BAL HARBOUR, FLA—“I’m not going to defend posttraumatic stress disorder. I think there are a lot of problems with the diagnosis and that we still have a lot of work to do in the field,” said Rachel Yehuda, PhD, in response to earlier presentations by an anthropologist and a historian who called into question the diagnosis and its utility to society as a whole. Speaking at the 15th Annual Meeting of the American Neuropsychiatric Association, Dr. Yehuda, Professor of Psychiatry at the Mount Sinai School of Medicine in New York City, weighed in on what she believed were the controversial issues in the field “as a scientist and as a mental health professional who has had the opportunity to speak with hundreds of trauma survivors” and went on to make the point that the perspective offered by anthropology or history may be different from that offered by mental health. Dr. Yehuda is also Founder and Director of the Traumatic Stress Studies Program at Mount Sinai and the Bronx Veterans Affairs Hospital.

WHAT’S IN A NAME?

Dr. Yehuda asserted that one of the most salient controversies in the field of posttraumatic stress disorder “has to do with the term ‘posttraumatic stress disorder’ itself, which is a highly ambiguous term since we have not decided whether to emphasize ‘posttraumatic stress’ or ‘disorder.’ ”

DEBUNKING THE DIAGNOSTIC CRITERIA

The diagnosis of posttraumatic stress disorder traces its origins to 1980 and is itself a source of continuing controversy. “The diagnosis of posttraumatic stress disorder is a good example of what happens when you try to create a description of something without an empiricial literature to guide you—you make assumptions that may not hold up.”

For example, Dr. Yehuda said, “Implicit in the diagnosis of posttraumatic stress disorder—as articulated in the DSM-III—were the following: that traumatic events were unusual or rare, that posttraumatic stress disorder is a prototype response to such events, that other psychiatric disorders would not share the exclusive relationship that trauma has with posttraumatic stress disorder, and that once people develop posttraumatic stress disorder, it would be hard to get rid of.” Subsequent research, however, “has demonstrated that each and every one of these assumptions is not true.”

Traumatic events are not unusual, Dr. Yehuda elaborated. “Kessler and colleagues demonstrated that 60% of people in the United States had been exposed to at least one event that met the criteria for a traumatic event. Posttraumatic stress disorder only occurred in a percentage of those exposed. So events like rape and child abuse are associated with a higher percentage of posttraumatic stress disorder than other events—but no matter what event we’re talking about, more people do not develop posttraumatic stress disorder than do.”

Combining the data from Kessler and colleagues would reveal quite a high prevalence of trauma exposure and quite a low prevalence of posttraumatic stress disorder to those events, she said. “Ninety-two percent of men and 80% of women did not develop posttraumatic stress disorder to these events.

“So we’ve just shattered two of the assumptions. What about the third one?” Data from a study by McFarlane and colleagues demonstrated that when you examine people prospectively from the moment of the traumatic event and follow them for several months, the majority of people do not develop psychiatric disorders, Dr. Yehuda said. “Among those who do, depression is just as likely an outcome as posttraumatic stress disorder. Drug abuse can be a likely outcome, and anxiety disorders other than posttraumatic stress disorder, panic disorders, or eating disorders can also occur in response to trauma,” she noted. “In other words, there’s no exclusive relationship between trauma and posttraumatic stress disorder, and as far as this being a disorder that doesn’t remit, what we now know from prospective studies and retrospective studies is that the majority of people who develop posttraumatic stress disorder do show a remission of symptoms.”

PARADIGM SHIFT

To help provide more clarity about the effects of trauma and posttraumatic stress disorder, Dr. Yehuda called for a paradigm shift in the consideration of posttraumatic stress disorder. “The new formulation might say that posttraumatic stress disorder is a specific response to trauma occurring under specific circumstances and in response to prespecified risk factors, rather than simply the psychological response resulting from a traumatic event,” she explained. Dr. Yehuda noted that although there has been very little discussion on the type of symptoms that should be represented by the posttraumatic stress disorder diagnosis, “less is known about why any given individual develops posttraumatic stress disorder.”

She noted that factors such as the degree of perceived controllability and predictability, plus feelings of shame, humiliation, guilt, and the sense that one could have prevented what happened and minimized damage and injury to others, could be important determinants. “Obviously how one feels in response to any event is in part going to be socially and culturally mediated, but only some will intensify pathologic responses,” she said. Another issue concerns defining pathologic responses and the time at which you make this decision posttrauma. “For example, in the immediate aftermath of 9/11, many people had symptoms, but is this pathology?” she asked. “What is gained by calling these reactions pathological versus stating that they are normal responses?”

IMPLICATIONS OF A FAILURE TO RECOVER

According to Dr. Yehuda, a critical question with respect to posttraumatic stress disorder is “Why do people seem to recover at different rates, and why do some people seem not to recover?” She stated that posttraumatic stress disorder appears to represent a failure to recover from the effects of a trauma but noted that “there are two ways to look at this.” One way is to view failure to recover as a function of time. The other way is that those who don’t recover have predetermined risk factors that show that the response to traumatic events may have been different from the outset and possibly could have been predicted, Dr. Yehuda clarified. The failure-to-recover model would compel clinicians “to search for posttraumatic factors that inhibit recovery,” and the risk model “would identify those with pretraumatic risk factors,” she said.

Depending on the model, there would be different treatment implications, Dr. Yehuda noted. “With a failure-to-recover model, one might wish to delay treatment and allow natural restitution or administer prophylactic treatments to everyone in the immediate aftermath of trauma. In a risk model, one would want to administer prophylactic treatment only to those at risk, and these would be different treatments,” she added.

