegetativa. Se estima que aproximadamente entre el 8 y 11 % de las personas autistas padecen catatonia. Es probable que haya un subregistro de catatonía, en especial en personas con autismo, debido a la falta de alerta sobre la misma, la heterogenicidad clínica y la similitud de muchos de sus síntomas con manifestaciones del autismo. Incluso muchas veces puede expresarse como una regresión autista tardía desde la pubertad a la vida adulta. Sus bases neurobiológicas aún no son claras y el tratamiento se basa en la administración de bensodiazepinas y la terapia electroconvulsiva, aunque es mucho el camino que aún queda por investigar en estos temas.

Abstract Autism is a neurodevelopmental disorder characterized by a qualitative alteration in social interac tion and communication, associated with restricted interests and stereotyped behaviors. It can be associated with medical problems such as epilepsy, gastrointestinal dysfunction, sleep disorders, other neurodevelopmental disorders such as language impairment, intellectual disability, sensory dysfunction, ADH/D, motor clumsiness, and/or neuropsychiatric disorders such as anxiety, depression, catatonia, schizophrenia, obsessive-compulsive disorders, behavioral and impulsive disorders, among others. Catatonia is recognized as a neuropsychiatric syn drome identified in all major mood and psychotic disorders, due to general medical conditions or as a syndrome not otherwise specified; this allows catatonia to be coded in the context of other psychiatric or neurodevelopmental disorders, such as obsessive-compulsive disorder or autism. It is characterized by abnormal motor, vocal, and behavioral symptoms, with impaired volition and vegetative function. It is estimated that approximately 8-11% of autistic people suffer from catatonia. It is probable that there is an underreporting of catatonia, especially in people with autism, due to the lack of alertness about it, the clinical heterogeneity and the similarity of many of its symptoms with manifestations of autism. Many times it can even express itself as a late autistic regression from puberty to adult life. Its neurobiological bases are still not clear and the treatment is based on the administration of bensodiazepines and electroconvulsive therapy although there is still a long way to go to investigate these issues.

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Autism is a neurodevelopmental disorder characterized by a qualitative alteration in social interaction and communication, associated with restricted interests and stereotyped behaviors. It can be associated with medical problems such as epilepsy, gastrointestinal dysfunction, sleep disorders, other neurodevelopmental disorders such as language impairment, intellectual disability, sensory dysfunction, ADH/D, motor clumsiness, and/or neuropsychiatric disorders such as anxiety, depression, catatonia, schizophrenia, obsessive-compulsive disorders, behavioral and impulsive disorders, among others. Catatonia is recognized as a neuropsychiatric syndrome identified in all major mood and psychotic disorders, due to general medical conditions or as a syndrome not otherwise specified; this allows catatonia to be coded in the context of other psychiatric or neurodevelopmental disorders, such as obsessive-compulsive disorder or autism. It is characterized by abnormal motor, vocal, and behavioral symptoms, with impaired volition and vegetative function. It is estimated that approximately 8-11% of autistic people suffer from catatonia. It is probable that there is an underreporting of catatonia, especially in people with autism, due to the lack of alertness about it, the clinical heterogeneity and the similarity of many of its symptoms with manifestations of autism. Many times it can even express itself as a late autistic regression from puberty to adult life. Its neurobiological bases are still not clear and the treatment is based on the administration of bensodiazepines and electroconvulsive therapy although there is still a long way to go to investigate these issues.

El autismo es un desorden del neurodesarrollo caracterizado por una alteración cualitativa en la interacción social y la comunicación, asociada a intereses restringidos y conductas estereotipadas. Puede asociarse a problemas médicos como epilepsia, disfunciones gastrointestinales, trastornos de sueño, otros trastornos del neurodesarrollo como deterioro del lenguaje, discapacidad intelectual, disfunciones sensoriales, TDA/H, torpeza motriz y/o trastornos neuropsiquiátricos como ansiedad, depresión, catatonia, esquizofrenia, trastornos obsesivo-compulsivo, trastornos de conducta e impulsividad, entre otros.La catatonía es reconocida como un síndrome neuropsiquiátrico identificado en todos los tra stornos psicóticos y del estado de ánimo mayor, debido a condiciones médicas generales o como un síndrome no especificado de otra manera; esto permite codificar la catatonia en el contexto de otros trastornos psiquiátricos o del neurodesarrollo, como el trastorno obsesivo compulsivo o el autismo. Se caracteriza por síntomas motores, vocales y conductuales anormales, con alteración de la volición y la función vegetativa. Se estima que aproximadamente entre el 8 y 11 % de las personas autistas padecen catatonia. Es probable que haya un subregistro de catatonía, en especial en personas con autismo, debido a la falta de alerta sobre la misma, la heterogenicidad clínica y la similitud de muchos de sus síntomas con manifestaciones del autismo. Incluso muchas veces puede expresarse como una regresión autista tardía desde la pubertad a la vida adulta. Sus bases neurobiológicas aún no son claras y el tratamiento se basa en la administración de bensodiazepinas y la terapia electroconvulsiva, aunque es mucho el camino que aún queda por investigar en estos temas.

