Abnormal Psychology

Anxiety Disorders 255

Brain Systems

The brain ultimately controls the body’s responses, and thus GAD must involve the

brain in some way. However, researchers are only beginning to identify the precise

ways in which large-scale brain mechanisms are altered to produce GAD (Nutt,

2001). For example, they have found that patients with GAD have more gray and

white matter in the superior temporal gyrus, an area used in hearing and language

comprehension, than do individuals who do not have this disorder. Moreover, this

brain area is strikingly larger in the right hemisphere than the left in patients with

GAD, and the size difference is more extreme for people who have more severe

anxiety (De Bellis et al., 2002). It is possible that this additional cortex leads people

with GAD to form certain associations (such as of being in danger when in common

situations or suffering dangerous consequences after performing common actions)

more easily than do other people, but at present this is only a hypothesis.

The role of the right hemisphere was also evident in an fMRI study in which

adolescent patients with GAD and adolescents in a control group viewed angry and

neutral faces (Monk et al., 2006). The researchers found that a key part of the right

frontal lobe was more strongly activated for the patients than for the controls when

the participants saw angry faces. However, patients who showed greater activation

in this area had less severe anxiety. These results are only suggestive, but might in-

dicate that this area is involved in a coping activity, such as attempting to regulate

bodily responses; in fact, the frontal lobes have many connections to the limbic

system, including connections to the amygdala, which plays a key role in fear (e.g.,

LeDoux, 1996, 2000), and to the autonomic nervous system (Gabbott et al., 2005;

Ghashghaei & Barbas, 2002; Teves et al., 2004).

The connections from the frontal lobes to the autonomic nervous system may

play a particular role in GAD—but, unlike most types of anxiety disorders, GAD

isn’t associated with cranked up sympathetic nervous system activity (Marten et al.,

1993). Instead, GAD is associated with decreased arousal that arises from an

unusually responsive parasympathetic nervous system. The parasympathetic ner-

vous system tends to cause effects opposite to those caused by the sympathetic

nervous system. So, for instance, heightened parasympathetic activity slows heart

rate, stimulates digestion and the bladder, and causes pupils to contract (Barlow,

2002a). When an individual with GAD perceives a threatening stimulus, his or her

subsequent worry temporarily reduces any arousal (Borkovec & Hu, 1990), sup-

presses negative emotions (see Figure 7.2), and produces muscle tension (Barlow,

2002a; Pluess, Conrad, & Wilhelm, 2009). These facts are in stark contrast to Earl

Campbell’s symptoms, which suggest that he did not have GAD.

Neural Communication

Although the frontal lobes of patients with GAD are normal in size, the dopamine in

the frontal lobes of these patients does not function normally (Stein, Westenberg, &

Liebowitz, 2002). In fact, numerous studies suggest that a wide range of

neurotransmitters, including gamma-aminobutyric acid (GABA), serotonin, and

norepinephrine, may not function properly in people with GAD (Nutt, 2001). These

neurotransmitters affect, among other things, people’s response to reward, their

motivation, and how effectively they can pay attention to stimuli and events.

Genetics

Studies of the genetics of GAD have produced solid evidence that GAD has a ge-

netic component. The heritability estimate for GAD is at least 15–20% (Hettema,

Prescott, & Kendler, 2001) and possibly almost 40% (Scherrer et al., 2000) and the

disorder is equally heritable for men and women (Hettema, Prescott, & Kendler,

2001). However, much of this disorder may rest on a tendency to become anxious,

which can be manifested in a number of different ways. For example, much of the

genetic basis of GAD is shared with panic disorder (Chantarujikapong et al., 2001;

Scherrer et al., 2000) and with posttraumatic stress disorder (Chantarujikapong

et al., 2001). Moreover, if one family member has GAD, other family members are

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