Neuroleptic malignant syndrome: Difference between revisions
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'''Neuroleptic malignant syndrome''' is "potentially fatal syndrome associated primarily with the use of neuroleptic agents (see [[antipsychotic agent]]s) which are in turn associated with [[Biogenic amine receptor|dopaminergic receptor]] blockade in the basal ganglia and hypothalamus, and sympathetic dysregulation. Clinical features include diffuse muscle rigidity; [[tremor]]; high [[fever]]; diaphoresis; labile blood pressure; cognitive dysfunction; and autonomic disturbances. Serum CPK level elevation and a leukocytosis may also be present."<ref>{{MeSH}}</ref><ref name="isbn0-07-067439-6">{{cite book |author=Ropper, Allan H.; Adams, Raymond Delacy; Victor, Maurice |title=Principles of Neurology |publisher=McGraw-Hill, Health Professions Division |location=New York |year=1997 |pages=1199 |isbn=0-07-067439-6 |oclc= |doi=}}</ref><ref name="pmid9735957">{{cite journal |author=Pelonero AL, Levenson JL, Pandurangi AK |title=Neuroleptic malignant syndrome: a review |journal=Psychiatr Serv |volume=49 |issue=9 |pages=1163-72 |year=1998 |pmid=9735957 |doi= |url=http://ps.psychiatryonline.org/cgi/pmidlookup?view=long&pmid=9735957}}</ref> | '''Neuroleptic malignant syndrome''' is "potentially fatal syndrome associated primarily with the use of neuroleptic agents (see [[antipsychotic agent]]s) which are in turn associated with [[Biogenic amine receptor|dopaminergic receptor]] blockade in the [[basal ganglia]] and [[hypothalamus]], and sympathetic dysregulation. Clinical features include diffuse muscle rigidity; [[tremor]]; high [[fever]]; diaphoresis; labile blood pressure; [[cognitive dysfunction]]; and autonomic disturbances. Serum CPK level elevation and a leukocytosis may also be present."<ref>{{MeSH}}</ref><ref name="isbn0-07-067439-6-p1199">{{cite book |author=Ropper, Allan H.; Adams, Raymond Delacy; Victor, Maurice |authorlink= |editor= |others= |title=Principles of Neurology |edition=6th |language=English |publisher=McGraw-Hill, Health Professions Division |location=New York |year=1997 |origyear= |pages=1199 |quote= |isbn=0-07-067439-6 |oclc= |doi= |url= |accessdate=}}</ref><ref name="pmid9735957">{{cite journal |author=Pelonero AL, Levenson JL, Pandurangi AK |title=Neuroleptic malignant syndrome: a review |journal=Psychiatr Serv |volume=49 |issue=9 |pages=1163-72 |year=1998 |pmid=9735957 |doi= |url=http://ps.psychiatryonline.org/cgi/pmidlookup?view=long&pmid=9735957}}</ref><ref name="pmid3892294">{{cite journal |author=Guzé BH, Baxter LR |title=Current concepts. Neuroleptic malignant syndrome |journal=N. Engl. J. Med. |volume=313 |issue=3 |pages=163-6 |year=1985 |pmid=3892294 |doi=}}</ref> | ||
Blockade of the [[Biogenic amine receptor|D2 receptors]], which may be predisposed by genetic polymorphisms of the allele, cause neuroleptic malignant syndrome.<ref name="pmid15094790">{{cite journal |author=Kishida I, Kawanishi C, Furuno T, Kato D, Ishigami T, Kosaka K |title=Association in Japanese patients between neuroleptic malignant syndrome and functional polymorphisms of the dopamine D(2) receptor gene |journal=Mol. Psychiatry |volume=9 |issue=3 |pages=293-8 |year=2004 |pmid=15094790 |doi=10.1038/sj.mp.4001422 |url=http://dx.doi.org/10.1038/sj.mp.4001422}}</ref> | Blockade of the [[Biogenic amine receptor|D2 receptors]], which may be predisposed by genetic polymorphisms of the allele, may cause neuroleptic malignant syndrome.<ref name="pmid15094790">{{cite journal |author=Kishida I, Kawanishi C, Furuno T, Kato D, Ishigami T, Kosaka K |title=Association in Japanese patients between neuroleptic malignant syndrome and functional polymorphisms of the dopamine D(2) receptor gene |journal=Mol. Psychiatry |volume=9 |issue=3 |pages=293-8 |year=2004 |pmid=15094790 |doi=10.1038/sj.mp.4001422 |url=http://dx.doi.org/10.1038/sj.mp.4001422}}</ref> | ||
==Diagnosis== | |||
Neuroleptic malignant syndrome usually shows fever, "lead-pipe" rigidity of muscles, mental status changes, and autonomic instability. | |||
===Differential diagnosis=== | |||