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BACKGROUND: Patients with anti-N-methyl-d-aspartate (NMDA) receptor encephalitis (ANMDARE) show a wide range of behavioral abnormalities and are often mistaken for primary psychiatric presentations. We aimed to determine the behavioral hallmarks of ANMDARE with the use of systematic neuropsychiatric and cognitive assessments. METHODS: A prospective study was conducted, with 160 patients admitted to the National Institute of Neurology and Neurosurgery of Mexico, who fulfilled criteria for possible autoimmune encephalitis and/or red flags along a time window of seven years. Cerebrospinal fluid (CSF) antibodies against the NR1 subunit of the NMDAR were processed with rat brain immunohistochemistry and cell-based assays with NMDA expressing cells. Systematic cognitive, neuropsychiatric, and functional assessments were conducted before knowing NMDAR antibodies results. A multivariate analysis was used to compare patients with and without definite ANMDARE according to antibodies in CSF. RESULTS: After obtaining the CSF antibodies results in 160 consecutive cases, 100 patients were positive and classified as having definite ANMDARE. The most frequent neuropsychiatric patterns were psychosis (81%), delirium (75%), catatonia (69%), anxiety-depression (65%), and mania (27%). Cognition was significantly impaired. A total of 34% of the patients had a predominantly neuropsychiatric presentation without seizures. After multivariate analysis, the clinical hallmarks of ANMDARE consisted of a catatonia-delirium comorbidity, tonic-clonic seizures, and orolingual dyskinesia. CONCLUSIONS: Our study supports the notion of a neurobehavioral phenotype of ANMDARE characterized by a fluctuating course with psychotic and affective symptoms, catatonic signs, and global cognitive dysfunction, often accompanied by seizures and dyskinesia. The catatonia-delirium comorbidity could be a distinctive neurobehavioral phenotype of ANMDARE.

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This review aims to describe the clinical spectrum of catatonia, in order to carefully assess the involvement of astrocytes, neurons, oligodendrocytes, and microglia, and articulate the available preclinical and clinical evidence to achieve a translational understanding of the cellular and molecular mechanisms behind this disorder. Catatonia is highly common in psychiatric and acutely ill patients, with prevalence ranging from 7.6% to 38%. It is usually present in different psychiatric conditions such as mood and psychotic disorders; it is also a consequence of folate deficiency, autoimmunity, paraneoplastic disorders, and even autistic spectrum disorders. Few therapeutic options are available due to its complexity and poorly understood physiopathology. We briefly revisit the traditional treatments used in catatonia, such as antipsychotics, electroconvulsive therapy, and benzodiazepines, before assessing novel therapeutics which aim to modulate molecular pathways through different mechanisms, including NMDA antagonism and its allosteric modulation, and anti-inflammatory drugs to modulate microglia reaction and mitigate oxidative stress, such as lithium, vitamin B12, and NMDAr positive allosteric modulators.

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BACKGROUND: Neuropsychiatric symptoms can be part of the clinical spectrum of COVID-19 infections. AIM: To devise an evidence based clinical algorithm as a guide for clinicians, to identify and treat underlying clinical syndromes of psychomotor agitation, such as delirium, catatonia or substance withdrawal in patients who are hospitalized and infected with SARS-CoV-2. MATERIAL AND METHODS: A review of the literature about the pharmacological management of neuropsychiatric manifestations of COVID-19 at the general hospital, to develop a clinical protocol based on a consensus from an interdisciplinary expert panel at a Clinical Hospital. Results: A consensual clinical algorithm for the management of delirium, catatonia, and substance withdrawal, manifested as psychomotor agitation in patients hospitalized with COVID-19, was developed as a clinical proposal for physicians at different levels of complexity in health services. CONCLUSIONS: Cooperation among different clinical units in the general hospital facilitated the implementation of a clinical algorithm for clinicians for the management of psychomotor agitation in COVID-19 patients.

