Catatonia and cognition: exploring the cognitive dimensions of catatonia as an overlooked aspect of schizophrenia.
A systematic review

Vjekoslav Peitl1,2, Frane Paleka2, Dalibor Karlović1,2

1School of Medicine, Catholic University of Croatia, Zagreb, Croatia; 2Department of Psychiatry, Sestre Milosrdnice University Hospital Center, Zagreb, Croatia.

Summary. Background and objectives. Catatonia, a complex neuropsychiatric condition, is frequently linked to psychiatric illnesses, especially schizophrenia. While its motor and behavioral signs are well-recognized, cognitive deficits in catatonia are insufficiently studied. This systematic review investigates whether catatonia involves impairments in attention, executive functioning, and other cognitive areas, particularly in psychiatric conditions like schizophrenia. Methods. We performed a systematic literature review following PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) framework. We searched PubMed, Scopus, and BioMed Central using terms related to catatonia and DSM-5 (Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition) cognitive domains, including only studies that specifically assessed cognitive deficits in individuals with catatonia. Results. Thirty studies were included, consistently revealing cognitive deficits in catatonia, especially in schizophrenia patients, affecting memory, executive functioning, attention, and perceptual skills. These deficits may reflect mechanisms shared with broader schizophrenia-related cognitive challenges. Conclusions. Cognitive deficits in catatonia, often neglected, are significant in schizophrenia, emphasizing the necessity for regular cognitive evaluations and further neurobiological research to enhance diagnosis and therapeutic strategies.

Key words. Attention disorders, cognitive deficits, cognitive screening, neuropsychiatric syndrome, perceptual abilities, PRISMA Guidelines.

Catatonia e cognizione: esplorare le dimensioni cognitive della catatonia come aspetto trascurato della schizofrenia. Una revisione sistematica.

Riassunto. Introduzione e obiettivi. La catatonia, una condizione neuropsichiatrica complessa, è frequentemente associata a malattie psichiatriche, in particolare alla schizofrenia. Sebbene i suoi sintomi motori e comportamentali siano ben noti, i deficit cognitivi associati alla catatonia non sono sufficientemente studiati. Questa revisione sistematica indaga se la catatonia comporti compromissioni dell’attenzione, delle funzioni esecutive e di altre aree cognitive, in particolare in condizioni psichiatriche come la schizofrenia. Metodi. È stata condotta una revisione sistematica della letteratura seguendo il framework PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses). Sono state effettuate ricerche su PubMed, Scopus e BioMed Central utilizzando termini correlati alla catatonia e ai domini cognitivi del DSM-5 (Diagnostic and Statistical Manual of Mental Disorders, Quinta Edizione), includendo solo studi che hanno valutato specificamente i deficit cognitivi negli individui con catatonia. Risultati. Sono stati inclusi 30 studi, che hanno costantemente rivelato deficit cognitivi nella catatonia, soprattutto nei pazienti schizofrenici, che influenzano la memoria, le funzioni esecutive, l’attenzione e le capacità percettive. Questi deficit potrebbero riflettere meccanismi condivisi con le più ampie sfide cognitive correlate alla schizofrenia. Conclusioni. I deficit cognitivi nella catatonia, spesso trascurati, sono significativi nella schizofrenia, il che sottolinea la necessità di valutazioni cognitive regolari e di ulteriori ricerche neurobiologiche per migliorare la diagnosi e le strategie terapeutiche.

Parole chiave. Capacità percettive, deficit cognitivi, disturbi dell’attenzione, linee guida PRISMA, screening cognitivo, sindrome neuropsichiatrica.

Introduction

Catatonia is a neuropsychiatric disorder marked by abnormal behaviors, movements, and withdrawal1. It is frequently observed in individuals with mood disorders, but also in various neurological and psychotic conditions1. Initially described as a motor syndrome associated with epilepsy, tuberculosis, and affective disorders2,3, catatonia is often not diagnosed or treated promptly4. It typically results from another primary illness, most commonly psychiatric disorders such as schizophrenia, bipolar disorder, and major depressive disorder1. The condition presents with symptoms such as catalepsy, negativism, mutism, muscle rigidity, and mannerisms, often accompanied by fever and autonomic instability4,5.

