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Treating Post-Holiday Let-Down & Depression
Depression continuing education MFT CEUs

Section 18
Generalized Anxiety Disorder Pathogenesis

CEU Question 18 | CEU Test | Table of Contents | Depression
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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.

Somatic Symptoms
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 temporal lobe.

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.


Personal 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 QUESTION 18
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 CEU Test.

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