{{Short description|Psychiatric behavioural syndrome}} {{About|the catatonic state}} {{Distinguish|Katatonia|cataplexy|catalepsy|Catalonia|Cataonia}} {{copy-paste|date=May 2026}} {{cs1 config|name-list-style=vanc}} {{Use dmy dates|date=February 2020}} {{Infobox medical condition | name = Catatonia | synonyms = Catatonic syndrome | image = Сatatonic stupor3.jpg | caption = A patient in catatonic stupor, 1914 | pronunciation = {{IPAc-en|ˌ|k|æ|t|ə|ˈ|t|oʊ|n|i|ə}} | field = Psychiatry, neurology | complications = Physical trauma, malignant catatonia (autonomic instability, life-threatening), dehydration, pneumonia, pressure ulcers due to immobility, muscle contractions, deep vein thrombosis (DVT)<ref name=Balaguer-Rivero2021>{{Cite journal |last1=Pérez-Balaguer |first1=Ana |last2=Sánchez-Rivero |first2=Irene |date=2021-12-22 |title=Electroconvulsive therapy, catatonia, deep vein thrombosis and anticoagulant treatment: a case report |journal=General Psychiatry |language=en |volume=34 |issue=6 |article-number=e100666 |doi=10.1136/gpsych-2021-100666 |issn=2517-729X |pmc=8705197 |pmid=35028525}}</ref> and pulmonary embolism (PE)<ref name=Balaguer-Rivero2021/> | onset = | duration = | causes = Underlying illness (psychiatric, neurologic, or medical), brain injury/damage, certain drugs/medications | risks = | diagnosis = Clinical, lorazepam challenge | differential = | prevention = | treatment = Benzodiazepines (lorazepam challenge), electroconvulsive therapy (ECT)<ref name=Balaguer-Rivero2021/> | prognosis = | medication = | frequency = | deaths = | alt = | symptoms = Immobility, mutism, staring, posturing, rigidity, low consciousness }}

'''Catatonia''' is a neuropsychiatric syndrome most commonly seen in people with underlying mood disorders such as major depressive disorder, or psychotic disorders such as schizophrenia.<ref name="Fink & Taylor 2009"/><ref name="Catatonia StatPearls"/> People with catatonia exhibit abnormal movement and behaviors that vary from person to person, and which may fluctuate in intensity within a single episode.<ref name="Heckers 2023"/>

People with catatonia appear withdrawn, with limited interaction with the outside world and difficulty processing information.<ref>{{Cite journal |last1=Edinoff |first1=Amber N. |last2=Kaufman |first2=Sarah E. |last3=Hollier |first3=Janice W. |last4=Virgen |first4=Celina G. |last5=Karam |first5=Christian A. |last6=Malone |first6=Garett W. |last7=Cornett |first7=Elyse M. |last8=Kaye |first8=Adam M. |last9=Kaye |first9=Alan D. |date=2021-11-08 |title=Catatonia: Clinical Overview of the Diagnosis, Treatment, and Clinical Challenges |journal=Neurology International |volume=13 |issue=4 |pages=570–586 |doi=10.3390/neurolint13040057 |doi-access=free |issn=2035-8385 |pmc=8628989 |pmid=34842777}}</ref> They may be nearly motionless for days on end or perform repetitive, purposeless movements. People may exhibit very different sets of behaviors and still be diagnosed with catatonia. Treatment with benzodiazepines or electroconvulsive therapy is most effective and leads to remission of symptoms in most cases.<ref name="Catatonia StatPearls" />

There are different subtypes of catatonia, which represent groups of symptoms that commonly occur together. These include stuporous/akinetic catatonia, excited catatonia, malignant catatonia, and periodic catatonia.<ref>{{Cite web |title=Catatonia treatment and prognosis |publisher=UpToDate |url=https://www.uptodate.com/contents/catatonia-treatment-and-prognosis |access-date=2024-11-22}}</ref>

Catatonia has historically been related to schizophrenia, but is most often seen in mood disorders.<ref name="Catatonia StatPearls"/> It is now known that catatonic symptoms are nonspecific and may occur in other mental, neurological, and medical conditions. The prognosis of catatonia is typically good, with complete remission in some patients; however, outcomes vary depending on the underlying disorder.<ref>{{Cite journal |last=Hirjak |first=Dusan |last2=Rogers |first2=Jonathan P. |last3=Wolf |first3=Robert Christian |last4=Kubera |first4=Katharina Maria |last5=Fritze |first5=Stefan |last6=Wilson |first6=Jo Ellen |last7=Sambataro |first7=Fabio |last8=Fricchione |first8=Gregory |last9=Meyer-Lindenberg |first9=Andreas |last10=Ungvari |first10=Gabor S. |last11=Northoff |first11=Georg |date=2024-07-18 |title=Catatonia |url=https://www.nature.com/articles/s41572-024-00534-w |journal=Nature Reviews Disease Primers |language=en |volume=10 |issue=1 |pages=49 |doi=10.1038/s41572-024-00534-w |issn=2056-676X|url-access=subscription }}</ref>

==Signs and symptoms== To properly diagnose catatonia, both the ICD-11 and DSM-5 require three or more of the symptoms defined in the table below. However, each person can have a different set of symptoms that may worsen, improve, and change in appearance throughout a single episode.<ref name="Heckers 2023">{{cite journal |last1=Heckers |first1=Stephan |last2=Walther |first2=Sebastian |date=9 November 2023 |title=Catatonia |journal=New England Journal of Medicine |volume=389 |issue=19 |pages=1797–1802 |doi=10.1056/NEJMra2116304 |pmid=37937779 |s2cid=265673511}}</ref> Symptoms may develop in varying amounts of time, presenting in hours, days, or even weeks.{{cn|date=April 2026}} {| class="wikitable" |+ !Symptom !Definition |- |Stupor |A marked lack of psychomotor activity; the individual appears immobile and unresponsive |- |Catalepsy |Passive induction of a posture held against gravity |- |Waxy flexibility |Slight resistance to positioning by the examiner, allowing limbs to remain in imposed positions |- |Mutism |Lack of verbal response despite apparent alertness |- |Negativism |Resistance or no response to external instructions or stimulus |- |Posturing |Voluntary assumption of inappropriate or bizarre postures |- |Mannerism |Odd, exaggerated movements or behaviors |- |Stereotypy |Repetitive, non-goal-directed movements or gestures |- |Agitation |Restlessness or excessive motor activity without external stimulus |- |Grimacing |Facial contortions or expressions unrelated to emotional context |- |Echolalia |Mimicking or repeating another person's speech |- |Echopraxia |Mimicking or imitating another person's movements |} Because most patients with catatonia have an underlying psychiatric illness, the majority will present with worsening depression, mania, or psychosis, followed by catatonia symptoms.<ref name="Catatonia StatPearls">{{cite book |last1=Burrow |first1=Jeffrey P. |url=https://www.ncbi.nlm.nih.gov/books/NBK430842/ |title=StatPearls |last2=Spurling |first2=Benjamin C. |last3=Marwaha |first3=Raman |date=2022 |publisher=StatPearls Publishing |chapter=Catatonia |pmid=28613592}}</ref> Even when they are unable to interact, patients presenting with catatonia should not be assumed to be unaware of their surroundings, as some can recall their catatonic state and their actions in detail.<ref name="Rasmussen Mazurek Rosebush 2016">{{cite journal |last1=Rasmussen |first1=Sean A |last2=Mazurek |first2=Michael F |last3=Rosebush |first3=Patricia I |date=2016-12-22 |title=Catatonia: Our current understanding of its diagnosis, treatment and pathophysiology |journal=World Journal of Psychiatry |volume=6 |issue=4 |pages=391–8 |doi=10.5498/wjp.v6.i4.391 |pmc=5183991 |pmid=28078203 |doi-access=free}}</ref>

<gallery> File:Image from page 110 of "Mental medicine and nursing - for use in training-schools for nurses and in medical classes and a ready reference for the general practitioner" (1915).jpg| File:Image from page 219 of "A treatise on mental diseases" (1900).jpg| File:Image from page 719 of "Diseases of the nervous system - a text-book of neurology and psychiatry" (1915).jpg| </gallery> === Subtypes === There are several subtypes of catatonia recognized: stuporous catatonia, excited catatonia, malignant catatonia, and periodic catatonia. Subtypes are defined by the group of symptoms and associated features that a person is experiencing or displaying. Although catatonia can be divided into subtypes, its presentation is often dynamic, and the same individual may exhibit different subtypes at different times.<ref>{{Cite book |last1=Shorter |first1=Edward |url=https://books.google.com/books?id=K_tdDwAAQBAJ&q=fink+catatonia+%22alternation%22&pg=PA119 |title=The Madness of Fear: A History of Catatonia |last2=Fink |first2=Max |date=2018 |publisher=Oxford University Press |isbn=978-0-19-088119-1 |language=en}}</ref>

'''Stuporous catatonia''' is characterized by immobility, mutism, and a lack of response to the world around them.<ref name="Fink & Taylor 2009">{{cite journal |last1=Fink |first1=Max |last2=Taylor |first2=Michael Alan |date=1 November 2009 |title=The Catatonia Syndrome: Forgotten but Not Gone |journal=Archives of General Psychiatry |volume=66 |issue=11 |pages=1173–7 |doi=10.1001/archgenpsychiatry.2009.141 |pmid=19884605}}</ref><ref name="Catatonia StatPearls"/> They may appear frozen in one position for long periods of time unable to eat, drink, or speak.

