Epidemiological studies on catatonia encounter several methodological challenges, and as a result, the historical epoch and clinical context must be carefully considered when estimating its incidence and prevalence. Over the past 70 years, the reported incidence and prevalence of catatonia have significantly declined, influenced by several key historical developments, including the widespread use of antipsychotic medications, shifts in diagnostic criteria, advances in psychiatric care, and changes in the clinical recognition of the disorder. The reclassification of catatonic symptoms as antipsychotic-induced motor side effects, along with the decentralization of psychiatric care and shorter patient observation periods, contributed to this decline. This chapter explores the limitations of epidemiological research on catatonia, particularly regarding its prevalence across diverse patient populations. It provides a detailed analysis of catatonia’s incidence and prevalence in different epochs, various clinical settings, considering factors such as sex ratios, age distribution, ethnicity, and recurrence rates, supported by the most recent scientific evidence.

In addition to the international classification systems such as DSM-5 and ICD-11 discussed in earlier chapters of this book, we will now introduce three further diagnostic steps essential for diagnosing catatonia: (1) clinical rating scales, (2) the lorazepam challenge test, and (3) laboratory and neuroimaging work-up. This chapter will first present the widely used clinical rating scales for assessing catatonia, highlighting their advantages, limitations, and their role in scientific studies. While these scales are valuable tools, it is important to emphasize that clinical judgment remains crucial, as some catatonic symptoms may not be fully captured by these scales. Following this, we will explore the lorazepam challenge test, evaluating its diagnostic utility in light of current evidence. Lastly, the chapter will discuss the importance of laboratory and neuroimaging work-ups, including blood tests, lumbar puncture to examine cerebrospinal fluid, electroencephalogram, and magnetic resonance imaging, for both diagnosing catatonia and guiding therapeutic decisions.

This chapter explores the diverse therapeutic approaches to catatonia, integrating insights from both national and international guidelines. The primary treatment typically include benzodiazepines, such as lorazepam and diazepam, which are widely recognized for their efficacy in alleviating catatonic symptoms. Electroconvulsive therapy (ECT) remains a cornerstone for more severe, treatment-resistant and malignant cases (e.g. febrile catatonia), with recent evidence suggesting its effectiveness across various psychiatric populations, including children, adolescents, older adults, and patients with dementia. However, in cases of ultra-resistant catatonia – where up to 40% of patients do not respond to benzodiazepines or ECT – new treatment options such as intranasal esketamine are emerging, showing promise in cases unresponsive to conventional therapies. Additionally, treatments such as dopamine receptors antagonists and partial agonists (=antipsychotics) must be used with caution, particularly in cases of substance-induced catatonia, where they may exacerbate symptoms. Noninvasive brain stimulation techniques like repetitive transcranial magnetic stimulation and transcranial direct current stimulation are also gaining attention for their potential therapeutic benefits in catatonia, though further research is needed. Finally, the chapter underscores the importance of individualized treatment plans, carefully considering the underlying cause of catatonia to optimize outcomes and ensure the most effective intervention.

This chapter explores the psychopathological signs associated with catatonia, aiming to clarify their definitions and support these with clinical studies. We focus on the complex nature of catatonic signs by: (1) describing the wide range of signs, (2) explaining catatonia subtypes, (3) discussing the diagnostic challenges, (4) listing the possible differential diagnoses of catatonia, and finally (5) addressing serious health risks, including circulatory collapse, respiratory failure, and renal failure with their implications for clinical diagnosis and therapy. This comprehensive overview serves as a vital resource for clinicians, providing tools to accurately diagnose and effectively treat catatonia. By understanding the subtypes, differential diagnoses, and severe complications such as circulatory collapse and respiratory failure, clinicians can better identify life-threatening conditions and implement timely appropriate therapeutic interventions.

Over the past three decades, catatonia research has experienced a remarkable renaissance, driven by the application of diverse methodologies and conceptual frameworks. This renewed interest has significantly reshaped our understanding of catatonia, a complex syndrome with multifactorial origins spanning epidemiology, historical context, phenomenology, genetics, immunology, and neurobiology. These advancements have offered a more comprehensive and nuanced perspective, culminating in the recognition of catatonia as a distinct diagnosis in the ICD-11 – a landmark development that underscores its clinical and scientific relevance. Despite these strides, several unresolved issues remain that require future research. Bridging these gaps is crucial not only to enhance our understanding of catatonia but also to identify the most effective treatments and uncover the mechanisms underlying their efficacy. Such advancements hold the promise of developing improved diagnostic markers and tailored therapeutic strategies, offering significant benefits to patients affected by this challenging condition. In this chapter, we explore the profound implications of catatonia research, spanning its impact on clinical psychiatry and neuroscience, as well as its broader contributions to our understanding of the intricate relationship between the brain and mind.

Karl Ludwig Kahlbaum (1828–1899), a German psychiatrist, is widely recognized for his seminal work Catatonia or Tension Insanity, published 1874, in which he first conceptualized catatonia as a distinct psychomotor disorder. However, the observation of catatonic signs in the context of mental illness predates Kahlbaum’s formal classification. Understanding the history and development of different clinical concepts of catatonia before and after Kahlbaum is paramount for grasping the intricacies of current classification systems such as ICD-11 and DSM-5. Historical perspectives provide valuable insights into the evolution of diagnostic criteria and conceptualizations of catatonia over time, highlighting the diverse array of clinical presentations and the challenges inherent in defining and categorizing this complex syndrome. Further, by studying historical perspectives, clinicians and researchers gain insight into the diverse ways in which catatonia has been perceived, defined, and categorized throughout history. This chapter includes previous work on the topic of the history of catatonia as well as more recent systematic research in electronic historical archives. It addresses the origins of catatonic signs during the eighteenth century and how the concept of catatonia has been embedded in historical psychiatric literature of the nineteenth century.