The distinction between [[serotonin syndrome]], [[neuroleptic malignant syndrome]], [[malignant hyperthermia]], and toxicity from [[cholinergic agent]]s has been reviewed ([http://content.nejm.org/cgi/content/full/352/11/1112/T2 see chart]).<ref name="pmid15784664">{{cite journal |author=Boyer EW, Shannon M |title=The serotonin syndrome |journal=N. Engl. J. Med. |volume=352 |issue=11 |pages=1112-20 |year=2005 |pmid=15784664 |doi=10.1056/NEJMra041867 |url=http://content.nejm.org/cgi/pmidlookup?view=short&pmid=15784664&promo=ONFLNS19}}</ref> The most difficult distinction is between serotonin syndrome and neuroleptic malignant syndrome as patients may be on drugs that could cause either disorder. Serotonin syndrome shows hyperkinesia, hyperreflexia, and hyperactive bowel sounds, while neuroleptic malignant syndrome shows bradykinesia, bradyreflexia and normal or diminished bowel sounds. A helpful guide is that "dopamine antagonists [such as used to sedate a [[psychosis]]] produce bradykinesia, whereas serotonin agonists [such as used to activate a [[depression]]] produce hyperkinesia".<ref name="pmid15784664"/> Lastly, neuroleptic malignant syndrome may develop over several days while serotonin syndrome develops faster. | |||
==References== | ==References== | ||
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==See also== | ==See also== | ||
* [[Serotonin syndrome]] | * [[Malignant hyperthermia]] | ||
* [[Serotonin syndrome]][[Category:Suggestion Bot Tag]] | |||
Latest revision as of 06:00, 25 September 2024
Neuroleptic malignant syndrome is "potentially fatal syndrome associated primarily with the use of neuroleptic agents (see antipsychotic agents) which are in turn associated with dopaminergic receptor blockade in the basal ganglia and hypothalamus, and sympathetic dysregulation. Clinical features include diffuse muscle rigidity; tremor; high fever; diaphoresis; labile blood pressure; cognitive dysfunction; and autonomic disturbances. Serum CPK level elevation and a leukocytosis may also be present."[1][2][3][4]
Blockade of the D2 receptors, which may be predisposed by genetic polymorphisms of the allele, may cause neuroleptic malignant syndrome.[5]
Diagnosis
Neuroleptic malignant syndrome usually shows fever, "lead-pipe" rigidity of muscles, mental status changes, and autonomic instability.
Differential diagnosis
The distinction between serotonin syndrome, neuroleptic malignant syndrome, malignant hyperthermia, and toxicity from cholinergic agents has been reviewed (see chart).[6] The most difficult distinction is between serotonin syndrome and neuroleptic malignant syndrome as patients may be on drugs that could cause either disorder. Serotonin syndrome shows hyperkinesia, hyperreflexia, and hyperactive bowel sounds, while neuroleptic malignant syndrome shows bradykinesia, bradyreflexia and normal or diminished bowel sounds. A helpful guide is that "dopamine antagonists [such as used to sedate a psychosis] produce bradykinesia, whereas serotonin agonists [such as used to activate a depression] produce hyperkinesia".[6] Lastly, neuroleptic malignant syndrome may develop over several days while serotonin syndrome develops faster.
References
- ↑ Anonymous (2024), Neuroleptic malignant syndrome (English). Medical Subject Headings. U.S. National Library of Medicine.
- ↑ Ropper, Allan H.; Adams, Raymond Delacy; Victor, Maurice (1997). Principles of Neurology (in English), 6th. New York: McGraw-Hill, Health Professions Division, 1199. ISBN 0-07-067439-6.
- ↑ Pelonero AL, Levenson JL, Pandurangi AK (1998). "Neuroleptic malignant syndrome: a review". Psychiatr Serv 49 (9): 1163-72. PMID 9735957. [e]
- ↑ Guzé BH, Baxter LR (1985). "Current concepts. Neuroleptic malignant syndrome". N. Engl. J. Med. 313 (3): 163-6. PMID 3892294. [e]
- ↑ Kishida I, Kawanishi C, Furuno T, Kato D, Ishigami T, Kosaka K (2004). "Association in Japanese patients between neuroleptic malignant syndrome and functional polymorphisms of the dopamine D(2) receptor gene". Mol. Psychiatry 9 (3): 293-8. DOI:10.1038/sj.mp.4001422. PMID 15094790. Research Blogging.
- ↑ 6.0 6.1 Boyer EW, Shannon M (2005). "The serotonin syndrome". N. Engl. J. Med. 352 (11): 1112-20. DOI:10.1056/NEJMra041867. PMID 15784664. Research Blogging.