'''Excited catatonia''' is characterized by odd mannerisms and gestures, purposeless or inappropriate actions, excessive motor activity, restlessness, stereotypy, impulsivity, agitation, and combativeness. Patients suffering from excited catatonia may have speech and actions that are repetitive or mimic another person's.<ref name="Fink & Taylor 2009"/><ref name="Catatonia StatPearls"/><ref name="Rasmussen Mazurek Rosebush 2016"/> This state is often characterized by hyperactivity, and the patient may have delusions and hallucinations.<ref>{{cite book |last1=Nolen-Hoeksema |first1=Susan |title=Abnormal Psychology |date=2014 |publisher=McGraw-Hill Education |isbn=978-1-259-06072-4 |page=224}}</ref>

'''Malignant catatonia''' is characterized by fever, dramatic and rapid changes in blood pressure, increased heart rate and respiratory rate, and excessive sweating.<ref name="Fink & Taylor 2009"/><ref name="Catatonia StatPearls"/> This condition is life-threatening, and the patient's laboratory tests may come back abnormal.{{cn|date=April 2026}}

'''Periodic catatonia''' is characterized by a person having recurrent episodes of catatonia. Individuals will experience multiple episodes over time, with no signs of catatonia between episodes. Historically, the Wernicke-Kleist-Leonhard school considered periodic catatonia a distinct form of "non-system schizophrenia", characterized by recurrent acute phases with hyperkinetic and akinetic features and often psychotic symptoms. There is also a residual state between these phases, characterized by low-level catatonic features and abulia of varying severity.{{cn|date=April 2026}}

== Causes == Catatonia develops in the presence of an underlying condition, including psychiatric and neurological disorders, other medical conditions, and substance use.

=== Neuropsychiatric === Mood disorders like bipolar disorder and clinical depression are the most common conditions underlying catatonia.<ref name="Catatonia StatPearls"/> Other psychiatric conditions that can cause catatonia include schizophrenia and other primary psychotic disorders,<ref name="Fink & Taylor">{{cite book |last1=Fink |first1=Max |title=Catatonia: A Clinician's Guide to Diagnosis and Treatment |last2=Taylor |first2=Michael Alan |date=2003 |publisher=Cambridge University Press |isbn=978-0-521-82226-8}}{{page needed|date=June 2022}}</ref> autism spectrum disorder, ADHD,<ref>{{cite book |last1=Dhossche |first1=Dirk Marcel |last2=Rout |first2=Ujjwal |chapter=Are Autistic and Catatonic Regression Related? A Few Working Hypotheses Involving Gaba, Purkinje Cell Survival, Neurogenesis, and ECT |title=International Review of Neurobiology |date=2006 |volume=72 |pages=55–79 |doi=10.1016/S0074-7742(05)72004-3 |pmid=16697291 |isbn=978-0-12-366873-8}}</ref> and post-traumatic stress disorder.<ref>{{Cite journal |last1=Ahmed |first1=Gellan K. |last2=Elbeh |first2=Khaled |last3=Karim |first3=Ahmed A. |last4=Khedr |first4=Eman M. |date=2021 |title=Case Report: Catatonia Associated With Post-traumatic Stress Disorder |journal=Frontiers in Psychiatry |volume=12 |article-number=740436 |doi=10.3389/fpsyt.2021.740436 |doi-access=free |issn=1664-0640 |pmc=8688766 |pmid=34950066}}</ref>

Psychodynamic theorists have historically interpreted catatonia as a psychological defense against the potentially destructive consequences of responsibility, with the passivity of the disorder providing relief.<ref>{{Cite book |last=Arieti |first=Silvano |title=Interpretation of schizophrenia |date=1994 |publisher=Jason Aronson |isbn=1-56821-209-7 |oclc=472906047}}</ref>

=== Other conditions === Catatonia is also seen in many medical disorders, including encephalitis, meningitis, autoimmune disorders,<ref name=Rogers19>{{cite journal |last1=Rogers |first1=Jonathan P |last2=Pollak |first2=Thomas A |last3=Blackman |first3=Graham |last4=David |first4=Anthony S |date=July 2019 |title=Catatonia and the immune system: a review |journal=The Lancet Psychiatry |volume=6 |issue=7 |pages=620–630 |doi=10.1016/S2215-0366(19)30190-7 |pmc=7185541 |pmid=31196793}}</ref> focal neurological lesions (including strokes),<ref>{{cite journal |last1=Haroche |first1=Alexandre |last2=Rogers |first2=Jonathan |last3=Plaze |first3=Marion |last4=Gaillard |first4=Raphaël |last5=Williams |first5=Steve CR |last6=Thomas |first6=Pierre |last7=Amad |first7=Ali |date=July 2020 |title=Brain imaging in catatonia: systematic review and directions for future research |url=https://discovery.ucl.ac.uk/id/eprint/10110277/ |journal=Psychological Medicine |volume=50 |issue=10 |pages=1585–97 |doi=10.1017/S0033291720001853 |pmid=32539902 |s2cid=219704600}}</ref> alcohol withdrawal,<ref name="Geoffroy-2012">{{cite journal |last1=Geoffroy |first1=Pierre Alexis |last2=Rolland |first2=Benjamin |last3=Cottencin |first3=Olivier |date=1 May 2012 |title=Catatonia and Alcohol Withdrawal: A Complex and Underestimated Syndrome |journal=Alcohol and Alcoholism |volume=47 |issue=3 |pages=288–290 |doi=10.1093/alcalc/agr170 |pmid=22278315 |doi-access=free}}</ref> abrupt or overly rapid benzodiazepine withdrawal,<ref>{{cite journal |author=Rosebush PI |author2=Mazurek MF |date=August 1996 |title=Catatonia after benzodiazepine withdrawal |journal=Journal of Clinical Psychopharmacology |volume=16 |issue=4 |pages=315–9 |doi=10.1097/00004714-199608000-00007 |pmid=8835707}}</ref><ref>{{cite journal |vauthors=Deuschle M, Lederbogen F |date=January 2001 |title=Benzodiazepine withdrawal-induced catatonia |journal=Pharmacopsychiatry |volume=34 |issue=1 |pages=41–42 |doi=10.1055/s-2001-15188 |pmid=11229621 |s2cid=260241781}}</ref><ref>{{cite journal |vauthors=Kanemoto K, Miyamoto T, Abe R |date=September 1999 |title=Ictal catatonia as a manifestation of de novo absence status epilepticus following benzodiazepine withdrawal |journal=Seizure |volume=8 |issue=6 |pages=364–6 |doi=10.1053/seiz.1999.0309 |pmid=10512781 |s2cid=17454162 |doi-access=free}}</ref> cerebrovascular disease, neoplasms, head injury,<ref name="DSM-5-introduction">{{Cite book |last=American Psychiatric Association |url=https://archive.org/details/diagnosticstatis0005unse/page/119 |title=Diagnostic and Statistical Manual of Mental Disorders |publisher=American Psychiatric Publishing |year=2013 |isbn=978-0-89042-555-8 |edition=Fifth |location=Arlington, VA |pages=[https://archive.org/details/diagnosticstatis0005unse/page/119 119–121]}}</ref> and some metabolic conditions (e.g.,homocystinuria, diabetic ketoacidosis, hepatic encephalopathy, and hypercalcaemia).<ref name="DSM-5-introduction"/>

==== Neurological ==== Catatonia can occur due to several neurological conditions. For instance, certain types of encephalitis can cause catatonia. Anti-NMDA receptor encephalitis is a form of autoimmune encephalitis known to cause catatonia, albeit very rarely. Additionally, encephalitic catatonia has been reported in cases of severe HIV and herpes simplex virus infections. A small amount of evidence suggests that catatonia can develop after traumatic brain injury in the absence of a primary psychiatric disorder.<ref>{{Cite journal |last1=Berthelot |first1=Jessica |last2=Cambre |first2=Jacob |last3=Erwin |first3=Madeline |last4=Phan |first4=Jennifer |date=2024-03-06 |editor-last=Inada |editor-first=Toshiya |title=Catatonia as a Result of a Traumatic Brain Injury |journal=Case Reports in Psychiatry |language=en |volume=2024 |pages=1–3 |doi=10.1155/2024/5184741 |doi-access=free |issn=2090-6838 |pmc=10937075 |pmid=38482162}}</ref> Similarly, there are several case reports of catatonia after a stroke, with some having catatonia-associated symptoms that were unexplainable by stroke itself and which improved after treatment with benzodiazepines.<ref>{{Cite journal |last1=Koprucki |first1=Shawna |last2=Morcos |first2=Roy |date=2024-09-18 |title=Acute Catatonia Following a Cerebellar Stroke: A Case Report |journal=Cureus |volume=16 |issue=9 |article-number=e69645 |language=en |doi=10.7759/cureus.69645 |doi-access=free |issn=2168-8184 |pmc=11488475 |pmid=39429282}}</ref><ref>{{Cite journal |last1=Hasan |first1=H. |last2=Abdo |first2=M. |last3=Rabei |first3=S. |date=March 2023 |title=Post Cerebrovascular Stroke Catatonic Psychosis: A Case Report |journal=European Psychiatry |language=en |volume=66 |issue=S1 |pages=S1058 |doi=10.1192/j.eurpsy.2023.2245 |issn=0924-9338 |pmc=10479261}}</ref> Parkinson's disease can cause catatonia for some people by impairing their ability to produce and secrete dopamine, a neurotransmitter which is thought to contribute to motor dysfunction in people with catatonia.

