Most of the available evidence on neuropsychological functioning in anxiety disorders is based on clinical samples, investigating persons affected by obsessive–compulsive disorder. Knowledge is sparse regarding cognitive functions in other types of anxiety disorders.
The aim of this study was to examine whether persons diagnosed with an anxiety disorder show neuropsychological impairments relative to healthy controls in tasks tapping episodic memory, verbal fluency, psychomotor speed, and executive functioning. Population-based samples comprising individuals affected by panic disorder with and without agoraphobia or agoraphobia (n = 33), social phobia (n = 32), generalised anxiety disorder (n = 7), obsessive–compulsive disorder (n = 16), and specific phobia (n = 24) were compared with healthy controls (n = 175) in test performance. Overall, the total anxiety disorder group exhibited significant impairments in episodic memory and executive functioning. Separate analyses on the respective anxiety subgroup indicated that panic disorder with and without agoraphobia, and obsessive–compulsive disorder were related to impairments in both episodic memory and executive functioning. In addition, social phobia was associated with episodic memory dysfunction. Verbal fluency and psychomotor speed were not affected by anxiety. Specific phobia and generalised anxiety disorder did not affect neuropsychological functioning
Anxiety disorders are common with the prevalence varying between 2% and 5% in population-based studies (APA, 1994). During the past decade, an increasing number of studies addressing neuropsychological functioning in anxiety disorders have been published. However, the majority of this research has focused on the less prevalent obsessive–compulsive disorder (OCD), whereas less attention has been paid to the other diagnostic and statistical manual of mental disorders (DSM-IV) ( APA, 1994) defined anxiety disorders, such as panic disorder (PD) and social phobia (SP).
Research focusing on cognitive functioning in OCD has demonstrated episodic memory impairments for both non-verbal (Dirson et al., 1995; Savage et al., 1996 and Savage et al., 1999) and verbal information (Savage et al., 2000; Zitterl et al., 2001). Also, reliable performance deficits have been obtained in tasks tapping executive functioning (Martinot et al., 1990; Purcell et al., 1998a and Purcell et al., 1998b; Veale et al., 1996; Head et al., 1989), although some research has reported normal executive functioning among persons affected by OCD (Boone et al., 1991; Christensen et al., 1992; Zielinski et al., 1991).
As noted above, only a few studies have addressed neuropsychological functioning in other DSM-IV defined anxiety disorders, and available evidence presents a mixed pattern of results. Regarding episodic memory, Lucas et al. (1991) reported that persons with PD exhibit reliable performance impairments for both visual and verbal information. In a similar vein, Asmundson et al. (1995) reported that both PD and SP were associated with significant recall deficits for verbal information, although individuals with PD performed as well as controls for visually based information. In addition to these findings, some research has established significant executive dysfunction in PD (Cohen et al., 1996). In contrast to these observations, other investigators found no evidence of an episodic memory dysfunction in PD, and this was true for both verbal and visual stimuli (Gladsjo et al., 1998). Also, Purcell et al., 1998a and Purcell et al., 1998b compared groups of OCD patients, PD, and major depression with healthy controls across a number of cognitive domains. The results indicated that only OCD patients exhibited impairments in executive functioning, attention, and episodic memory, whereas the PD and major depression groups performed as well as the healthy controls. It is highly likely that these inconsistent findings are a function of methodological differences between the studies regarding selection of participants, patient status, materials used in the memory tasks, and memory performance assessment (e.g. recall vs. recognition).
Evidence from neurobiological studies suggests that brain structures subserving episodic memory functioning are affected in anxiety disorders. For example, positron emission tomography studies demonstrate abnormal blood flow in medial temporal lobe including amygdala and hippocampus in symptom provoked SP patients (Tillfors et al., 2001), and an involvement of the hippocampal and parahippocampal areas in PD (Bisaga et al., 1998). In addition, magnetic resonance imaging study reported abnormalities in temporal lobe structures in PD subjects (Vythilingam et al., 2000). Further, neuroimaging studies in patients with OCD suggest a frontal-subcortical circuit involvement (Kwon et al., 2003).
The main objective of this research was to extend our knowledge on neuropsychological functioning in persons affected by an anxiety disorder in a population. In contrast to most previous research addressing this topic, the present investigation is based on population-based samples of persons meeting the DSM-IV criteria for an anxiety disorder. We compared different anxiety subgroups with non-anxious healthy controls across a number of different tasks tapping various cognitive domains including episodic memory for verbal information, verbal fluency, psychomotor speed, and executive functioning. In this way, we were able to examine cognitive functioning in population-based samples of persons suffering from an anxiety disorder, and to determine whether cognitive performance varied as a function of anxiety subgroup.