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INTRODUCTION: Autoimmune encephalitis (AIE) is a group of immune-mediated inflammatory processes of the brain with marked psychiatric features. Although relatively rare, they might offer difficult differential diagnosis with psychiatric conditions, especially catatonia and psychotic syndromes. Anti-N-methyl-d-aspartate receptor (NMDAR) encephalitis is the most common AIE, presenting with psychiatric syndromes in 90% of cases. The associated psychopathology is complex, pleomorphic, and best characterized when there is involvement of a psychiatrist in the assessment. AREAS COVERED: This text will review the main aspects of AIE to psychiatrists and/or neuropsychiatrists. EXPERT OPINION: Immune system dysfunction has been implicated in the pathophysiology of psychiatric symptoms and disorders. The use of diagnostic criteria for possible AIE, especially when specific antibodies of AIE are not available, allows early diagnosis and prompt treatment which are associated with better clinical outcomes. The study of the psychiatric aspects of AIE can broaden our knowledge of the underlying mechanisms of various psychiatric manifestations.

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Baclofen was approved for medical use in the United States in 1977 by Food and Drug Administration. Serious adverse effects associated with this medication are uncommon at usually prescribed doses. Herein, we present a case of baclofen-induced catatonia in a young-adult female with back pain receiving oral baclofen. A 20-year-old female presented to the emergency department with possible seizure-like activity. It was reported that the patient was suffering from acute back pain and was prescribed baclofen three times a day by her general physician one day before her presentation. Upon further discussion, it was known that following an altercation with her family member, she had attempted suicide by consuming 200 mg of baclofen and then developed rapidly progressive symptoms of aphasia, mutism, and decreased oral intake. Laboratory tests, cerebrospinal fluid analysis, and neuroimaging were unremarkable. Electroencephalogram was normal. Bush-Francis Catatonia Rating Scale score was 27. She showed significant improvement following low-dose lorazepam administration. There are four reports in the literature of catatonia secondary to baclofen. The present report is the first to describe the occurrence of catatonia in a previously healthy individual. Analysis of these cases suggests a relationship between a history of psychotic symptoms and catatonia. All the reports were classified as probable by the Naranjo algorithm.

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Animal models are important tools for studying neuropsychological disorders. Considering their limitations, a more extensive translational research must encompass data that are generated from several models. Therefore, a comprehensive characterization of these models is needed in terms of behavior and neurophysiology. The present study evaluated the behavioral responses of Carioca Low-conditioned Freezing (CLF) rats to haloperidol and methylphenidate. The CLF breeding line is characterized by low freezing defensive responses to contextual cues that are associated with aversive stimuli. CLF rats exhibited a delayed response to haloperidol at lower doses, needing higher doses to reach similar levels of catatonia as control randomly bred animals. Methylphenidate increased freezing responses to conditioned fear and induced motor effects in the open field. Thus, CLF rats differ from controls in their responses to both haloperidol and methylphenidate. Because of the dopamine-related molecular targets of these drugs, we hypothesize that dopaminergic alterations related to those of animal models of hyperactivity and attention disorders might underlie the observed phenotypes of the CLF line of rats.

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RESUMEN Fundamento: la catatonía es una de las presentaciones psiquiátricas más dramáticas, es muy rara en niños y adolescentes, por lo que puede ser mal diagnosticada al confundirse con cuadros psicóticos y provocar la muerte si no es tratada de manera adecuadada. Objetivo: presentar el caso inusual de una adolescente gambiana diagnosticada como un síndrome catatónico. Presentación del caso: adolescente de 14 años de edad, gambiana, femenina, fue ingresada en el Hospital Pediátrico de Banjul; debido a negarse a ingerir alimentos, agua y hablar por una semana. El examen físico reveló aumento de la frecuencia cardíaca, signos de deshidratación moderada, nivel de conciencia estuporoso y rigidez generalizada del cuerpo. Los estudios analíticos e fonomenológicos fueron normales. Se diagnosticó como un síndrome catatónico y luego de recibir tratamiento con lorazepam durante 10 días, fue dada de alta con evolución satisfactoria. Conclusiones: a pesar de ser la catatonía una rara afección, el médico general debe conocer esta enfermedad, con el fin de poner el tratamiento adecuado, para evitar su agravamiento y así preservar la vida de estos pacientes.

