Monday, July 6, 2009

Neuroleptic Malignant Syndrome

22 of the 23 Psychiatric Poisons in our FDA Adverse Reaction section feature Neuroleptic Malignant Syndrome as an FDA reported Adverse Reaction with each Drug Individually identified as 'The Primary Suspect Drug' responsible for that Adverse Reaction.

Abilify: Neuroleptic Malignant Syndrome
Adderall: Neuroleptic Malignant Syndrome
Celexa: Neuroleptic Malignant Syndrome
Clozapine: Neuroleptic Malignant Syndrome
Cymbalta: Neuroleptic Malignant Syndrome
Depakote: Neuroleptic Malignant Syndrome
Effexor: Neuroleptic Malignant Syndrome
Geodon: Neuroleptic Malignant Syndrome
Klonopin: Neuroleptic Malignant Syndrome
Lamactil: Neuroleptic Malignant Syndrome
Lexapro: Neuroleptic Malignant Syndrome
Neurontin: Neuroleptic Malignant Syndrome
Paxil: Neuroleptic Malignant Syndrome
Prozac: Neuroleptic Malignant Syndrome
Risperdal: Neuroleptic Malignant Syndrome
Ritalin/Concerta: Neuroleptic Malignant Syndrome
Seroquel: Neuroleptic Malignant Syndrome
Strattera: Neuroleptic Malignant Syndrome
Tegretol: Neuroleptic Malignant Syndrome
Wellbutrin:
Xanax: Neuroleptic Malignant Syndrome
Zoloft: Neuroleptic Malignant Syndrome
Zyprexa: Neuroleptic Malignant Syndrome


Wiki has Neuroleptic Malignant Syndrome in 0.2% of patients within 30 days.

1 in 500.

How many people have to be Poisoned to Sell $40 Billion Dollars of Psych Drugs, ...... last year alone? 8 Million Americans have already been 'Diagnosed'. They are NOT being cured. They are BUYING drugs.

Neuroleptic Malignant Syndrome

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Neuroleptic malignant syndrome
Classification and external resources
ICD-10 G21.0
ICD-9 333.92
DiseasesDB 8968
eMedicine emerg/339 med/2614 ped/1581
MeSH D00945

Neuroleptic malignant syndrome (NMS) is a neurological disorder most often caused by an adverse reaction to neuroleptic or antipsychotic drugs. It generally presents with muscle rigidity, fever, autonomic instability and cognitive changes such as delirium, and is associated with elevated creatine phosphokinase (CPK). Treatment is generally supportive.

Contents

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Causes

It is believed to be triggered by blockade of dopaminergic receptors in the corpus striatum, resulting in spasticity of skeletal muscle (which, in turn, leads to excessive heat generation), coupled with impaired hypothalamic thermoregulation. NMS can be caused by all types of neuroleptics (typical and atypical antipsychotic drugs). The higher the dosage of the antipsychotic, the more common the occurrence. Rapid and large increases in dosage can also trigger the development of NMS. Other drugs, environmental or psychological factors, hereditary conditions, and specific demographics may cause greater risk, but to date no conclusive evidence has been found to support this. The disorder typically develops within two weeks of the initial treatment with the drug, but may develop at any time the drug is being taken. NMS may also occur in people (such as patients with Parkinson's disease) who are taking a class of drugs known as dopaminergics (e.g., Levodopa) when the dosage is abruptly reduced. In addition, other drugs which are not used as neuroleptics, but which have anti-dopaminergic activity, can induce NMS (eg, metoclopramide [Reglan]). Even drugs which do not have known anti-dopaminergic activity (e.g., amoxampine [Ascendin] and lithium) have been associated with NMS.

Incidence

Occurs in 0.2% of patients receiving neuroleptic agents (e.g., butyrophenones [especially haloperidol], phenothiazines, thioxanthenes) within the initial 30 days of therapy.

Pathophysiology

The mechanism is thought to depend on decreased levels of dopamine due to:

However, the failure of D2 dopamine receptor antagonism or dopamine receptor dysfunction to fully explain the presenting symptoms and signs of NMS, as well as the occurrence of NMS with atypical antipsychotic drugs with lower D2 dopamine activity, has led to the hypothesis of sympathoadrenal hyperactivity as an etiological mechanism for NMS. There is also thought to be considerable overlap between malignant catatonia and NMS in their pathophysiology, the former being idiopathic and the latter being drug-induced form of the same syndrome.

Signs and symptoms

The first symptom to develop is usually muscular rigidity, followed by high fever, symptoms of instability of the autonomic nervous system such as unstable blood pressure, and changes in cognition, including agitation, delirium and coma. Other symptoms may include muscle tremors and pharyngitis. Once symptoms do appear, they rapidly progress and can reach peak intensity in as little as three days. These symptoms can last anywhere from eight hours to forty days.

