Attention A T users. To access the menus on this page please perform the following steps. 1. Please switch auto forms mode to off. 2. Hit enter to expand a main menu option (Health, Benefits, etc). 3. To enter and activate the submenu links, hit the down arrow. You will now be able to tab or arrow up or down through the submenu options to access/activate the submenu links.

PTSD: National Center for PTSD

Menu
Menu

Quick Links

Veterans Crisis Line Badge
My healthevet badge
EBenefits Badge
 

Clinician's Guide to Medications for PTSD

 

Professional

This section is for Researchers, Providers, & Helpers

This section is for Researchers, Providers, and Helpers

Clinician's Guide to Medications for PTSD

Matt Jeffreys, MD

Overview

Each case of posttraumatic stress disorder (PTSD) has unique biological, psychological, and social determinants with differing treatment implications. Medications can be used to ameliorate the biological basis for PTSD symptoms along with co-occurring psychiatric diagnoses, and indirectly may benefit psychological and social symptoms as well. Studies suggest that cognitive behavioral therapies (CBT) such as Prolonged Exposure (PE) therapy and Cognitive Processing Therapy (CPT) have greater effects on relieving PTSD symptoms than medications, but there have been few head-to-head comparisons, and some people may prefer medications or may benefit from receiving a medication in addition to psychotherapy.

It is crucial to consider the level of evidence available for specific medication interventions being considered. Trials which are randomized, placebo-controlled, and double blinded are the gold standard for guiding pharmacotherapy decision making. Less strongly supported evidence includes open trials and case reports. It is vital for the clinician to question the level of evidence supporting the medications being prescribed for PTSD, because there are a variety of influences on prescribing, including marketing, patient preferences, and clinical custom, all of which can be inconsistent with the current evidence base.

The current evidence base for PTSD psychopharmacology is strongest for the selective serotonin reuptake inhibitors (SSRIs), and currently only sertraline (Zoloft) and paroxetine (Paxil) are approved by the Food and Drug Administration (FDA) for PTSD (1, 2). From the FDA perspective, all other medication uses are off label, though there are differing levels of evidence supporting their use. From the VA/DoD Clinical Practice Guideline for PTSD perspective, these SSRIs, as well as the SSRIs fluoxetine and paroxetine along with the serotonin and norepinephrine reuptake inhibitor (SNRI) venlafaxine are first-line recommended treatments.

When discussing treatment options for individuals under their care, clinicians recognize that each individual brings unique biological, social, and psychological backgrounds to his or her treatment. Thus, clinicians recognize the need to tailor the treatment guidelines to the needs of the individual patient. For example:

  • PTSD carries high comorbidities with major depressive disorder and substance use disorders. There are times when medications used for PTSD treatment may positively or negatively impact these co-occurring disorders.
  • Highly resilient individuals have responded more quickly to medications than those who are less resilient (4)
  • Veterans naïve to treatment recruited from the community respond as well as civilians in some studies (5) while Veterans with persistent PTSD symptoms (especially older Veterans who have received PTSD treatment for decades) may not respond as well to new treatments (6).
  • Older individuals appear to have a less robust response to medications for PTSD than younger patients (7).
  • Patients with personality disorders may be treated effectively, but medications alone are unlikely to address all of the needs for those with more complex trauma histories (8,9).

Back to top

What core PTSD symptoms are medications targeting?

The four main PTSD symptom clusters of the DSM-5 criteria are listed below:

  • Intrusion. Examples include nightmares, unwanted thoughts of the traumatic events, flashbacks, and reacting to traumatic reminders with emotional distress or physiological reactivity.
  • Avoidance. Examples include avoiding triggers for traumatic memories including places, conversations, or other reminders.
  • Negative alterations in cognitions and mood. Examples include distorted blame of self or others for the traumatic event, negative beliefs about oneself or the world, persistent negative emotions (e.g., fear, guilt, shame), feeling alienated, and constricted affect (e.g., inability to experience positive emotions).
  • Alterations in arousal and reactivity. Examples include angry, reckless, or self-destructive behavior, sleep problems, concentration problems, increased startle response, and hypervigilance.

These symptoms may improve at differing rates with differing medications. For example, a study of venlafaxine ER demonstrated early resolution in irritability (week 2), a later decrease in intrusive recollections (week 4), and no differences for sleep, dreams, and some avoidance symptoms at week 12 (10).

Back to top

What is the current understanding of the biological disturbances found in PTSD?

The biological disturbances in PTSD can be conceptualized as a dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis and the balance between excitatory and inhibitory brain neurocircuitry. There is a resultant dysregulation of adrenergic mechanisms that mediate the classical fight-flight or freeze response. Yehuda and Bierer (2008) have found that patients with PTSD have abnormal HPA function as compared to patients without PTSD and have a much greater variation in their levels of adrenocorticoids (11).

Other researchers have found differences between patients with PTSD and those without in both brain structures and brain circuits that process threatening input. It is not known for certain whether these changes were present before the traumatic event and predisposed the person to developing PTSD or if these changes were the result of the PTSD. The fear circuitry exhibits excessive activation in PTSD and is no longer integrated well with the executive planning and judgment centers in the prefrontal cortex (12). Even minor stresses may then trigger the "fight or flight" response, which leads to activation of the brain's adrenergic circuitry as well as increased heart rate, sweating, rapid breathing, tremors, and other symptoms of hyperarousal in patients with PTSD. The HPA system and other components of the human stress response are also mobilized in response to threat or other stressful stimuli (13). Conversely, overactivity of the prefrontal cortex could lead to a "freeze" response and emotional detachment.

Back to top

How do medications help regulate these responses?

The medications prescribed for treating PTSD symptoms act upon neurotransmitters related to the fear and anxiety circuitry of the brain including serotonin, norepinephrine, gamma-aminobutyric acid (GABA), excitatory amino acids such as N-methyl-D-aspartate (NMDA), and dopamine, among many others. There is great interest in developing agents with novel and more specific mechanisms of action than are currently available to target the PTSD symptoms described earlier while also minimizing potential side effects.

Studies show that a number of medications are helpful in minimizing PTSD symptoms. Most of the time, medications do not entirely eliminate symptoms but provide symptom reduction and could be more effective when used in conjunction with an ongoing program of trauma specific psychotherapy for patients, such as PE or CPT (14).

Back to top

What are current clinical tools to measure treatment outcomes?

