Evidence map›Paper›PMID 36966063›Full record

ArticleSchizophrenia research2024

Molecular and immunological origins of catatonia.

Scott R Beach, James Luccarelli, Nathan Praschan, Mark Fusunyan, Gregory L Fricchione

Registry-linked trialOpen access · greenAbstract read
In one paragraph

Article in Schizophrenia research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT07315386 (Catatonic Syndrome in Adult Patients at Basurto Hospital), which is not on this map. Cited by 16 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 2 pooled it
4.7field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

NCT07315386 recruitingnot on this map

Catatonic Syndrome in Adult Patients at Basurto Hospital: A Descriptive Study of Incidence, Comorbidity, and Short-Term Outcomes

TypeobservationalSponsorBeatriz Rodriguez CaboRan2024 to 2030Enrolled40ConditionsCatatonia
3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Genetics of catatonia: a systematic review of case reports and a gene pathway analysis.European psychiatry : the journal of the Association of European Psychiatrists · 2025
    Pooled it
  3. Article
  4. Article
  5. Electrographic Features of Catatonia With or Without Comorbid Delirium.The Journal of neuropsychiatry and clinical neurosciences · 2026
    Article
  6. Article
  7. Article
  8. Difficult to Treat Catatonia: A Case Series.Indian journal of psychological medicine · 2025
    Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Catatonia.Nature reviews. Disease primers · 2024
    Review
  14. Review
  15. Article
  16. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Scott R BeachDepartment of Psychiatry, Massachusetts General Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA. Electronic address: Sbeach1@mgh.harvard.edu.
James LuccarelliDepartment of Psychiatry, Massachusetts General Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA.
Nathan PraschanDepartment of Psychiatry, Massachusetts General Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA.
Mark FusunyanDepartment of Psychiatry, Santa Clara Valley Medical Center, San Jose, CA, USA.
Gregory L FricchioneDepartment of Psychiatry, Massachusetts General Hospital, Boston, MA, USA; Harvard Medical School, Boston, MA, USA.
Massachusetts General Hospital · USHarvard University · USSanta Clara Valley Medical Center · US

Funding

Translational Neuroscience Training for CliniciansT32MH112485 · NIMH · MASSACHUSETTS GENERAL HOSPITAL · PI BUCKNER, RANDY L, ROFFMAN, JOSHUA LAWRENCE · 2018 to 2022
$1.7M
NIMH NIH HHS T32 MH112485
6 · The paper itself

Abstract

Catatonia occurs secondary to both primary psychiatric and neuromedical etiologies. Emerging evidence suggests possible linkages between causes of catatonia and neuroinflammation. These include obvious infectious and inflammatory etiologies, common neuromedical illnesses such as delirium, and psychiatric entities such as depression and autism-spectrum disorders. Symptoms of sickness behavior, thought to be a downstream effect of the cytokine response, are common in many of these etiologies and overlap significantly with symptoms of catatonia. Furthermore, there are syndromes that overlap with catatonia that some would consider variants, including neuroleptic malignant syndrome (NMS) and akinetic mutism, which may also have neuroinflammatory underpinnings. Low serum iron, a common finding in NMS and malignant catatonia, may be caused by the acute phase response. Cellular hits involving either pathogen-associated molecular patterns (PAMP) danger signals or the damage-associated molecular patterns (DAMP) danger signals of severe psychosocial stress may set the stage for a common pathway immunoactivation state that could lower the threshold for a catatonic state in susceptible individuals. Immunoactivation leading to dysfunction in the anterior cingulate cortex (ACC)/mid-cingulate cortex (MCC)/medial prefrontal cortex (mPFC)/paralimbic cortico-striato-thalamo-cortical (CSTC) circuit, involved in motivation and movement, may be particularly important in generating the motor and behavioral symptoms of catatonia.

Indexed as

CatatoniaNeuroleptic Malignant SyndromeHumansAkinetic mutismCatatoniaImmunoactivationInflammationNeuroleptic malignant syndrome

Identifiers

PMID36966063
PMCPMC10517087
OpenAlexW4360612877

What Socratic holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.