==== Metabolic and endocrine ==== Abnormal thyroid function may result in the development of catatonia when the thyroid overproduces (hyperthyroidism) or underproduces thyroid hormones (hypothyroidism). This is thought to occur due to the impact of thyroid hormones on metabolism, including in the cells of the nervous system. Abnormal electrolyte levels have also been shown to cause catatonia in rare cases. Most notably, low blood sodium levels can cause catatonia in some people.<ref>{{Cite journal |last1=McGuire |first1=Eimear |last2=Yohanathan |first2=Mythily |last3=Lally |first3=Leona |last4=McCarthy |first4=Geraldine |date=2017-07-14 |title=Hyponatraemia-associated catatonia |journal=BMJ Case Reports |language=en |pages=bcr–2017–219487 |doi=10.1136/bcr-2017-219487 |issn=1757-790X |pmc=5534696 |pmid=28710304}}</ref><ref>{{Cite journal |last1=Peritogiannis |first1=Vaios |last2=Rizos |first2=Dimitrios V. |date=2021-05-24 |title=Catatonia Associated with Hyponatremia: Case Report and Brief Review of the Literature |url=https://clinical-practice-and-epidemiology-in-mental-health.com/VOLUME/17/PAGE/26/ |journal=Clinical Practice & Epidemiology in Mental Health |language=en |volume=17 |issue=1 |pages=26–30 |doi=10.2174/1745017902117010026 |issn=1745-0179 |pmc=8227445 |pmid=34249136}}</ref><ref>{{Cite journal |last1=Mehta |first1=Vishal |last2=Sharma |first2=Akhya |last3=Sharma |first3=Chandra Bhushan |last4=Guria |first4=Rishi Tuhin |date=December 2021 |title=Cerebral Salt Wasting Induced Hyponatraemia Presenting as Catatonia |url=https://journals.sagepub.com/doi/10.4997/jrcpe.2021.413 |journal=Journal of the Royal College of Physicians of Edinburgh |language=en |volume=51 |issue=4 |pages=377–9 |doi=10.4997/jrcpe.2021.413 |pmid=34882138 |issn=1478-2715|url-access=subscription}}</ref><ref>{{Cite journal |last1=Krueger |first1=Anna |last2=Shebak |first2=Shady S. |last3=Kavuru |first3=Bush |date=2015-11-12 |title=Catatonia in the Setting of Hyponatremia |url=https://www.psychiatrist.com/pcc/catatonia-setting-hyponatremia/ |journal=The Primary Care Companion for CNS Disorders |language=English |volume=17 |issue=6 |page=26803 |doi=10.4088/PCC.15l01808 |pmid=27057405 |pmc=4805406 |issn=2155-7780}}</ref>

==== Infectious ==== Certain infections are known to cause catatonia, either by directly impairing brain function or by increasing a person's susceptibility to other diseases that can do so. HIV and AIDS can cause catatonia by predisposing one to infections in the brain, including different types of viral encephalitis.<ref>{{Cite journal |last1=Volkow |first1=N D |last2=Harper |first2=A |last3=Munnisteri |first3=D |last4=Clother |first4=J |date=1987-01-01 |title=AIDS and catatonia. |journal=Journal of Neurology, Neurosurgery & Psychiatry |language=en |volume=50 |issue=1 |page=104 |doi=10.1136/jnnp.50.1.104-a |issn=0022-3050 |pmc=1033262 |pmid=3819740}}</ref><ref>{{Cite journal |last1=Hisamoto |first1=Yoshimi |last2=Gabriel |first2=Genevieve |last3=Verma |first3=Sonam |last4=Karakas |first4=Cemal |last5=Chari |first5=Geetha |date=2017-04-18 |title=Catatonia as a rare manifestation of HIV associated psychosis in adolescents. (P6.208) |url=https://www.neurology.org/doi/10.1212/WNL.88.16_supplement.P6.208 |journal=Neurology |language=en |volume=88 |issue=16_supplement |article-number=P6.208 |doi=10.1212/WNL.88.16_supplement.P6.208 |issn=0028-3878|url-access=subscription}}</ref> ''Borrelia burgdorferi'' causes Lyme disease, which has been shown to cause catatonia by infecting the brain and causing encephalitis.<ref name=Rogers19/><ref>{{Cite journal |last1=Pfister |first1=H.-W. |last2=Preac-Mursic |first2=V. |last3=Wilske |first3=B. |last4=Rieder |first4=G. |last5=Förderreuther |first5=S. |last6=Schmidt |first6=S. |last7=Kapfhammer |first7=H.-P. |date=February 1993 |title=Catatonic syndrome in acute severe encephalitis due to Borrelia burgdorferi infection |url=https://www.neurology.org/doi/10.1212/WNL.43.2.433 |journal=Neurology |language=en |volume=43 |issue=2 |pages=433–5 |doi=10.1212/WNL.43.2.433 |pmid=8437717 |issn=0028-3878|url-access=subscription}}</ref><ref>{{Cite journal |last1=Neumärker |first1=K. J. |last2=Dudeck |first2=U. |last3=Plaza |first3=P. |date=February 1989 |title=[Borrelia encephalitis and catatonia in adolescence] |journal=Der Nervenarzt |volume=60 |issue=2 |pages=115–9 |issn=0028-2804 |pmid=2716930}}</ref><ref>{{Cite journal |last1=Ford |first1=Lenzie |last2=Tufts |first2=Danielle M. |date=2021-06-15 |title=Lyme Neuroborreliosis: Mechanisms of B. burgdorferi Infection of the Nervous System |journal=Brain Sciences |volume=11 |issue=6 |page=789 |doi=10.3390/brainsci11060789 |doi-access=free |issn=2076-3425 |pmc=8232152 |pmid=34203671}}</ref>

=== Medications === Disulfiram, a drug used to treat alcoholism, can cause catatonia. It is theorized that the medication can cause alterations in dopamine metabolism, as it blocks dopamine beta-hydroxylase. Additionally, phencyclidine, corticosteroids, and antipsychotics, among other drugs, are known to cause catatonia.<ref>{{Cite book |url=https://books.google.com/books?id=4cPp3Uj_xlYC |title=Catatonia: From Psychopathology to Neurobiology |date=3 May 2007 |publisher=American Psychiatric Pub |isbn=978-1-58562-712-7 |editor-last=Carrof |editor-first=Stanley N. |pages=133–136 |editor-last2=Mann |editor-first2=Stephan C. |editor-last3=Francis |editor-first3=Andrew |editor-last4=Fricchione |editor-first4=Gregory L.}}</ref>

== Pathogenesis == The mechanisms underlying brain catatonia are poorly understood.<ref name="Rasmussen Mazurek Rosebush 2016"/><ref>{{cite journal |last1=Walther |first1=Sebastian |last2=Stegmayer |first2=Katharina |last3=Wilson |first3=Jo Ellen |last4=Heckers |first4=Stephan |title=Structure and neural mechanisms of catatonia |journal=The Lancet Psychiatry |date=July 2019 |volume=6 |issue=7 |pages=610–9 |doi=10.1016/S2215-0366(18)30474-7 |pmid=31196794 |pmc=6790975}}</ref> Currently, there are two main categories of explanations for the brain pathology of catatonia. The first is a disruption of normal neurotransmitter production or release in certain brain areas, preventing normal cognitive function and leading to behavioral and motor symptoms associated with catatonia.<ref>{{Cite web |title=Sage Journals: Discover world-class research |url=https://journals.sagepub.com/action/cookieAbsent |access-date=2026-04-05 |website=Sage Journals |language=en |doi=10.12788/acp.0116}}</ref> The second claims that disruption of communication between different areas of the brain causes catatonia.<ref>{{Cite web |title=Sage Journals: Discover world-class research |url=https://journals.sagepub.com/action/cookieAbsent |access-date=2026-04-05 |website=Sage Journals |language=en |doi=10.1177/02698811231158232 |pmc=10101189 |pmid=37039129}}</ref>

