Examine the evidence for a relationship between pregabalin effect on pain and baseline anxiety and depressive symptoms in patients with fibromyalgia (FM).

Chronic pain and concomitant anxiety and depressive symptoms are common in patients with FM, as well as in other chronic pain disorders. Pregabalin was effective for treating pain in FM patients in three parallel group RCTs (105, 1056, 1077) where data for anxiety and depressive symptom levels were collected.

Patients meeting ACR criteria for FM with a pain VAS score ≥40 mm were followed for 8-14 weeks in 3 randomized, double-blind, placebo-controlled trials. Patients (N=2022) received 150, 300, 450 or 600mg/d pregabalin or placebo. The primary efficacy parameter was change in endpoint Mean Pain Score (MPS) (range 0 [no pain]-10[worst possible pain]). Regression analyses evaluated whether changes in pain bore any relation to the baseline Hospital Anxiety and Depression Scales (HADS-A) and (HADS-D) levels.

Pregabalin 300, 450, and 600 mg/d, but not 150 mg/d, showed statistically significant improvements in pain compared with placebo (p<0.0001). For each pregabalin treatment group, improvements in pain at endpoint were not found to have a statistically significant association with baseline levels of anxiety or depressive symptoms. Adverse events (AEs) were consistent with known side effects of pregabalin; dizziness and somnolence, mild to moderate in intensity, were the most frequently reported AEs for pregabalin patients.

Pregabalin treatment demonstrated significant improvements in pain regardless of baseline anxiety or depressive symptom levels for patients with FM.

Study funded by Pfizer, Inc

To compare the anxiolytic efficacy and speed of onset of pregabalin (PGB) and venlafaxine-XR (VXR) in patients with GAD.

Adult outpatients with DSM-IV GAD and a HAM-A score >20 were randomized to 8-weeks of flexible-dose double-bind treatment with PGB 300-600mg/d (n=121), VXR 75-225mg/d (n=125), or placebo (PBO; n=128). Primary outcome: LOCF-endpoint change in HAM-A total score. Secondary outcomes included the Clinical Global Impression, Severity scale (CGI-S).

Study groups were similar at baseline, or PGB, VXR, and PBO, respectively, in terms of gender, mean age, and baseline HAM-A (27.6±0.4 vs. 27.4±0.4 vs. 26.8±0.4. Treatment with PGB was associated with significantly greater improvement than placebo at LOCF-endpoint, with onset of treatment effect beginning by day 4. HAM-A-total scores for PBO, PGB, and VXR at day 4 were: -3.4±0.5, -5.3±0.5 (P=.008), and -2.9±0.6 (P=.070), respectively; corresponding LOCF-endpoint HAM-A-total scores were: -11.7±0.9, -14.5±0.9 (P=.03), and -12.0±0.9 (P=.097). LOCF-endpoint CGI-S scores for PBO, PGB, and VXR were: -1.5±0.2, -2.0±0.2 (P=.02), and -1.7±0.2 (P=.36),

Severe AE rates were: PGB (9.1%), VXR (20.0%), and PBO (7.8%). Discontinuation due to AEs were: PGB (12.4%), VXR (17.6%), and PBO (5.5%).

Pregabalin was safe and effective, demonstrating significantly earlier onset of anxiolytic activity against GAD than venlafaxine-XR. Venlafaxine-XR did not demonstrate significant efficacy, possibly due to a relatively high placebo response.

Funded by Pfizer Inc

To assess the speed of onset of anxiolytic efficacy of a single-dose of pregabalin (PGB) in a dental-anxiety model.

Adult outpatients in this double-blind, parallel-group study received a single-dose PGB 150mg (n=27), alprazolam 0.5mg (n=31; ALP), or placebo (n=31; PBO) 4 hours before a dental procedure. Inclusion criteria included Dental Anxiety Total score ≥12 (moderate-to-severe) without presence of DSM-IV anxiety disorder. Efficacy and safety assessments (at 2, 2.5, 3, 3.5, and 4 hours post-dose) included: 100-mm Visual Analogue Scale for Anxiety (VAS-A; primary outcome); 100-mm VAS-Sedation (VAS-S); and Time-to-Onset of Action Scale (TOAS), which rates anti-anxiety drug benefit (0-10, no–full benefit).

