Intifada and the Continuous Terror Paradigm

August 31st, 2010

I would like to introduce the concept of “Continuous Terror Paradigm”, proposed by Dr. Shalev and colleagues from Hadassah University Hospital.

While many studies in psychological literature evaluate PTSD following a discrete traumatic occurrence, the recent article by Dr. Shalev and colleagues evaluates the effect of continuous terror by examining the occurrence of general distress, PTSD symptoms, and full-blown PTSD in two suburbs of Jerusalem (Shalev, et al. Am. J. Psychiatry, 2006).

Efrat (the directly exposed community) and Bet Shemesh (an indirectly exposed community) are located at similar distances from Jerusalem (11 miles for Efrat and 15 miles for Bet Shemesh). During the eight months preceding the data collection, the directly exposed community was practically under siege, whereas the indirectly exposed community was not.  Specifically, shooting incidents occurred frequently, and erratically blocked the roads leading to Efrat.

Stoning of cars occurred daily.  Snipers killed and wounded several residents.  While stress exposure was far more pervasive in the directly exposed community of Efrat, the prevalence of PTSD symptoms (26.95%) for the directly exposed community sample compared with that of 21.35% for the indirectly exposed community was not statistically significant. These findings reflect a high frequency of traumatic anxiety in neighborhood communities exposed either directly or indirectly to continuous threat.

When comparing the effects of circumscribed catastrophic events with those of a continuous terror paradigm, a spectrum emerges representing two contrasting stress models with differing psychological, behavioral, neurobiological, and sociological implications.

In fact, the fear conditioning model has guided the neurocircuitry theories of PTSD and its pathophysiology (Southwick. Psychiatric Annals, August 1998).

Previous exposure to trauma is the important risk factor for PTSD. Furthermore, studies have shown that previous history of stressors may alter the HPA axis response to subsequent stressors.

Fear conditioning leads to heightened threat responsiveness, overgeneralization of fear responses, and failure of extinction. Kindling and sensitization within the amygdala is the accumulative result of multiple traumas and predicts the development of PTSD (Davis, M. “The Role of Amygdala in Fear and Anxiety.” Annual Rev. Neurosc., 1992).

In the Continuous Terror model, because of sensitization to repeated fear-conditioned cues and neurological kindling, PTSD is more likely to endure (McEwen. “The Effects of Stress on Structural and Functional Plasticity in the Hippocampus.” Neurobiology of Mental Illness. Oxford University Press, 1999).

The mechanisms involved here may include both long-term potentiation as well as lasting changes in the genetic regulation of neurotransmitters, intracellular messengers, and cellular structures. These changes affect primarily the amygdala, hippocampus, and medial prefrontal cortex — the triad of structures implicated in fear conditioning.

In “The Continuous Terror Study” conducted by Dr. Shalev and colleagues, the investigators expressed concern regarding the implications of living under continuous terror, where recuperation may not occur as it does following a discrete occurrence.

These observations are consistent with the findings of the “Cross-Sectional and Longitudinal Aging Study (CALAS), funded by the U.S. National Institute on Aging.” Thirteen hundred and sixty-nine Holocaust survivors interviewed from the Israel National Population Registry reported a high incidence of cumulative life events distress, a lower level of lifestyle activity, and poorer social functioning ( Shmotkin and colleagues. “A Broad-Scope View of Holocaust Survivors in Late Life.” Journal of Consulting and Clinical Psychology, 2003).

Overall, the findings indicated that older Holocaust survivors randomly approached in a nonclinical setting still endure the sequelae of their trauma.  These findings are consistent with the theory of sensitization, and are particularly pertinent to the Continuous Terror model posed by Dr. Shalev and colleagues.

Not only does this bode poorly for life quality on a long-term time trajectory, but also raises concern for the potential impact in the U.S of a major national disaster of the magnitude of a September 11th event in a pre-traumatized population.

In fact, Solomon and Prager reported this vulnerability to re-traumatization, when survivors of the Nazi Holocaust showed more pronounced psychological symptoms following the SCUD missile attacks during the Persian Gulf War than the rest of the population (Am. J. Psychiatry, 1992).

Dr. Shalev responds:

Dr. Trappler expands the implications of our study of the effects of continuous terror by commenting on the potential long-term effects of repeated trauma exposure.

These are very important points because our study only concerned reactions during adversity, whereas Dr. Trappler’s comment implies that there might be a hidden sensitizing effect masked by an external resilience. This could lead to currently resilient survivors becoming more sensitive to subsequent stressors and developing PTSD in the future.

The debate regarding the sensitizing or immunizing effect of exposure has not been resolved. A study of Israeli soldiers exposed to two successive wars (Yom Kippur War of 1973 and Lebanon I in 1982) supports both views (Solomon, et al. “Reactivation of Combat-related PTSD.” Am J Psych, 1987).

Those who developed combat stress reactions during the first war were more likely to develop PTSD in 1982 (a sensitizing effect). In contrast, soldiers who did not develop combat stress showed lower stress reactions in 1982 than newly exposed combatants (an immunizing effect).

