It is becoming clear that the current criteria are fre- quently inadequate for characterizing GAD in older pa- tients. Diagnosing anxiety in this population can be dif- ficult. Comorbid psychiatric conditions that can mask and/or produce anxiety in the elderly include mood dis- orders and dementia (Alexopoulos 1991; Reisberg et al. 1987). An additional complication is that a primary medical condition (e.g., endocrine abnormality, nutri- tional deficiency, or secreting tumor) may be causal (McCullough 1992).
Evidence indicates that clinically significant anxiety problems in the elderly often elude identification by conventional methods, and are actually more prevalent than in the young (Kessler et al. 2005). Surveys that fo- cus on anxiety symptoms rather than anxiety disorders indicate steadily increasing rates of anxiety as individu- als age (Sallis and Lichstein 1982). Use of anxiolytic drugs increases with age (Rifkin et al. 1989; Salzman 1985), with some studies showing that as many as 20% of the noninstitutionalized elderly and 30% of the med- ically hospitalized elderly use benzodiazepines (Parry et al. 1973; Salzman 1991; Shaw and Opit 1976). Also, 20%–25% of the elderly experience insomnia “often” or “always.” Research indicates that anxiety is the factor most often associated with insomnia in the elderly (Morgan et al. 1988); therefore, a significant proportion of nighttime benzodiazepine use in elderly patients may reflect anxiety in addition to a sleep problem. Finally, the elderly are subjected to an increasing number of real-life stressors (e.g., illness, disability, widowhood, fi- nancial decline, and social isolation) that are known to foster anxiety (Hassan and Pollard 1994). These stres- sors have been shown to predict ill health among the elderly, particularly stress-related disorders such as headache, gastrointestinal distress, hypertension, and cardiovascular disease (Deberry 1982). Often, ill health brings the elderly patient to the attention of the medical practitioner, and the concomitant or underlying anxiety disorder is frequently overlooked (Turnbull 1989). In sum, the unique manifestations of GAD in older pa- tients will require modified diagnostic criteria.
Symptoms
The symptoms of GAD are numerous and highly vari- able. Signs of motor tension, autonomic hyperactivity, and hyperarousal are frequently the presenting prob-
lems. Patients complain of restlessness, inability to re- lax, and fatigue. The motor tension results in frequent headaches and chronic muscle pain in the shoulder, neck, and lower back. A DSM-IV-TR companion book provides a case vignette describing a typical patient with GAD (Papp 2004).
Pathological worry has been identified as the patho- gnomonic feature of GAD. The nature of pathological worry, however, has been subjected to research only re- cently. Therefore, only limited data are available on the characteristics of worry in actual clinical samples. GAD patients consistently report a greater number of worry areas compared with patients with other anxiety dis- orders and nonanxious control subjects, but the partic- ular patterns of worry content are highly variable and do not consistently identify patients with GAD (Roe- mer et al. 1997). Studies show that patients with GAD share the same concerns as nonanxious control subjects, such as concerns about family and interpersonal rela- tionships, work, school, finances, and health (Craske et al. 1989; Roemer et al. 1997; Sanderson and Barlow 1990).
Some investigators suggest that the manifest content of the worry is unimportant. They argue that the worry is simply a distraction and serves to protect patients from their “real” problems. Indeed, GAD subjects do believe that worry serves to distract them from more emotional topics (Borkovec and Roemer 1995). The role of emotional trauma in the pathogenesis of GAD may also be supported by the finding that these patients have more exposure to potentially traumatizing events in their pasts than nonanxious control subjects (Roemer et al. 1996). This hypothesis, akin to the “unconscious conflict” paradigm of psychodynamic thinking, needs further support.
GAD worry has been distinguished from “normal” worry by being perceived as significantly more uncon- trollable and unrealistic. Patients with GAD spend more of the day worrying than nonanxious control sub- jects (60% vs. 18%). Reliance on the perception of con- trol alone, however, may be misleading. An objective measure of thought suppression has shown that al- though patients with GAD have significantly less men- tal control over intrusive thoughts concerning their “main worry” than they do over their own neutral cog- nitions, contrary to expectation, they have no more ac- tual “main worry” intrusions than do nonanxious con- trol subjects (Becker et al. 1998).