VAS-A scores at baseline were higher on PGB (70.2) compared to ALP (57.4) or PBO (64.1). On a mixed-model analysis, VAS-A improvement slopes were greater for PGB (t= -2.47; P=0.014) and ALP (t= -2.39; P=0.018) vs PBO. Significant improvement on TOAS was seen at hour 2 and hour 3 through endpoint for ALP and PGB subjects, respectively (P≤0.05 vs PBO, both groups). VAS-S scores were significantly higher vs PBO for PGB at hours 2.5-4.0, and at hours 2 until endpoint for ALP (P≤0.05 both groups). Spearman analysis showed similar levels of correlation between the TOAS and VAS-S (r= +0.58) and VAS-A (r= -0.50), suggesting that the VAS-S may be measuring an efficacy outcome in this model. Both PGB and ALP were well-tolerated.

Clinically meaningful anxiolytic effect occurred within 3-4 hours after single-dose PGB in this dental-anxiety model.

were consistent with national studies but showed higher figures to neighbouring countries. It was consistent with figures in United Kingdom before 1950.

Patient's satisfaction is a vital part of the assessment of quality of health care. Patient's mental health situation may influence service satisfaction and vice versa. The aim of this study was to evaluate relationship between anxiety and depression and service satisfaction, in a group of patients that were admitted in a general hospital.

Four hundred patients who were admitted in Dr. Shariati Hospital were included in the study consecutively. Participants were recruited from medical and surgical wards. The Hospital Anxiety and Depression Scale (HADS) was used to determine depression and anxiety and 18 items Patient Satisfaction Questionnaire (PSQ-18) was used to measure service satisfaction. Other variables that were measured included: demographic variables, duration of disease, time passed from admission, ward of admission, pattern of referral to hospital, type of insurance and the way of payment.

Patient with anxiety and depression were less satisfied with services. Service satisfaction according to PSQ-18 scores had a reverse significant relation with anxiety score of HADS. There was no significant relationship between service satisfaction and age, sex, education, duration of disease, time passed from admission, ward of admission, pathway of referral, type of insurance and the way of payment.

Psychological profile of hospitalized patients may play important role in their satisfaction with services. Careful management of mental health problem may be necessary to improve service satisfaction of medical inpatients. On the other hand improvement in quality of care and increasing service satisfaction may reduce mental health problem of the patients.

Generalized Anxiety Disorder (GAD) is classified as an anxiety disorder. High co-morbidity with other anxiety and depressive disorders blurs boundaries between these disorders, clinically as in research. This is particularly relevant for genetic research into causes of these disorders.

We attempt to clarify where GAD belongs in the anxiety/depression spectrum disorders.

The cohort is based on a population-wide screening for anxiety and depression in Iceland as part of a genetic research project. Following the screening participants underwent the Composite International Diagnostic Interview (CIDI) for possible ICD-10 diagnoses. Odds ratios (OR) were calculated by logistic regression analysis for GAD and the other disorders. The phobias (simple, social and agoraphobia) were pooled together in the analysis.

A total of 3.150 participants underwent the CIDI. The OR between GAD and dysthymia was 2.99 (2.37-3,78), Panic disorder, PD, 2.03 (1.59-2.59); any phobia 1.15 (0.92-1.42) and Major Depressive Disorder, MDD, 1.07 (0.84-1.37). The OR between dysthymia, MDD and GAD is very high, . The OR, with co-morbidity accounted for by logistic regression analysis, is slightly lowered for all except dysthymia.

Our results show that GAD is significantly associated with dysthymia, followed by PD, but non-significant with the phobias and MDD. Dysthymia, on the other hand, has a robust relationship both to GAD and MDD, 2.97 and 2.91 respectively. Logistic regression confirms the strong link between GAD and dysthymia and gives these disorders the possible role of a genetic bridge between anxiety and depressive disorders.

To assess the impact of high levels of insomnia on response to pregabalin (PGB) in patients with GAD.