A raised creatine phosphokinase (CPK) plasma concentration will be reported due to increased muscular activity and rhabdomyolysis (destruction of muscle tissue). The patient may suffer hypertensive crisis and metabolic acidosis. A non-generalised slowing on an EEG is reported in around 50% of cases. White blood cells go up in the blood.

Unfortunately, symptoms are sometimes misinterpreted by doctors as symptoms of mental illness, delaying treatment. NMS is less likely if a person has previously been stable for a period of time on antipsychotics, especially in situations where the dose has not been changed and there are no issues of noncompliance or consumption of psychoactive substances known to worsen psychosis.

Synopsis of symptoms

  • Increased body temperature >100.4 degrees °F, or >38 °C
  • Confused or altered consciousness
  • Diaphoresis "sweat shock"
  • Rigid muscles
  • Autonomic imbalance

Mnemonic

A mnemonic used to remember the features of NMS is FEVER.

Prognosis

As with most illnesses, the prognosis is best when identified early and treated aggressively. In these cases NMS is usually not fatal, although there is currently no agreement on the exact mortality rate for the disorder. Studies have given the disorder a mortality rate as low as 5% and as high as 76%, although most studies agree that the correct percentage is in the lower spectrum, perhaps 10–15%.[citation needed] Re-introduction to the drug that originally caused NMS to develop may also trigger a recurrence, although in most cases it does not.

Treatment

NMS is often an emergency, and can cause death if it goes untreated. The first step in treatment is generally to remove the patient from any neuroleptic or antipsychotic drugs being taken and to treat fever aggressively, such as, with ice packs to front, axillae, and groin. Many cases require intensive care, or some kind of supportive care at the minimum. Depending on the severity of the case, patients may require other treatments to contend with specific effects of the disorder. These include circulatory and ventilatory support, the drugs dantrolene sodium, bromocriptine, apomorphine. Benzodiazepines may also be of great benefit as muscle relaxants. Highly elevated CPK can damage the kidneys, therefore patients may need to be aggressively hydrated to help the kidneys eliminate the excessive amount of CPK.

NMS and serotonergic syndrome

The clinical features of NMS and serotonergic syndrome are very similar. This can make differentiating them very difficult.

Features, classically present in NMS, that are useful for differentiating the two syndromes are:

  • bradykinesia
  • Muscle rigidity
  • Laboratory values (WBC & CK)

History

NMS was known about as early as 1956, shortly after the introduction of the first phenothiazines, and is derived from the French syndrome malin des neuroleptiques.

References

  1. ^ Theodore I. Benzer, MD, PhD (2005). "Neuroleptic Malignant Syndrome". Emedicine. http://www.emedicine.com/EMERG/topic339.htm.
  2. ^ Mihara K, Kondo T, Suzuki A, et al. (2003). "Relationship between functional dopamine D2 and D3 receptors gene polymorphisms and neuroleptic malignant syndrome". Am. J. Med. Genet. B Neuropsychiatr. Genet. 117 (1): 57–60. doi:10.1002/ajmg.b.10025. PMID 12555136.
  3. ^ Ananth J, Parameswaran S, Gunatilake S, Burgoyne K, Sidhom T (2004). "Neuroleptic malignant syndrome and atypical antipsychotic drugs". J. Clin. Psychiatry 65 (12): 1722–3. PMID 15119907.
  4. ^ Gurrera RJ (1999). "Sympathoadrenal hyperactivity and the etiology of neuroleptic malignant syndrome". Am. J. Psychiatry 156 (2): 169–81. PMID 9989551.
  5. ^ Stacy Milbouer, "Quest for the truth", Nashua Telegraph http://www.nashuatelegraph.com/apps/pbcs.dll/article?AID=/20050424/NEWS01/104240081
  6. ^ Identify neuroleptic malignant syndrome. schizophrenia.com URL:http://www.schizophrenia.com/sznews/archives/002054.html. Accessed: July 2, 2006.
  7. ^ Christensen V, Glenthøj B (2001). "[Malignant neuroleptic syndrome or serotonergic syndrome]". Ugeskr Laeger 163 (3): 301–2. PMID 11219110.
  8. ^ Birmes P, Coppin D, Schmitt L, Lauque D (2003). "Serotonin syndrome: a brief review.". CMAJ 168 (11): 1439–42. PMID 12771076. Full Free Text.
  9. ^ Friedberg JM. Neuroleptic malignant syndrome. URL: http://www.idiom.com/~drjohn/biblio.html. Accessed: July 3, 2006.

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