What causes PTSD?
Post-traumatic stress disorder
In one sense, the cause of PTSD is obvious: a specific trauma. And yet this is only part of the explanation. Why is it that some people who are raped or badly beaten up develop PTSD and others do not?
Of the psychological attempts to answer that question, arguably the most influential is the one formulated by Anke Ehlers and David Clark.
The theory is nicely illustrated by a research study carried out by Ehlers and colleagues. For six months, they tracked the progress of 147 people who’d been injured in motor vehicle accidents. Two weeks after the accident, 33 (22.4%) met the criteria for a diagnosis of PTSD (except, of course, the stipulation that symptoms have lasted more than a month); six months later, 17 (12.1%) were affected.
The individuals who developed PTSD tended to share certain characteristics:
• Before the accident: a history of emotional problems and previous traumatic experiences.
• During the accident: a focus on the sensations evoked by the trauma, rather than the meaning of what was happening (this is called ’data-driven processing’); the feeling that the accident was happening to someone else (a lack of ’self-referential thinking’); a sensation of detachment or numbness or that the accident wasn’t real.
• After the accident: a pessimistic view of the trauma; an inability to clearly recall what had gone on; a perceived lack of support from friends and family; constant thoughts of the accident and its consequences or, conversely, avoidance of all reminders; adoption of safety behaviours (for instance, refusing to travel by car).
Ehlers and Clark argue that PTSD arises when the person believes they are still seriously threatened in some way by the trauma they’ve experienced. Why should someone assume they are still endangered by an event that happened months or even years previously? Ehlers and Clark identify two factors.
First is a negative interpretation of the trauma and the normal feelings that follow, for example:
• Nowhere is safe.
• I attract disaster.
• I can’t cope with stress.
• I’m going mad.
• I’ll never be able to get over this.
• No one is there for me.
These interpretations can make the person feel in danger physically (the world seems fundamentally unsafe), or psychologically (their self-confidence and sense of wellbeing seem irreparably damaged).
Second are problems with the memory of the trauma. Because of the way the person reacts during the event, the memory somehow fails to acquire a properly developed context and meaning. As a result, it constantly intrudes, triggered automatically by the slightest reminder of the trauma (a colour, or smell, or vague physical resemblance). Ehlers and Clark liken the traumatic memory to:
a cupboard in which many things have been thrown in quickly and in a disorganised fashion, so it is impossible to fully close the door and things fall out at unpredictable times.
(In a related theory, Chris Brewin argues that PTSD develops when unconscious, situationally accessible memories (SAMs) of the trauma — which largely comprise sensory information — fail to be incorporated in conscious, verbally accessible memory (VAMs).)
PTSD is maintained by exactly the kind of behaviours adopted by the individuals in the traffic accident study. Thus, cognitive therapy aims to persuade the person to drop these behaviours, and to tackle the negative beliefs and incomplete memories that provoke them.
PTSD seems to be marked by problems in the limbic system of the brain, and specifically the relationship between the:
• amygdala, the storehouse of unconscious fear memories;
• anterior cingulate cortex (ACC), which helps control our fear reactions;
• hippocampus, which stores contextual memories (for example, where we were and what we were doing when a frightening event occurred), and can therefore help us judge whether a situation is truly dangerous or merely resembles aspects of a previously threatening event.
In people suffering from PTSD, the amygdala may be overactive and the ACC and hippocampus underactive. Indeed, there’s evidence to suggest that the ACC and hippocampus are actually smaller in people with PTSD, though whether that’s a result of the illness or a cause is unclear. (In fact, it may not be the whole hippocampus that is affected; recent research has highlighted atrophy in a specific region of the hippocampus in people with PTSD.)
Without the moderating influence of the ACC and hippocampus, the amygdala may perceive threat where there is none — a hallmark of PTSD, and indeed of anxiety disorders in general.
It’s been suggested that the hippocampus may shrink through the effects of the hormone cortisol. Cortisol, and related neurochemicals, are released via the hypothalamic-pituitary-adrenal (HPA) axis in order to key up the body to respond to potential threat. Scientists are investigating the idea that dysfunction in the HPA axis may play an important role in PTSD. So far, however, no consistent pattern has emerged.
Research into the genetics of PTSD is scarce. What there is suggests only moderate heritability (around the 30—35% mark). Interestingly, there seems to be some overlap between genetic susceptibility to PTSD and to some types of the trauma that trigger the illness. This may be a result of the individual’s personality. Murray Stein and colleagues have speculated:
an individual’s genetically influenced propensity toward neuroticism would lead the individual to experience more anger and irritability, making that person 1) more likely to get into fights (thereby increasing the risk of experiencing assaultive trauma) and 2) more likely to become highly emotionally aroused as a result of experiencing such traumata (thereby increasing the risk for PTSD symptoms).
In some cases, then, personality may partly influence the likelihood of a person experiencing a trauma and of then developing PTSD. But we shouldn’t get carried away: most traumatic events occur out of the blue and regardless of the individual’s personality.