Tomas Furmark

Internet-based self-help with therapist feedback and in vivo group exposure for social phobia: A randomized controlled trial.

Sixty-four individuals with social phobia (social anxiety disorder) were assigned to a multimodal cognitive-behavioral treatment package or to a waiting list control group. Treatment consisted of a 9-week, Internet-delivered, self-help program that was combined with 2 group exposure sessions in real life and minimal therapist contact via e-mail. Results were analyzed on an intention-to-treat basis, including all randomized participants. From pre- to posttest, treated participants in contrast to controls showed significant improvement on most measured dimensions (social anxiety scales, general anxiety and depression levels, quality of life). The overall within- and between-groups effect sizes were Cohens d = 0.87 and 0.70, respectively. Treatment gains were maintained at 1-year follow-up. The results from this study support the continued use and development of Internet-distributed, self-help programs for people diagnosed with social phobia.

Social phobia: Overview of community surveys.

Objective: Social phobia has in recent years been recognized as a considerable public health concern. This paper presents an overview of community studies that have estimated the prevalence of social phobia, its subtypes, and specific social fears in the adult general population. Sociodemographic findings are also summarized.

Social phobia in the general population: prevalence and sociodemographic profile

Background: The present study examined the prevalence of social phobia in the Swedish general population and demographic characteristics associated with this anxiety disorder. Methods: Data were obtained by means of a postal survey administrated to 2000 randomly selected adults. A questionnaire, validated against clinical interviews and established social phobia scales, was used to assess social distress in a broad range of phobic situations, as well as the diagnostic criteria for social phobia corresponding to DSM-IV. Interpretable questionnaires were obtained from 1202 respondents (60.1%). Results: The point prevalence of social phobia was estimated at 15.6%, but prevalence rates varied between 1.9 and 20.4% across the different levels of distress and impairment used to define cases. Public speaking was the most common social fear. Social phobia was associated with female gender, low educational attainment, psychiatric medication use, and lack of social support. Conclusions: Although the exact diagnostic boundaries for social phobia are difficult to determine, it can be concluded that social anxiety is a distressing problem for a considerable proportion of the general population.

Size and burden of social phobia in Europe

This paper provides a critical review of the prevalence of social phobia in European countries, a description of associated disability and burden and of clinical correlates and risk factors associated with social phobia. On the basis of a comprehensive literature search we identified 21 community studies and two primary care studies. The median lifetime and 12-month prevalence rates of social phobia in community samples referring to DSM-III-R and DSM-IV criteria were 6.65% and 2.0%, respectively. Younger individuals showed the highest rates, and women were more frequently affected than men. Social phobia was shown to be a persistent condition with a remarkably high degree of comorbid conditions, associated impairment and disability. Research deficits lie in a lack of data for most EU countries and in a lack of studies in children and the elderly. No data are available addressing met and unmet needs for intervention and costs, and data for vulnerability and risk factors of malignant course are scarce.

Serotonin transporter polymorphism related to amygdala excitability and symptom severity in patients with social phobia

A functional polymorphism in the promoter region of the human serotonin transporter (5-HTT) gene has been related to negative affect and amygdala activity. We studied amygdala activation during social anxiety provocation in relation to affective ratings and 5-HTT genetic variation. [H2(15)O]positron emission tomography was used to estimate amygdala blood flow during private and public speaking (baseline and anxiety conditions) in 17 patients with social phobia. Genotyping identified patients with long and short alleles in the promoter region of the 5-HTT. Individuals with one or two copies of the short allele exhibited significantly increased levels of anxiety-related traits, state anxiety, and enhanced right amygdala responding to anxiety provocation, compared with subjects homozygous for the long allele. Thus, 5-HTT genetic variation was associated with symptom severity and amygdala excitability in social phobia.

Cerebral blood flow during anticipation of public speaking in social phobia: a PET study

BACKGROUND The aim was to examine the neural correlates of anxiety elicited by the anticipation of public speaking in individuals with social phobia. Positron emission tomography and (15)O-water was used to measure regional cerebral blood flow in subjects with DSM-IV defined social phobia during anxiety anticipation. Heart rate and subjective anxiety were also recorded. While being scanned, subjects were speaking alone either before or after speaking in public. To evaluate anticipatory anxiety we compared individuals speaking alone before they were speaking in front of an audience with those who did the reverse. RESULTS Heart rate and subjective anxiety measures confirmed anticipatory anxiety in social phobics who performed their private speech before their public. This was accompanied by enhanced cerebral blood flow in the right dorsolateral prefrontal cortex, left inferior temporal cortex, and in the left amygdaloid-hippocampal region. Brain blood flow was lower in the left temporal pole and bilaterally in the cerebellum in the anticipation group. CONCLUSIONS Brain regions with altered perfusion presumably reflect changes in neural activity associated with worry about anticipated public performance. We speculate that anticipatory anxiety in social phobics originates in an affect sensitive fear network encompassing the amygdaloid-hippocampal region, prefrontal, and temporal areas.

Cerebral blood flow changes after treatment of social phobia with the neurokinin-1 antagonist GR205171, citalopram, or placebo.