There are a number of self-rating scales and structured clinical interviews to monitor the effects of treatment. Two examples include the Posttraumatic Stress Disorder Checklist for DSM-5 (PCL-5) and the Clinician-Administered PTSD Scale for DSM-5 (CAPS-5). The PCL-5 is an example of a patient self-rating scale, while the CAPS-5 is an example of a structured clinical interview including Criterion A stressor information recorded on the Life Events Checklist. The CAPS-5 may provide a much richer dialogue between the clinician and the person being treated regarding the severity and nature of the PTSD symptoms and is considered the gold standard for PTSD evaluation. For further information or to obtain these measures, see the Assessments Section.

While the CAPS-5 is preferred for initial evaluation, there is literature supportive of a strong correlation between the two measures, and the PCL-5 has the advantage of being quick and easy to administer as a follow up measure for PTSD symptom severity. Both the PCL-5 and the CAPS-5 provide a quantitative measure of the patient's PTSD symptoms and response to treatment over time. This information enhances the clinical assessment and interview with the patient, and is consistent with measurement based care.

Back to top

What is the evidence for specific classes of medications used for PTSD treatment?

Selective Serotonin Reuptake Inhibitors (SSRIs)

The neurotransmitter serotonin has a well-recognized role in the modulation of a number of mood and anxiety disorders. A deficiency in amygdala serotonin transport has been identified in some individuals with PTSD (15). The level of this neurotransmitter in both the peripheral and central nervous systems can be modulated by the selective serotonin reuptake inhibitors (SSRIs). The SSRIs are the only medications approved by the FDA for PTSD, and have the strongest empirical evidence for reducing PTSD symptoms in randomized controlled trials (RCTs). They are the preferred initial class of medications used in PTSD treatment (1, 2). Exceptions may occur for patients based upon their individual histories of side effects, response, comorbidities, and personal preferences.

An example of an exception would be a PTSD patient with co-occurring bipolar disorder where an antidepressant could cause mood instability which could be mitigated with a mood stabilizing medication (such as lithium or an anti-epileptic medication) before prescribing SSRIs. However, there is evidence that different antidepressants have varying effects on destabilizing mood in bipolar disorder (16). Another example would be intolerable sexual dysfunction or gastrointestinal side effects due to the effects of increased serotonin levels in the peripheral nervous system. Each patient varies in their response and ability to tolerate a specific medication and dosage, so medications must be tailored to individual needs.

Research indicates that maximum benefit from SSRI treatment depends upon adequate dosages and duration of treatment, and ensuring treatment adherence is key to successful pharmacotherapy for PTSD. Some typical dosage ranges for SSRIs, side effects, and initial mechanisms of action in the treatment of PTSD are listed below. It is not fully understood how medications affect differing brain circuitry to improve symptoms. For example, it has been hypothesized that the long term effect of antidepressants on mood and anxiety is related to the downregulation of the targeted serotonin synaptic receptors. In PTSD, one mechanism of action might be to stimulate neuronal connections through brain-derived neurotropic factor (BDNF) based upon animal and clinical studies (17,18).

  • Sertraline (Zoloft) 50 mg to 200 mg daily
  • Paroxetine (Paxil) 20 to 60 mg daily
  • Fluoxetine (Prozac) 20 mg to 60 mg daily

Note: Only sertraline and paroxetine have been approved for PTSD treatment by the FDA. All other medications described in this guide are being used "off label" and have empirical support and practice guideline support only.

Back to top

Other antidepressants for PTSD

Antidepressants that affect the balance of serotonergic and noradrenergic neurotransmission or which alter serotonin neurotransmission through other mechanisms of action are also helpful in PTSD. Venlafaxine acts primarily as a serotonin reuptake inhibitor at lower dosages and as a combined serotonin and norepinephrine reuptake inhibitor at higher dosages. It is now a recommended first-line treatment for PTSD in the revised VA/DoD Clinical Practice Guideline for PTSD based upon large multi-site RCTs (19).

There have been smaller RCTs with mirtazapine as well as open trials (20). Mirtazapine has a unique mechanism of action affecting both serotonin and norepinephrine through blockade of the pre-synaptic alpha-2 adrenergic inhibitory autoreceptor for norepinephrine and blockade of post-synaptic 5-HT2 and 5-HT3 receptors. Because of its mechanism of action, it may cause less sexual dysfunction than the SSRIs. Mirtazapine may be particularly helpful for treatment of insomnia in PTSD. A recent small trial of mirtazapine as an add-on to sertraline demonstrated significantly more improvement in depressive symptoms as compared to placebo but no significant difference for PTSD symptoms (21). Trazodone is also commonly used for insomnia in PTSD even though there is little empirical evidence available for its use.

Nefazodone affects serotonin by blocking the post-synaptic 5-HT2 receptor as well as blocking pre-synaptic reuptake (like an SSRI). It is still available in a generic form but carries a black box warning regarding liver failure (1 per 250,000 patient-years), so liver function tests need to be monitored and precautions taken as recommended in the medication's prescribing information (22,23). Nefazodone causes less sexual dysfunction than the SSRIs and enhances sleep.

Examples of antidepressants with novel mechanisms of action prescribed for PTSD and some typical dosage ranges are listed below:

  • Mirtazapine (Remeron) 7.5 mg to 45 mg daily
  • Venlafaxine (Effexor) 75 mg to 300 mg daily
  • Nefazodone (Serzone) 200 mg to 600 mg daily

All of the antidepressants described above are also effective in treating comorbid major depressive disorder (MDD) which depending upon the study, accompanies PTSD about fifty percent of the time. While bupropion is useful in treating comorbid MDD, it has not been shown effective for PTSD in controlled trials (24).

Back to top

Mood stabilizers for PTSD

These medications, also known as anticonvulsants or anti-epileptic drugs, affect the balance between the excitatory neurotransmitter glutamate the most common neurotransmitter in the central nervous system and the inhibitory neurotransmitter GABA by acting indirectly to affect these neurons when their neuronal receptor sites are activated. Topiramate has demonstrated promising results in randomized controlled trials with civilians and Veterans with PTSD, but currently is listed as having no demonstrated benefit in the VA/DoD Clinical Practice Guideline for PTSD.

There are two double-blind, placebo-controlled trials evaluating topiramate as monotherapy in civilians with PTSD (25,26). The trial published in 2007 included 38 participants and found no significant difference in total CAPS scores between topiramate and placebo. The 2010 trial included 35 participants and demonstrated a significant decrease in total CAPS scores. There are also two published double-blind, placebo-controlled trials evaluating topiramate as adjunctive treatment for PTSD in Veterans (27,28). The trial published in 2004 included 67 participants and found a significant decrease in the total CAPS score. The 2007 trial included 40 participants and showed no significant decrease in total CAPS scores.