Mood disorders like bipolar disorder and depression are frequently linked to catatonia1, while schizophrenia is the psychotic disorder most associated with it1,4. Historically, schizophrenia diagnoses were based on catatonic symptoms, though DSM-5 now separates the two conditions6. However, catatonic symptoms can also arise from other medical etiologies such as stroke, neoplasms, Parkinson’s disease, autoimmune disorders, metabolic conditions, and certain medications7,8. Disruptions in GABA, glutamate, serotonin, and dopamine neurotransmission are linked to the onset and progression of catatonic symptoms1,7.

Cognition involves mental actions or processes like using and acquiring knowledge9, with domains including memory, language, executive functions, attention, social cognition, and motor functions9. Cognitive deficits, defined as impairments in these domains, can be short-term or long-term10, while cognitive disorders, such as neurocognitive disorders, impair daily functioning6,10. These impairments vary in severity, with mild deficits often noticed by healthcare professionals and family members, while severe cases lead to reduced independence4,10. Aging is a primary risk factor, with Alzheimer’s disease being a well-known cause of cognitive impairment4,10.

Cognitive disorders such as delirium and major neurocognitive disorder (formerly dementia) are characterized by significant declines in cognitive abilities11-13. While neurocognitive disorders primarily affect older adults, they often present with memory loss, psychosis, agitation, and mood changes11-13.

In catatonia, cognitive impairments are challenging to assess due to the overlap with abnormal behaviors and movements1,5,14. Systematic evaluation often includes the Bush-Francis Catatonia Rating Scale (BFCRS)15, and the lorazepam challenge test helps confirm the diagnosis14,16. However, cognitive dysfunction is rarely assessed in standard evaluations17. The clock drawing test is a commonly used tool for quick assessment of cognitive status in catatonia18. Comprehensive evaluation often requires multiple tests, including neuropsychological evaluations, to accurately identify and plan treatment for cognitive impairments in catatonia19.

Cognitive deficits are a significant concern in chronic psychotic disorders, particularly schizophrenia, and are strong predictors of functional outcomes15,19. Similarly, in mood disorders such as bipolar disorder and major depressive disorder, cognitive impairments in domains like attention, memory, and executive functioning are prevalent and can worsen functional outcomes, particularly when catatonia is present. These deficits often persist beyond acute episodes, complicating recovery and treatment adherence15,19,20,21 Catatonia, when co-occurring with schizophrenia, complicates the clinical presentation and treatment due to the additional cognitive impairments, particularly in attention and executive functioning15,19. While some studies have shown improvements in cognitive functioning with antipsychotic treatments22, the effect of pharmacological interventions on cognitive outcomes remains unclear. Research into COMT polymorphisms, especially the Met/Met genotype, and the interaction with MTHFR, has shown promising associations with cognitive functions, suggesting COMT may be a potential cognitive biomarker in schizophrenia23.

Objective

The objective of the research is to investigate the relationship between catatonia and cognitive deficits in individuals diagnosed with catatonia.

Methods

A literature search was conducted according to the guidelines of Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA)24. Databases such as PubMed, Scopus, and BioMed Central were searched up to May 2024. Search terms were selected based on the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) classification of cognitive domains to standardize the evaluation of cognitive impairments in catatonia. The search combined “catatonia” with DSM-5 domain terms using the “AND” operator, including: cognition, cognitive impairment, perceptual-motor function, language, learning and memory, social cognition, executive functions, and complex attention.

Inclusion and exclusion criteria

Original papers (case reports, research, meta-analyses) were included if they: 1) examined cognitive impairments in individuals diagnosed with catatonia, 2) were published in English, and 3) appeared in peer-reviewed journals. No time limit was set for publication dates, and no restrictions applied to sample characteristics. Papers were excluded if they: lacked full-text access (n=528), did not specifically address cognitive deficits in catatonia (n=200), provided insufficient data on cognitive outcomes (n=80), or were only tangentially related to psychiatric disorders (n=44). Title and abstract filters were applied in PubMed and Scopus to enhance relevance.

