Severity of generalized social anxiety disorder correlates with low executive functioning

Highlights

• We evaluate neurocognitive functions of patients with social anxiety disorder.

• The WCST performance was lower than that of healthy controls.

• Performance of the WCST correlates with the LSAS score.

• Social anxiety disorder has low executive function correlates with the severity.

Abstract

To evaluate neurocognitive functions of patients with social anxiety disorder (SAD) without comorbidity using neuropsychological assessments and to investigate the relation between neurocognitive functions and clinical severity of SAD, this study assessed 30 SAD patients (10 female, 20 male) without comorbidity and 30 healthy subjects matched on gender, education level, and age. The neuropsychological assessment consisted of the Wisconsin card sorting test (WCST), the continuous performance test, the trail-making test, the word fluency test, and the auditory verbal learning test. On the WCST, patients showed lower performance than healthy controls did. The Liebowitz Social Anxiety Scale score correlated significantly with the numbers of perseverative errors of the WCST, although the State anxiety score of State-Trait Anxiety Inventory and the Beck Depression Inventory – Second Edition score showed no correlation with neuropsychological test scores. Results show that the executive functioning of patients with SAD was low and that the low functioning correlates with the SAD symptom severity.

Introduction

Social anxiety disorder (SAD) is characterized by a persistent fear of one or more social or performance situations. The prevalence of this disorder is high: approximately 1.4–12.1% of the population meets DSM-IV TR criteria [4] for SAD over their lifetime [1], [19], [20], [27], [30]. A person with SAD, although recognizing that the fear is unreasonable or excessive, usually cannot resolve it and deflect attention away from the fear.

According to the cognitive model of SAD, self-focused attention is an important factor in maintaining the illness. A person with SAD tends to increase access to self-referent negative thoughts and feelings that interfere with performance, thereby preventing the individual from observing external information that might disprove the thoughts and feelings of patients with SAD [11]. Presumably, this inflexibility of informational processes is based on neurocognitive dysfunction. The dysfunction of executive functioning, attention and memory is frequently reported in relation to anxiety disorders [10]. Executive functioning is defined as a set of general-purpose control mechanisms, often linked to the pre-frontal cortex of the brain, that regulate the dynamics of human cognition and action [28]. Unlike psychotic or mood disorders, little is known about the neurocognitive impairment of anxiety disorders except for obsessive–compulsive disorder and posttraumatic stress disorder. The impairment of executive functioning, visual memory, attention and processing speed has been reported as associated with obsessive–compulsive disorder. The dysfunction of executive functioning, attention, verbal and visual memory has been reported as associated with posttraumatic stress disorder. However, few reports describe studies of SAD patients’ neurocognitive functions [10], [13].

Several studies have examined threat biases by which individuals with SAD devote selective attention to socially threatening situations [26], [32], [41], [42]. Results do not necessarily support threat biases. Nevertheless, few studies have targeted cognitive functions independently of social context. Among such studies that have assessed potential cognitive impairment in SAD, one found that patients with SAD were more impaired than healthy controls in terms of verbal memory [3]. Another study revealed that patients with SAD had lower executive functioning and visual memory scores than healthy controls had [12]. Based on these studies, patients with SAD might show low performance in tasks of verbal memory, visual memory, and executive functioning. However, results of these studies were not congruent, perhaps because of comorbidities, especially major depressive disorder.

Generally speaking, SAD is frequently comorbid with major depressive disorder, with estimated frequency of 44–70% [9], [23], [33]. In connection with major depressive disorder, many reports have described that memory, learning, attention, motor function, and problem-solving might be affected [5], [40]. Therefore, it is possible that depressive symptoms affect the neurocognitive functions of patients with SAD. Actually, one study demonstrated that verbal memory impairment is correlated with the Beck Depression Inventory score [7]. The impairment of verbal memory might be influenced by comorbid depression. Moreover, another study set their exclusion criterion as 16 points (and above) on the Hamilton rating scale for depression (HAM-D) [15], presented the possibility that some of their subjects had mild depression.

However, one report has described that comorbid depressed versus non-depressed SAD patients respond uniquely to stress in terms of their neuropsychological function [14]. We were unable to find a report in the relevant literature describing the evaluation of a relation between clinical severity and neurocognitive functions in patients with SAD who had few depressive symptoms, but who nevertheless had severe social anxiety symptoms for which they had sought clinical treatment.

For this study, we recruited outpatients without comorbidity to exclude effects of depressive symptoms. This study was conducted to evaluate neurocognitive functions in SAD patients without comorbidity, and to investigate the relation between clinical severity and neurocognitive functions.