S. Michelle Barnett

Running Head: Therapeutic Drug Use

As someone who has struggled with post-traumatic stress disorder (PTSD) for nearly 15 years, I have chosen to focus my research into therapeutic drug use regarding this disorder. According to the Diagnostic and Statistical Manual of Mental Disorders (DSM5), diagnostic criteria for PTSD include a history of exposure to a traumatic event that meets specific stipulations and symptoms from each of four symptom clusters: intrusion, avoidance, negative alterations in cognitions and mood, and alterations in arousal and reactivity. The sixth criterion concerns duration of symptoms; the seventh assesses functioning; and, the eighth criterion clarifies symptoms as not attributable to a substance or co-occurring medical condition. The diagnostic criteria are as follows:

Criterion A: stressor – The person was exposed to: death, threatened death, actual or threatened serious injury, or actual or threatened sexual violence, as follows: (one required)

  1. Direct exposure.
  2. Witnessing, in person.

Criterion B: intrusion symptoms – The traumatic event is persistently re-experienced in the following way(s): (one required)

  4. Intense or prolonged distress after exposure to traumatic reminders.

Criterion C: avoidance – Persistent effortful avoidance of distressing trauma-related stimuli after the event: (one required)

  1. Trauma-related thoughts or feelings.

Criterion D: negative alterations in cognitions and mood – Negative alterations in cognitions and mood that began or worsened after the traumatic event: (two required)

  7. Constricted affect: persistent inability to experience positive emotions.

Criterion E: alterations in arousal and reactivity- Trauma-related alterations in arousal and reactivity that began or worsened after the traumatic event: (two required)

  1. Irritable or aggressive behavior
  2. Self-destructive or reckless behavior
  3. Hypervigilance
  4. Exaggerated startle response
  5. Problems in concentration
  6. Sleep disturbance

Criterion F: duration- Persistence of symptoms (in Criteria B, C, D, and E) for more than one month.

Criterion G: functional significance- Significant symptom-related distress or functional impairment (e.g., social, occupational).

Criterion H: exclusion- Disturbance is not due to medication, substance use, or other illness.

It is important to note that full diagnosis is not met until at least six months after the trauma(s), although onset of symptoms may occur immediately (American Psychiatric Association, 2013). The prevalence of PTSD, based on the U.S. population, is as follows:

  • About 8 million adults have PTSD during a given year.
  • About 10 of every 100 women (or 10%) develop PTSD sometime in their lives compared with about 4 of every 100 men (or 4%) (PTSD, 2007).

What causes PTSD? There are biological, genetic, sociological and behavioral factors that are associated with PTSD. I will start first with biological. Because only a percentage of people exposed to traumatic events develop PTSD, it is important to explain the factors that increase the risk for the development of PTSD following trauma exposure. Recent data has implicated biological and familial risk factors for PTSD. For example, recent studies have shown an increased prevalence of PTSD in the adult children of Holocaust survivors, even though these children, as a group, do not report a greater exposure to life-threatening events. At risk family members, such as children, may be more vulnerable to PTSD because they witnessed the extreme suffering of a parent with chronic PTSD rather than because of inherited genes (National Center for Biotechnology Information, 2017). It is possible that when combined, the person’s psychological history, the nature of the trauma, and the availability of support post-trauma can cause PTSD symptoms to develop after a traumatic event. However, someone without risk factors who is exposed to a traumatic event also may develop symptoms. The amygdala is part of the limbic system that is involved in the expression of emotion, autonomic reactions, and emotional memory. Dysfunction in the amygdala may produce symptoms of PTSD. I discovered an article on the Health Communities website in relation to PTSD that states:

“Overwhelming trauma can cause changes in brain function that produce symptoms of PTSD: hyperarousal, numbing, sleep disturbance, irritability, intrusive emotions and memories, flashbacks, outbursts, and memory impairment. The body responds to stress and trauma by releasing several stress hormones. When a person is subjected to repeated or severe trauma, the physiological stress response becomes hyperactive and hyperarousal and intrusive symptoms of PTSD develop. There also may be a biological component to numbing and other dissociative symptoms of PTSD. Some studies show that when people who have been exposed to prolonged or repeated trauma are exposed to any stimulus reminiscent of the trauma, the brain releases opiates that can produce emotional non-responsiveness, or numbing, and amnesia. Serotonin depletion may result from repeated exposure to severe stress and trauma, which may be a factor in the development of irritability and violent or angry outbursts in people with PTSD” (PTSD causes, 2017).