Based upon the current studies, topiramate could provide a useful option for clinicians in treatment of PTSD symptoms in patients who fail first-line pharmacotherapy. Further studies are needed regarding the place of topiramate in PTSD treatment (29). A recent meta-analysis showed strong support for the use of topirimate in PTSD finding it to be similar to paroxetine in its efficacy (30). Additionally, topiramate has been found helpful in reducing alcohol consumption in those with an alcohol use disorder and could prove beneficial in the PTSD patient dually diagnosed with an alcohol use disorder (31,32).

The published results for other mood stabilizers are mixed or negative for their effects on PTSD symptoms. Despite some promising open label data, there have been two negative RCTs for divalproex and one negative RCT for tiagabine in treating PTSD (33-35). A small trial of lamotrigine in 15 individuals with PTSD demonstrated possible benefit (36). In summary, the effectiveness of mood stabilizers, as a class, remains uncertain.

These medications are definitely indicated for bipolar disorder whether or not it is comorbid with PTSD, for mood stabilization of the bipolar disorder. Divalproex and carbamazepine require regular lab work to monitor side effects, but neither lamotrigine nor topiramate require lab work but must be titrated slowly according to package insert directions to avoid potentially serious side effects. Examples are given below:

  • Carbamazepine (Tegretol). Requires monitoring of white blood cell counts due to risk of agranulocytosis. Will self-induce its own metabolism and increase the metabolism of other medications including oral contraceptives.
  • Divalproex (Depakote). Requires monitoring of liver function tests due to risk of hepatotoxicity and platelet levels due to risk of thrombocytopenia. Target dosage is 10 times the patient's weight in pounds.
  • Lamotrigine (Lamictal). Requires slow titration according to the package insert due to risk of serious rash.
  • Topiramate (Topimax). Requires clinical monitoring for glaucoma, sedation, dizziness and ataxia.

Back to top

Atypical antipsychotics for PTSD

While originally developed for patients with a psychotic disorder, there has been an interest in these medications as treatment for many other psychiatric disorders including PTSD. This would seem reasonable given their effects on the balance between dopaminergic and serotonergic neurotransmitter systems. The dopaminergic system has well established effects on reward and gratification and the serotonin system on mood and anxiety. The antipsychotics ameliorate psychotic symptoms in PTSD patients. The real question is whether these medications are useful for core PTSD symptoms when psychotic symptoms are not present.

Previously, a number of small single-site studies suggested that atypical antipsychotic agents were effective adjunctive treatment for PTSD patients who had poor responses to first-line SSRIs or SNRIs (37). A recent large-scale multi-site trial of risperidone as an adjunctive agent for SSRI poor/partial responders showed that there was no benefit (in comparison with a placebo group) for adjunctive use of this agent (38). It should be noted that the patients receiving adjunctive risperidone had failed 2 SSRI trials and adjusting for combat era did not change the results, though the study was not specifically designed to address differing responses to treatment based upon combat era. The VA/DoD PTSD Clinical Practice Guideline makes the following recommendations regarding the use of atypical antipsychotics:

  • Atypical antipsychotics are not recommended as monotherapy for PTSD.
  • Risperidone (Risperdal) is contraindicated for use as an adjunctive agent - potential harm (side effects) exceeds benefits.
  • There is insufficient evidence to recommend any other atypical antipsychotic as an adjunctive agent for PTSD.

At this time, atypical antipsychotics are recommended as treatment for co-occurring psychotic symptoms and mood disorders in PTSD.

Back to top

Other medications for PTSD

There are a number of other medications that can be helpful for specific PTSD symptoms or that have been used as second line agents including the following:

  • Prazosin (Minipress)
  • Tricyclic Antidepressants (such as Imipramine)
  • Monoamine Oxidase Inhibitors (MAOIs) (such as Phenelzine)

Prazosin has been found to be effective in decreasing nightmares in PTSD. This is logical given its blockade of the neurotransmitter norepinephrine at the post-synaptic alpha-1 receptor. Research results for the effectiveness of prazosin for PTSD symptoms other than nightmares have been mixed (39,40). However, a recent trial with military personnel using prazosin during the day in addition to bedtime for nightmares shows a significant reduction in daytime PTSD symptoms as well as nightmares (41). Because of prazosin's short half-life, divided dosage schedules may be necessary. This research provides a pathway to further research to possibly extend the therapeutic effects of prazosin in PTSD. Additionally, prazosin demonstrated a significant beneficial effect on alcohol cravings and sobriety in two small pilot studies of newly abstinent individuals with alcohol dependence (42,43). The first study did not address PTSD symptoms specifically, and the second study did not demonstrate an improvement in PTSD symptoms including nightmares. The author hypothesized it may have been due to the bedtime prazosin dosage being relatively low at 8 mg.

The tricyclic antidepressants and MAOIs act on multiple neurotransmitters including serotonin and norepinephrine. The tertiary tricyclics such as imipramine and amitriptyline which are more serotonergic were thought to be more beneficial in PTSD treatment than the secondary amines such as nortriptyline and desipramine which are more adrenergic (44). However, a recent study demonstrated no difference between desipramine and paroxetine in reducing PTSD symptoms (45). While there are RCTs supporting their use, these medications are not used as first-line agents due to their safety and side effect profiles. This is because tricyclics can cause ventricular arrhythmias through QT prolongation especially in overdose. On the other hand, they do not usually cause the sexual side effects seen with SSRIs. There is evidence that some SSRIs such as citalopram can have similar cardiac side effects. If patients fail to respond to first line treatments with the SSRIs or SNRI medication, then tricyclics used with these precautions in mind may be a viable alternative.

The MAOI phenezine has been shown to be effective in PTSD (46). The MAOIs increase a number of neurotransmitters, such as serotonin, norepinephrine, and dopamine, through inhibition of their degradation by the enzyme monoamine oxidase (MAO). Careful management of the MAOIs and strict dietary controls are important because they can cause potentially fatal hypertensive reactions when taken with other medications or certain foods rich in tyramine. They are contraindicated for patients who take stimulants therapeutically (e.g., for ADHD) or illicitly. MAOIs can also provoke the potentially fatal serotonin syndrome when used concurrently with SSRIs.

Buspirone and beta blockers are sometimes used adjunctively in treatment of hyperarousal symptoms, though there is little empirical evidence in support of their use. Buspirone is an agonist at the pre-synaptic serotonin 5-HT(1A) receptor and a partial agonist at the post-synaptic serotonin 5-HT(1A) receptor and might reduce anxiety in PTSD without sedation or addiction. There are some case reports but no randomized trials supporting its use. Beta blockers provide post-synaptic blockade of norepinephrine at synapses and blockade of adrenalin (epinephrine) at the organs such as the heart, sweat glands, and muscles. There is interest in using beta blockers to prevent PTSD, though the evidence at the current time does not support this. Beta blockers reduce both central and peripheral manifestations of hyperarousal and may reduce aggression as well. They may be used for comorbid conditions such as performance anxiety in the context of social anxiety disorder.

