|Classification and external resources|
Catatonia is a state of neurogenic motor immobility and behavioral abnormality manifested by stupor. It was first described in 1874 by Karl Ludwig Kahlbaum, in Die Katatonie oder das Spannungsirresein (Catatonia or Tension Insanity).
In the current Diagnostic and Statistical Manual of Mental Disorders published by the American Psychiatric Association (DSM-5) 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, 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 and abrupt or overly rapid benzodiazepine withdrawal.
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. Electro-convulsive therapy is also sometimes used. There is growing evidence for the effectiveness of NMDA antagonists for benzodiazepine resistant catatonia. Antipsychotics are sometimes employed but require caution as they can worsen symptoms and have serious adverse effects.
Patients with catatonia may experience an extreme loss of motor skill or even constant hyperactive motor activity. Catatonic patients will sometimes hold rigid poses for hours and will ignore any external stimuli. Patients with catatonic excitement can suffer from exhaustion if not treated. Patients may also show stereotyped, repetitive movements.
They may show specific types of movement such as waxy flexibility, in which they maintain positions after being placed in them through someone else in which they resist movement in proportion to the force applied by the examiner. They may repeat meaningless phrases or speak only to repeat what the examiner says.
While catatonia is only identified as a symptom of schizophrenia in present psychiatric classifications, it is increasingly recognized as a syndrome with many faces. It appears as the Kahlbaum syndrome (motionless catatonia), malignant catatonia (neuroleptic malignant syndrome, toxic serotonin syndrome), and excited forms (delirious mania, catatonic excitement, oneirophrenia). It has also been recognized as grafted on to autism spectrum disorders.
- 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., slight, even resistance to positioning by examiner)
- 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)
- mannerism (i.e., odd, circumstantial caricature of normal actions)
- stereotypy (i.e., repetitive, abnormally frequent, non-goal-directed movements)
- agitation, not influenced by external stimuli
- echolalia (i.e., mimicking another's speech)
- echopraxia (i.e., mimicking another's movements)
- 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. It is commonly cited as one of the most dangerous mental states in psychiatry.
- Malignant catatonia is an acute onset of excitement, fever, autonomic instability, delirium and may be fatal.
Fink and Taylor developed a catatonia rating scale to identify the syndrome. 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 1–2 mg 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.
Electroconvulsive therapy (ECT) is an effective treatment for catatonia as well as for most of the underlying causes (e.g. psychosis, mania, depression). 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.
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.
- Disorganized schizophrenia
- Oneiroid syndrome
- Paranoid schizophrenia
- Persistent vegetative state
- Tonic immobility
- Awakenings-1990 film with Catatonia as a plot topic
- http://web.archive.org/web/20080209213229/http://www.entwicklung-der-psychiatrie.de/seiten/24.1_kahlbaum_die_katatonie.htm, Archived copy (Internet Archive)
- Geoffroy PA, Rolland B, Cottencin O. (may–jun 2012). "Catatonia and alcohol withdrawal: a complex and underestimated syndrome.". Alcohol Alcohol. 47 (3): 288–90. doi:10.1093/alcalc/agr170. PMID 22278315. Check date values in:
- 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.
- Deuschle M, Lederbogen F (January 2001). "Benzodiazepine withdrawal-induced catatonia". Pharmacopsychiatry 34 (1): 41–2. doi:10.1055/s-2001-15188. PMID 11229621.
- 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.
- 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.
- Fink M, Taylor MA: CATATONIA: A Clinician's Guide to Diagnosis and Treatment, Cambridge U Press, 2003"
- Dhossche D et al.: Catatonia in Autism Spectrum Disorders, Elsevier, Amsterdam, 2006
- American Psychiatric Association (2013). Diagnostic and Statistical Manual of Mental Disorders (Fifth ed.). Arlington, VA: American Psychiatric Publishing. p. 119. ISBN 978-0-89042-555-8.
- Nolen-Hoeksema. Abnormal psychology. (6th ed., p. 224)
- Maric, J. (2000). Clinical Psychiatry. Nolit, Belgrade.
- Semple,David."oxford hand book of psychiatry" Oxford press. 2005.
- 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.