Pharmacologic reduction of CNS noradrenergic activity in PTSD: the case for clonidine and prazosin

J Psychiatr Pract. 2007 Mar;13(2):72-8. doi: 10.1097/01.pra.0000265763.79753.c1.


This article reviews the neurobiologic rationale for and presents clinical guidance concerning the use of medications that reduce central nervous system noradrenergic activity in the treatment of intrusive symptoms of posttraumatic stress disorder. The authors reviewed neurobiological studies, nonclinical studies using animal models, clinical case reports, open-label drug studies, and blinded, placebo-controlled drug studies. This review of the basic science and clinical literature, and the authors' clinical experience with culturally and demographically diverse populations, indicate that clonidine and prazosin can play a useful role in treating sleep disturbance and hyperarousal in posttraumatic stress disorder, with minimal adverse effects and low financial cost.

Publication types

  • Case Reports

MeSH terms

  • Adrenergic alpha-Antagonists / adverse effects
  • Adrenergic alpha-Antagonists / therapeutic use*
  • Adult
  • Arousal / drug effects*
  • Arousal / physiology
  • Brain / drug effects*
  • Brain / physiopathology
  • Clonidine / adverse effects
  • Clonidine / therapeutic use*
  • Controlled Clinical Trials as Topic
  • Dose-Response Relationship, Drug
  • Dreams / drug effects
  • Dreams / physiology
  • Female
  • Humans
  • Male
  • Middle Aged
  • Norepinephrine / antagonists & inhibitors*
  • Norepinephrine / metabolism
  • Practice Guidelines as Topic
  • Prazosin / adverse effects
  • Prazosin / therapeutic use*
  • Stress Disorders, Post-Traumatic / drug therapy*
  • Stress Disorders, Post-Traumatic / physiopathology
  • Sympatholytics / adverse effects
  • Sympatholytics / therapeutic use*


  • Adrenergic alpha-Antagonists
  • Sympatholytics
  • Clonidine
  • Norepinephrine
  • Prazosin