ABSTRACT Background: catatonia is one of the most dramatic psychiatric presentations, it is a very rare condition in children and adolescents, it could be misdiagnosed as a psychotic disorder, and could cause death if not treated properly. Objective: to discuss an unusual case of a Gambian female teenager diagnosed of catatonic syndrome. Case report: a 14-year-old Gambian female teenager was admitted to Banjul Pediatric Hospital because she refused to eat, drink or speak for one week. On physical examination she was found to have an increased heart rate, moderate signs of dehydration, stuporous level of consciousness and generalized rigidity of the body. The analytical and phonomenological studies were normal. After being diagnosed of catatonic syndrome and treated with Lorazepam for 10 days, she improved enough and she was satisfactorily discharged. Conclusions: despite the fact that catatonia is a rare condition, the general practitioner must know this pathology, in order to impose the appropriate treatment, avoid its aggravation and thus preserve the life of these patients.

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Catatonic patients may develop deep vein thrombosis (DVT) and pulmonary embolism (PE) due to prolonged periods of immobility. These life-threatening conditions demand prompt recognition and management. We describe the case of a patient with catatonia who presented to anesthesia for electroconvulsive therapy (ECT) at the outset of the current coronavirus disease 2019 pandemic. She complained of breathing difficulty and was suspected to have COVID-19 infection. On further evaluation, she was found to have DVT and PE and required oxygen therapy and intensive care management. The diagnostic delay in our patient would have probably not occurred, had it not been for the existing pandemic situation.

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Catatonia is a psychomotor syndrome common to several medical and neuropsychiatric disorders. Here, we report on the case of a 95-year-old woman who underwent a radical change in personality characterized by sexual disinhibition, and physical and verbal aggressiveness. Over several months, she developed verbal stereotypies, gait deterioration, and double incontinence. She eventually developed mutism and an active opposition to all attempts to be fed or cared for. Benzodiazepines, olanzapine and electroconvulsive therapy were of no benefit. Magnetic resonance imaging revealed asymmetric (more severe on the right) frontotemporal, parietal, and upper brainstem atrophy. She died from sepsis without recovering from stupor seven years after the onset of symptoms. We believe that the initial behavioral disinhibition was related to the frontotemporal injury, whereas catatonic stupor reflected the progression of the degenerative process to the parietal cortices. Our case adds to the small number of cases of catatonia as a symptom of degenerative dementia. It also supports the idea that damage to the parietal cortex gives rise to pathological avoidance of which catatonic stupor represents an extreme form.

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Abstract Background There is growing evidence of subclinical inflammation in mental disorders. Objective The aim of this study was to investigate frequency of symptoms of catatonia and the newly diagnosed subclinical inflammatory markers which are neutrophil/lymphocyte (NLR), platelet/lymphocyte (PLR), monocyte/lymphocyte (MLR) ratios in catatonia patients due to mental disorders. Methods: Patients who were admitted to psychiatry clinic with the diagnosis of catatonia according to DSM 5 in the last two years and equal number of control group were included in this retrospective study. Univariate analysis of covariance controlled for possible confounders was used to compare NLR, PLR, MLR ratios between patients and the control group. Results A total of 34 catatonia patients and 34 healthy controls were included in the study. Patients' mean age was 30.88 + 13.4. NLR value was significantly higher in the patient group than control group. There was no significant difference between the patients and control group according to PLR, MLR values. Discussion The presence of subclinical inflammation in catatonic syndrome due to mental disorders should be considered. Subclinical inflammation that was observed in numerous mental disorders continues in catatonia due to mental disorders. Large-scale studies are needed to determine the role of inflammation in catatonia.

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BACKGROUND: Previous case reports showed that delirious mania could be one of the many neuropsychiatric presentations of Anti-N-methyl-d-aspartate receptor encephalitis (ANMDARE). OBJECTIVE: To evaluate the frequency of delirious mania and its associated factors in ANMDARE. METHOD: A prospective study, including all patients with ANMDARE admitted to the National Institute of Neurology and Neurosurgery of Mexico, from January 2014 to April 2019. The diagnosis of delirious mania was established when diagnostic criteria for mania and delirium were fulfilled simultaneously. RESULTS: 79 patients with definitive ANMDARE were included. Delirious mania was identified in 20 (25.3%) of these patients. Catatonia, psychomotor agitation, disinhibition, impulsivity, and grandiose delusions were significantly associated with delirious mania. Also, a lower frequency of EEG abnormalities, absence of extreme delta brush, and a shorter hospital stay was observed in these patients. CONCLUSION: Delirious mania proved to be a frequent neuropsychiatric presentation of ANMDARE, and its presence should warn the physician about the possibility of this diagnosis. It was mainly associated with higher rates of catatonia, psychomotor agitation, disinhibition, and psychotic symptoms. The lack of recognition of delirious mania as a neuropsychiatric presentation in ANMDARE may be a source of diagnostic and therapeutic errors, as most physicians associate this with bipolar disorder.