Since the initial clinical delineation of catatonia in 1874, two distinct conceptual frameworks have emerged: one viewing catatonia as a psychomotor disorder, rooted in Kahlbaum’s legacy, and the other interpreting it as a primarily motor phenomenon, aligned with the perspectives of Kraepelin and Bleuler. This historical dichotomy is reflected in contemporary investigations into the pathophysiological mechanisms of catatonia. Neuroimaging studies utilizing motor and behavioral rating scales, such as the Bush-Francis Catatonia Rating Scale, have highlighted alterations in dopamine-mediated cortical and subcortical motor circuits – specifically the basal ganglia, supplementary motor area, primary motor cortex, and cerebellum – as key neuronal correlates of catatonia. In contrast, studies employing the Northoff Catatonia Rating Scale, a scale integrating affective, motor, and behavioral criteria within a psychomotor framework, have identified disruptions in higher-order frontoparietal networks, including the prefrontal, orbitofrontal, and primary motor cortices, as well as the limbic system. These networks appear to be dysregulated by imbalances in glutamatergic and gamma-aminobutyric acid transmission, underscoring the complex interplay between motor, affective, and cognitive domains in the pathophysiology of catatonia. This chapter introduces the pathophysiology of catatonia from a systemic (network-based) perspective, irrespective of its association with mental or medical disorders.

This chapter illustrates different psychopathological presentations, highlights key aspects crucial for catatonia management, explores the subjective experiences of catatonia patients, and proposes novel approaches to address various symptoms while deriving therapeutic options. We present five catatonia patients, four of them were treated at the Central Institute of Mental Health (CIMH) in Mannheim, Germany, by Dr. Hirjak, one patient was treated by Dr. Northoff at the Department of Psychiatry in Magdeburg, Germany. This chapter focuses on their catatonic and other psychopathological symptoms, subjective experiences, treatment outcomes, and follow-up assessments in the outpatient departments of CIMH and Magdeburg. The patient case examples are structured as follows: (1) introduction and background on the significance and relevance of the case, (2) case presentation, (3) treatment, (4) follow-up and outcomes, and (5) discussion. Patient examples, including statements from a first-person perspective, will be provided, and new clinical rating scales on the subjective experience of catatonia patients will be discussed.

Prognosis of catatonia has received little attention and remains an unsettled area of debate in clinical psychiatry. This chapter examines various outcome measures in catatonia patients and explores the associations between these outcomes and demographic, clinical, and neuropsychological variables. Both historical and contemporary studies are discussed, as they are crucial to understanding why catatonia should be recognized and treated in a timely manner. Historically, catatonia was linked to relatively favorable outcomes in some patients, while others experienced chronic symptoms or complications. Contemporary research further underscores the variability in prognosis depending on early recognition and intervention. This chapter is based on a narrative search of the scientific literature, providing a comprehensive view of catatonia prognosis and offering insights into factors that may influence recovery. Understanding these perspectives can aid clinicians in improving their approach to timely diagnosis and treatment, ultimately improving patient outcomes.

Since the initial description of catatonia in 1874, three different distinct clinical and neurobiological frameworks have emerged. The first emphasizes psychomotor and affective aspects, building on Karl Ludwig Kahlbaum’s legacy. The second focuses on motor symptoms alone, influenced by the work of Emil Kraepelin and Eugen Bleuler. The third introduces the Wernicke–Kleist–Leonhard concept of psychomotor abnormalities such as catatonia as a significant neuropsychiatric framework. This chapter critically examines all three frameworks from both scientific and clinical perspectives, highlighting their advantages and disadvantages in research and treatment. The chapter will also delve into common synergies between neurobiological and clinical studies, discussing how these can inform the day-to-day management of catatonia. Furthermore, we will analyze the current classification systems of DSM-5 and ICD-11 and their relation to the described frameworks, with a focus on their strengths and weaknesses in diagnosing catatonia. Finally, this chapter will introduce a novel approach that links neural correlates and subjective experience of catatonia through their spatial (space) and temporal (time) patterns. This chapter will provide a comprehensive overview of diagnostic approaches and their clinical implications.

In recent years, research has highlighted the significant role of the immune system in the pathophysiology of catatonia. Emerging evidence indicates that autoimmune encephalitis, such as anti-N-methyl-D-aspartate (anti-NMDA), anti-gamma-aminobutyric acid-A receptor (anti-GABA-AR), and anti-dopamine-2 receptor (anti-D2 R) encephalitis, plays a crucial role in the development of different movement disorders in general and catatonia in particular. In this chapter, we will present three of the most prominent forms of autoimmune encephalitis associated with catatonia depending on their frequency – anti-NMDA, anti-GABA-AR, and anti-D2 R encephalitis. These three neurotransmitter systems, glutamate, GABA, and dopamine, are essential for understanding the pathophysiology of catatonia. Given the rapidly evolving nature of research on autoimmune encephalitis, we aim to inform and sensitize clinicians about the potential association between catatonia (and its signs) and autoimmune encephalitides targeting pathophysiologically relevant neurotransmitters. Our goal is to equip clinicians with the latest findings to improve the recognition and treatment of catatonia in the context of these autoimmune conditions. Finally, we will present the most common red flags that can help identify encephalitis and catatonia early, while emphasizing the need for continued research to better understand the molecular mechanisms and improve treatment options for this complex condition.