2012
DOI: 10.1682/jrrd.2011.09.0183
|View full text |Cite
|
Sign up to set email alerts
|

Pharmacotherapy for posttraumatic stress disorder: Review with clinical applications

Abstract: Abstract-Posttraumatic stress disorder (PTSD) is a prevalent psychiatric diagnosis among veterans and has high comorbidity with other medical and psychiatric conditions. This article reviews the pharmacotherapy recommendations from the 2010 revised Department of Veterans Affairs/Department of Defense Clinical Practice Guideline (CPG) for PTSD and provides practical PTSD treatment recommendations for clinicians. While evidence-based, trauma-focused psychotherapy is the preferred treatment for PTSD, pharmacother… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

0
46
0
4

Year Published

2012
2012
2016
2016

Publication Types

Select...
5
1
1

Relationship

1
6

Authors

Journals

citations
Cited by 81 publications
(51 citation statements)
references
References 82 publications
0
46
0
4
Order By: Relevance
“…Of note, ketamine demonstrated a superior effect to that of midazolam, despite the fact that midazolam may have a potential acute benefit in a study of patients with chronic PTSD, because it is also a well-known anxiolytic. Although practice guidelines recommend against the use of benzodiazepines for the treatment of PTSD, 4 The biological mechanisms underlying the effects of ketamine, a glutamate NMDA receptor antagonist, in patients with PTSD are unknown. The role of glutamate in memory formation, including trauma-related memories, and in the pathophysiology of PTSD has recently received increased attention.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Of note, ketamine demonstrated a superior effect to that of midazolam, despite the fact that midazolam may have a potential acute benefit in a study of patients with chronic PTSD, because it is also a well-known anxiolytic. Although practice guidelines recommend against the use of benzodiazepines for the treatment of PTSD, 4 The biological mechanisms underlying the effects of ketamine, a glutamate NMDA receptor antagonist, in patients with PTSD are unknown. The role of glutamate in memory formation, including trauma-related memories, and in the pathophysiology of PTSD has recently received increased attention.…”
Section: Discussionmentioning
confidence: 99%
“…[3][4][5] Accumulating evidence for the role of glutamate, the most widely distributed excitatory neurotransmitter, in mediating stress responsivity, the formation of traumatic memories, and the pathophysiology of PTSD, suggests a potential benefit for novel pharmacotherapeutic interventions for this disorder. 6,7 Recently, intravenous (IV) ketamine, an antagonist of the glutamate N-methyl-D-aspartate (NMDA) receptor, has emerged as an effective, rapidly acting intervention for patients with treatment-resistant depression when administered at subanesthetic doses of 0.5 mg/kg.…”
mentioning
confidence: 99%
“…Drugs showing varying treatment success are from diverse pharmacological classes, e.g., selective serotonin reuptake inhibitors, α-adrenergic antagonists, anticonvulsants, mood stabilizers, antipsychotics, β-blockers, benzodiazepines, glucocorticoids, tricyclic antidepressants, and monoamine oxidase inhibitors [40,41].…”
Section: Pathophysiology and Pharmacotherapeutic Strategiesmentioning
confidence: 99%
“…Therefore, a number of pharmacological agents that either inhibit the release of monoamines or block the effects of monoamines released during stress are employed with varying success and side-effect profiles across individuals in the treatment of PTSD and its comorbidities. These medications, which have been sorely understudied using traditional multisite methods that rely on average population responses, as well as with regard to individualized predictors of response, include the serotonin-selective reuptake inhibitors (SSRIs), norepinephrine antagonists such as prazosin, and other agents that may target and block serotonergic, noradrenergic, and dopaminergic receptors in the cortex and amygdala, so as to restore appropriate amygdala/PFC balance (Jeffreys, Capehart, & Friedman, 2012).…”
Section: Neurobiological Risk Factorsmentioning
confidence: 99%