Worry is the major cognitive component of GAD
(Generalized Anxiety Disorder). People who have GAD tend to worry most of the
day, nearly every day. However, worry in itself is not pathological. It is an
attempt to predict future danger and/or an attempt to gain control over events
that appear uncontrollable (and usually negative or dangerous). However, it is
clear that pathological worry is dysfunctional in that it is, by definition, excessive
and/or unrealistic and feels uncontrollable. As a result, patients overpredict
the likelihood of negative events and exaggerate consequences if the events were
to occur. In a study by Abel and Borkovec (1995), 100% of patients with GAD described
their worry as uncontrollable, whereas none of the nonanxious control subjects
did. In addition, anxious subjects tend to selectively attend to threatening,
personally relevant stimuli (Mathews 1990). Frequently, there is an implied belief
that worry will make the world more controllable and predictable. Consistent with
this, worriers report five major functions of worry: 1) superstitious avoidance
of catastrophes, 2) actual avoidance of catastrophes, 3) avoidance of deeper emotional
topics, 4) coping preparation, and 5) motivating devices (Borkovec 1994).
Research supports the idea that pathological worry has a functional role
for people with GAD. Ironically, worry inhibits autonomic arousal in patients
with GAD when they arc shown aversive imagery. Worrying may cause the avoidance
of aversive imagery, which is associated with an even greater emotional arousal
(Borkovecet al. 1991). Thus, worry may be maintained by both the avoidance of
certain affective states and the reduction of anxious states through the decrease
in arousal that occurs along with worry or by the latter alone. Research has recently
supported the role of worry in avoidance of emotions (Mennin et al. 2003; Roemer
and Orsillo 2002). Counterintuitively, relaxation has been shown to increase the
amount of worry in some patients with GAD (Borkovec et al. 1991). It may be that
for these patients relaxation signals a lack of control, triggering an increase
in anxiety, or that patients sit quietly with their thoughts, causing greater
exposure to their worries.
In addition to worry, patients with GAD experience unpleasant somatic sensations.
Although these usually increase during the course of a worry episode, both the
worry and the somatic sensations can be described as relatively persistent and
pervasive. The most common somatic symptom reported by patients with GAD is muscle
tension. Patients may experience other symptoms often associated with worry and
tension, including irritability, restlessness, feeling keyed up or on edge, difficulty
sleeping, fatigue, and difficulty concentrating.
Multiple neurochemicals and neurotransmitter systems have been implicated as potential
contributors to the development of GAD. These include the y-aminobutyric acid
(GABA)-benzodiazepine (BZ) complex, serotonin (5-HT), norepinephrine, cholecystokinin,
corticotropin-releasing factor, the hypothalamic-pituitary-adrenal axis, and neurosteriods
(Connor and Davidson 1998). Work on the GABA-BZ complex and the serotonin system
is perhaps particularly relevant to the clinical setting and to current pharmacological
treatments of GAD.
Indeed, in view of the link between early
antianxiety treatments and GABA, it was logical to focus on the role of the GABA-BZ
complex in GAD. Studies have shown a lower number of peripheral BZ binding sites
on platelets and lymphocytes in patients with GAD. This finding was reversed when
patients were treated with a BZ (Rocca eta1. 1991; Weizman et al. 1987). The development
of BZ ligands has allowed work demonstrating decreased BZ binding in the left
A range ofpreclinical studies demonstrate that
the 5-HT system plays an important role in mediating anxiety. Patients with GAD
have a decrease of 5-HT in the cerebrospinal fluid (Brewerton et al. 1995) and
reduced platelet paroxetine binding (Iny et al. 1994). Patients with GAD demonstrate
exacerbation of anxiety symptoms after administration of the serotonin agonist
mchlorophenylpiperazine. In addition, several serotonergic agents are effective
in the treatment of GAD.
- Stein, Dan J., Clinical Manual of Anxiety Disorders,
American Psychiatric Publishing: London, 2004.
The article above contains foundational information. Articles below contain optional updates.
Reflection Exercise #6
The preceding section contained information
about the pathogenesis of generalized anxiety disorder. Write three case study
examples regarding how you might use the content of this section in your practice.
Online Continuing Education
What is an attempt to predict future danger and/or an attempt to gain
control over events that appear uncontrollable? Record the letter of the correct
answer the .