Pooled data were analyzed from 6 double-blind, placebo-controlled, 4- to 6-week trials of outpatients who met DSM-IV criteria for GAD with a minimum Hamilton rating scale for anxiety (HAM-A) score ≥18. Response was evaluated for 3 fixed-dose PGB groups: 150mg/d, 300-450mg/d, and 600mg/d. A "high-insomnia" subgroup was defined by a baseline HAM-D insomnia factor score ≥4 (maximum=6).

At baseline, 482 (31%) patients met criteria for the high-insomnia subgroup, and 1073 (69%) for the low-insomnia subgroup. Mean baseline HAM-A scores were non-significantly higher (approx. 1-point) in high-insomnia vs low-insomnia patients. In high-insomnia patients, PGB produced significantly greater improvement in HAM-A total scores at LOCF-endpoint vs placebo—PGB 150mg/d (-10.3±1.01), PGB 300-450mg/d (-12.4±0.88), PGB 600mg/d (-11.6±0.72), and placebo (-8.4±0.66) (P<0.0001, all comparisons). Effect sizes for endpoint HAM-A change were higher in high-insomnia than low-insomnia subgroups (0.47 vs 0.32). Endpoint HAM-A-score changes were the same (-12.0) on PGB in both insomnia subgroups; placebo response was higher in low-insomnia patients. Significantly more high-insomnia patients on PGB were insomnia responders (reduction to minimal-to-no insomnia) (75.2%, all doses combined) vs placebo (61.5%; P<0.005). Rates of treatment-emergent insomnia were 4.7% for all PGB doses combined vs 5.4% for placebo.

Pregabalin was well tolerated, and improved overall anxiety symptoms, while specifically improving insomnia in patients with GAD presenting with high levels of concurrent insomnia.

Panic attacks are psychopathological phenomena with a strong emotional component that often induce an adaptive response with anticipatory anxiety and phobic avoidance. There are evidences of the presence of biases in emotional processing in patients with panic disorder. The aims of this study were to compare Emotional Intelligence (EI) between patients with PD and control subjects and to investigate if this construct is related to the severity of agoraphobia.

Fifty-one patients with PD and 50 healthy controls were assessed for their EI with the Mayer-Salovey-Caruso Emotional Intelligence Scale and their phobic avoidance with the Mobility Inventory for Agoraphobia. Data were analysed by not parametric statics.

The Strategic Emotional Intelligence area showed lower scores in patients with PD compared to healthy controls (median 80 vs 84.9, z =-3.37, p<.0008). Among the subscales of this area, this difference was significant (median 80 vs 85.3, z =-2.61, p<.009) for the “Understanding emotions” branch. The severity of agoraphobia correlated with the “Facilitating thought with emotion” branch of Experiential EI area.

Patients with PD show a lower strategic EI. Some aspect of experiential EI seem to be related to the severity of agoraphobia. A training focused on the development of the strategic component of emotional intelligence might help patients with PD.

Mayer J., Caruso D., Salovey P. Emotional Intelligence Meets Traditional Standards for an Intelligence. Intelligence 2000; 27: 267–298.

Recent studies indicate that Adult Separation Anxiety Disorder (ASAD) may represent a discrete diagnostic entity worthy of attention. Adults with ASAD report estreme anxiety and fear about separations from major attachment figures. These symptoms lead to severe impairment in social relationships and are not better accounted for by the presence of agoraphobia. In a previous study, we found platelet expression reduction of the 18 kDa Translocator Protein (TSPO) in patients with panic disorder with associated ASAD.

To explore whether separation anxiety might be a factor differentiating TSPO expression in a sample of patients with major depression.

The equilibrium binding parameters of the specific TSPO ligand [3H]PK 11195 were estimated on platelet membranes from 40 adult outpatients with MDD, with or without separation anxiety symptoms, and 20 healthy controls. Patients were assessed by SCID-I, HAM-D, the Structured Clinical Interview for Separation Anxiety Symptoms (SCI-SAS) and the Adult Separation Anxiety Self-report Checklist (ASA-27).

A significant reduction of platelet TSPO density mean value was found in depressed patients with associated ASAD, while no significant differences were found between depressed patients without ASAD and the control group. Individual TSPO density values were significantly and negatively correlated with both SCI-SAS-A and ASA-27 total scores, but not with HAM-D total score or HAM-D anxiety/somatization factor score.

