Post-traumatic Stress Disorder and Fear Responses

The authors' research on post-traumatic stress disorder builds upon previous psychophysiological studies and their effects on human behavior. Post-traumatic stress disorder (PTSD) is a psychiatric disorder caused by traumatic life events. Approximately 8% of Americans have experienced some form of PTSD in their lives. PTSD heightens fear responses, hinders restrictions on conditioned fear, and inhibits the body's ability to distinguish between safety and fear signaling cues. Since this disorder varies case by case, not all individuals can be successfully treated through conventional methods.

Michopoulos et al. hope to find alternative ways to treat affected individuals by looking at how PTSD influences specific parts of the body.

Patients with this disorder have impaired automatic stress response systems that are responsible for fear stimuli. These stress responses occur in the hypothalamic-pituitary-adrenal (HPA) axis, which functions as the control center for the body’s autonomic system. Searching for potential ways to target the HPA axis, the authors found dexamethasone. Dexamethasone is a glucocorticosteroid used for relieving symptoms related to intracranial pressure, but its long-term use can suppress cortisol and the HPA axis. This means that the suppression of cortisol and the HPA axis should theoretically suppress stress and fear responses. Michopoulos, et al. devised a study to test their hypothesis that dexamethasone and cortisol suppression would decrease fear expression and increase fear extinction in PTSD patients.

To test the effectiveness of dexamethasone treatment, the authors studied 68 willing patients from Grady Memorial Hospital over the course of two and a half years. Figure 1 shows the design model for the double-blind, randomized, crossover study. The study participants took 4 unique self-reports to measure PTSD symptoms. Participants who scored higher on trauma exposure were identified as PTSD+, while those who scored lower were labeled PTSD- (Table 1). Groups were randomized and given their respective pills to take at night, one half receiving dexamethasone (DEX) and the other receiving placebos (PBO). The next morning, their blood samples were taken and assayed for cortisol measurements. Fear-potential startle sessions were performed shortly after to measure fear acquisition and extinction between DEX and PBO participants. A week later, participants were given the opposite pill and underwent fear-potential startle sessions again.

The fear acquisition paradigm focused on learning a conditioned fear response. It included both reinforced conditioned (CS+) and non-reinforced conditioned (CS-) stimuli, followed by an unconditioned (US) stimulus. The conditioned stimuli consisted of colored shapes shown on a monitor, while the unconditioned stimuli involved an air blast to the larynx to induce a potentially fear-inducing startle. This tested the participants’ ability to distinguish between safety (CS+) and danger cues (CS-). The fear extinction paradigm represented a decline in fear-conditioned responses, using the same methods as for fear acquisition. However, these potentially fear-inducing startles were performed in early and late extinction blocks to determine if there was a significant difference in response. Both fear acquisition and extinction tests were conducted to observe the efficacy of dexamethasone treatment in PTSD patients.

PTSD+ and PTSD- patients had no significant differences in fear-conditioned learning between PBO and DEX treatment (Fig. 2). This showed dexamethasone having no effect on fear expression. For safety discrimination, fear-potential startle responses in PTSD- patients remained constant for DEX and PBO treatment as they were able to differentiate between safety (CS+) and danger (CS-) cues. However, PTSD+ patients who received PBO treatment could not distinguish safety from danger cues while DEX treated patients could distinguish between the two (Fig. 3). Fear-potential startle responses from the fear extinction session in Figure 4 showed increased fear extinction prevalent in all PTSD- patients. PTSD+ participants who received PBO treatment showed decreased fear extinction as opposed to participants with DEX treatment who showed increased fear extinction, similar to the PTSD- group. Low fear extinction suggests that affected individuals have difficulty unlearning conditioned fear responses. The results from the authors' study suggest that dexamethasone usage may facilitate fear extinction and discrimination in PTSD patients. Notably, dexamethasone may also be used as a pharmacological agent to assist with extinction-based therapies.

Analysis.

The authors' study's hypothesis was valid. Previous studies provided evidence for PTSD symptoms such as increased fear responses and decreased safety discrimination. Michopoulos et al. built upon the existing evidence on PTSD to discover alternative methods to medicine. However, much is still unknown about the treatment of psychiatric disorders, which leaves room for further studies.

The sociodemographic characteristics between PTSD+ and PTSD- individuals were consistent (Table 1). Age, race, and gender were within a similar range to eliminate external factors that could affect data. The design model (Fig. 1) clearly showed the complete study.

Certain limitations, such as self-reporting measures, may alter data collection since individuals interpret trauma differently. This establishes a bias on the PTSD diagnoses as patients control the information they give. The absence of medical history makes it difficult to factor in other disorders and pre-existing conditions that may negatively affect data. Michopoulos et al. have stated the possible problems listed above, so they are aware of these limitations.

Although there was the possibility of self-report bias from the participants, the authors presented an unbiased interpretation of their results. The study was placebo-controlled, randomized, and double-blinded to ensure fairness. The results showed dexamethasone facilitating fear extinction and discrimination (Fig. 3 & 4), which proved their hypothesis to be partially true as fear expression remained unaffected (Fig. 2). These findings have prompted Michopoulos et al. to suggest the further viability of dexamethasone and its suppression of cortisol levels. The authors propose dexamethasone as a possible pharmacological agent to assist in extinction-based therapy. This provides supplementary evidence that the field of PTSD treatment is open to interpretation. Future research could focus on new ways of looking at PTSD to seek alternative methods of treatment.

Did you like this example?

341

18