Essentially, Dr. Yehuda said, the problem is “how do we distinguish from a fundamentally normal response that is possibly prolonged and a response that is fundamentally different from the outset that leads the person on a different trajectory of recovery?”

ALL ABOUT THE AMYGDALA?

Understanding the biology of posttraumatic stress disorder and how it develops longitudinally provides a potential way of addressing the question of what constitutes a pathologic response to trauma, Dr. Yehuda said. She focused on the importance of the amygdala as a brain structure that is very important in the fear response and explained how the amygdala is activated in response to sensory information about danger.

The physiologic responses initiated by the amygdala include the activation of the hypothalamus-pituitary-adrenal axis, as well as other responses in the sympathetic nervous system, the latter of which is responsible for the release of adrenaline. However, in addition to responses that turn on the stress responses, there are also reactions that are involved in the containment of this response. “For example,” she noted, “cortisol is one of the hormones that’s also involved with the containment of that stress response —the ‘Off’ switch.”

All things being equal, “the response to stressors is not prolonged: People return to baseline within hours,” Dr. Yehuda remarked. “Long-term effects are observed only after exposure to a subsequent stressor.”

THE BIOLOGY OF POSTTRAUMATIC STRESS

Stress theory “can take us down the wrong path” in the consideration of posttraumatic stress disorder, Dr. Yehuda observed. However, the problem in posttraumatic stress disorder is understanding why the person still has biologic reactions to an event that has long since stopped occurring, she noted. “In stress theory, the biologic responses usually reverse themselves when the stressor is no longer present. When investigators initially looked at the biology of posttraumatic stress disorder, they saw a lot of things that made us think of stress response, such as increased activation of the amygdala in response to the fear-related stimulus, but at the same time, a reduced functioning of the anterior cingulate was observed.” What this means, Dr. Yehuda added, “is that it isn’t simply that the amygdala’s activated but also that the brain region that normally asserts an inhibition on the amygdala isn’t functioning exactly right. Catecholamine levels are high in patients with posttraumatic stress disorder under baseline conditions, but in the same blood sample cortisol levels are low.”

These cortisol-related alterations “seem to be unique in posttraumatic stress disorder but it won’t surprise me if exposure to trauma or premorbid histories will result in similar biologic alterations that have been observed in this disorder,” Dr. Yehuda said, “because we don’t really know whether biologic alterations in posttraumatic stress disorder relate to the disorder or preexisting risk factors. The point is, however, that the biology of posttraumatic stress disorder is not simply the biology of stress. It seems to also have to do with the biology of a stress response that has not been properly contained.”

POSTTRAUMATIC STRESS COHORTS

Persons who were studied in the immediate aftermath of rape showed lower cortisol levels if they had a prior history of rape or assault, suggesting “that it would be very important to study all our biologic measures in persons who are at risk for the development of posttraumatic stress disorder,” Dr. Yehuda said. She and her colleagues conducted such a study in a cohort of adult children of Holocaust survivors.

The children of Holocaust survivors were three times more likely to develop posttraumatic stress disorder in response to their own traumatic events compared with Jewish demographically matched controls, according to Dr. Yehuda. “The risk factor appears to be posttraumatic stress disorder in the mother,” she said. “And then if you look, for example, at cortisol levels, you can see that in the high-risk group people who are children of Holocaust survivors with posttraumatic stress disorder but not their own traumatic event, their cortisol levels are slightly lower.”

Such findings lead to one possible trajectory for posttraumatic stress disorder, Dr. Yehuda said. “Let’s say you have low cortisol levels due to a preexisting risk factor and then a traumatic event occurs. You might have increased adrenaline or increased catecholamine levels. This might lead to an overconsolidation repairing of memories of distress. It would make traumatic reminders distressing; the distress could lead to further pairing with nonspecific stimuli. This could result in the failure of habituation and extinction. Survival would be anxious, and there would be other behavioral consequences.”

A CULTURE OF VICTIMIZATION

“I completely agree with Ben Shephard’s comment that we’re creating a culture of victimization to the extent that we give people the message that they will develop posttraumatic stress disorder following trauma exposure, rather than explaining posttraumatic stress disorder as a rare response to trauma,” Dr. Yehuda said, referring to an earlier presentation at the meeting. “Here’s how to not create a culture of victimization: We can provide a proper educational message that suggests that individuals have capacities for being able to overcome adversities and demonstrating resilience,” she asserted.

“My main message is that while short-term responses to trauma are universal, chronic responses to trauma appear to develop because of failure to recover from the normal effects of stress,” Dr. Yehuda said. “This may be due in some measure to prior experiences, such as how one interprets what’s going on. It could be influenced by personality disorder, low IQ, lack of cognitive flexibility, your parents—any or all of these factors—but the point here is that long-lasting responses to trauma result not simply from the experience of fear or helplessness but from how your body interprets these responses,” she explained.

“The reaction to stress is biological, but it is fundamentally influenced by what you think at the time of the trauma, which is influenced by pretrauma factors, which is influenced by cultural factors,” Dr. Yehuda noted. “Mental health treatment is about figuring out what gets in the way of stress recovery,” she concluded.

—C. Justin Romano

Suggested Reading
Ballenger JC, Davidson JR, Lecrubier Y, et al. Consensus statement update on posttraumatic stress disorder from the International Consensus Group on Depression and Anxiety. J Clin Psychiatry. 2004;65 suppl 1:55-62.
Kessler RC, Sonnega A, Bromet E, et al. Posttraumatic stress disorder in the National Comorbidity Survey. Arch Gen Psychiatry. 1995;52:1048-1060.
Yehuda R, Golier JA, Halligan SL, Harvey PD. Learning and memory in Holocaust survivors with posttraumatic stress disorder. Biol Psychiatry. 2004; 55:291-295.

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