Editing Catatonia (section)

=== Catatonia-specific treatments ===
The specifics of treating catatonia itself can vary from region to region, hospital to hospital, and individual to individual, but typically involves the use of benzodiazepines. In fact, in some cases it is unclear whether a person has catatonia or another condition which may present similarly. In these cases a "benzodiazepine challenge" is often done. During a "benzodiazepine challenge" a healthcare provider will give a moderate dose of a benzodiazepine to the patient and monitor them. If a person has catatonia they will often have improvements in their symptoms within 15 to 30 minutes. If the person does not improve within 30 minutes they are given a second dose and the process is repeated once more. If the person responds to either of the doses then they can be given benzodiazepines at a consistent dose and timing until their catatonia resolves. Depending on the person, a person may need to reduce their dosing slowly over time in order to prevent reoccurrence of their symptoms.

ECT is also commonly used to treat catatonia in people who do not improve with medication alone or whose symptoms reoccur whenever the dose of medications are reduced. ECT is usually administered with multiple sessions per week over two to four weeks.<ref>{{Cite web |title=Catatonia treatment and prognosis: Search |publisher=UpToDate |url=https://www.uptodate.com/contents/catatonia-treatment-and-prognosis?search=catatonia&source=search_result&selectedTitle=1~63&usage_type=default&display_rank=1 |access-date=2024-11-15 }}</ref> ECT has a success rate of 80% to 100%.<ref name=Luchini15>{{cite journal |vauthors=Luchini F, Medda P, Mariani MG, Mauri M, Toni C, Perugi G |title=Electroconvulsive therapy in catatonic patients: Efficacy and predictors of response |journal=World J Psychiatry |volume=5 |issue=2 |pages=182–92 |date=June 2015 |pmid=26110120 |pmc=4473490 |doi=10.5498/wjp.v5.i2.182 |doi-access=free }}</ref> ECT is effective for all subtypes of catatonia, however people who have catatonia with an underlying neurological condition show less improvement with ECT treatment.<ref name=Luchini15 /><ref name="Sienaert Dhossche Vancampfort et al 2014" />

Excessive [[glutamate]] activity is believed to be involved in catatonia;<ref name="sciencedirect.com">{{Cite journal |last1=Saini |first1=Aman |last2=Begum |first2=Nazifa |last3=Matti |first3=James |last4=Ghanem |first4=Dory Anthony |last5=Fripp |first5=Laurie |last6=Pollak |first6=Thomas A. |last7=Zandi |first7=Michael S. |last8=David |first8=Anthony |last9=Lewis |first9=Glyn |last10=Rogers |first10=Jonathan |date=2022-09-15 |title=Clozapine as a treatment for catatonia: A systematic review |url=https://discovery.ucl.ac.uk/10156362/1/Lewi_Clozapine%20as%20a%20treatment%20for%20catatonia_AOP.pdf |journal=Schizophrenia Research |language=en |volume=263 |pages=275–281 |doi=10.1016/j.schres.2022.09.021 |issn=0920-9964 |pmid=36117082 |s2cid=252276294 |doi-access=free}}</ref> when first-line treatment options fail, [[NMDA antagonists]] such as [[amantadine]] or [[memantine]] may be 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.<ref name="Carroll-2007">{{cite journal |last1=Carroll |first1=Brendan T. |last2=Goforth |first2=Harold W. |last3=Thomas |first3=Christopher |last4=Ahuja |first4=Niraj |last5=McDaniel |first5=William W. |last6=Kraus |first6=Marilyn F. |last7=Spiegel |first7=David R. |last8=Franco |first8=Kathleen N. |last9=Pozuelo |first9=Leopold |last10=Muñoz |first10=Camilo |date=October 2007 |title=Review of Adjunctive Glutamate Antagonist Therapy in the Treatment of Catatonic Syndromes |journal=The Journal of Neuropsychiatry and Clinical Neurosciences |volume=19 |issue=4 |pages=406–412 |doi=10.1176/jnp.2007.19.4.406 |pmid=18070843}}</ref>