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Other namescatatonic syndrome

Catatonia is a state of psycho-motor immobility and behavioral abnormality manifested by stupor. It was first described in 1874 by Karl Ludwig Kahlbaum, in German: Die Katatonie oder das Spannungsirresein[1] (Catatonia or Tension Insanity).

Though catatonia has historically been related to schizophrenia (catatonic schizophrenia), it is now known that catatonic symptoms are nonspecific and may be observed in other mental disorders and neurological conditions. In the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM), catatonia is not recognized as a separate disorder, but is associated with psychiatric conditions such as schizophrenia (catatonic type), bipolar disorder, post-traumatic stress disorder, depression and other mental disorders, narcolepsy, as well as drug abuse or overdose (or both). It may also be seen in many medical disorders including infections (such as encephalitis), autoimmune disorders, focal neurologic lesions (including strokes), metabolic disturbances, alcohol withdrawal[2] and abrupt or overly rapid benzodiazepine withdrawal.[3][4][5] In the fifth edition of the DSM, it is written that a variety of medical conditions may cause catatonia, especially neurological conditions: encephalitis, cerebrovascular disease, neoplasms, head injury.[6] Moreover, metabolic conditions: homocystinuria, diabetic ketoacidosis, hepatic encephalopathy, hypercalcaemia.[6]

It can be an adverse reaction to prescribed medication. It bears similarity to conditions such as encephalitis lethargica and neuroleptic malignant syndrome. There are a variety of treatments available; benzodiazepines are a first-line treatment strategy. Electroconvulsive therapy is also sometimes used. There is growing evidence for the effectiveness of NMDA receptor antagonists for benzodiazepine-resistant catatonia.[7] Antipsychotics are sometimes employed but require caution as they can worsen symptoms and have serious adverse effects.[8]

Signs and symptoms[edit]

Catatonia can be stuporous or excited. Stuporous catatonia is characterised by immobility during which people may hold rigid poses (stupor), an inability to speak (mutism), as well as waxy flexibility, in which they maintain positions after being placed in them by someone else. Mutism may be partial and they may repeat meaningless phrases or speak only to repeat what someone else says. People with stuporous catatonia may also show stereotyped, repetitive movements (stereotypy). Excited catatonia is characterised by bizarre, non-goal directed hyperactivity and impulsiveness.

Catatonia is a syndrome that can occur in various psychiatric disorders, including major depressive disorder, bipolar disorder, schizophrenia, schizoaffective disorder, schizophreniform disorder, brief psychotic disorder, and substance-induced psychotic disorder. It appears as the Kahlbaum syndrome (motionless catatonia), malignant catatonia (neuroleptic malignant syndrome, toxic serotonin syndrome), and excited forms (delirious mania, catatonic excitement, oneirophrenia).[8] It has also been recognized as grafted on to autism spectrum disorders.[9]


According to the DSM-5, "Catatonia Associated with Another Mental Disorder (Catatonia Specifier)" (code 293.89 [F06.1]) is diagnosed if the clinical picture is dominated by at least three of the following:[6]

  • stupor (i.e., no psychomotor activity; not actively relating to environment)
  • catalepsy (i.e., passive induction of a posture held against gravity)
  • waxy flexibility (i.e., allow positioning by examiner and maintain position)
  • mutism (i.e., no, or very little, verbal response [exclude if known aphasia])
  • negativism (i.e., opposition or no response to instructions or external stimuli)
  • posturing (i.e., spontaneous and active maintenance of a posture against gravity)
  • mannerisms (i.e., odd, circumstantial caricature of normal actions)
  • stereotypy (i.e., repetitive, abnormally frequent, non-goal-directed movements)
  • agitation, not influenced by external stimuli
  • grimacing (i.e. making a grimace like children)
  • echolalia (i.e., mimicking another's speech)
  • echopraxia (i.e., mimicking another's movements)

Other disorders (used additional code 293.89 [F06.1] to indicate the presence of the comorbid catatonia):

If catatonic symptoms are present but they don't form the catatonic syndrome, a medication-induced or substance-induced aetiology should first be considered.[10]


  • Stupor is a motionless, apathetic state in which one is oblivious or does not react to external stimuli. Motor activity is nearly non-existent. Individuals in this state make little or no eye contact with others and may be mute and rigid. One might remain in one position for a long period of time, and then go directly to another position immediately after the first position.
  • Catatonic excitement is a state of constant purposeless agitation and excitation. Individuals in this state are extremely hyperactive, although, as aforementioned, the activity seems to lack purpose. The individual may also experience delusions or hallucinations.[11] It is commonly cited as one of the most dangerous mental states in psychiatry.[12]
  • Malignant catatonia is an acute onset of excitement, fever, autonomic instability, delirium and may be fatal.[13]

Rating scale[edit]

Fink and Taylor developed a catatonia rating scale to identify the syndrome.[8] A diagnosis is verified by a benzodiazepine or barbiturate test. The diagnosis is validated by the quick response to either benzodiazepines or electroconvulsive therapy (ECT). While proven useful in the past, barbiturates are no longer commonly used in psychiatry; thus the option of either benzodiazepines or ECT.