Quality assessment

Data extraction was conducted independently by three authors, who reviewed and documented each study’s aims, methods, and findings. Quality was assessed manually, evaluating study design, sample size, data collection methods, and outcome reporting. Discrepancies were resolved through consensus, ensuring reliability without automation tools.

Search results and analysis

The search yielded 1,224 potentially relevant manuscripts (PubMed: 108, BioMed Central: 395, Scopus: 721). After removing 342 duplicates, 882 records remained. Title and abstract screening excluded 528 closed-access studies, leaving 354 full-text articles for eligibility assessment. Of these, 324 were excluded due to the reasons above, resulting in 30 studies included in the final analysis. The research strategy is detailed in figure 1.




Results

Our search strategy revealed a total of 1,224 potentially relevant manuscripts, from which 30 studies were ultimately included after applying inclusion and exclusion criteria. A complete overview of the search strategy and study selection process is provided in figure 1. Several studies demonstrated cognitive impairments in individuals diagnosed with catatonia, notably in domains such as memory, executive functioning, attention, and visuospatial abilities.

In total, 30 articles directly focusing on the relationship between catatonia and cognitive impairments were included in the analysis and are summarized across table 19,20,21,25-44 and table 21,4,5,9,10,45-47.







The studies are categorized based on whether the sample size was provided. Table 1 includes 22 studies with a clearly defined sample size, while table 2 presents 8 studies where the sample size was not specified.

Our search strategy identified 30 studies that met the inclusion criteria, as detailed in figure 1. These studies, summarized in table 1 and table 2, revealed cognitive impairments in catatonia across domains such as executive functions, attention, memory, and visuospatial abilities. Assessments commonly employed tools such as the Bush-Francis Catatonia Rating Scale15, clock drawing test18, Mini-Mental State Examination (MMSE), and Montreal Cognitive Assessment (MoCA), with research spanning Europe, the United States, and Asia. No demographic variables were set as inclusion criteria, allowing for a broad scope of participants. The studies predominantly focused on schizophrenia, with fewer exploring depression and other psychiatric disorders, and none were addressed somatic comorbidities in relation to catatonia.

Discussion

The relationship between catatonia and cognitive deficits in psychiatric patients, particularly those with schizophrenia, requires careful consideration due to the complex interplay between motor symptoms and cognitive impairments. Catatonia is defined as a psychomotor syndrome that frequently occurs in psychiatric patients, characterized by affective and neurological disturbances, exaggerated and bizarre movements, and immobility1,4,5. This paper has reviewed studies investigating the relationship between catatonia and cognitive deficits, highlighting the consistent presence of impairments in key cognitive domains such as attention, memory, executive functioning, and visuospatial abilities across conditions like schizophrenia, depression, and dementia. These findings align with prior literature, such as Walther et al.5, which emphasizes the neural mechanisms underlying catatonia, and Northoff19, who proposed deficits in top-down modulation as a key feature. Our review confirms that cognitive deficits are a pervasive feature of catatonia, often more pronounced in schizophrenia with a prevalence ranging from 9 to 32%48, and provides a comprehensive synthesis that strengthens the case for routine cognitive screening to address these overlooked impairments in clinical settings5,19.

Given the current gaps in assessment, we recommend implementing cognitive screening in cases of catatonia. This would enable clinicians to monitor therapeutic response more effectively and track improvements across specific cognitive domains, such as attention and executive functioning, using tools like the clock drawing test38 or Montreal Cognitive Assessment (MoCA) alongside the Bush-Francis Catatonia Rating Scale15. Such an approach would provide a more targeted evaluation of treatment effectiveness, allowing for a systematic focus on cognitive symptoms that may otherwise go unaddressed in standard clinical practice. Most studies show that patients diagnosed with catatonia are diagnosed with schizophrenia spectrum disorders or psychotic disorders4,5,9,25-30. Depression20,47 and bipolar disorder38,40 are also common. One study discusses the connection between frontotemporal dementia and catatonia, but the partial overlap of diagnostic criteria for these two conditions presents a limiting factor in assessment45.

