318 CHAPTER 7
2004). The abnormal structure and function of the hippocampus in PTSD patients
is important because that brain structure plays a crucial role in storing information
in memory (Squire & Kandel, 2000), and thus an impaired hippocampus should
impair memory. And, in fact, as expected, PTSD patients have trouble recalling au-
tobiographical memories (McNally et al., 1995).
Note that correlation does not imply causation; perhaps the brain abnormal-
ity predisposes people to PTSD, or perhaps PTSD leads to the brain abnormality
(McEwen, 2001; Pitman, Shin, & Rauch, 2001). A twin study provides an impor-
tant hint about what causes what: In this study, researchers compared the sizes of
the hippocampi in veterans who had served in combat and had PTSD with the sizes
of hippocampi in their identical twins who had not served in combat and did not
have PTSD. The results were clear: In both twins, the hippocampi were smaller
than normal (Gilbertson et al., 2002). This fi nding implies that the trauma does not
cause the hippocampus to become smaller, but rather the smaller size is a risk factor
(or is correlated with some other factor that produces the risk) that makes a person
vulnerable to the disorder.
Neuroimaging studies have focused not only on the hippocampus but also on
the entire brain, in an effort to discover more generally which brain functions have
been disrupted by PTSD (Rauch et al., 1996; Rauch, Shin & Phelps, 2006; Shin
et al., 1999). For example, in some studies, researchers either show patients pic-
tures of trauma-related stimuli (such as jungle scenes in Vietnam for Vietnam-war
vets) or ask them to visualize such scenes. When PTSD patients visualize their own
traumatic events, parts of the limbic system and related areas are activated, which
is not surprising given the role these areas play in emotion. In addition, areas of the
brain involved in visual perception are highly activated, which may indicate that
these patients have particularly vivid visual mental images (Kosslyn, Thompson, &
Ganis, 2006).
In addition, some studies have found that when PTSD patients see faces with
fearful expressions (which can be presented so quickly that the participants aren’t
consciously aware of seeing them), their amygdalas become abnormally highly ac-
tivated (Pitman, Shin, & Rauch 2001; Rauch, Shin, & Phelps, 2006; Rauch et
al., 2000). Moreover, curiously, in three of these studies, patients with PTSD had
less activation in Broca’s area (in the left frontal lobe) when visualizing traumatic
stimuli (Broca’s area plays a key role in language production). Shin and colleagues
(1997) suggest that these patients may be “scared speechless,” which dampens
down activity in this area. In fact, the more activated the amygdala, the less acti-
vated this area of the frontal lobe tends to be in these patients (Shin et al., 2005).
It is possible that people who don’t develop PTSD can use language to reinterpret
trauma, and thereby lessen its impact—but PTSD patients may be overwhelmed
by the sensory images, which interfere with using language in this way.Neural Communication
Initially, researchers thought of PTSD as an extreme response to stressful situations.
If so, then the brain would produce abnormal amounts of stress-related hormones,
such as cortisol (Yehuda et al., 1991). But this turned out not to be the case—in
fact, patients with PTSD actually have lower-than-normal levels of this hormone
(Yehuda et al., 1995, 1996), even immediately after the traumatic event (McFarlane,
Atchison, & Yehuda, 1997).
Even though the initial theory turned out not to be correct, it contained a grain
of truth: PTSD patients do experience stress when they recall the traumatic event,
and the brain does respond to stress in specific ways. In particular, when animals
are forced to confront stressors, the locus coeruleus (a small structure in the brain-
stem) produces norepinephrine, a neurotransmitter that may be involved in PTSD
(Charney et al., 1993; Southwick et al., 1994). Southwick and colleagues (1993)
provided support for this theory. They gave a drug that allows norepinephine levels
to surge to volunteers with and without PTSD. When norepinephrine levels became very
high, 70% of the PTSD patients had a panic attack, and 40% of them had a fl ashback