Neuroleptic malignant syndrome

From Citizendium
Revision as of 06:00, 25 September 2024 by Suggestion Bot (talk | contribs)
(diff) ← Older revision | Latest revision (diff) | Newer revision → (diff)
Jump to navigation Jump to search
This article is a stub and thus not approved.
Main Article
Discussion
Related Articles  [?]
Bibliography  [?]
External Links  [?]
Citable Version  [?]
 
This editable Main Article is under development and subject to a disclaimer.

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

  1. Anonymous (2024), Neuroleptic malignant syndrome (English). Medical Subject Headings. U.S. National Library of Medicine.
  2. 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. 
  3. Pelonero AL, Levenson JL, Pandurangi AK (1998). "Neuroleptic malignant syndrome: a review". Psychiatr Serv 49 (9): 1163-72. PMID 9735957[e]
  4. Guzé BH, Baxter LR (1985). "Current concepts. Neuroleptic malignant syndrome". N. Engl. J. Med. 313 (3): 163-6. PMID 3892294[e]
  5. 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. 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.

See also