Since catatonia is associated with frontal dysfunction, catatonic symptoms in frontotemporal dementia are not uncommon34. Research has also shown that catatonia can occur without a pre-existing psychiatric disorder or in the presence of neurological diseases or other health conditions42,45, such as autism41, autoimmune disorders46, or critical illness42. Some conditions where catatonia may appear include changes in the limbic system and anomalies in dopaminergic and GABAergic circuits that result in a lack of top-down modulation19. The most commonly investigated cognitive areas in the literature are executive functions, complex attention, perceptual functions, and visual-spatial abilities, as evidenced by our review of 30 studies summarized in table 1 and table 2. Studies with defined sample sizes (table 1), ranging from single cases such as Graziane et al.40 (n=1) to large cohorts such as Wing & Shah41 (n=969), offer robust evidence, while those without sample sizes (table 2) provide valuable insights but limit generalizability due to unreported participant numbers. This variability in sample size highlights the need for standardized reporting to better assess the prevalence and severity of cognitive impairments.

Research focused on behavioral mechanisms underlying catatonia in schizophrenia has shown specific differences in patients with catatonia who have and do not have a schizophrenia diagnosis. Differences were observed in the areas of intelligence, complex attention, executive, and perceptual functions19. Dean et al. conducted a study examining cognitive ability differences in patients with schizophrenia without catatonia, schizophrenia with catatonia, and healthy patients. They demonstrated that patients with schizophrenia have significantly lower scores in all areas of cognition compared to healthy patients, but patients with a history of catatonia showed significantly lower scores in the areas of language and executive functions30. In contrast, Northoff et al. reported no significant differences in executive function impairments among catatonic patients, irrespective of their psychiatric disorder status. However, catatonic patients showed distinct deficits in perceptual abilities compared to both psychiatric and healthy control groups and demonstrated significantly poorer performance in tasks involving complex attention32. Northoff et al. further demonstrated significantly lower regional cerebral perfusion in the right inferior prefrontal and parietal cortex in catatonia compared to other psychiatric patients and healthy controls, as well as poorer results in perceptual abilities related to right parietal function33. Docx et al. conducted a study on patients with medically stable schizophrenia but was unable to establish an association between test results in processing speed, executive functioning, complex attention, language, and memory35. Similarly, Kontaxaki et al. found that cognitive deficits in domains such as processing speed, executive functioning, attention, and memory were not correlated with clinical features like catatonia in schizophrenia spectrum disorders36. These discrepancies may reflect differences across conditions: schizophrenia-related catatonia may involve prefrontal and parietal dysfunction33, while depression-related catatonia, as seen in Starkstein et al.20 and Baker et al.47, shows greater memory and attention deficits, potentially linked to limbic alterations.

The brain structures affected by catatonia are not fully established, but most neuroimaging studies indicate dysfunction in the frontal and parietal cortex14. Studies on brain structure in schizophrenia patients with catatonia did not clearly show which brain structures are affected by catatonia. One study showed a cluster in the VII cerebellar lobule in catatonic patients, while another linked catatonia with the striatum, thalamus, cerebellum, and several cortical areas5,37. Northoff et al. highlighted a diffuse network of brain regions involved in catatonia, such as the cerebellum and parietal cortex, through functional brain imaging34. Contrary to this, Dean et al. tested gray matter volume in schizophrenia and catatonia, but their study did not prove abnormalities in brain volume and structures in patients with and without a schizophrenia diagnosis30. These inconsistencies, compounded by differences in assessment timing and tools, suggest that catatonia’s cognitive profile varies by condition and methodology, necessitating further research.