=== Neurotransmitters === The neurotransmitters that are most strongly associated with catatonia are GABA, dopamine, and glutamate. GABA is the primary inhibitory neurotransmitter of the brain, meaning it slows down the activity of the systems it acts on. In catatonia, people have low levels of GABA, which causes them to be overly activated, especially in areas of the brain that normally inhibit activity. This is thought to cause the behavioral symptoms associated with catatonia, including withdrawal.<ref> Daniels J. Catatonia: Clinical Aspects and Neurobiological Correlates. The Journal of Neuropsychiatry and Clinical Neurosciences 2009;21:371–80. https://doi.org/10.1176/jnp.2009.21.4.371.‌</ref> Dopamine can increase or decrease the activity of the area of the brain it acts on, depending on where in the brain it is. Dopamine is lower than normal in people with catatonia, which is thought to cause many of the motor symptoms, because dopamine is the main neurotransmitter that activates the parts of the brain responsible for movement.<ref name="Rasmussen Mazurek Rosebush 2016"/> Glutamate is an excitatory neurotransmitter, meaning that it increases the activity of the areas of the brain it acts on. Notably, glutamate tells the neuron it acts on to fire by binding to the NMDA receptor. People with anti-NMDA receptor encephalitis can develop catatonia because their antibodies attack the NMDA receptor, reducing the brain's ability to activate different areas through glutamate.<ref> {{Cite journal |last=Rogers |first=Jonathan P. |last2=Pollak |first2=Thomas A. |last3=Blackman |first3=Graham |last4=David |first4=Anthony S. |date=2019-07-01 |title=Catatonia and the immune system: a review |url=https://www.thelancet.com/journals/lanpsy/article/PIIS2215-0366(19)30190-7/fulltext |journal=The Lancet Psychiatry |language=English |volume=6 |issue=7 |pages=620–630 |doi=10.1016/S2215-0366(19)30190-7 |issn=2215-0366 |pmid=31196793|pmc=7185541 }}</ref>

=== Neurological pathways === Several brain pathways have been studied, and they seem to contribute to catatonia when they are not functioning properly.<ref>{{cite journal |last1=Dhossche |first1=Dirk M. |last2=Stoppelbein |first2=Laura |last3=Rout |first3=Ujjwal K. |date=December 2010 |title=Etiopathogenesis of Catatonia: Generalizations and Working Hypotheses |journal=The Journal of ECT |volume=26 |issue=4 |pages=253–8 |doi=10.1097/YCT.0b013e3181fbf96d |pmid=21076339}}</ref> However, these studies were unable to determine if the abnormalities they observed were the cause of catatonia or if the catatonia caused the abnormalities. Furthermore, it has been hypothesized that pathways connecting the basal ganglia with the cortex and thalamus are involved in the development of catatonia.<ref>{{cite journal |last1=Northoff |first1=Georg |title=What catatonia can tell us about 'top-down modulation': A neuropsychiatric hypothesis |journal=Behavioral and Brain Sciences |date=October 2002 |volume=25 |issue=5 |pages=555–577 |doi=10.1017/s0140525x02000109 |pmid=12958742 |s2cid=20407002}}</ref>

==Diagnosis== Catatonia is diagnosed when a person exhibits at least three key symptoms simultaneously.

These can include: * not moving or speaking (stupor or mutism) * unusual body positions * repeating words or actions * sudden restlessness * other, less common symptoms<ref name="Smith Holmes 2023">{{Cite journal |last1=Smith |first1=Alyssa C. |last2=Holmes |first2=Emily G. |date=2023-12-01 |title=Catatonia: A Narrative Review for Hospitalists |journal=American Journal of Medicine Open |volume=10 |article-number=100059 |doi=10.1016/j.ajmo.2023.100059 |doi-access=free|pmid=39035239 |issn=2667-0364|pmc=11256243 }}</ref>

The DSM-5 and ICD-11, global manuals for mental health conditions, describe catatonia and its various types. Catatonia can occur with other mental illnesses, like depression or schizophrenia. It may also be a reaction to certain drugs or a medical condition. While often linked to psychiatric disorders, about one in five cases of catatonia are due to medical conditions.<ref>{{Cite journal |last1=Rogers |first1=Jonathan P |last2=Zandi |first2=Michael S |last3=David |first3=Anthony S |date=May 2023 |title=The diagnosis and treatment of catatonia |journal=Clinical Medicine |language=en |volume=23 |issue=3 |pages=242–245 |doi=10.7861/clinmed.2023-0113 |pmc=11046566 |pmid=37236789}}</ref>

There is not a definitive consensus regarding diagnostic criteria. In the fifth edition of the American Psychiatric Association's ''Diagnostic and Statistical Manual of Mental Disorders'' (DSM-5, 2013) and the eleventh edition of the World Health Organization's ''International Classification of Diseases (''ICD-11, 2022), the classification is more homogeneous than in earlier editions. Prominent researchers in the field have other suggestions for diagnostic criteria.<ref>{{Cite book|last=Fink|first=Max|title=Catatonia: a clinician's guide to diagnosis and treatment|date=2003|publisher=Cambridge University Press|others=Michael Alan Taylor|isbn=0-511-06198-6|location=Cambridge|oclc=57254202}}{{page needed|date=August 2022}}</ref> Still, diagnosing catatonia can be challenging. Evidence suggests that there is as high as a 15-day average delay to diagnosis for people with catatonia.

===DSM-5 ===

The DSM-5 does not classify catatonia as an independent disorder. Instead, it classifies it as:

* catatonia associated with another mental disorder * due to another medical condition * unspecified catatonia.<ref name="DS">{{Cite book |last=American Psychiatric Association |title=Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision |publisher=American Psychiatric Association |year=2022 |isbn=978-0-89042-575-6 |location=Washington, DC |doi=10.1176/appi.books.9780890425787|s2cid= 249488050}}</ref><ref>{{cite book|last1=Jeste|first1=Dilip V. |last2=Lieberman|first2=Jeffrey A.|last3=Benson|first3=R Scott|last4=Young|first4=Melinda L.|last5=Akaka|first5=Jeffrey|last6=Bernstein|first6=Carol A.|last7=Crowley|first7=Brian|last8=Everett|first8=Anita S|last9=Geller|first9=Jeffrey|last10=Graff|first10=Mark David|last11=Greene|first11=James A.|last12=Kashtan|first12=Judith F.|last13=Mcvoy|first13=Molly K.|last14=Nininger|first14=James E.|last15=Oldham|first15=John M.|last16=Schatzberg|first16=Alan F.|last17=Widge|first17=Alik S.|last18=Vanderlip|first18=Erik R.|url=https://archive.org/details/dsm-5_202110/mode/2up |title=Diagnostic and Statistical Manual of Mental Disorders Fifth Edition DSM-5<sup><sup><small>TM</small></sup></sup> |date=2013|publisher=American Psychiatric Association |access-date=8 December 2023 |quote=}}</ref> {{Rp|pages=134–5}}

Diagnosis requires the presence of '''three or more''' of the following twelve psychomotor symptoms in association with a mental disorder, medical condition, or unspecified:<ref name="DS"/>{{Rp|pages=|page=135}} * stupor: absence of psycho-motor activity; not actively relating to the environment * catalepsy: passive induction of a posture held against gravity * waxy flexibility: maintaining positions imposed by the examiner * mutism: minimal or absent verbal response (not due to aphasia) * negativism: resistance or lack of response to instructions or external stimuli * posturing: spontaneous and active maintenance of a posture against gravity * mannerisms: odd or exaggerated caricatures of normal actions * stereotypy: repetitive, abnormally frequent, non-goal-directed movements * agitation: excessive activity not influenced by external stimuli * grimacing: sustained facial expression * echolalia: mimicking another's speech * echopraxia: mimicking another's movements

Other disorders (additional code 293.89 [F06.1] to indicate the presence of the co-morbid catatonia): * Catatonia associated with autism spectrum disorder<ref name="DS"/>{{Rp|pages=|page=57}} * Catatonia associated with schizophrenia spectrum and other psychotic disorders ** Catatonia associated with brief psychotic disorder<ref name="DS"/>{{Rp|pages=|page=109}} ** Catatonia associated with schizophreniform disorder<ref name="DS"/>{{Rp|pages=|page=111}} ** Catatonia associated with schizoaffective disorder<ref name="DS"/>{{Rp|pages=|page=121}} ** Catatonia associated with a substance-induced psychotic disorder * Catatonia associated with bipolar and related disorders<ref name="DS"/>{{Rp|pages=|page=142}} * Catatonia associated with major depressive disorder<ref name="DS"/>{{Rp|pages=|page=185}} * Catatonic disorder due to another medical condition<ref name="DS"/>{{Rp|pages=136–7}}

If catatonic symptoms are present but do not form the catatonic syndrome, a medication- or substance-induced aetiology should be considered first.<ref name="DSM-5Differential">{{cite book |author=Michael B. First |title=DSM-5® Handbook of Differential Diagnosis |url=https://books.google.com/books?id=haOvBAAAQBAJ&pg=PA49 |date=2013 |publisher=American Psychiatric Publishing |isbn=978-1-58562-998-5 |page=49}}</ref>

===ICD-11===

The ICD-11 defines catatonia as a syndrome of psychomotor disturbances, characterized by the co-occurrence of several symptoms such as stupor, catalepsy, waxy flexibility, mutism, negativism, posturing, mannerisms, stereotypies, psychomotor agitation, grimacing, echolalia, and echopraxia. Catatonia may occur in the context of specific mental disorders, including mood disorders, schizophrenia or other primary psychotic disorders, and neurodevelopmental disorders. It may also be induced by psychoactive substances, including medications, or caused by a medical condition not classified under mental, behavioral, or neurodevelopmental disorders. {| class="wikitable" |+Table 1: '''DSM-5 vs. ICD-11criteria:''' !Features !DSM-5 (2013) !ICD-11 (2022) |- |Status of catatonia |Not an independent disorder; specified with another condition |Recognized as a syndrome that can occur across disorders |- |Required symptoms |≥3 of 12 psychomotor features |Several psychomotor features occurring simultaneously |- |Associated conditions |Mental disorders, medical conditions, unspecified |Mood disorders, schizophrenia, neurodevelopmental disorders, substance use, or medical conditions |}

=== Assessment and physical examination === Catatonia is often overlooked and under-diagnosed.<ref name="Serra-Mestres & Jaimes-Albornoz 2018" /> Most patients present with an underlying psychiatric disorder, which can obscure recognition of catatonia. For example, psychotic symptoms may dominate the clinical picture, while classic catatonic features (such as mutism or posturing) are absent. Motor abnormalities can also be misleading; in mania, increased motor activity is typically goal-directed, whereas in excited catatonia, activity is non–goal-directed and repetitive.<ref name="Catatonia StatPearls" /> Careful observation of motor behavior is therefore crucial for diagnosis.