Back to top

Benzodiazepines and PTSD

Benzodiazepines enhance activity of GABA at the GABA-A receptor which produces CNS depression. This is the only potentially addictive group of medications discussed. Limited studies have not shown them to be useful in treating the core PTSD symptoms (47,48). There are several other concerns about the use of benzodiazepines including potential disinhibition, difficulty integrating the traumatic experience, interfering with the mental processes needed to benefit from psychotherapy, increased falls and mental clouding in the elderly, and addiction. In a recent study combining PE and alprazolam, the group receiving alprazolam had a poorer outcome in PTSD symptom reduction than the group receiving PE alone (49). Furthermore, a recent meta-analysis found benzodiazepines to worsen symptom outcome for patients with PTSD (50). Because of these potentially negative effects, it is recommended that benzodiazepines not be used in PTSD. Any acute use should be short term (e.g., no more than five days) with frequent re-evaluation for side effects. Examples of commonly used benzodiazepines are listed below:

  • Lorazepam (Ativan)
  • Clonazepam (Klonopin)
  • Alprazolam (Xanax)
  • Diazepam (Valium)

Back to top

What are some future research directions for pharmacotherapy?

The pathophysiological mechanism of PTSD in the nervous system is unknown, but there are several interesting neurotransmitters and pathways that could lead to new drug development for the treatment or the prevention of PTSD. There are competing hypotheses about the role of glucocorticoids following trauma and their effects on the brain. It might be possible to intervene at some level in the HPA axis or at the level of the glucocorticoid receptors in the brain to modulate the effects of stress and the development of PTSD. Some research suggests the potential ability of supplemental cortisol in reducing PTSD symptoms (51). Furthermore, cortisol administered prior to PE demonstrated significantly better retention in treatment especially among those patients with increased sensitivity to glucocorticoids. The authors cite several actions of glucocorticoids including: potentiating glutamate at NMDA receptors, decreased retrieval of fear memories, and interactions with noradrenergic systems, as potential mechanisms of action on brain pathways affecting PTSD (52).

In addition to corticotropin releasing factor (CRF) and adrenocorticotropin hormone (ACTH), other neuropeptides such as Substance P and Neuropeptide-Y (NPY) appear to play a role in PTSD (53). Combat troops exposed to stress have been found to have lower levels of NPY while resilient Special Forces troops exhibit elevated NPY levels (54). Perhaps potentiation of this neuromodulator could improve the resiliency of the brain's capacity to cope with trauma. One challenge with this new focus of research is dealing with the blood-brain barrier for introducing neuropeptides into the brain, but researchers have delivered the neuropeptide oxytocin intranasally through the olfactory pathway in veterans with PTSD and have demonstrated a decrease in hyperarousal symptoms (55).

D-cycloserine (DCS) has been used in panic disorder, specific phobia and social anxiety disorder, to enhance the effects of exposure therapy (56). It is a partial agonist of the glutamatergic N-methyl-D-aspartate (NMDA) receptor. Based upon animal research supporting the use of DCS to facilitate extinction of conditioned fear, it is hypothesized that use of DCS in conjunction with exposure therapy may reduce the number of psychotherapy sessions required (57). A recent study of DCS did not demonstrate a significant treatment benefit by adding the drug to PE. There were some interesting other findings in this study; DCS reduced cortisol and startle reactivity more than placebo when combined with PE (58). Clearly further research is needed, though this line of research shifts the focus from pharmacotherapy as the major treatment modality for reducing PTSD symptoms, to an adjunctive role for medication used to facilitate CBT psychotherapy, especially with regard to PE.

A recent study compared methylphenidate and the acetylcholinesterase inhibitor galantamine to placebo and found that methylphenidate, but not galantamine, improved cognitive complaints as well as PTSD symptom severity in patients with mild traumatic brain injury (mTBI) and/or PTSD. The authors propose larger randomized controlled trials to further evaluate improving cognition in those with PTSD and co-occurring mTBI (59).

Ketamine is an anesthetic agent which modulates the balance between glutamanergic activity at the NMDA receptor and serotonergic activity at the 5-HT receptors. This agent is showing promise for treatment of refractory depression in research trials currently (60). A recent trial showed beneficial effects in PTSD as well (61). The limitations so far include a short term benefit of a few weeks and the anesthetic nature of the drug and potential for addiction. However, this could lead to a new line of medication research and to newer agents with mechanisms of action distinct from serotonin and norepinephrine for treatment of PTSD.

The endocannabinoid system is another potential area of interest in moderating depressive, anxiety, and PTSD symptoms. Abnormalities at cannabinoid (CB-1) receptors coupled with reduced levels of anandamide (an endogenous cannabinoid) have been found in PTSD patients (62,63). While direct stimulation of the cannabinoid type 1 receptor (e.g. with marijuana) would likely lead to addiction and adverse side effects, indirect influences on this pathway could prove beneficial. Studies of direct stimulation of the system through cannabis have demonstrated negative effects on PTSD outcomes (64,65).

Baclofen is used clinically as a muscle relaxant and has GABA-B receptor agonist activity. A small randomized study of 23 Iranian combat Veterans with PTSD randomized to citalopram and baclofen (n=13) or citalopram and placebo (n=10) found that those on the combination of citalopram and baclofen had significantly more reduction in PTSD symptoms than the citalopram and placebo group (66). This is an area of potential future research.

There is ongoing interest in the possibility of early intervention and promoting resiliency following trauma with psychotherapy, pharmacotherapy, or some combination that would prevent the development of PTSD. There are no currently recognized medications which prevent the development of PTSD after trauma.

Back to top

What are common clinical barriers to successful medication treatment?

There are several common barriers to effective medication treatment for PTSD which are listed below. These need to be addressed with individuals receiving treatment in an ongoing dialogue with their prescribing clinician. Side effects need to be examined and discussed, weighing the risks and the benefits of continued medication treatment. Patient education about the side effects, necessary dosages, duration of treatment, and adherence can improve outcomes to medications. Simple interventions, such as setting up a pill organizer weekly or enlisting family/caregiver support, can go a long way to improve adherence.

