European archives of psychiatry and clinical neuroscience · 2026
Frozen emotions, frozen bodies: a systematic review of limbic system alterations in catatonia.
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Marcolini Federica, Beghelli Valentina, Tartarini Damiano, Di Giacomo Valentina, Tempia Valenta Silvia, Mastellari Tomas, De Ronchi Diana, Atti Anna Rita
Аннотация
INTRODUCTION: Catatonia is a complex neuropsychiatric syndrome characterized by psychomotor and affective symptoms. While current neurobiological models have focused on cortical and cerebellar dysfunctions, the limbic system—crucial for emotional regulation and motivation—remains comparatively underexplored. Emerging evidence suggests that limbic abnormalities may contribute to the pathophysiology of catatonia, offering a more integrated understanding of its clinical manifestations.
AIMS: This systematic review aims to synthesize current evidence on neurobiological abnormalities within the limbic system in individuals with catatonia and to identify which structures may be implicated in symptom development.
METHODS: Following PRISMA guidelines, systematic searches were conducted across MEDLINE, Web of Science, PsycINFO, and Scopus without date restrictions. Eligible studies included patients with a codified catatonia diagnosis undergoing instrumental or biological investigations involving limbic structures. Data extraction covered study design, diagnostic criteria, limbic regions assessed, and neuroanatomical or functional findings.
RESULTS: A total of 1792 studies were identified through database searching, of which 54 full-text articles were assessed; 14 studies met the inclusion criteria and were included. Six additional studies were identified through reference screening, resulting in 20 included articles: 13 observational studies and seven case reports. Most investigations highlighted alterations in the anterior cingulate cortex, including abnormal gyrification, grey matter reduction, and perfusion changes associated with catatonic symptoms. Orbitofrontal cortex abnormalities—though not classically part of the limbic system—were also frequently reported. Evidence regarding other regions was heterogeneous and included volumetric abnormalities of the amygdala and hypothalamus, as well as genetic or acquired factors affecting limbic biochemical regulation.
CONCLUSIONS: This systematic review highlights the available neuroanatomical findings in patients with catatonia, supporting the involvement of limbic structures in the development and maintenance of this syndrome. However, variability in catatonia assessment, small sample sizes and study designs limit definitive conclusions. Future studies are needed to better understand the neural underpinnings of catatonia and inform treatment strategies.
AIMS: This systematic review aims to synthesize current evidence on neurobiological abnormalities within the limbic system in individuals with catatonia and to identify which structures may be implicated in symptom development.
METHODS: Following PRISMA guidelines, systematic searches were conducted across MEDLINE, Web of Science, PsycINFO, and Scopus without date restrictions. Eligible studies included patients with a codified catatonia diagnosis undergoing instrumental or biological investigations involving limbic structures. Data extraction covered study design, diagnostic criteria, limbic regions assessed, and neuroanatomical or functional findings.
RESULTS: A total of 1792 studies were identified through database searching, of which 54 full-text articles were assessed; 14 studies met the inclusion criteria and were included. Six additional studies were identified through reference screening, resulting in 20 included articles: 13 observational studies and seven case reports. Most investigations highlighted alterations in the anterior cingulate cortex, including abnormal gyrification, grey matter reduction, and perfusion changes associated with catatonic symptoms. Orbitofrontal cortex abnormalities—though not classically part of the limbic system—were also frequently reported. Evidence regarding other regions was heterogeneous and included volumetric abnormalities of the amygdala and hypothalamus, as well as genetic or acquired factors affecting limbic biochemical regulation.
CONCLUSIONS: This systematic review highlights the available neuroanatomical findings in patients with catatonia, supporting the involvement of limbic structures in the development and maintenance of this syndrome. However, variability in catatonia assessment, small sample sizes and study designs limit definitive conclusions. Future studies are needed to better understand the neural underpinnings of catatonia and inform treatment strategies.