Catatonia remains a clinical diagnosis with no specific laboratory test to diagnose it. However, supportive investigations may help identify underlying causes:

* EEG: usually shows diffuse slowing; can detect seizure activity if present * CT or MRI: do not demonstrate catatonia directly, but may reveal structural or metabolic causes * Laboratory tests (metabolic panels, inflammatory markers, autoantibodies): can identify reversible medical contributors<ref name="Catatonia StatPearls" />

Vital signs should be frequently monitored as catatonia can progress to malignant catatonia, which is a life-threatening condition characterized by fever, hypertension, tachycardia, and tachypnea.<ref name="Catatonia StatPearls" />

===Rating scale=== Several rating instruments have been developed, but their utility in clinical practice remains debated .<ref>{{cite journal |last1=Sienaert |first1=Pascal |last2=Rooseleer |first2=Jonas |last3=De Fruyt |first3=Jürgen |title=Measuring catatonia: A systematic review of rating scales |journal=Journal of Affective Disorders |date=December 2011 |volume=135 |issue=1–3 |pages=1–9 |doi=10.1016/j.jad.2011.02.012 |pmid=21420736}}</ref> The most commonly used scale is the '''Bush-Francis Catatonia Rating Scale (BFCRS)'''.<ref>{{cite journal |last1=Bush |first1=G. |last2=Fink |first2=M. |last3=Petrides |first3=G. |last4=Dowling |first4=F. |last5=Francis |first5=A. |title=Catatonia. I. Rating scale and standardized examination |journal=Acta Psychiatrica Scandinavica |date=February 1996 |volume=93 |issue=2 |pages=129–136 |doi=10.1111/j.1600-0447.1996.tb09814.x |pmid=8686483 |s2cid=20752576}}</ref> The scale consists of 23 items. The first 14 serve as a screening tool; if 2 of the 14 are positive, this prompts for further evaluation and completion of the remaining 9 items.

Diagnostic certainty may also be supported by:

* lorazepam challenge<ref name="Sienaert Dhossche Vancampfort et al 2014">{{cite journal |last1=Sienaert |first1=Pascal |last2=Dhossche |first2=Dirk M. |last3=Vancampfort |first3=Davy |last4=De Hert |first4=Marc |last5=Gazdag |first5=Gábor |title=A Clinical Review of the Treatment of Catatonia |journal=Frontiers in Psychiatry |date=9 December 2014 |volume=5 |page=181 |doi=10.3389/fpsyt.2014.00181 |pmid=25538636 |pmc=4260674 |doi-access=free}}</ref> * zolpidem challenge<ref>{{cite journal |title=Catatonia in French Psychiatry: Implications of the Zolpidem Challenge Test |journal=Psychiatric Annals |date=January 2007 |volume=37 |issue=1 |pages=00485713–20070101–02 |article-number=00485713-20070101-02 |doi=10.3928/00485713-20070101-02}}</ref>

Historically, barbiturates were used, but today benzodiazepines and electroconvulsive therapy (ECT) are the main options chosen for treatment.{{cn|date=April 2026}}

=== Laboratory findings === Laboratory abnormalities are most relevant in malignant catatonia rather that in other forms of catatonia, and may include:

* elevated creatine kinase * leukocytosis * low serum iron

These findings overlap with neuroleptic malignant syndrome (NMS). Therefore, it is essential to make careful correlation with clinical history, medications, and physical findings.{{cn|date=April 2026}} {| class="wikitable" |+Table 2: Malignant catatonia vs. neuroleptic malignant syndrome (NMS) !Feature !Malignant catatonia !NMS |- |Trigger |Spontaneous or due to psychiatric illness |Typically after antipsychotics (esp. first-gen) |- |Motor |Posturing, stereotypy, echolalia possible |Rigidity, tremor |- |Labs |↑ CK, leukocytosis, low iron (variable) |↑ CK, leukocytosis, low iron (more consistent) |- |Treatment |Benzodiazepines, ECT |Stop antipsychotics, supportive care, benzodiazepines |}