  • Fear of possible medication side effects including sexual side effects
  • Feeling medication is a "crutch" and that taking it is a weakness
  • Fear of becoming addicted to medications
  • Taking the medication only occasionally when symptoms get severe
  • Not being sure how to take the medication
  • Keeping several pill bottles and not remembering when the last dosage was taken
  • Using "self-medication" with alcohol or drugs with prescribed medications

Back to top

Other Important Considerations

  • Patients with PTSD or anxiety disorders may be very aware of their somatic reactions, and it is important to start low and go slow on dosage adjustments to improve patient adherence.
  • Be sure to ask female patients of childbearing age about contraception and pregnancy when prescribing medication. And be aware of medications that are contraindicated during pregnancy because of teratogenic effects.
  • Be sure to ask all patients about substance abuse as well.
  • Once medications are started, it is crucial that the provider remember to discontinue medications which are not proving efficacious and to simplify the number and types of medications used whenever possible.

Back to top

Final thoughts about medications for treatment of PTSD

A more comprehensive discussion of pharmacotherapy can be found online in the VA/DoD PTSD Clinical Practice Guideline.

Although CPT and PE may be more effective, pharmacotherapeutic monotherapy may be sufficient to ameliorate PTSD for some patients. Furthermore, there are many more prescribing clinicians available then qualified CPT or PE therapists. Finally, some patients prefer medication to psychotherapy, although when given the choice, the majority choose psychotherapy (67). Based upon current knowledge, most prescribing clinicians view pharmacotherapy as an important adjunct to the evidenced based psychotherapies for PTSD. While there are few direct comparisons of pharmacotherapy and psychotherapy, the greatest benefits of treatment appear to come from evidenced based therapies such as CPT and PE based upon the effect sizes in the literature. Patients need to be informed of the risks and benefits of the differing treatment options along with the risks of no treatment.

When using a combined approach of medication and therapy, it is important to keep several practices in mind. If treatment is being provided by a therapist and a prescriber, it is important for the clinicians to discuss treatment response and to coordinate efforts. It is important for the prescribing clinician to have an ongoing dialogue with the patient about their medications and side effects. It is important for the patient to take an active role in his or her treatment rather than feeling they are a passive recipient of medications to alleviate their symptoms. There is emerging evidence that when given a choice, most patients will select psychotherapy treatment for their PTSD symptoms rather than medications.

