How to Quickly Diagnose Catatonia, and a Farewell Salute to Max Fink, MD

We dedicate this editorial to Max Fink, MD, who died on June 15, 2025 at 102. Max was a paragon of psychiatry, an astute practitioner and researcher, prolific writer, fierce polemist, and advocate for electroconvulsive therapy (ECT), and generous mentor to younger colleagues, including both of us. Max was the strongest advocate for catatonia as an independent syndrome across many disorders and conditions, and inspired the making of The Catatonia Foundation, https://www.thecatatoniafoundation.org, a new organization established in 2022 by a parent in the aftermath of her daughter's significantly delayed catatonia diagnosis and lifesaving course of ECT in order to bring sorely needed awareness about catatonia and connect patients and families globally with treatment providers.

Max made several contributions to Acta Psychiatrica Scandinavica, including the 1996 papers [1, 2] establishing the Bush Francis Catatonia Rating Scale (BFCRS) and Bush Francis Catatonia Screening Instrument (BFCSI) as standards worldwide and promoting benzodiazepines (BZDs) and ECT as their primary treatments.

Almost 30 years later, Luccarelli et al. [3] have distilled a list of 4 catatonic symptoms (excitement, mutism, staring, and posturing) from the original 14-item BFCSI. The presence of only one of those four symptoms assures 97% sensitivity compared to the BFCSI. This makes the new screening instrument, coined the Catatonia Quick Screen (CQS) a perfect tool to improve recognition, diagnosis, and treatment of catatonia.

Catatonia has a storied history. Catatonia was likely first formally described in 16th century England by Phillip Barrough who wrote Of congelation or taking and mostly aptly commented upon the “lethargic” and “frenetic” poles of a disorder now recognized to often be characterized by both psychomotor agitation and retardation [4]. King Henry VI may have suffered from catatonia, with historians noting that he was unable to speak, walk or hold up his head after being informed of a military loss in Gascony in 1453, furthermore described as “smitten with a frenzy and his wit and reason withdrawn.” Catatonia may also have been present since the early days of humankind, with the potential for catatonia underscored in Lot's Wife, the Prophet Ezekiel and the unfortunate individuals who gazed upon Medusa and turned into stone [5]. Vagal intimations and the role of the fight, flight or freeze response in evolution further suggests that catatonia may be an intimate part of the human experience [6] and opens up new vistas on the role of psychological, traumatic, environmental, and social risk factors in catatonia [7].

The formal term catatonia was coined in 1874 by Kahlbaum [8] as a novel clinical entity with distinct motor, vocal, and behavioral symptoms that he observed in the Reimer Sanitarium in Gorlitz, then part of the Kingdom of Prussia and now part of modern-day Germany. Unfortunately, catatonia was quickly subsumed along with hebephrenia and paranoia into Emil Kraepelin's dementia praecox diagnosis and later Eugene Bleuler's schizophrenia. The fact that Kahlbaum's catatonic patients presented with more affective, neurological, or postencephalitic symptomology remained unknown for decades, possibly given that his manuscript was only translated into English in 1973. This led to over a century of erroneous blanket ascription of catatonia to schizophrenia until their official diagnostic divorce in the Diagnostic and Statistical Manual, fifth edition (DSM5) in 2013 [9]. The catatonia diagnosis was also a near casualty of the expectation that the advent of antipsychotic medications beginning with chlorpromazine in 1954 would herald the end of schizophrenia and psychosis. However, the clinical limits of antipsychotic medications were quickly recognized, along with the curious appearance of antipsychotic-induced motor, thermoregulatory, and cardiovascular disturbance, initially termed neuroleptic malignant syndrome and later recognized as a drug-induced form of malignant catatonia, a potentially lethal condition first identified by Stauder in 1934 [10].

A smattering of manuscripts had reported the presence of catatonia in pediatric patients by the end of the 20th century; in 2000, Wing and Shah [11] documented the presence of catatonia in up to 17% of adolescents and young adults with autism, then a relatively novel neurodevelopmental disorder of childhood whose incidence has skyrocketed in the Western world such that the Centers for Disease Control presently estimates that 1 in 32 US children carry an autism spectrum diagnosis.

Catatonia has quite literally crawled out of the clinical woodwork in the past quarter century, with current recognition of the myriad psychiatric, neurological, somatic medical, and drug-related etiologies of this disorder [12]. Catatonia has been recognized as a common comorbidity of anti-NMDA receptor encephalitis and other autoimmune encephalitides, echoing Kahlbaum's earliest reflections and raising questions surrounding the individual and tandem treatment roles of BZDs, ECT, and immunomodulatory therapies.

Catatonia has also been found in an ever-expanding group of neurodevelopmental disorders of discrete genetic etiology, including Phelan-McDermid, Down, Fragile X, Prader-Willi, and velocardiofacial syndromes, as well as SYNGAP-1, CACNA1C, SCN2A, mTOR, and MED13L variant syndromes where modern science is now able to identify precise physiological errors such as channelopathies and disturbances in synaptic communication. These specific genetic findings offer potential insight into the molecular pathology not only of catatonia but also of their associated developmental disturbances with great potential for future research and therapeutic impact.

Catatonia remains, however, underdiagnosed and undertreated. Why? The new CQS surely will make it easier to screen for catatonia. The high sensitivity provided by the presence of a single symptom attests to the validity of catatonia as a syndrome, that is, the strong tendency of catatonic symptoms to “hang together.” Will more screening lead to increased recognition and diagnosis, decreased mortality, decreased morbidity, faster recovery, better functional outcome, and more frequent early treatment with BZDs and ECT? That is the crux.

A thorny issue is the vilification of BZDs, especially in high doses, and ECT. These primary treatments for catatonia are often subject to complicated legal and administrative regulatory restrictions. Both treatments may also be frowned upon by colleagues and administrators and relegated to treatment of last resort. Limited access to ECT services is another obstacle, especially in youth and those with neurodevelopmental disability [13]. We find that the optimal implementation of the lorazepam challenge test in patients with suspected catatonia may require more education. A strongly positive response to lorazepam or another BZD strengthens the diagnosis of catatonia. However, a negative response to lorazepam or other BZDs does not exclude the diagnosis of catatonia; rather, it should prompt an ECT referral. More studies are needed to assess optimal doses of lorazepam, other BZDs, and zolpidem to be used in the BZD challenge test in catatonia.

Once catatonia is diagnosed, the pursuit of early and optimal treatment with BZDs and ECT is not for the faint of heart, requiring a deliberate and focused BZD challenge test and championing access to ECT. It is understandable that these hurdles can become intimidating for clinicians and invite procrastination to formally diagnose catatonia. We believe that these factors are still at play and that more education, research, and advocacy are needed to fully disclose the importance of catatonia.

The development and preliminary validation of a rapid screening tool such as the QCS is a stellar suggestion that can be considered akin to the mental health screening measures surrounding mood, suicidality, substance abuse, and safety that have become de rigueur for most medical visits across the lifespan. The QCS is quick, simple, and free and can accurately raise a radar and bring suffering patients one step closer to care. We look forward to its integration and widespread application into medical practice coupled with lessening resistance to BZD and ECT treatment for catatonia, and with more studies and hopefully novel treatments.

The authors declare no conflicts of interest.