Reduction of platelet TSPO density in our sample of patients with depression was specifically related to the presence of ASAD. These data suggest that TSPO expression evaluation is a useful biological marker of ASAD.

Anxiety disorders are associated with impairment in social functioning and poor quality of life, with personal impairment affecting many areas. Instead of collapsing together symptoms and functioning, the Kennedy Axis V is designed to assess seven dimensions.

Thirty-five outpatients consecutively admitted to our Anxiety Disorders Unit were evaluated before starting treatment by a set of instruments including: Mobility Inventory for Agoraphobia (MIA), Self-rating Anxiety State (SAS), Anxiety Status Inventory (ASI), Penn State Worry Questionnaire (PSWQ), Symptom Check List 90 Revised (SCL-90-R), Brief-COPE, and Kennedy Axis V (K Axis).

Sample characteristics: age 38.5±10.9, males 36.1%, current substance use 14.3%, previous drug treatment 82.9%, previous psychotherapy 28.6%. Symptom scores (mean±SD): MIA 7.41±6.84, PSWQ 46.59±12.15, ASI 58.97±10.53, SAS 59.43±11.85; as for the SCL-90-R subscales and indexes: Somatization (SOM) 1.62±0.76, Obsessive-Compulsive (O-C) 1.48±0.70, Interpersonal Sensivity (I-S) 1.38±0.85, Depression (DEP) 2.02±0.90, Anxiety (ANX) 1.94±0.79, Hostility (HOS) 1.14±0.84, Phobic Anxiety (PHOB) 1.52±1.11, Paranoid Ideation (PAR) 1.33±0.87, Psychoticism (PSYC) 0.88±0.72; General Symptomatic Index (GSI) 1.55±0.59, Positive Symptom Total (PST) 58.84±15.42, Positive Symptom Distress Index (PSDI) 2.19±0.57. The results of the K Axis subscale for psychological functioning (PSY) was 54.00±4.97; all the remaining subscales scored 90 or more. Significant correlations between symptom scales and psychological functioning were (Spearman's Rho, α=.05): PSY vs. PSDI -0.526 (p=.002), PSY vs. PSYC -0.446 (p=.008), PSY vs. DEP -0.43 (p=.011), PSY vs. GSI -0.427 (p=.012), PSY vs. I-S -0.425 (p=.001).

Scores on the self-rated symptomatic scales are inversely correlated with the clinician-attributed score of PSY, suggesting construct validity.

analyse the presence of comorbid symtoms as assessed by Hamilton Anxiety scale in outpatients followed in Psychiatric clinics.

Multicentre, cross-sectional study enrolling subjects above 18 years-old with GAD according with ICD-10. Participants were chosen at ramdon by quotes and weighted geographically, but patients were enrolled consecutively. HAM-A and CGI-S were administered to determine clinical status and comorbid symptoms (scoring > 3 in HAM-A). QoL was assessed by SF-36 questionnaire.

A total of 792 patients; 15.7% naives (GADn), 68.9% women, mean (SD) age of 40.0 (12.9) years were included. Symptoms of imsomnia were presented in 30.1% of subjects; 42.3% in GADn vs 27.8% on-treatment (GADt), p=0.001. Symptoms of cognitive function deterioration were showed in 21.1% (25.2% in GADn vs. 20.3% in GADt, p=0.220) and depressive symptoms in 15.5% (15.4% in GADn vs 15.5 in GADt, p=0.991). Moderate to excruciating pain was presented in 46.7% of subjects; 50.5% in GADn vs 46.1% in GADt, p=0.705. Overall, psychic and somatic anxiety symptoms scoring were higher in GADn than in GADt; 26.8 (7.3) vs 22.4 (9.6), p<0.0001, 14.2 (3.6) vs 12.0 (5.0), p<0.0001, and 12.6 (4.5) vs 10.4 (5.2), p<0.0001, respectively. No age or sex differences were found.

Pain, symptoms of depression and cognitive deterioration were comorbid conditions presented in a considerable proportion of GAD patients irrespective of time of evolution, age or sex. Frecuency of insomnia was also high, mainly in naïve patients. This study shows that more attention should be devoted to comorbid condition associated with GAD.

analyse the impact of comorbid depression on clinical and self-perceived health status in outpatients with GAD in Spain.