Back to top

References

  1. Brady, K., Pearlstein, T., Asnis, G. M., Baker, D., Rothbaum, B., Sikes, C. R., & Farfel, G. M. (2000). Efficacy and safety of sertraline treatment of posttraumatic stress disorder: A randomized controlled trial. Journal of the American Medical Association, 283, 1837-1844. doi: 10.1001/jama.283.14.1837
  2. Marshall, R. D., Beebe, K. L., Oldham, M., & Zaninelli, R. (2001). Efficacy and safety of paroxetine treatment for chronic PTSD: A fixed-dose, placebo-controlled study. American Journal of Psychiatry, 158, 1982-1988. doi: 10.1176/appi.ajp.***********
  3. Hoskins, M., Pearce, J., Bethell, A., Dankova, L., Barbui, C., Tol, W. A., & Bisson, J. I. (2015). Pharmacotherapy for post-traumatic stress disorder: Systematic review and meta-analysis. The British Journal of Psychiatry : The Journal of Mental Science, 206 (2), 93-100. doi:10.1192/bjp.bp.114.148551
  4. Davidson, J., Stein, D. J., Rothbaum, B. O., Pedersen, R., Szumski, A., & Baldwin, D. S. (2012). Resilience as a predictor of treatment response in patients with posttraumatic stress disorder treated with venlafaxine extended release or placebo. Journal of Psychopharmacology, 26, 778-783. doi:10.1177/0269881111413821
  5. Martenyi, F., Brown, E. B., Zhang, H., Koke, S. C., & Prakash, A. (2002). Fluoxetine v. placebo in prevention of relapse in post-traumatic stress disorder. The British Journal of Psychiatry : The Journal of Mental Science, 181, 315-320.
  6. Friedman, M. J., Marmar, C. R., Baker, D. G., Sikes, C. R., & Farfel, G. M. (2007). Randomized, double blind comparison of sertraline and placebo for posttraumatic stress disorder in Department of Veterans Affairs setting. Journal of Clinical Psychiatry, 68, 711-720. doi: 10.4088/JCP.v68n0508
  7. Wetherell, J. L., Petkus, A. J., Thorp, S. R., Stein, M. B., Chavira, D. A., Campbell-Sills, L., & Roy-Byrne, P. (2013). Age differences in treatment response to a collaborative care intervention for anxiety disorders. The British Journal of Psychiatry : The Journal of Mental Science, 203, 65-72. doi:10.1192/bjp.bp.112.118547
  8. Walter, K. H., Bolte, T. A., Owens, G. P., & Chard, K. M. (2012). The impact of personality disorders on treatment outcome for Veterans in a posttraumatic stress disorder residential treatment program. Cognitive Therapy Research, 36, 576-584. doi:10.1007/s10608-011-9393-8
  9. Laddis, A. (2011). Medication for complex posttraumatic stress disorders. Journal of Aggression, Maltreatment & Trauma, 20, 645-668. doi: 10.1080/10926771.2011.596137
  10. Stein, D. J., Pedersen, R., Rothbaum, B. O., Baldwin, D. S., Ahmed, S., Musgnung, J., & Davidson, J. (2009). Onset of activity and time to response on individual CAPS-SX17 items in patients treated for post-traumatic stress disorder with venlafaxine ER: A pooled analysis. The International Journal of Neuropsychopharmacology / Official Scientific Journal of the Collegium Internationale Neuropsychopharmacologicum (CINP), 12, 23-31. doi:10.1017/S1461145708008961
  11. Yehuda, R., & Bierer, L. M. (2008). Transgenerational transmission of cortisol and PTSD risk. Progress in Brain Research, 167, 121-135. doi: 10.1016/S0079-6123(07)67009-5
  12. Lanius, R. A., Vermetten, E., Loewenstein, R. J., Brand, B., Schmahl, C., Bremner, J. D., & Spiegel, D. (2010). Emotion modulation in PTSD: Clinical and neurobiological evidence for a dissociative subtype. American Journal of Psychiatry, 167, 640-647. doi: 10.1176/appi.ajp.2009.09081168
  13. Friedman, M. J. (2014). The human stress response. In N. C. Bernardy & M. J. Friedman (Eds.), A Practical Guide to PTSD Treatment: Pharmacological and Psychotherapeutic Effects (pp. 9-20). Washington D. C.: American Psychological Association.
  14. Watts, B. V., Schnurr, P. P., Mayo, L., Young-Xu, Y., Weeks, W. B., & Friedman, M. J. (2013). Meta-analysis of the efficacy of treatments for posttraumatic stress disorder. The Journal of Clinical Psychiatry, 74, e541-550. doi:10.4088/JCP.12r08225
  15. Murrough, J. W., Huang, Y., Hu, J., Henry, S., Williams, W., Gallezot, J. D., Bailey, C. R., Krystal, J. H., Carson, R. E., & Neumeister, A. (2011). Reduced amygdala serotonin transporter binding in posttraumatic stress disorder. Biological Psychiatry, 170, 1033-1038. doi: 10.1016/j.biopsych.2011.07.003
  16. McElroy, S. L., Weisler, R. H., Chang, W., Olausson, B., Paulsson, B, Brecher, M., Agambaram, V., Merideth, C., Nordenhem, A., & Young, A. H. (2010). A double-blind, placebo-controlled study of quetiapine and paroxetine as monotherapy in adults with bipolar depression (EMBOLDEN II). Journal of Clinical Psychiatry, 71, 163-74. doi: 10.4088/JCP.08m04942gre
  17. Duman, R. S., Heninger, G. R., & Nestler, E.J. (1997). A molecular and cellular theory of depression. Archives of General Psychiatry, 54, 597-606.
  18. Vermetten, E., Vythilingam, M., Southwick, S. M., Charney, D. S., & Bremner, J. D. (2003). Long-term treatment with paroxetine increases verbal declarative memory and hippocampal volume in posttraumatic stress disorder. Biological Psychiatry, 54, 693-702. doi:S0006322303006346
  19. Davidson, J., Baldwin, D., Stein, D. J., Kuper, E., Benattia, I., Ahmed, S., Pedersen, R., & Musgnung, J. (2006). Treatment of posttraumatic stress disorder with venlafaxine extended release: A 6-month randomized controlled trial. Archives of General Psychiatry, 63, 1158-1165. doi: 10.1001/archpsyc.63.10.1158
  20. Chung, M. Y., Min, K. H., Jun, Y. J., Kim, S. S., Kim, W. C., & Jun, E. M. (2004). Efficacy and tolerability of mirtazapine and sertraline in Korean Veterans with posttraumatic stress disorder: A randomized open label trial. Human Psychopharmacology, 19, 489-94. doi: 10.1002/hup.615
  21. Schneier, F. R., Campeas, R., Carcamo, J., Glass, A., Lewis-Fernandez, R., Neria, Y., Sanchez-Lacay, A., Vermes, D. & Wall, M. M. (2015). Combined mirtazapine and SSRI treatment of PTSD: A placebo-controlled trial. Depression and Anxiety, 32, 570-579. doi:10.1002/da.22384
  22. Davis, L. L., Jewell, M. E., Ambrose, S., Farley, J., English, B., Bartolucci, A., & Petty, F. (2004). A placebo-controlled study of nefazodone for the treatment of chronic posttraumatic stress disorder: A preliminary study. Journal of Clinical Psychopharmacology, 24, 291-297. doi: 10.1097/01.jcp.0000125685.82219.1a
  23. McRae, A. L., Brady, K. T., Mellman, T. A., Sonne, S. C., Killeen, T. K., Timmerman, M. A., & Bayles-Dazet, W. (2004). Comparison of nefazodone and sertraline for the treatment of posttraumatic stress disorder. Depression & Anxiety, 19, 190-196. doi: 10.1002/da.20008
  24. Becker, M. E., Hertzberg, M. A., Moore, S. D., Dennis, M. F., Bukenya, D. S., & Beckham, J. C. (2007). A placebo-controlled trial of bupropion SR in the treatment of chronic posttraumatic stress disorder. Journal of Clinical Psychopharmacology, 27, 193-197. doi: 10.1097/JCP.0b013e318032eaed