=== Differential diagnosis === Because catatonia overlaps with many psychiatric and neurological conditions a careful and detailed history, medication review, and physical exam are key to diagnosing catatonia and differentiating it from other conditions. Furthermore, some of these conditions can themselves lead to catatonia. The differential diagnosis is as follows: * Neuroleptic malignant syndrome (NMS) and catatonia are both life-threatening conditions that share many of the same characteristics including fever, autonomic instability, rigidity, and delirium.<ref name="Neuroleptic Malignant Syndrome StatPearls">{{cite book |last1=Simon |first1=Leslie V. |last2=Hashmi |first2=Muhammad F. |last3=Callahan |first3=Avery L. |title=StatPearls |date=2022 |publisher=StatPearls Publishing |url=https://www.ncbi.nlm.nih.gov/books/NBK482282/ |chapter=Neuroleptic Malignant Syndrome |pmid=29489248}}</ref> Lab values of low serum iron, elevated creatine kinase, and white blood cell count are also shared by the two disorders, further complicating the diagnosis. There are features of malignant catatonia (posturing, impulsivity, etc.) that are absent from NMS and the lab results are not as consistent in malignant catatonia as they are in NMS. Some experts consider NMS to be a drug-induced condition associated with antipsychotics, particularly first generation antipsychotics,<ref name="Neuroleptic Malignant Syndrome StatPearls"/> but it has not been established as a subtype.<ref>{{cite journal |last1=Northoff |first1=G. |title=Catatonia and neuroleptic malignant syndrome: psychopathology and pathophysiology |journal=Journal of Neural Transmission |date=1 December 2002 |volume=109 |issue=12 |pages=1453–67 |doi=10.1007/s00702-002-0762-z |pmid=12486486 |s2cid=12971112 |citeseerx=10.1.1.464.9266}}</ref> Therefore, discontinuing antipsychotics and starting benzodiazepines is a treatment for this condition, and similarly it is helpful in catatonia as well. (See table 2 above). * Anti-NMDA receptor encephalitis is an autoimmune disorder characterized by neuropsychiatric features and the presence of IgG antibodies.<ref name="Anti-NMDA Receptor Encephalitis StatPearls">{{cite book |last1=Samanta |first1=Debopam |last2=Lui |first2=Forshing |title=StatPearls |date=2022 |publisher=StatPearls Publishing |url=https://www.ncbi.nlm.nih.gov/books/NBK551672/ |chapter=Anti-NMDA Receptor Encephalitis |pmid=31869136}}</ref> The presentation of anti-NMDA encephalitis has been categorized into 5 phases: ** prodromal phase. ** psychotic phase. ** unresponsive phase. ** hyperkinetic phase. ** recovery phase. The psychotic phase progresses into the unresponsive phase characterized by mutism, decreased motor activity, and catatonia.<ref name="Anti-NMDA Receptor Encephalitis StatPearls" /> * serotonin syndrome: Triggered by serotonergic drugs (ex: SSRI); features include delirium, hyperreflexia, myoclonus, GI symptoms (N/V/D), autonomic instability, hyperthermia, and rigidity.<ref>{{Cite journal|last1=Foong|first1=Ai-Leng|last2=Grindrod|first2=Kelly A.|last3=Patel|first3=Tejal|last4=Kellar|first4=Jamie|author2-link=Kelly Grindrod|date=October 2018|title=Demystifying serotonin syndrome (or serotonin toxicity)|journal=Canadian Family Physician|volume=64|issue=10|pages=720–7 |pmc=6184959|pmid=30315014}}</ref> * Malignant hyperthermia: A hereditary disorder of skeletal muscle, triggered by anesthetics or muscle relaxants like succinylcholine.; associated with metabolic acidosis, hyperkalemia, and arrhythmias.<ref>{{cite book |last1=Watt |first1=Stacey |last2=McAllister |first2=Russell K. |title=StatPearls |date=2022 |publisher=StatPearls Publishing |url=https://www.ncbi.nlm.nih.gov/books/NBK430828/ |chapter=Malignant Hyperthermia |pmid=28613578}}</ref> * Akinetic mutism is a neurological disorder associated with structural damage in a variety of brain, it is characterized by immobility and mutism but intact awareness; lacks echolalia/echopraxia. Furthermore, it is unresponsive to benzodiazepines.<ref>{{cite journal |last1=Arnts |first1=Hisse |last2=van Erp |first2=Willemijn S. |last3=Lavrijsen |first3=Jan C.M. |last4=van Gaal |first4=Simon |last5=Groenewegen |first5=Henk J. |last6=van den Munckhof |first6=Pepijn |title=On the pathophysiology and treatment of akinetic mutism |journal=Neuroscience & Biobehavioral Reviews |date=May 2020 |volume=112 |pages=270–8 |doi=10.1016/j.neubiorev.2020.02.006 |pmid=32044373 |doi-access=free |hdl=11245.1/c438b878-4d5b-4f13-887c-7f01df095324 |hdl-access=free}}</ref> Patients may present with apathy, and may seem indifferent to pain, hunger, or thirst.<ref>{{cite journal |last1=Ackermann |first1=H. |last2=Ziegler |first2=W. |title=Akinetischer Mutismus – eine Literaturübersicht |journal=Fortschritte der Neurologie · Psychiatrie |date=February 1995 |volume=63 |issue=2 |pages=59–67 |doi=10.1055/s-2007-996603 |pmid=7705740 |s2cid=260156218}}</ref> * Selective mutism has an anxious etiology but has also been associated with personality disorders.<ref>{{cite journal |last1=Holka-Pokorska |first1=Justyna |last2=Piróg-Balcerzak |first2=Agnieszka |last3=Jarema |first3=Marek |title=The controversy around the diagnosis of selective mutism – a critical analysis of three cases in the light of modern research and diagnostic criteria |journal=Psychiatria Polska |date=30 April 2018 |volume=52 |issue=2 |pages=323–343 |doi=10.12740/PP/76088 |pmid=29975370 |doi-access=free}}</ref> Patients with this disorder fail to speak with some individuals but will speak with others. Likewise, they may refuse to speak in certain situations; in another word it is anxiety-driven; speech restriction limited to certain contexts, without catatonic signs. for example, a child who refuses to speak at school but is conversational at home. This disorder is distinguished from catatonia by the absence of any other signs/symptoms. * Nonconvulsive status epilepticus is seizure activity with no accompanying tonic-clonic movements.<ref>{{cite book |last1=Wylie |first1=Todd |last2=Sandhu |first2=Divyajot S. |last3=Murr |first3=Najib |title=StatPearls |date=2022 |publisher=StatPearls Publishing |url=https://www.ncbi.nlm.nih.gov/books/NBK430686/ |chapter=Status Epilepticus |pmid=28613459}}</ref> It can present with stupor, similar to catatonia, and they both respond to benzodiazepines. Nonconvulsive status epilepticus is diagnosed by the presence of seizure activity seen on electroencephalogram (EEG).<ref>{{cite journal |last1=Sutter |first1=Raoul |last2=Kaplan |first2=Peter W. |title=Electroencephalographic criteria for nonconvulsive status epilepticus: Synopsis and comprehensive survey: EEG Criteria for NCSE |journal=Epilepsia |date=August 2012 |volume=53 |pages=1–51 |doi=10.1111/j.1528-1167.2012.03593.x |pmid=22862158 |s2cid=24014621}}</ref> Catatonia, on the other hand, is associated with normal EEG or diffuse slowing. * Delirium is characterized by fluctuating disturbed perception and consciousness in the ill individual.<ref>{{cite book |title=Delirium: prevention, diagnosis and management |series=National Institute for Health and Care Excellence: Guidelines |date=2019 |publisher=National Institute for Health and Care Excellence (NICE) |isbn=978-1-4731-2992-4 |url=https://www.ncbi.nlm.nih.gov/books/NBK553009/ |pmid=31971702}}</ref> It has hypoactive and hyperactive or mixed forms. People with hyperactive delirium present similarly to those with excited catatonia and have symptoms of restlessness, agitation, and aggression. Those with hypoactive delirium present with similarly to stuporous catatonia, withdrawn and quiet. However, catatonia also includes other distinguishing features including posturing and rigidity as well as a positive response to benzodiazepines. * Patients with locked-in syndrome present with immobility and mutism; however, unlike patients with catatonia who are unmotivated to communicate, patients with locked-in syndrome try to communicate with eye movements and blinking. Furthermore, locked-in syndrome is caused by damage to the brainstem.<ref>{{cite book |last1=M Das |first1=Joe |last2=Anosike |first2=Kingsley |last3=Asuncion |first3=Ria Monica D. |title=StatPearls |date=2022 |publisher=StatPearls Publishing |url=https://www.ncbi.nlm.nih.gov/books/NBK559026/ |chapter=Locked-in Syndrome |pmid=32644452}}</ref> * Stiff-person syndrome and catatonia are similar in that they may both present with rigidity, autonomic instability, and a positive response to benzodiazepines.<ref>{{cite journal |last1=Balint |first1=Bettina |last2=Meinck |first2=Hans-Michael |title=Pragmatic Treatment of Stiff Person Spectrum Disorders: Pragmatic Treatment of SPSD |journal=Movement Disorders Clinical Practice |date=July 2018 |volume=5 |issue=4 |pages=394–401 |doi=10.1002/mdc3.12629 |pmid=30363317 |pmc=6174384}}</ref> However, stiff-person syndrome may be associated with anti-glutamic acid decarboxylase (anti-GAD) antibodies<ref>{{cite journal |last1=Baizabal-Carvallo |first1=José Fidel |last2=Jankovic |first2=Joseph |title=Stiff-person syndrome: insights into a complex autoimmune disorder |journal=Journal of Neurology, Neurosurgery & Psychiatry |date=August 2015 |volume=86 |issue=8 |pages=840–8 |doi=10.1136/jnnp-2014-309201 |pmid=25511790 |s2cid=19981869}}</ref><ref>{{cite journal |last1=Sarva |first1=Harini |last2=Deik |first2=Andres |last3=Ullah |first3=Aman |last4=Severt |first4=William L. |title=Clinical Spectrum of Stiff Person Syndrome: A Review of Recent Reports |journal=Tremor and Other Hyperkinetic Movements |date=4 March 2016 |volume=6 |page=340 |doi=10.7916/D85M65GD |pmid=26989571 |pmc=4790195}}</ref> and other catatonic signs such as mutism and posturing are not part of the syndrome. * Untreated late-stage Parkinson's disease may present similarly to stuporous catatonia with symptoms of immobility, rigidity, and difficulty speaking. Further complicating the diagnosis is the fact that many patients with Parkinson's disease will have major depressive disorder, which may be the underlying cause of catatonia. Parkinson's disease can be distinguished from catatonia by a positive response to levodopa. Catatonia, on the other hand, will show a positive response to benzodiazepines. * Extrapyramidal side effects of antipsychotic medication, especially dystonia and akathisia, can be difficult to distinguish from catatonic symptoms, or may confound them in the psychiatric setting. Extrapyramidal motor disorders usually do not involve social symptoms like negativism, while individuals with catatonic excitement typically do not have the physically painful compulsion to move that is seen in akathisia.<ref name="Rasmussen Mazurek Rosebush 2016"/> * Certain stimming behaviors and stress responses in individuals with autism spectrum disorders can present similarly to catatonia. In autism spectrum disorders, chronic catatonia is distinguished by a lasting deterioration of adaptive skills from the background of pre-existing autistic symptomatology that cannot be easily explained. Acute catatonia is usually clearly distinguishable from autistic symptoms.<ref name="Vaquerizo-Serrano Salazar De Pablo Singh Santosh 2022">{{cite journal |last1=Vaquerizo-Serrano |first1=J. |last2=Salazar De Pablo |first2=G. |last3=Singh |first3=J. |last4=Santosh |first4=P. |date=2022 |title=Catatonia in autism spectrum disorders: A systematic review and meta-analysis |journal=European Psychiatry |volume=65 |issue=1 |pages=e4 |doi=10.1192/j.eurpsy.2021.2259 |pmc=8792870 |pmid=34906264}}</ref> * The diagnostic entities of obsessional slowness and psychogenic parkinsonism show overlapping features with catatonia, such as motor slowness, gegenhalten (oppositional paratonia), mannerisms, and reduced or absent speech. However, psychogenic parkinsonism involves tremor which is unusual in catatonia.<ref>{{cite book |doi=10.1016/B978-0-12-801772-2.00022-9 |chapter=Psychogenic (Functional) parkinsonism |title=Functional Neurologic Disorders |series=Handbook of Clinical Neurology |year=2016 |last1=Thenganatt |first1=M.A. |last2=Jankovic |first2=J. |volume=139 |pages=259–262 |pmid=27719845 |isbn=978-0-12-801772-2}}</ref> Obsessional slowness is a controversial diagnosis, with presentations ranging from severe but common manifestations of obsessive compulsive disorder to catatonia.<ref>{{cite journal |last1=Ganos |first1=Christos |last2=Kassavetis |first2=Panagiotis |last3=Cerdan |first3=Maria |last4=Erro |first4=Roberto |last5=Balint |first5=Bettina |last6=Price |first6=Gary |last7=Edwards |first7=Mark J. |last8=Bhatia |first8=Kailash P. |title=Revisiting the Syndrome of "Obsessional Slowness" |journal=Movement Disorders Clinical Practice |date=June 2015 |volume=2 |issue=2 |pages=163–9 |doi=10.1002/mdc3.12140 |pmid=30713890 |pmc=6353487 |s2cid=73414098}}</ref> * Down syndrome disintegrative disorder (or Down Syndrome Regression Disorder, DSDD / DSRD) is a chronic condition characterized by loss of previously acquired adaptive, cognitive and social functioning occurring in persons with Down syndrome, usually during adolescence or early adulthood. The clinical picture is variable, but often includes catatonic signs, which is why it was called "catatonic psychosis" in initial reports in 1946.<ref>{{cite journal|pmid=32471843 |date=2020 |last1=Rosso |first1=M. |last2=Fremion |first2=E. |last3=Santoro |first3=S. L. |last4=Oreskovic |first4=N. M. |last5=Chitnis |first5=T. |last6=Skotko |first6=B. G. |last7=Santoro |first7=J. D. |title=Down Syndrome Disintegrative Disorder: A Clinical Regression Syndrome of Increasing Importance |journal=Pediatrics |volume=145 |issue=6 |pages=e20192939 |doi=10.1542/peds.2019-2939 |s2cid=219104019 |doi-access=free}}</ref> DSDD seems to phenotypically overlap with obsessional slowness (see above)<ref>{{cite web |first=B. |last=Chicoine |title=Obsessional Slowness |date=December 2022 |publisher=Adult Down Syndrome Center, Advocate Medical Group |url=https://adscresources.advocatehealth.com/resources/obsessional-slowness/#:~:text=The%20persistent%20stress%20of%20the%20rapidly%20moving%20environment,slowness%2C%20which%20we%20have%20also%20labeled%20%E2%80%9CThe%20Pace.%E2%80%9D;}}</ref> and catatonia-like regression occurring in ASD.<ref>{{cite journal|pmid=31959555 |date=2020 |last1=Lyons |first1=A. |last2=Allen |first2=N. M. |last3=Flanagan |first3=O. |last4=Cahalane |first4=D. |title=Catatonia as a feature of down syndrome: An under-recognised entity? |journal=European Journal of Paediatric Neurology |volume=25 |pages=187–190 |doi=10.1016/j.ejpn.2020.01.005 |s2cid=210841869 |doi-access=free}}</ref>