Multicentre, cross-sectional study enrolling subjects above 18 years-old with GAD according with ICD-10. Participants were chosen at ramdon by quotes and weighted geographically, but patients were enrolled consecutively. HAM-A and CGI-S were administered to determine clinical status and SF-36 and Sheehan disability scales for health status assessment.

Seven-hundred-ninety-two patients; 15.7% naives (GADn), 68.9% women, mean (SD) age of 40.0 (12.9) years were included. Ninety (11,4%) fulfilled criteria for comorbid depression with GAD. Depressive subjects were older [49.5 (11.3) vs. 43.7 (13.2) years, p=0.0001], female (78.7% vs 67.6%, p=0.034) and received lorazepan and lormetazepan more frequently (30.0% vs. 18.5%, p=0.015, and 15.6% vs. 5.0%, p=0.0002, respectively), but not antidepressatns, and received higher number of drugs; 2.3 (0.8) vs. 2.0 (0.8), p=0.011. Overall, psychic and somatic anxiety symptoms scoring (HAM-A) were higher in depressive; 26.4 (8.2) vs 22.7 (9.5), p=0.0003, 14.1 (4.1) vs 12.1 (4.9), p<0.0001, and 12.3 (4.7) vs 10.6 (5.2), p=0.0023, respectively. Depressive showed more severe symptoms of anxiety; 62.2% vs. 43.0%, p=0.0031, and scoring in CGI; 4.2 (0.9) vs 3.7 (1.1), p<0.0001. Depressives also showed higher scoring of disability; 19.7 (6.0) vs. 15.6 (7.0)%, p<0.0001, and lower values in physical and mental summary subscales of SF-36; 38,6 (7,9) vs 43.9 (9.0), p<0.0001, and 26.6 (9.5) vs. 30.4 (11.6), p=0.0008.

Comorbid depression enlarges deterioration in clinical status, level of functioning and quality of life of outpatients with GAD.

analyse GAD impact on clinical and self-perceived health status in outpatients followed in Psychiatric clinics.

Multicentre, cross-sectional study enrolling subjects above 18 years-old with GAD according with ICD-10. Participants were chosen at ramdon by quotes and weighted geographically, but patients were enrolled consecutively. HAM-A and CGI-S were administered to determine clinical status and SF-36 and Sheehan disability scales for health status assessment.

A total of 792 patients; 15.7% naives (GADn), 68.9% women, mean (SD) age of 40.0 (12.9) years were included. Time to effective diagnosis and start up of treatment were, respectively, 2.3 (4.9) and 2.6 (4.7) years. Severe symtoms of anxiety (HAM-A > 24) were presented in 45.2%; 56.9% in GADn vs 43.0% on-treatment (GADt), p<0.001. CGI-S was 3.7 (1.1) in GADn vs. 4.2 (0.8) in GADt, p<0.001. The 77,7% of GADt were receiving 2 or more drugs: 94.1% ansiolytics and/or antidepressants. The 39.3% of subjects showed high/extreme disability for work; 44.4% GADn vs 38.5% GADt, p=0.33, 34.5% for daily-living domestic activities; 39.7% vs 33.7% respectively, p=0.082, and 41.8% for social life; 43.1% vs 41.7% respectively, p=0,145. Mental composite summary of SF-36 was below normal; 30,0 (11,4), much lower in GADn: 25,4 (8,5) vs. 30,8 (11,7), p<0.001. No gender differences were found.

This study showed that a considerable proportion of GAD patients still need for additional medical remedies which should improve the level of disability caused by the diasease and counteract the deteriorated mental health observed in such patients.

Tobacco consumption has been related to the onset of panic attacks (PA), panic disorder (PD) and agoraphobia, to panic symptoms and to features related to PD. The relationship that links tobacco and panic is not clear, and some models have been proposed to explain it (causal, neuroticism as a vulnerability factor).

Our aim was to study the relationship that tobacco consumption before the onset of PD has with some features of the disorder and to clarify the relationship that links tobacco and panic.