Golubovic´ et al.49 emphasize the importance of identifying risk factors for depression in patients with schizophrenia, such as poor social support, loneliness, and low socioeconomic status. These factors are strongly associated with the severity of depressive symptoms, which in turn complicate the clinical picture of schizophrenia by exacerbating cognitive deficits and reducing treatment adherence. Their findings underscore the need for early detection of these socio-environmental factors to prevent the onset of depressive symptomatology, which may further impair cognitive functions in affected individuals. This aligns with the broader understanding of catatonia and schizophrenia, where cognitive impairments and social isolation interplay to create a challenging clinical scenario that requires holistic management49. In depression, Baker et al. demonstrated through a case study that major depression and catatonia are associated with long-term memory and executive function impairments47, while Starkstein et al. found that 20% of depressed patients had catatonic symptoms, with more severe cognitive impairments compared to those without catatonia50. In dementia, Cahn-Weiner et al. reported that patients with Lewy body dementia were more prone to conceptual errors compared to Alzheimer’s and Parkinson’s diseases when assessed with the clock drawing test44. Mahgoub et al. linked catatonia with melancholia in major depressive disorder and bipolar disorder, noting overlapping symptoms like psychomotor retardation and perseveration21.

Despite these studies being conducted on patients with schizophrenia and catatonia, there are differences and variability in the obtained results. This can be explained by differences in data interpretation and the fact that authors used various instruments and scales for patient assessment. What is important to note is that the percentage of catatonic patients in the total investigated sample was much higher than the reported number of catatonic patients and varied from 9 to 32%, suggesting that in clinical practice more care should be taken about the presence of catatonia48. While some cases, like Baker et al.’s report of depression-related catatonia, indicate persistent deficits, most studies suggest variability rather than permanence, highlighting the need for cautious interpretation and longitudinal studies to explore recovery potential47.

Limitations

Despite the comprehensive nature of this review, several limitations must be acknowledged. First, the inconsistent reporting of sample sizes, particularly in studies from table 2 where participant numbers are often omitted48, reduces the ability to generalize findings compared to the more robust data in table 1. Second, the use of varied assessment tools, such as those seen in Medina et al.38 versus Docx et al.35, alongside differences in evaluation timing5,14, hinders direct comparisons across studies. Third, an overrepresentation of schizophrenia-related research4,5,9,25-30 may limit insights into cognitive deficits in other disorders like depression or neurological conditions45. Finally, the absence of longitudinal studies restricts conclusions about the duration or reversibility of cognitive impairments48, leaving significant gaps in understanding catatonia’s long-term impact. These issues underscore the need for standardized methodologies and broader research scopes in future investigations.

Conclusions

Despite significant research, the behavioral mechanisms of catatonia remain inadequately understood. Catatonia is marked by complex symptoms, including motor disturbances and cognitive dysfunctions, complicating psychiatric conditions like schizophrenia, bipolar disorder, and depression. These cognitive deficits, particularly in executive functions, attention, and memory, emphasize the need for a more comprehensive understanding of catatonia’s cognitive impact.

Historically, catatonia’s connection to cognitive deficits was recognized as early as Kahlbaum’s work in the 19th century. However, despite this longstanding awareness, systematic research exploring these links remains limited. Cognitive dysfunctions, although essential to diagnosis, are often overlooked during clinical assessments. While standardized diagnostic tools like the Bush-Francis Catatonia Rating Scale are crucial, they should be complemented by cognitive assessments, such as the clock-drawing test, to provide a fuller picture of the patient’s cognitive profile.

Future research should prioritize exploring the neurobiological mechanisms underlying these cognitive deficits to enhance diagnostic and therapeutic strategies for catatonia. Additionally, there is a pressing need for the development and implementation of cognitive screening tools specific to catatonia. Such tools would facilitate more accurate diagnosis, allow clinicians to monitor therapeutic responses across cognitive domains, and ultimately contribute to a more comprehensive, patient-centered approach to managing catatonia.

Conflict of interests: the authors declare no conflicts of interest related to the content or publication of this manuscript. All authors have reviewed and approved the final version of the manuscript, and there are no financial, personal, or professional interests that could influence the objectivity of this review.

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