==Treatment==

Treatment is most effective when it is early and aggressive.<ref name="Sienaert Dhossche Vancampfort et al 2014"/> Patients may face issues such as poor nutrition, infections, and skin breakdown. Immobility can lead to pressure ulcers, muscle contractions, and the formation of blood clots in the legs (deep vein thrombosis) and the lungs (pulmonary embolism). Other complications also include the development of pneumonia and neuroleptic malignant syndrome.<ref name="Catatonia StatPearls" /><ref name="CC">{{Cite journal |last1=Clinebell |first1=Kimberly |last2=Azzam |first2=Pierre N. |last3=Gopalan |first3=Priya |last4=Haskett |first4=Roger |date=2014-06-15 |title=Guidelines for Preventing Common Medical Complications of Catatonia: Case Report and Literature Review |url=https://www.psychiatrist.com/jcp/guidelines-preventing-common-medical-complications |journal=The Journal of Clinical Psychiatry |volume=75 |issue=6 |pages=644–651 |doi=10.4088/JCP.13r08870 |pmid=25004188 |issn=0160-6689}}</ref><ref name=Balaguer-Rivero2021/><ref name="EB">{{Cite journal |last1=Rogers |first1=Jonathan P. |last2=Oldham |first2=Mark A. |last3=Fricchione |first3=Gregory |last4=Northoff |first4=Georg |last5=Ellen Wilson |first5=Jo |last6=Mann |first6=Stephan C. |last7=Francis |first7=Andrew |last8=Wieck |first8=Angelika |last9=Elizabeth Wachtel |first9=Lee |last10=Lewis |first10=Glyn |last11=Grover |first11=Sandeep |last12=Hirjak |first12=Dusan |last13=Ahuja |first13=Niraj |last14=Zandi |first14=Michael S. |last15=Young |first15=Allan H. |date=April 2023 |title=Evidence-based consensus guidelines for the management of catatonia: Recommendations from the British Association for Psychopharmacology |journal=Journal of Psychopharmacology |volume=37 |issue=4 |pages=327–369 |doi=10.1177/02698811231158232 |issn=1461-7285 |pmc=10101189 |pmid=37039129}}</ref><ref name="Smith Holmes 2023"/>

The first choice of treatment for catatonia is benzodiazepines, particularly lorazepam, which may be used as a diagnostic tool via the "lorazepam challenge". Patients are given a dose of lorazepam and their condition monitored; if there is an improvement within minutes, catatonia is likely. Patients who require a rapid response or do not respond to benzodiazepines may undergo a course of electroconvulsive therapy.<ref name="Sienaert Dhossche Vancampfort et al 2014"/> This has been shown to produce favorable response rates, particularly in patients with malignant catatonia, and often succeeds where medication does not.<ref>{{cite journal |last1=Hawkins |first1=John M |last2=Archer |first2=Katharine J |last3=Strakowski |first3=Stephen M |last4=Keck |first4=Paul E |title=Somatic Treatment of Catatonia |journal=The International Journal of Psychiatry in Medicine |date=December 1995 |volume=25 |issue=4 |pages=345–369 |doi=10.2190/X0FF-VU7G-QQP7-L5V7}}</ref>

Catatonia may be caused by external factors such as medical problems, side effects of certain medications, and psychiatric disorders such as depression and schizophrenia. The cause can affect treatment and outcomes: for example, catatonia associated with schizophrenia may respond less effectively to benzodiazepines.<ref name="Catatonia StatPearls"/><ref>{{cite journal |last1=Rosebush |first1=Patricia I |last2=Mazurek |first2=Michael F |title=Catatonia and Its Treatment |journal=Schizophrenia Bulletin |date=March 2010 |volume=36 |issue=2 |pages=239–242 |doi=10.1093/schbul/sbp141 |pmid=19969591 }}</ref>

== Prognosis ==

Twenty-five percent of psychiatric patients with catatonia will have more than one episode throughout their lives.<ref name="Heckers 2023"/> Treatment response for patients with catatonia is 50–70%, with treatment failure being associated with a poor prognosis. Many of these patients will require long-term and continuous mental health care. The prognosis for people with catatonia due to schizophrenia is much worse compared to other causes.<ref name="Catatonia StatPearls"/> In cases of malignant catatonia, the mortality rate is as high as 20%.<ref>{{cite journal |last1=Park |first1=Julia |last2=Tan |first2=Josh |last3=Krzeminski |first3=Sylvia |last4=Hazeghazam |first4=Maryam |last5=Bandlamuri |first5=Meghana |last6=Carlson |first6=Richard W |title=Malignant Catatonia Warrants Early Psychiatric-Critical Care Collaborative Management: Two Cases and Literature Review |journal=Case Reports in Critical Care |date=30 January 2017 |volume=2017 |issue=1 |pages=1–4 |doi=10.1155/2017/1951965 |doi-access=free |pmc=5303832 }}</ref>

== Epidemiology == Catatonia has been historically studied in psychiatric patients.<ref>{{cite book |title=Diagnostic and Statistical Manual of Mental Disorders |year=2022 |doi=10.1176/appi.books.9780890425787 |isbn=978-0-89042-578-7 |url=https://dsm.psychiatryonline.org/doi/book/10.1176/appi.books.9780890425787 |last1=American Psychiatric Association |s2cid=249488050 |page=103}}</ref> Catatonia is under-recognized because the features are often mistaken for other disorders, including delirium or the negative symptoms of schizophrenia. The prevalence has been reported to be as high as 10% in those with acute psychiatric illnesses, and 9–30% in the setting of inpatient psychiatric care.<ref name="Heckers 2023" /><ref>{{cite journal |last1=Solmi |first1=Marco |last2=Pigato |first2=G Giorgio |last3=Roiter |first3=Beatrice |last4=Guaglianone |first4=Argentina |last5=Martini |first5=Luca |last6=Fornaro |first6=Michele |last7=Monaco |first7=Francesco |last8=Carvalho |first8=Andrè F |last9=Stubbs |first9=Brendon |last10=Veronese |first10=Nicola |last11=Correll |first11=Christoph U |title=Prevalence of Catatonia and Its Moderators in Clinical Samples: Results from a Meta-analysis and Meta-regression Analysis |journal=Schizophrenia Bulletin |date=20 August 2018 |volume=44 |issue=5 |pages=1133–50 |doi=10.1093/schbul/sbx157 |pmid=29140521 |pmc=6101628}}</ref><ref name="Rasmussen Mazurek Rosebush 2016"/> The incidence of catatonia is 10.6 episodes per 100 000 person-years, which essentially means that in a group of 100,000 people, the group as a whole would experience 10 to 11 episodes of catatonia per year.<ref name="Rogers Pollak Begum et al 2021">{{cite journal |last1=Rogers |first1=Jonathan P. |last2=Pollak |first2=Thomas A. |last3=Begum |first3=Nazifa |last4=Griffin |first4=Anna |last5=Carter |first5=Ben |last6=Pritchard |first6=Megan |last7=Broadbent |first7=Matthew |last8=Kolliakou |first8=Anna |last9=Ke |first9=Jessie |last10=Stewart |first10=Robert |last11=Patel |first11=Rashmi |last12=Bomford |first12=Adrian |last13=Amad |first13=Ali |last14=Zandi |first14=Michael S. |last15=Lewis |first15=Glyn |last16=Nicholson |first16=Timothy R. |last17=David |first17=Anthony S. |title=Catatonia: demographic, clinical and laboratory associations |journal=Psychological Medicine |date=2 November 2021 |volume=53 |issue=6 |pages=2492–2502 |doi=10.1017/S0033291721004402 |pmid=35135642 |pmc=10123832 |s2cid=242076501 |doi-access=free}}</ref> Catatonia can occur at any age, but is most commonly seen in adolescence or young adulthood or in older adults with existing medical conditions. It occurs in males and females in approximately equal numbers.<ref>{{cite journal |last1=Parsanoglu |first1=Zozan |last2=Balaban |first2=Ozlem Devrim |last3=Gica |first3=Sakir |last4=Atay |first4=Ozge Canbek |last5=Altin |first5=Ozan |title=Comparison of the Clinical and Treatment Characteristics of Patients Undergoing Electroconvulsive Therapy for Catatonia Indication in the Context of Gender |journal=Clinical EEG and Neuroscience |date=May 2022 |volume=53 |issue=3 |pages=175–183 |doi=10.1177/15500594211025889 |pmid=34142904 |s2cid=235471133}}</ref><ref name="Rogers Pollak Begum et al 2021"/> Around 20% of all catatonia cases can be attributed to a general medical condition.<ref name="Oldham 333–340">{{Cite journal |last=Oldham |first=Mark A. |date=2018-07-01 |title=The Probability That Catatonia in the Hospital has a Medical Cause and the Relative Proportions of Its Causes: A Systematic Review |url=https://linkinghub.elsevier.com/retrieve/pii/S0033318218301828 |journal=Psychosomatics |volume=59 |issue=4 |pages=333–340 |doi=10.1016/j.psym.2018.04.001 |issn=0033-3182 |pmid=29776679 |url-access=subscription}}</ref><ref name="Serra-Mestres & Jaimes-Albornoz 2018">{{cite journal |last1=Serra-Mestres |first1=Jordi |last2=Jaimes-Albornoz |first2=Walter |title=Recognizing Catatonia in Medically Hospitalized Older Adults: Why It Matters |journal=Geriatrics |date=29 June 2018 |volume=3 |issue=3 |page=37 |doi=10.3390/geriatrics3030037 |pmid=31011075 |pmc=6319219 |doi-access=free}}</ref> {| class="wikitable" |+ !Underlying condition !Proportion of catatonia cases |- |Mood disorders |20–40% |- |Major depressive disorder |15–20% |- |Bipolar disorder |15–20% |- |Psychotic disorders |20–30% |- |Schizophrenia |10–15% |- |Schizoaffective disorder |5–10% |- |Autism spectrum disorder |5–10% |- |Medical conditions |~20% |}

