 |
 |
 |
 |
 |
 |
 |
|
|
|
|||||||||
|
|||||||||||
Clinical Instructor, Department of Psychiatry, College of Medicine, University of Cincinnati, Box 0559, Cincinnati, Ohio 45267, fax 513/487-6696, strawnjr{at}uc.edu, Research and Psychiatry Services, Cincinnati Veterans Affairs Medical Center, Cincinnati
Published Online, October 2, 2007. www.theannals.com, DOI 10.1345/aph.1H588a
1-receptor antagonist
prazosin in the treatment of nightmares related to posttraumatic stress
disorder (PTSD). It seems appropriate to augment this thorough review with a
discussion of the central role of norepinephrine in PTSD and several comments
regarding other antiadrenergic agents that are increasingly being used in the
treatment of this disorder. Given the central role of norepinephrine in mediating the human stress response, it is not surprising that symptom-linked hypernoradrenergic abnormalities have been implicated in the pathophysiology of PTSD. A number of brain structures that are thought to be involved in the production of PTSD symptoms (eg, hyperarousal, intrusive symptoms) are heavily innervated by noradrenergic fibers and contain dense populations of adrenergic receptors.2 In addition, cerebrospinal fluid concentrations of norepinephrine directly correlate with the severity of symptoms in veterans with combat-related PTSD.3
As might be expected, drugs that suppress the hyperactive noradrenergic
state associated with PTSD have been used to decrease PTSD symptoms for
several
decades.2 In
addition to the studies of prazosin that were reviewed by Dierks et
al.,1 a
number of centrally acting 2-receptor agonists (eg,
clonidine, guanfacine) as well as centrally acting ß-receptor antagonists
have been examined in open-label trials of patients with PTSD and were found
to reduce hyperarousal, hypervigilance, and
nightmares.2
Of particular interest is the nonselective ß-receptor antagonist
propranolol, which not only reduces chronic PTSD symptoms but may have utility
as a means of secondary prevention. In 2 recent controlled trials of acute
posttraumatization treatment with propranolol, significantly fewer
propranolol-treated patients developed PTSD symptoms at the end of the studies
compared with untreated
patients.4,5
Clearly, larger trials are needed to replicate these preliminary findings and
to evaluate other antiadrenergic drugs as potential
"PTSD-blocking" interventions.
In the context of substantial evidence for noradrenergic activation in PTSD, it is not surprising that antiadrenergic agents have therapeutic potential. Nonetheless, the specific roles of these drugs remain unclear, although they may prove to have primary or adjunctive roles in either the treatment of PTSD or the secondary prevention of this disorder.
References
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
 |
 |
 |
 |
 |
 |
 |
