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Neuroleptic Malignant Syndrome - Diagnosis
Neuroleptic Malignant Syndrome - Diagnosis
Date Created: 27/03/1999 Last Modified: 15/01/2000 Last Checked: 03/01/2003
Neuroleptic malignant syndrome would appear to be a state of extreme blockade of dopamine receptors, where progressive bradykinesia results in a state of immobilisation, akinesia and ‘stupor’ accompanied by ‘lead pipe’ rigidity, fever, autonomic instability and increased creatine phosphokinase (CPK). It is of particular interest to note that no reviews of NMS include bradykinesia as a diagnostic criterion, which is curious since it is the essence of Parkinsonism.
The only prospective series (Rosebush and Stewart), where most patients were under close observation in hospital, showed that transient agitation, followed by bradykinesia and immobility, which prostrated patients, was the usual course.
Despite frequent assertions in the literature that serotonin syndrome and neuroleptic malignant syndrome are similar it is now clear that their clinical pictures are quite different in almost all respects.
These differences are summarised below ***.
NMS and SS
NMS, slow onset (days) and slow progression
SS, both rapid onset and rapid progression (minutes to hours)
NMS, bradykinesia and lead pipe rigidity versus
SS, hyperkinesia and clonus.
NMS, an idiosyncratic reaction to therapeutic dosages versus
SS, a manifestation of toxicity (usually to a combination of drugs) to which everyone is liable.
In summary the precipitating drug defines the syndrome: dopamine (DA) receptor blockers produce bradykinesia whereas serotonergic drugs produce hyperkinesia.
*** from Gillman, P.K., Serotonin Syndrome: History and Risk. Fundamental and Clinical Pharmacology, 1998. 12(5): p. 482-491. [Review]
All text ©Dr Ken Gillman MRC Psych - PsychoTropical Research®
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