Clarifying these issues is of particular relevance in an era where US soldiers may be called for second or third tour of duty in Iraq or Afghanistan.

Moreover, some specifics of current warfare and terrorism (including the vivid visual communication of suffering) significantly extends the circle of those affected by these traumatic events.

Theory suggests that controllable stress tends to immunize, whereas uncontrollable stress sensitizes (Brewin. J Consult Clin Psychol, 2000).

Poor social support after a trauma is a major risk factor for PTSD (Liu. Science, 1997).

A series of animal studies have established the role of soothing body contact in reversing the stress-sensitizing effects of early maternal separation (Coplan, Rosenblum, Gorman, Nemeroff. “Increased CRF Concentrations in the Spinal Fluid of Non-Human Primates Exposed to Adverse Experiences as Infants.” Proceedings for the National Academy of Science, 1996).

We therefore come back to the old adage: Hug a veteran today.

It behooves us during these dire times to protect and support those among us who have been repeatedly exposed to stress by giving them as much personal support as we can.

This might not prevent exposure to stress, but helps those already exposed.

Dr. Trappler responds:

My comments on the Continuous Terror model proposed by Dr. Shalev focused on a continuous compounding effect of repeated trauma exposure.

Neurological kindling theory would suggest that the sympathetic nervous system becomes more prone to both hyper-arousal, and more likely to heighten stress-responses to trauma triggers.

What Dr. Shalev identified was two subgroups of combat exposed veterans. The subgroup that developed controlled stress was “immunized,” while the subgroup that experienced “uncontrolled stress” became “sensitized.”

This is relevant in terms of predicting which victims are more prone to PTSD in the long run.

There are important neurobiological ramifications to this concept which will determine the long-term prognosis (in terms of life quality) of trauma survivors.

I found two interesting publications that illustrate “controlled” versus “uncontrolled” stress in terrorist situations.

In a study on the “Psychiatric Aspects of Terrorist Violence in Northern Ireland,” Peter Curran found that what began in the late 1960’s as legitimate unrest soon gave way to widespread street rioting, evolving into social upheaval as thousands scurried to the comparative safety of ghettos within which paramilitary organizations constellated.

When the British Army entered the scene as “peacemakers,” the IRA launched a campaign of bombing targets throughout Northern Ireland and Great Britain.

As the killings rose from indiscriminate bombings and sectarian executions, former Home Secretary Reginald Maudling imposed direct rule from Westminster as he tightened control to “an acceptable level of violence.”

At the 18 year follow-up, Curran found that, except for the small proportion of actual victims, the rest of the community rebounded to a state of psychological well-being (Br J Psychiatry, 1988).

In contrast, David Kinzie and colleagues found that previously traumatized Bosnian and Somali refugees living in New York showed significant deterioration in their sense of safety and security following the 9/11 attacks.

These previously traumatized refugees also experienced PTSD reactivation in response to widely televised images of the Twin Tower bombings (Journal of Nervous and Mental Disease, 2002).

While Curran’s IRA study demonstrates the effect of stress-containment leading to an “immunizing” effect, Kinzie’s study illustrates the “sensitizing effect” of an uncontrolled stress (the idea that nowhere is safe).

Another valuable point mentioned by Dr. Shalev is the issue of “duration of exposure” by veterans within the combat theatre, suggesting that the current extended tours in combat theatre raise the risk of PTSD in comparison to shorter tours of active duty with longer periods of respite.

This very short turnaround between active tours of duty will certainly put returning veterans from Iraq and Afghanistan at greater risk.

The clinical significance returns to the physiology of stress circuitry and the imperative to shorten periods of sustained “stress activation” in order to protect limbic brain structures from the deleterious effects of toxic stress-induced neurohormones.

Victims with extended trauma exposure, as described in Shalev’s Continuous Trauma syndrome, may become prone to chronic over-arousal, a failure to regulate affective responses, and social skill deficits (Herman. Trauma and Recovery. Basic Books, 1992).

In the Middle East, where there is a continuous terror threat, the pervasive threat may simulate the Type II, or Complex Trauma paradigm.

According to Marylene Cloitre, victims of chronic trauma first need “Skill Training in Affective Regulation” (known by the acronym “STAIR”) in order to help identify their fears, learn how to self-soothe, and regain a sense of autonomy (Cloitre, et al. Treating Survivors of Childhood Abuse.  Guilford Press, 2006).

Adequate self-function, affective regulation and skill training may become critical to prepare trauma victims prior to exposure to their specific trauma narratives.

When “sensitized” patients are “therapeutically challenged” to revisit “split off” traumatic memory fragments, they might experience the unmanageable dread for which Cloitre advocates the STAIR method.

Ultimately, the most effective way of restoring a personal sense of security is by creating a safe holding environment, one with a secure boundary that keeps the predator well away.

When it comes to terrorism, as we have learned only too painfully, an ounce of U.N. and USA prevention is better than a pound of care.”

 

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3 Responses to “Intifada and the Continuous Terror Paradigm”

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