PTSD is a prevalent, disabling anxiety disorder that constitutes a major health care burden. Despite intensive research efforts during the past few decades, PTSD remains poorly understood in terms of etiology and shows modest response to current treatment interventions. If the specific genes associated with PTSD risk can be identified, this could provide insight into the cause of PTSD that could lead to the development of new diagnostic and therapeutic strategies. An article found on the National Center for Biotechnology Information (NCBI) website states the following:

“Although recent years have seen an exponential increase in the number of studies examining the influence of candidate genes on PTSD diagnosis and symptomatology, most studies have been characterized by relatively low rates of PTSD, with apparent inconsistencies in gene associations linked to marked differences in methodology” (National Center for Biotechnology Information, 2017).

There is evidence to that shows that social support, social cognition, and attachment organization contribute to emotion regulation under conditions of traumatic stress and contribute to risk for PTSD. Individuals that have social bonds may receive or develop a sense of safety, which is necessary to recovery from PTSD. The process of therapy may be considered one type of social bonding (PTSD, 2009).

The National Center for PTSD states that evidence for PTSD pharmacology is strongest for specific selective serotonin reuptake inhibitors (SSRIs), such as sertraline (Zoloft), paroxetine (Paxil), and fluoxetine (Prozac), and also a serotonin norepinephrine reuptake inhibitor (SNRI) called venlafaxine (Effexor). At this time, only sertraline and paroxetine are approved by the Food and Drug Administration (FDA) for PTSD (PTSD: National Center for PTSD, 2007). As also noted by The National Center for PTSD:

“The risks of taking SSRIs and SNRIs are mild to moderate side effects such as upset stomach, sweating, headache, and dizziness. Some people have sexual side effects, such as decreased desire to have sex or difficulty having an orgasm. Some side effects are short-term, though others may last as long as you are taking the medication” (PTSD, 2009).

“The 2017 VA/DoD Clinical Practice Guideline for PTSD suggests other antidepressants for PTSD treatment if the four strongly recommended medications are ineffective, unavailable, or not tolerated by the individual. These medications are the serotonin potentiator, nefazodone (Serzone); the tricyclic antidepressant, imipramine (Tofranil); and the mono-amine oxidase inhibitor, phenelzine (Nardil). Both nefazodone and phenelzine require careful management as they carry potentially serious toxicities” (PTSD, 2007).

The 2017 VA/DoD Clinical Practice Guideline for PTSD recommends trauma-focused psychotherapy as the first-line treatment for PTSD over pharmacotherapy. For patients who prefer pharmacotherapy or who do not have access to psychotherapy, medications remain a treatment option. PTSD also carries high levels of psychiatric co-morbidities which may be treated with medications. Even though every case of PTSD has different biological, psychological, and social factors with different treatment options, there are empirically supported treatments that can reduce symptoms. Most studies show that cognitive behavioral therapies (CBT) such as Prolonged Exposure (PE), Cognitive Processing Therapy (CPT), and Eye Movement Desensitization and Reprocessing (EMDR) have greater effects on relieving PTSD symptoms than medications, but many unanswered questions remain when it comes to the role of pharmacotherapy (PTSD, 2007).

In conclusion, as a combat Veteran who has dealt with PTSD for nearly 15 years, my experience is that a combination of the right medication and trauma-focused psychotherapy, specifically CBT and CPT, has been the best option for me. The medication assists me with being able to have less nightmares, anxiety, and depression, and the therapy has taught me valuable coping skills which the medication cannot cure. Although I dislike having to take medication daily, I have discovered that not doing so actually hampers my ability to think clearly and to utilize the coping skills I have learned in therapy.



(5th ed.). Washington, DC: Author.

National Center for Biotechnology Information. (n.d.). Retrieved December 05, 2017, from




PTSD: National Center for PTSD. (2007, July 05). Retrieved December 05, 2017, from


PTSD causes. (n.d.). Retrieved December 05, 2017, from


PTSD: National Center for PTSD. (2009, January 07). Retrieved December 05, 2017, from



PTSD: National Center for PTSD. (2007, January 01). Retrieved December 05, 2017, from