Initial treatment is aimed at providing symptomatic relief. Benzodiazepines are the first line of treatment, and high doses are often required. A test dose of intramuscular lorazepam will often result in marked improvement within half an hour. In France, zolpidem has also been used in diagnosis, and response may occur within the same time period. Ultimately the underlying cause needs to be treated.[8]

Electroconvulsive therapy (ECT) is an effective treatment for catatonia, however, it has been pointed out that further high quality randomized controlled trials are needed to evaluate the efficacy, tolerance, and protocols of ECT in catatonia.[14]

Antipsychotics should be used with care as they can worsen catatonia and are the cause of neuroleptic malignant syndrome, a dangerous condition that can mimic catatonia and requires immediate discontinuation of the antipsychotic.[8]

Excessive glutamate activity is believed to be involved in catatonia; when first-line treatment options fail, NMDA antagonists such as amantadine or memantine are used. Amantadine may have an increased incidence of tolerance with prolonged use and can cause psychosis, due to its additional effects on the dopamine system. Memantine has a more targeted pharmacological profile for the glutamate system, reduced incidence of psychosis and may therefore be preferred for individuals who cannot tolerate amantadine. Topiramate is another treatment option for resistant catatonia; it produces its therapeutic effects by producing glutamate antagonism via modulation of AMPA receptors.[15]

See also[edit]


  1. ^ "Archived copy (Internet Archive)". Archived from the original on 2008-02-09. Retrieved 2017-06-29.CS1 maint: BOT: original-url status unknown (link)
  2. ^ Geoffroy PA, Rolland B, Cottencin O (May–June 2012). "Catatonia and alcohol withdrawal: a complex and underestimated syndrome". Alcohol Alcohol. 47 (3): 288–90. doi:10.1093/alcalc/agr170. PMID 22278315.
  3. ^ Rosebush PI; Mazurek MF. (August 1996). "Catatonia after benzodiazepine withdrawal". Journal of Clinical Psychopharmacology. 16 (4): 315–9. doi:10.1097/00004714-199608000-00007. PMID 8835707.
  4. ^ Deuschle M, Lederbogen F (January 2001). "Benzodiazepine withdrawal-induced catatonia". Pharmacopsychiatry. 34 (1): 41–2. doi:10.1055/s-2001-15188. PMID 11229621.
  5. ^ Kanemoto K, Miyamoto T, Abe R (September 1999). "Ictal catatonia as a manifestation of de novo absence status epilepticus following benzodiazepine withdrawal". Seizure. 8 (6): 364–6. doi:10.1053/seiz.1999.0309. PMID 10512781.
  6. ^ a b c American Psychiatric Association (2013). Diagnostic and Statistical Manual of Mental Disorders (Fifth ed.). Arlington, VA: American Psychiatric Publishing. pp. 119–121. ISBN 978-0-89042-555-8.
  7. ^ Daniels, J. (2009). "Catatonia: clinical aspects and neurobiological correlates". J Neuropsychiatry Clin Neurosci. 21 (4): 371–80. doi:10.1176/appi.neuropsych.21.4.371. PMID 19996245.
  8. ^ a b c d e Fink M, Taylor MA: CATATONIA: A Clinician's Guide to Diagnosis and Treatment, Cambridge U Press, 2003"
  9. ^ Dhossche D et al.: Catatonia in Autism Spectrum Disorders, Elsevier, Amsterdam, 2006
  10. ^ Michael B. First (2013). DSM-5® Handbook of Differential Diagnosis. American Psychiatric Publishing. p. 49. ISBN 978-1-58562-998-5.
  11. ^ Nolen-Hoeksema. Abnormal psychology. (6th ed., p. 224)
  12. ^ Maric, J. (2000). Clinical Psychiatry. Nolit, Belgrade.
  13. ^ Semple, David. "Oxford hand book of psychiatry" Oxford press. 2005.
  14. ^ Leroy, Arnaud; Naudet, Florian; Vaiva, Guillaume; Francis, Andrew; Thomas, Pierre; Amad, Ali (2017-06-21). "Is electroconvulsive therapy an evidence-based treatment for catatonia? A systematic review and meta-analysis". European Archives of Psychiatry and Clinical Neuroscience. 268 (7): 675–687. doi:10.1007/s00406-017-0819-5. ISSN 0940-1334. PMID 28639007.
  15. ^ Carroll, BT.; Goforth, HW.; Thomas, C.; Ahuja, N.; McDaniel, WW.; Kraus, MF.; Spiegel, DR.; Franco, KN.; et al. (2007). "Review of adjunctive glutamate antagonist therapy in the treatment of catatonic syndromes". J Neuropsychiatry Clin Neurosci. 19 (4): 406–12. doi:10.1176/appi.neuropsych.19.4.406. PMID 18070843. Archived from the original on 2007-12-13.

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