  25. Tucker, P., Trautman, R. P., Wyatt, D. B., Thompson, J., We,S. C., Capece, J. A., & Rosenthal, N. R. (2007). Efficacy and safety of topiramate monotherapy in civilian posttraumatic stress disorder: A randomized, double-blind, placebo-controlled study. Journal of Clinical Psychiatry, 68, 201-206. doi: 10.4088/JCP.v68n0204
  26. Yeh, M. S., Mari, J. J., Costa, M. C., Andreoli, S. B., Bressan, R. A., & Mello, M. F. (2011). A double-blind randomized controlled trial to study the efficacy of topiramate in a civilian sample of PTSD. Clinical Neuroscience & Therapeutics, 17, 305-310. doi: 10.1111/j.1755-5949.2010.00188.x
  27. Akuchekian, S., & Amant, S. (2004). The comparison of topiramate and placebo in the treatment of posttraumatic stress disorder: a randomized, double-blind study. Journal of Research in Medical Sciences, 9, 240-244.
  28. Lindley, S. E., Carlson, E. B., & Hill, K. (2007). A randomized, double-blind, placebo-controlled trial of augmentation topiramate for chronic combat-related posttraumatic stress disorder. Journal of Clinical Psychopharmacology, 27, 677-681. doi: 10.1097/jcp.0b013e31815a43ee
  29. Andrus, M. R., & Gilbert, E. (2010). Treatment of civilian and combat-related posttraumatic stress disorder with topiramate. Annals of Pharmacotherapy, 44, 1810-1816. doi: 10.1345/aph.1P163
  30. Jonah, D. E., Cusack, K., Fomeris, C. A., Forneris, C. A., Wilkins, T. M., Sonis, J., Middleton, J. C., Feltner, C., Meredith, D., Cavanaugh, J., Brownley, K. A., Olmsted, K. R., Greenblat, A., Weil, A., & Gaynes, B. N. (2013). Psychological and pharmacological treatments for adults with posttraumatic stress disorder (PTSD). Comparative Effectiveness Reviews, 92. Retrieved from http://www.ncbi.nlm.nih.gov/books/NBK137702/
  31. Johnson, B. A., Rosenthal, N., Capece, J. A., Wiegand, F., Mao, L., Beyers, K., McKay, A., Ait-Daoud, N., Addolorato, G., Anton, R. F., Ciraulo, D. A., Kranzler, H. R., Mann, K., O'Malley, S. S., & Swift, R. M. (2008). Improvement of physical health and quality of life of alcohol-dependent individuals with topiramate treatment: U.S. multisite randomized controlled trial. Archives of Internal Medicine, 169, 1188-1199. doi: 10.1001/archinte.***********
  32. Batki, S. L., Pennington, D. L., Lasher, B., Neylan, T. C., Metzler, T., Waldrop, A., Delucchi, K., & Herbst, E. (2014). Topiramate treatment of alcohol use disorder in Veterans with posttraumatic stress disorder: A randomized controlled pilot trial. Alcoholism, Clinical and Experimental Research, 38, 2169-2177. doi:10.1111/acer.12496
  33. Davis, L. L., Davidson, J. R., Ward, L. C., Bartolucci, A., Bowden, C. L., & Petty, F. (2008). Divalproex in the treatment of posttraumatic stress disorder: a randomized, double-blind, placebo-controlled trial in a Veteran population. Journal of Clinical Psychopharmacology, 28, 84-88. doi: 10.1097/JCP.0b013e318160f83b
  34. Hamner, M. B., Faldowski, R. A., Robert, S., Ulmer, H. G., Horner, M. D., & Lorberbaum, J. P. (2009). A preliminary controlled trial of divalproex in posttraumatic stress disorder. Annals of Clinical Psychiatry, 21, 88-94.
  35. Davidson, J. R., Brady, K., Mellman, T. A., Stein, M. B., & Pollack, M. H. (2007). The efficacy and tolerability of tiagabine in adult patients with post-traumatic stress disorder. Journal of Clinical Psychopharmacology, 27, 85-88. doi:10.1097/JCP.0b013e31802e5115
  36. Hertzberg, M. A., Butterfield, M. I., Feldman, M. E., Beckham, J. C., Sutherland, S. M., & Connor, K. M. (1999). A preliminary study of lamotrigine for the treatment of posttraumatic stress disorder. Biological Psychiatry, 45, 1226-1229. doi: 10.1016/S0006-3223(99)00011-6
  37. Pae, C. U., Lim, H. K., Peindl, K., Ajwani, N., Serretti, A., Patkar, A. A., & Lee, C. (2008). The atypical antipsychotics olanzapine and risperidone in the treatment of posttraumatic stress disorder: A meta-analysis of randomized, double-blind, placebo-controlled clinical trials. International Clinical Psychopharmacology, 23, 1-8. doi: 10.1097/YIC.0b013e32825ea324
  38. Krystal, J. H., Rosenheck, R. A., Cramer, J.A., Vessicchio, J. C., Jones, K. M., Vertrees, J. E., Horney, R. A., Huang, G. D., & Stock, C. (2011). Adjunctive risperidone treatment for antidepressant-resistant symptoms of chronic military service-related PTSD. Journal of the American Medical Association, 306, 493-502. doi: 10.1001/jama.2011.1080
  39. Raskind, M. A., Peskind, E. R., Hoff, D. J., Hart, K. L., Holmes, H. A., Warren, D., Shofer, J., O'Connell, J., Taylor, F., Gross, C., Rohde, K., & McFall, M. E. (2007). A parallel group placebo controlled study of prazosin for trauma nightmares and sleep disturbance in combat Veterans with post-traumatic stress disorder. Biological Psychiatry, 61, 928-934. doi: 10.1016/j.biopsych.2006.06.032
  40. Kachatryan, D., Groll, D., Booij, L., Sepehry, A. A., & Schütz, C. G. (in press). Prazosin for treating sleep disturbances in adults with posttraumatic stress disorder: A systematic review and meta-analysis of randomized controlled trials. General Hospital Psychiatry.
  41. Raskind, M. A., Peterson, K., Williams, T., Hoff, D. J., Hart, K., Holmes, H., Homas, D., Hill, J., Daniels, C., Calohan, J., Millard, S. P., Rohde, K., O'Connell, J., Pritzl, D., Feiszli, K., Petrie, E. C., Gross, C., Mayer, C. L., Freed, M. C., Engel, C., & Peskind, E. R. (2013). A trial of prazosin for combat trauma PTSD with nightmares in active-duty soldiers returned from Iraq and Afghanistan. American Journal of Psychiatry, 170, 1003-10. doi: 10.1176/appi.ajp.2013.12081133
  42. Fox, H. C., Anderson, G. M., Tuit, K., Hansen, J., Kimmerling, A., Siedlarz, K. M., Morgan, P. T., & Sinha, R. (2012). Prazosin effects on stress- and cue-induced craving and stress response in alcohol-dependent individuals: Preliminary findings. Alcoholism, Clinical and Experimental Research, 36, 351-360. doi:10.1111/j.1530-0277.2011.01628.x
  43. Simpson, T.L., Malte, C.A., Dietel, B., Tell, D., Pocock, I., Lyons, R., Varon, D., Raskind, M., & Saxon, A.J. (2015). A pilot trial of prazosin, an alpha-1 adrenergic antagonist, for comorbid alcohol dependence and posttraumatic stress disorder. Alcoholism: Clinical and Experimental Research, 39, 808-817. doi: 10.1111/acer.12703
  44. Davidson, J., Kudler, H., Smith, R., Mahorney, S. L., Lipper, S., Hammett, E., Saunders, W. B., & Cavenar, J. O. Jr. (1990). Treatment of posttraumatic stress disorder with amitriptyline and placebo. Archives of General Psychiatry, 47, 259-266. doi: 10.1001/archpsyc.1990.01810150059010
  45. Petrakis, I. L., Ralevski, E., Desai, N., Trevisan, L., Gueorguieva, R., Rounsaville, B., & Krystal, J. H. (2012). Noradrenergic vs serotonergic antidepressant with or without naltrexone for Veterans with PTSD and comorbid alcohol dependence. Neuropsychopharmacology, 37, 996-1004. doi: 10.1038/npp.2011.283
  46. Frank, J. B., Kosten, T. R., Giller, E. L. Jr., & Dan, E. (1998). A randomized clinical trial of phenelzine and imipramine for posttraumatic stress disorder. American Journal of Psychiatry, 145, 1289-1291.