== History ==

=== Ancient history === There have been reports of stupor-like and catatonia-like states in people throughout the history of psychiatry.<ref>{{cite journal | pmid=7034030 | date=1981 | last1=Berrios | first1=G. E. | title=Stupor: A conceptual history | journal=Psychological Medicine | volume=11 | issue=4 | pages=677–688 | doi=10.1017/s0033291700041179 | s2cid=26932116}}</ref> In ancient Greece, the first physician to document stupor-like or catatonia-like states was Hippocrates, in his ''Aphorisms.<ref>{{Citation |last=Roccatagliata |first=Giuseppe |chapter=The Idea of Melancholia in Classical Culture |date=1985 |title=Psychiatry: The State of the Art |volume=8 |pages=89–93 |editor-last=Pichot |editor-first=P. |chapter-url=https://link.springer.com/chapter/10.1007/978-1-4757-1853-9_12 |access-date=2024-11-18 |place=Boston, MA |publisher=Springer US |language=en |doi=10.1007/978-1-4757-1853-9_12 |isbn=978-1-4757-1853-9 |editor2-last=Berner |editor2-first=P. |editor3-last=Wolf |editor3-first=R. |editor4-last=Thau |editor4-first=K.|chapter-url-access=subscription}}</ref>''<ref>{{Cite journal |last=Scholtz |first=M. |date=December 1940 |title=Hippocrates' Aphorisms |journal=California and Western Medicine |volume=53 |issue=6 |page=272 |issn=0093-4038 |pmc=1634189 |pmid=18745795}}</ref> He never defined the syndrome, but seemingly observed these states in people he was treating for melancholia. In ancient China, the first descriptions of people that appear in the Huangdi Neijing (The Yellow Emperor's Inner Canon),<ref>{{Cite book |last=Veith |first=Ilza |title=The Yellow Emperor's Classic of Internal Medicine |date=2015-12-15 |publisher=University of California Press |doi=10.1525/9780520963245 |isbn=978-0-520-96324-5}}</ref> the book which forms the basis of Traditional Chinese Medicine. It is thought to have been compiled by many people over the course of centuries during the Warring States Period (475-221 BCE) and the early Han Dynasty (206 BCE-220 CE).{{cn|date=April 2026}}

=== Modern history === {{More citations needed section|date=August 2025}} The term "catatonia" was first used by German psychiatrist Karl Ludwig Kahlbaum in 1874, in his book ''Die Katatonie oder das Spannungsirresein'', which translates to "Catatonia or Tension Insanity".<ref>{{cite web |title=Zur Entwicklung der Psychiatrie - ein Internet-Atlas von Dr. Hans-Peter Haack |url=http://www.entwicklung-der-psychiatrie.de/seiten/24.1_kahlbaum_die_katatonie.htm |archive-url=https://web.archive.org/web/20080209213229/http://www.entwicklung-der-psychiatrie.de/seiten/24.1_kahlbaum_die_katatonie.htm |archive-date=2008-02-09 |access-date=2017-06-29 |language=de}}</ref> He viewed catatonia as its own illness, which would get worse over time in stages of mania, depression, and psychosis leading to dementia. This work heavily influenced another German psychiatrist, Emil Kraeplin, who was the first to classify catatonia as a syndrome. Kraeplin associated catatonia with a psychotic disorder called dementia praecox, which is no longer used as a diagnosis, but heavily informed the development of the concept of schizophrenia.

Kraeplin's work influenced two other notable German psychiatrists, Karl Leonhard and Max Fink, and their colleagues to expand the concept of catatonia as a syndrome which could occur in the setting of many mental illnesses, not just psychotic disorders. They also laid the groundwork to describe different subtypes of catatonia still used today, including Stuporous Catatonia, Excited Catatonia, Malignant Catatonia, and Periodic Catatonia. Additionally, Leonhard and his colleagues categorized catatonia as either systematic or unsystematic, based on whether or not symptoms happened according to consistent and predictable patterns. These ways of thinking shaped the way that psychologists and psychiatrists thought of catatonia well into the 20th century. In fact, catatonia was a subtype of schizophrenia as recently as the DSM-III, and was not revised to be able to be applied to mood disorders until 1994 with the release of the DSM-IV.

In the latter half of the 20th century, clinicians observed that catatonia occurred in various psychiatric and medical conditions, not exclusively in schizophrenia. Max Fink and colleagues advocated for recognizing catatonia as an independent syndrome, highlighting its frequent association with mood disorders and responsiveness to treatments like benzodiazepines and ECT.

== Society and culture ==

=== Popular conceptions and origins === {{Unreferenced section|date=April 2026}} Catatonia has been subject to shifting perceptions in society. Since the 19th century, it was often linked exclusively to schizophrenia, perpetuating misconceptions. These historical misunderstandings have shaped the public opinion on catatonia. This has contributed to a lack of understanding about catatonia, and its broader association with other mental disorders and medical conditions.

Popular culture and media have played a significant role in shaping societal perceptions of catatonia. In many cases, media portrayals reduce it to a stereotypical "frozen state," similar to a coma, failing to capture the complexity of symptoms like stupor, agitation, and mutism. These oversimplifications have greatly affected the public perception of catatonia.

==See also== {{div col}} * Acquiescence * Akinetic mutism * Autistic catatonia * ''Awakenings'' (1990 biopic about catatonic patients, based on Oliver Sacks's book of the same name) * Blank expression * Botulism * Clouding of consciousness * Disorganized schizophrenia * ''Homecoming'' (features catatonia as a main plot point) * Karolina Olsson * Oneiroid syndrome * Vegetative state * Resignation syndrome * Sensory overload * Tonic immobility * Sleep paralysis {{div col end}}

==References== {{Reflist}}

== External links == {{Commons}} * [https://web.archive.org/web/20171013152335/http://ccpweb.wustl.edu/pdfs/2013barchcatatonia.pdf Catatonia in DSM-5] * [http://www.minddisorders.com/Br-Del/Catatonic-disorders.html Encyclopedia of Mental Disorders — Catatonic Disorders] * [https://archive.org/details/schizophreniacatatonictype "Schizophrenia: Catatonic Type"] video by Heinz Edgar Lehmann, 1952 * [https://www.mdcalc.com/bush-francis-catatonia-rating-scale Bush-Francis Catatonia Rating Scale]

{{Medical condition classification and resources | ICD11 = {{ICD11|6A40}}, {{ICD11|6A41}} | ICD10 = {{ICD10|F06.1}} | ICD9 = {{ICD9|293.89}} | MeshID = D002389 | SNOMED CT = 247917007 }}

{{Mental and behavioral disorders|selected = symptoms}} {{Authority control}}

Category:Mood disorders Category:Symptoms of schizophrenia Category:Psychopathological syndromes Category:Catatonia