BACKGROUND Evidence is accumulating that pharmacological blockade of the substance P preferring neurokinin-1 (NK1) receptor reduces anxiety. This study compared the effects of an NK1 receptor antagonist, citalopram, and placebo on brain activity and anxiety symptoms in social phobia. METHODS Thirty-six patients diagnosed with social phobia were treated for 6 weeks with the NK1 antagonist GR205171 (5 mg), citalopram (40 mg), or matching placebo under randomized double-blind conditions. GR205171 was administered for 4 weeks preceded by 2 weeks of placebo. Before and after treatment, regional cerebral blood flow (rCBF) during a stressful public speaking task was assessed using oxygen-15 positron emission tomography. Response rate was determined by the Clinical Global Impression Improvement Scale. RESULTS Patients improved to a larger extent with the NK1 antagonist (41.7% responders) and citalopram (50% responders), compared with placebo (8.3% responders). Within- and between-group comparisons showed that symptom improvement was paralleled by a significantly reduced rCBF response to public speaking in the rhinal cortex, amygdala, and parahippocampal-hippocampal regions. The rCBF pattern was corroborated in follow-up analyses of responders and subjects showing large state anxiety reduction. CONCLUSIONS Short-term administration of GR205171 and citalopram alleviated social anxiety. Neurokinin-1 antagonists may act like serotonin reuptake inhibitors by attenuating neural activity in a medial temporal lobe network.

Disruption of Reconsolidation Erases a Fear Memory Trace in the Human Amygdala

Removing Fear Memories Disruption of reconsolidation of an activated fear memory prevents subsequent fear expression. After a memory reminder, extinction training can disrupt fear memory. In rodents, this process is dependent on a brain area called the amygdala. Agren et al. (p. 1550) used functional magnetic resonance imaging and a fear conditioning paradigm to show in humans that, after an associative fear memory was formed, reactivation and reconsolidation left a signature in the basolateral amygdala. This memory trace predicted later fear expression, which was linked to activity in areas forming the fear circuit of the brain. Extinction alone did not change this signal. However, extinction in the reconsolidation window blocked fear expression by erasing the fear memory trace in the amygdala and weakened the connection in the wider fear circuit of the brain. Interfering with memory formation at the right moment removes the signature of fear memories in human brain imaging studies. Memories become labile when recalled. In humans and rodents alike, reactivated fear memories can be attenuated by disrupting reconsolidation with extinction training. Using functional brain imaging, we found that, after a conditioned fear memory was formed, reactivation and reconsolidation left a memory trace in the basolateral amygdala that predicted subsequent fear expression and was tightly coupled to activity in the fear circuit of the brain. In contrast, reactivation followed by disrupted reconsolidation suppressed fear, abolished the memory trace, and attenuated fear-circuit connectivity. Thus, as previously demonstrated in rodents, fear memory suppression resulting from behavioral disruption of reconsolidation is amygdala-dependent also in humans, which supports an evolutionarily conserved memory-update mechanism.

Internet administration of self-report measures commonly used in research on social anxiety disorder: A psychometric evaluation

The Internet has become increasingly popular as a way to administer self-report questionnaires, especially in the field of Internet delivered psychological treatments. Collecting questionnaire data over the Internet has advantages, such as ease of administration, and automated scoring. However, psychometric properties cannot be assumed to be identical to the paper-and-pencil versions. The aim of this study was to test the equivalence of paper-and-pencil and Internet administered versions of self-report questionnaires used in social phobia research. We analyzed data from two trials in which samples were recruited in a similar manner. One sample (N=64) completed the paper-and-pencil version of questionnaires and the second sample (N=57) completed the same measures online. We included the Liebowitz Social Anxiety Scale-self-assessment (LSAS-SR), the Social Interaction and Anxiety Scale (SIAS), and the Social Phobia Scale (SPS) as measures of social anxiety. Also included were the Montgomery Asberg Depression Rating Scale-self-assessment (MADRS-S), the Beck Anxiety Inventory (BAI), and the Quality of Life Inventory (QOLI). Results showed equivalent psychometric properties across administration formats. Cronbachs @a ranged between 0.77 and 0.94. There was an indication of a somewhat higher construct validity when participants filled out questionnaires using paper-and-pencil. We conclude that the LSAS-SR, SIAS, and SPS can be administered via the Internet with maintained psychometric properties.

A Link between Serotonin-Related Gene Polymorphisms, Amygdala Activity, and Placebo-Induced Relief from Social Anxiety

Placebo may yield beneficial effects that are indistinguishable from those of active medication, but the factors underlying proneness to respond to placebo are widely unknown. Here, we used functional neuroimaging to examine neural correlates of anxiety reduction resulting from sustained placebo treatment under randomized double-blind conditions, in patients with social anxiety disorder. Brain activity was assessed during a stressful public speaking task by means of positron emission tomography before and after an 8 week treatment period. Patients were genotyped with respect to the serotonin transporter-linked polymorphic region (5-HTTLPR) and the G-703T polymorphism in the tryptophan hydroxylase-2 (TPH2) gene promoter. Results showed that placebo response was accompanied by reduced stress-related activity in the amygdala, a brain region crucial for emotional processing. However, attenuated amygdala activity was demonstrable only in subjects who were homozygous for the long allele of the 5-HTTLPR or the G variant of the TPH2 G-703T polymorphism, and not in carriers of short or T alleles. Moreover, the TPH2 polymorphism was a significant predictor of clinical placebo response, homozygosity for the G allele being associated with greater improvement in anxiety symptoms. Path analysis supported that the genetic effect on symptomatic improvement with placebo is mediated by its effect on amygdala activity. Hence, our study shows, for the first time, evidence of a link between genetically controlled serotonergic modulation of amygdala activity and placebo-induced anxiety relief.