  47. Braun, P., Greenberg, D., Dasberg, H., & Lerer, B. (1990). Core symptoms of posttraumatic stress disorder unimproved by alprazolam treatment. Journal of Clinical Psychiatry, 51, 236-238.
  48. Gelpin, E., Bonne, O., Peri, T., Brandes, D., & Shalev, A. Y. (1996). Treatment of recent trauma survivors with benzodiazepines: A prospective study. Journal of Clinical Psychiatry, 57, 390-394.
  49. Rothbaum, B. O., Price, M., Jovanovic, T., Norrholm, S. D., Gerardi, M., Dunlop, B., Davis, M., Bradley, B., Duncan, E. J., Rizzo, A., & Ressler, K. J. (2014). A randomized, double-blind evaluation of d-cycloserine or alprazolam combined with virtual reality exposure therapy for posttraumatic stress disorder in Iraq and Afghanistan War Veterans. American Journal of Psychiatry, 171, 640-648. doi 10.1176/appi.ajp.2014.13121625
  50. Guina, J., Rossetter, S. R., DeRHODES, B. J., Nahhas, R. W., & Welton, R. S. (2015). Benzodiazepines for PTSD: A systematic review and meta-analysis. Journal of Psychiatric Practice, 21, 281-303. doi:10.1097/PRA.0000000000000091
  51. Aerni, A., Traber, R., Hock, C., Roozendaal, B., Schelling, G., Papassotiropoulos, A., Nitsch, R. M., Schnyder, U., & de Quervain, D. J. (2004). Low-dose cortisol for symptoms of posttraumatic stress disorder. American Journal of Psychiatry, 161, 1488-90. doi: 10.1176/appi.ajp.161.8.1488
  52. Yehuda, R., Bierer, L. M., Pratchett, L. C., Lehrner, A., Koch, E. C., Van Manen, J. A., Flory, J. D., Makotkine, I., & Hildebrandt, T. (2015). Cortisol augmentation of a psychological treatment for warfighters with posttraumatic stress disorder: Randomized trial showing improved treatment retention and outcome. Psychoneuroendocrinology, 51, 589-597. doi:10.1016/j.psyneuen.2014.08.004
  53. Morales-Medina, J. C., Dumont, Y., & Quirion, R. (2010). A possible role of neuropeptide-Y in depression and stress. Brain Research, 1314, 194-205. doi: 10.1016/j.brainres.2009.09.077
  54. Morgan, C. A., 3rd, Wang, S., Southwick, S. M., Rasmusson, A., Hazlett, G., Hauger, R. L., & Charney, D. S. (2000). Plasma neuropeptide-Y concentrations in humans exposed to military survival training. Biological Psychiatry, 47, 902-909. doi:S0006-3223(99)00239-5
  55. Pitman, R. K., Orr, S. P., & Lasko, N. B. (1993). Effects of intranasal vasopressin and oxytocin on physiologic responding during personal combat imagery in Vietnam Veterans with posttraumatic stress disorder. Psychiatry Research, 48, 107-17.
  56. Otto, M. W., Tolin, D. F., Simon, N. M., Pearlson, G. D., Basden, S., Meunier, S. A., Hofmann, S. G., Eisenmenger, K., Krystal, J. H., & Pollack, M. H. (2010). Efficacy of d-cycloserine for enhancing response to cognitive-behavior therapy for panic disorder. Biological Psychiatry, 67, 365-70. doi: 10.1016/j.biopsych.2009.07.036
  57. Ressler, K. J., Rothbaum, B. O., Tannenbaum, L., Anderson, P., Graap, K., Zimand, E., Hodges, L., & Davis, M. (2004). Cognitive enhancers as adjuncts to psychotherapy: Use of D-cycloserine in phobic individuals to facilitate extinction of fear. Archives of General Psychiatry, 61, 1136-1144. doi: 10.1001/archpsyc.61.11.1136
  58. Rothbaum, B. O., Gerardi, M., Bradley, B., & Friedman, M. J. (2011). Evidence-based treatments for posttraumatic stress disorder in Operation Enduring Freedom and Operation Iraqi Freedom military personnel. In J. I. Ruzek, P. P. Schnurr, J. J. Vasterling, & M. J. Friedman (Eds.), Caring for Veterans with Deployment-Related Stress Disorders (pp. 215-239). Washington DC: American Psychological Association.
  59. McAllister, T. W., Zafonte, R., Jain, S., Flashman, L. A., George, M. S., Grant, G. A., He, F., Lohr, J. B., Andaluz, N., Summerall, L., Paulus, M. P., Raman, R., & Stein, M. B. (2015). Randomized placebo-controlled trial of methylphenidate or galantamine for persistent emotional and cognitive symptoms associated with PTSD and/or traumatic brain injury. Neuropsychopharmacology : Official Publication of the American College of Neuropsychopharmacology, doi:10.1038/npp.2015.282
  60. Caddy, C., Giaroli, G., White, T. P., Shergill, S. S., & Tracy D.K. (2014). Ketamine as the prototype glutamatergic antidepressant: Pharmacodynamic actions, and a systematic review and meta-analysis of efficacy. Therapuetic Advances in Psychopharmacology, 4, 75-99. doi: 10.1177/2045125313507739
  61. Feder, A., Parides, M. K., Murrough, J. W., Perez, A. M., Morgan, J. E., Saxena, S., Kirkwood, K., Aan Het Rot, M., Lapidus, K. A., Wan, L. B., Iosifescu, D., & Charney, D. S. (2014). Efficacy of intravenous ketamine for treatment of chronic posttraumatic stress disorder: A randomized clinical trial. JAMA Psychiatry, 71, 681-688. doi: 10.1001/jamapsychiatry.2014.62
  62. Neumeister, A. (2013). The endocannabinoid system provides an avenue for evidence-based treatment development for PTSD. Depression and Anxiety, 30, 93-96. doi:10.1002/da.22031
  63. Neumeister, A., Normandin, M. D., Pietrzak, R. H., Piomelli, D., Zheng, M. Q., Gujarro-Anton, A., Potenza, M. N., Vailey, C. R., Lin, S. F., Najafzadeh, S., Ropchan, J., Henry, S., Corsi-Travali, S., Carson, R. E., & Huang, Y. (2013). Elevated brain cannabinoid CB1 receptor availability in post-traumatic stress disorder: A positron emission tomography study. Molecular Psychiatry, 18, 1034-1040. doi:10.1038/mp.2013.61
  64. Bonn-Miller, M. O., Boden, M. T., Vujanovic, A. A., & Drescher, K. D. (2013). Prospective investigation of the impact of cannabis use disorders on posttraumatic stress disorder symptoms among Veterans in residential treatment. Psychological Trauma: Theory, Research, Practice, and Policy, 52, 193-200. doi: 10.1037/a0026621
  65. Betthauser, K., Pilz, J., & Vollmer, L. E. (2015). Use and effects of cannabinoids in military Veterans with posttraumatic stress disorder. American Journal of Health-System Pharmacy : AJHP : Official Journal of the American Society of Health-System Pharmacists, 72, 1279-1284. doi:10.2146/ajhp140523
  66. Akhoundpour, A. M., Hebrani, P., Mortezania, M., Haghighi, M. B., & Javanbakht, A. (2014). Baclofen add-on to citalopram in treatment of posttraumatic stress disorder. Journal of Clinical Psychopharmacology, 34, 240-243. doi: 10.1097/JCP.0000000000000089
  67. Simiola, V., Neilson, E. C., Thompson, R., & Cook, J. M. (2015). Preferences for trauma treatment: A systematic review of the empirical literature. Psychological Trauma, 7, 516-524. doi: 10.1037/tra0000038.

Back to top

Date this content was last updated is at the bottom of the page.

Share this page

Search Pilots

Search PILOTS*, the largest citation database on PTSD.
What is PILOTS?

The National Center for PTSD does not provide direct clinical care, individual referrals or benefits information.

PTSD Information Voice Mail:
(802) 296-6300
Contact Us: ncptsd@va.gov
Also see: VA Mental Health

FacebookTwitterYouTube