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Generalized Anxiety disorder (GAD) is a widespread psychiatric syndrome involving significant consequences on people's health. However, recent data show that this disorder has received little attention when compared to other anxiety disorders. A review of the publication on GAD also stated that the majority of research has been conducted on descriptive issues, whereas etiological factors received lower rates of publication. This may be explained by the fact that changes in the conceptualization of GAD slowed down the progression of researches focussing on the identification of factors implicated in the development and the maintenance of its symptoms. For example, in the third version of the Diagnostic and Statistical Manual of Mental disorders (DSM) published in 1980, GAD could only be assigned if patients had a persistent anxiety without reporting specific symptoms of other anxiety disorders (eg Specific Phobias, Panic Disorder, Obsessive-Compulsive Disorder). With DSM III-R and DSM IV, excessive worry became the central feature of GAD, which increased its diagnostic validity. Taking that into account, where do we stand in the comprehension of GAD? What are the etiological factors identified as playing a role in the development and the maintenance of GAD and its central feature, excessive and uncontrollable worry? The goal of this article consists to provide answers to these questions by reviewing the literature of the current knowledge of GAD and examining various theories and explanatory models available. Firstly, many studies suggest that environmental factors are implicated in the development and maintenance of GAD. However, the majority of researches rests on an out-of-date conceptualization of GAD. Furthermore, the nature of experimental designs used in researches limits their conclusion. The first environmental factor documented is negative life events. Researchers noted that the occurrence of one or more negative life events being significant and appearing in an unexpected way was associa-ted with an increase in the risk to develop a GAD (eg. Familial problems (eg conflicts, abuses), considered as chronic stress-inducing situations, have also been suggested as etiological factor of GAD. Among the other environmental factors identified are separation during childhood, role inversion during childhood, lack of social interactions, poor life satisfaction, and modeling of a relative having an anxiety disorder. The cognitive and behavioral approach has been widely used during the last two decades to precise the etiology of GAD. First of all, some studies have pointed out the function of worry, which is to suppress images associated with negative thoughts (eg. Thus, GAD patients seem to develop excessive worries in order to prevent more negative feeling associated with the images of a thought. Other authors suggested that a deficit of attention might be responsible of excessive worry. Finally, some cognitive variables such as intolerance of uncertainty, false beliefs about worry, negative problem orientation and cognitive avoidance have been suggested as playing a determinant role in the development and maintenance of GAD. In order to resume the empirical findings available in the literature, an etiological model gathering the cognitive, behavioral, and environmental factors implicated in GAD is proposed. This model suggests that GAD is the result of a psychological vulnerability activated by a tension resulting from a negative event. Finally, recommendations are brought concerning future researches on GAD and its central characteristic, excessive and uncontrollable worry.

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Because there is a large overlap between HIV manifestations and somatic symptoms of anxiety and depression, it is crucial to use measures that do not contain somatic items to validly and reliably assess these psychological states in HIV-infected patients. The purpose of this study was to assess the psychometric properties of the Hospital Anxiety and Depression Scale (HADS), a questionnaire that does not include any somatic items, in HIV-seropositive individuals. Because the study was conducted among French Canadian individuals, the quality of the translation was 1st subjectively and empirically assessed. Then, the psychometric properties of the HADS were evaluated in 162 HIV-seropositive patients, who, in addition to the HADS, also completed the Beck Depression Inventory (BDI) and the State-Trait Anxiety Inventory. The French Canadian version used was found to be subjectively and empirically equivalent to the original English version. Moreover, results of this study demonstrated a bifactorial structure with factors corresponding to the HADS subscales, an excellent internal consistency and test-retest reliability, a very good convergent validity, and an acceptable discriminant validity. Strikingly, in contrast to the BDI, HADS scores were found to be unconfounded by the presence of HIV symptomatology. The HADS appears to represent the best currently available self-report scale to reliably and validly assess anxiety and depression in HIV-infected patients. The HADS is simple and brief to administer (14 items) and may therefore be easily implemented in routine HIV care.

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A repertoire of reliable and valid self-report instruments to assess panic and panic disorder would help both researchers and clinicians. This review presents a description and an analysis of the available instruments. Following a comprehensive search of the literature, 14 instruments with published information on reliability and validity were reviewed. The following information is reported for each instrument: brief description of the instrument and its development, mean and standard deviation for clinical and nonclinical samples, and psychometric properties. Four types of instruments are presented: general assessment and information (n = 2), severity of panic disorder (n = 2), body sensations (n = 2) and cognitive dimensions of panic (n = 8). Overall, it would seem that panic measures have moderate to excellent psychometric qualities. However, the comparison between the instruments is difficult because the amount of empirical support available varies widely from one instrument to the other.

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The aim of this study was to assess the rate of change on clinical, behavioral and cognitive variables during exposure therapy and cognitive restructuring in the treatment of panic disorder with agoraphobia. A total of 28 Ss who received a diagnosis of panic disorder with agoraphobia were randomly assigned to either of two treatment conditions: exposure therapy or cognitive restructuring. Treatment conditions were kept as distinct as possible from each other. Subjects were assessed on five occasions: pretreatment, after 5, 10, and 15 (posttreatment) sessions of treatment and at a 6-month follow-up. Analyses of outcome data revealed strong and significant time effects on all measures. However, no group x time interaction reached statistical significance, suggesting that both strategies operate at the same pace. Furthermore, power analyses suggest that any difference that might exist in the rate of improvement between exposure and cognitive restructuring in the treatment of panic disorder with agoraphobia is marginal.

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Controlled studies indicate that cognitive-behavioral therapy eliminates panic attacks in greater than 80% of patients who suffer from panic disorder. However, because most of the screening procedures used in those studies called for excluding patients who were depressed, a question arises as to the extent to which these results apply to patients who are clinically depressed in addition to having panic attacks. Accordingly, an attempt was made in the present study to determine whether or not panic patients who are clinically depressed could be treated as successfully as those who are not clinically depressed. Two multiple baseline A-A1-A-B across-subjects designs were used, one to test 8 panic Ss with major depression and the second to test 7 panic Ss without major depression. In Baseline (A), Ss monitored their panic attacks daily. During the A1 phase, a program of information on panic attacks presented as psychotherapy was instituted to assess the effects of nonspecific factors, followed by a second baseline phase (A). Cognitive-behavioral therapy (B) was then introduced. Results showed that cognitive-behavioral therapy was significantly superior to information-based therapy in the reduction of panic attacks. No significant differences were found between depressed and nondepressed patients.

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