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Resumen El Síndrome de Cotard es una condición neuropsiquiátrica poco frecuente, descrito inicialmente por Jules Cotard como un delirio hipocondríaco y luego como Delirio de negación, en que el paciente niega la existencia de partes de su cuerpo, la propia existencia y/o del mundo entero. La aparición de un Síndrome Catatónico junto al Síndrome de Cotard es aún más infrecuente. Se presenta el caso de una paciente de 72 años con una Depresión psicótica, que desarrolla un Síndrome de Cotard y posteriormente Catatonía. Logra buena respuesta tras la adición de Lorazepam y Venlafaxina al esquema farmacológico en curso, por lo que se desestima el uso de Terapia Electroconvulsiva. Se constata remisión total de síntomas y posterior recuperación funcional ad integrum, siendo evaluada a través de entrevista clínica, Hamilton Depression Rating Scale, Bush-Francis Catatonia Rating Scale e Índice de Barthel. Además, se revisan otros reportes de caso sobre esta comorbilidad, y a diferencia de la mayoría de éstos, se destaca la favorable evolución de la paciente sin necesidad de Terapia Electroconvulsiva. Aún no se ha dilucidado la relación entre ambos síndromes, aunque algunos autores han planteado la hipótesis de vías neurobiológicas compartidas y otros han postulado la aparición de síntomas catatónicos como la progresión del Síndrome de Cotard. Para aclarar estas interrogantes, son necesarios más estudios al respecto que permitan conocer la etiopatogenia de esta inusual combinación.

Cotard's Syndrome is a rare neuropsychiatric condition, initially described by Jules Cotard as a hypochondriacal delusion and then as Delusion of negation, in which the patient denies the existence of parts of his body, his own existence and / or the entire world. The appearance of a Catatonic Syndrome together with Cotard Syndrome is even more infrequent. We present the case of a 72-year-old patient with a psychotic depression, who developed Cotard's Syndrome and later Catatonia. She achieves good response after the addition of Lorazepam and Venlafaxine to the current pharmacological treatment, so the use of Electroconvulsive Therapy is dismissed. Total remission of symptoms and subsequent functional recovery ad integrum was observed, being evaluated through clinical interview, Hamilton Depression Rating Scale, Bush-Francis Catatonia Rating Scale and Barthel Index. In addition, other case reports on this comorbidity are reviewed, and unlike most of these, the favorable evolution of the patient stands out without the need for Electroconvulsive Therapy. The relationship between the two syndromes has not been elucidated, although some authors have proposed the hypothesis of shared neurobiological pathways and others have postulated the appearance of catatonic symptoms such as the progression of Cotard's Syndrome. To clarify these questions, more studies are needed in order to know the etiopathogenesis of this unusual combination.

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BACKGROUND: Ketamine's application in psychiatry have expanded, but it appears never to have been previously used to diagnose and treat patients with catatonia-like syndrome that occasionally present to emergency departments. CASE REPORT: A 23-year-old male was observed to suddenly stop talking. His ED GCS was 8 and had normal vital signs. While verbally unresponsive, he refused to open his eyes, demonstrated waxy flexibility of his arms, but the balance of his physical, neurological, and laboratory exams were normal. Strongly suspecting a catatonic state, they needed to rapidly confirm that diagnosis or begin evaluating him for potentially life-threatening non-psychiatric illnesses. Lacking other diagnostic modalities, they administered low-dose ketamine boluses. Ketamine 25 mg (1 mL) was diluted in 9 mL NS (2.5 mg/mL). Based on similar protocols, 1 mL of the solution (0.03 mg/Kg) was given intravenously every few minutes. After 12.5 mg ketamine, he was conscious and verbal. Subsequent history confirmed a prior episode requiring an extensive, non-productive medical evaluation. Psychiatry later confirmed the diagnosis. WHY SHOULD AN EMERGENCY PHYSICIAN BE AWARE OF THIS?: Patients with catatonia-like states pose a difficult diagnostic and therapeutic dilemma. Multiple interventions have been used with varying success. Optimal interventions provide a rapid resolution (or demonstrate that a psychiatric cause is not likely), be safe, encompass few contraindications, and be familiar to the clinician. In our patient, subanesthetic doses of ketamine fulfilled these criteria and successfully resolved the condition. If shown effective in other cases, ketamine would be a valuable addition to our psychiatric armamentarium.

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