The one content area that has consistently distin- guished GAD patients from others is excessive worry
over minor matters (e.g., daily hassles and time manage- ment) (Craske et al. 1989; Roemer et al. 1997; Sander- son and Barlow 1990). This criterion has proven to be a necessary, if not sufficient, feature for a diagnosis of GAD. A negative answer to the question “Do you worry excessively about minor matters?” effectively ruled out the diagnosis of (DSM-IV ) GAD in subjects (0.94 negative predictive power vs. 0.36 positive predictive power) (R. DiNardo, unpublished analysis, cited in Brown 1993). On the other hand, patients who do not consider their worry excessive or uncontrollable, fre- quently suffer from GAD that is otherwise indistin- guishable from and just as disabling as a full-symptom GAD. The excessive nature of the worry may not be a necessary criterion of GAD; it is not required by ICD- 10. Similarly, the duration criterion of 6 months may exclude patients with an otherwise identical condition. Many consider GAD a chronic but fluctuating illness with several active episodes occurring for as briefly as 1 month (Rickels and Rynn 2001a, 2001b).
GAD patients do not lack problem-solving skills but do have poorer problem orientation (i.e., response-set involving sense of control, problem-solving confidence, and approach vs. avoidance), and have significantly more difficulty tolerating ambiguity, compared with control subjects (Davey 1994; Ladouceur et al. 1998). Low tolerance of uncertainty might also predict more severity and could differentiate GAD from other anxi- ety and mood disorders (Dugas et al. 2005, 2007). In- dividuals with GAD also show a cognitive bias for threat-related information. Studies employing the modified Stroop task, in which a subject’s speed at nam- ing the colors that different words are printed in is mea- sured, consistently revealed that patients with GAD were slower than nonanxious control subjects in color- naming negative or threat-related words (Martin et al. 1991; Mathews and MacLeod 1985; Mogg et al. 1989, 1995).
Comorbidity
The symptoms of generalized anxiety are present in most anxiety and mood disorders, but only about 20% of the patients with depression and 10% of those with an- other anxiety disorder meet the criteria for the full syn- drome of GAD. More than two-thirds of patients with the principal diagnosis of GAD have an additional Axis I disorder, with social phobia, depression, or panic leading the list (Borkovec et al. 1995; Wittchen et al. 1994). A recent survey among primary care patients showed that 89% of those with GAD met criteria for a
comorbid psychiatric disorder as well (Olfson et al. 1997).
A New Zealand birth cohort study of 1,037 males and females followed to age 32 years showed that both pure GAD and GAD comorbid with major depression, but not pure major depression, were preceded by most of the 13 risk factors chosen to assess domains of family history, early trauma, childhood behavior, and person- ality (Moffitt et al. 2007a). Comorbidity was also asso- ciated with early onset, more recurrence, and more treatment, suggesting that the diagnosis of GAD, with or without depression, was associated with more sever- ity. In the comorbid group, each condition, depression or GAD alone or comorbid GAD and depression, oc- curred first in about one-third of the cases (Moffitt et al. 2007b). These findings are at variance with the theory that a more disabling and more severe depression usu- ally follows a relatively less severe GAD. If these results were confirmed, major depression should not warrant the primary designation when comorbid with GAD. Comorbidity is also discussed in this chapter in the sec- tions “Epidemiology” and “Differential Diagnosis.”
Course
The course of GAD is chronic, with fluctuating severity and symptom patterns (see Chapter 14, “Psychotherapy for Generalized Anxiety Disorder,” in this volume). It usually begins in a person’s early 20s, but, because of the overwhelmingly retrospective data, there is much con- troversy about age at onset. Although most agree that onset after age 60 years is rare, some investigators be- lieve onset could occur much earlier than in the 20s. Pa- tients with onset of GAD before age 10 years may rep- resent a separate category that characterizes a more malignant type of the disorder. Although questions re- main about whether these various types are sufficiently distinct, late-onset GAD is usually characterized by rapid onset following a clearly identifiable major stress. Early-onset GAD is more likely to develop gradually, presents with comorbid depression and other Axis I and Axis II disorders (Shores et al. 1992), and follows a more chronic course. These patients have a frequent history of childhood fears, school problems, and behav- ioral inhibition. Middle-aged patients report, on aver- age, a 20-year history of significant baseline anxiety with frequent exacerbations. When GAD remains untreated, prolonged remission is unusual. Treated or untreated, the long-term outcome of GAD is variable. Severity is dependent on several factors, including the existence of GAD with comorbid Axis I and Axis II
disorders, environmental support, the biology of the disorder, and the duration of the illness.