A sample of 82 naïve PD patients was included. Patients were extensively evaluated (Mini Neuropsychiatric Interview–MINI-, Panic Disorder Severity Scale–PDSS-, State-Trait Anxiety Inventory–STAI-, Beck Depression Index–BDI-; Anxiety Sensitivity Index–ASI-, Mobility Inventory of Agoraphobia–MIA-, Clinical Global Impression-CGI-, NEO-Five Factor Inventory–NEO-FFI). Tobacco consumption was retrospectively assessed by asking the patients the consumption they had the week before suffering the first panic attack.

The condition of smoker before the onset of PA showed significant relationships with earlier age of onset of PD (p=0.04), less frequency of PA (p=0.04), and higher scores in BDI (p=0.04) and NEO-FFI neuroticism (p=0.02). After analysis with multiple logistic regression, neuroticism did not show considerably influence on any of these associations.

Being a smoker before the onset of PA is related, in the early phases of PD, to higher neuroticism and depressive symptoms, less frequency of PA and PD onset at a younger age.

Although proposed as a common vulnerability factor, neuroticism does not influence the observed associations.

The association between Mitral Valve Prolapse (MVP) and anxiety disorders, particularly Panic disorder (PD) and Social Anxiety disorder (SAD), attracted considerable interest in the 1980 and 1990 decades but the published results were not sufficient to definitely establish or to exclude an association between MVP and PD or SAD, with prevalences ranging from 0 to 57%.

According to a recent literature review on this topic, there are no studies about this possible association using current MVP criteria.

The study consisted of echocardiographic evaluation of 232 volunteers previously diagnosed with SAD (N=126), PD (N=41) or Control (N=65). The exams were performed by two cardiologists specialized in echocardiography who were blind to the psychiatric diagnosis of the participants.

There were no statistical differences between groups in MVP prevalence (SAD=4.0%, PD=2.4% and Control=0.0%), with values similar to the prevalence currently estimated for the normal population (2-4%). When the data were evaluated using the M-mode, the method used in most of the previous studies but currently considered of questionable validity, the prevalence was higher in the SAD group (8.7%) compared to control (0.0%).

Regarding the other morphological characteristics of the mitral valve, no significant differences were detected between groups in terms of the presence of mitral insufficiency, mean valve thickness and mean valvar dislocation in any two-dimensional echocardiographic view.

If any relationship does actually exist among SAD, PD and MVP, it could be said that it is infrequent and that it mainly occurs in subjects with minor variants of MVP.

The Social Anxiety Disorder (SAD) is a highly incapacitating condition that can cause considerable subjective suffering, with a negative impact on psychosocial functioning. However, few data are available in the literature about the influence of SAD severity and of SAD subtypes or the presence of comorbidities on psychosocial functioning, and the possible extent of this impairment in individuals with subclinical signs and symptoms.

The study consisted of the evaluation of psychosocial functioning using the Disability Profile (DP) in 355 volunteers, all of them college students who had been diagnosed in a previous study as SAD (N=141), Controls (N=92) or Subclinical (N=122), the last ones being defined as having unreasonable fear of a social situation but not fulfilling the criteria of avoidance or functional/occupational impairment due to this fear.

The groups were balanced regarding age, sex and socioeconomic level.

The SAD group had higher scores than the other two groups in all domains of DP, both on a lifetime basis and during the last two weeks. Subjects with subclinical SAD presented intermediate values.

The impairment of psychosocial functioning was also significantly related to the severity of the disorder. Regarding subtype, generalized SAD causes more harm, and the presence of comorbidities is associated with greater impairment of psychosocial functioning in each group.

The impairment of psychosocial functioning progressively increases along the spectrum of social anxiety. Further studies are needed to evaluate the consequences of this association.

Most patients with Social Anxiety Disorder (SAD) present other psychiatric disorders. The lifetime prevalence of comorbidities has been reported to range from 52% to 92% in epidemiological studies. There is some evidence showing that the frequency of comorbidities varies according to subtype and severity of SAD and those subjects with subclinical SAD present intermediate values.

The study consisted of the evaluation of psychiatric comorbidities in 355 volunteers, all of them college students who had been diagnosed as SAD (N=141), Controls (N=92) or Subclinical (N=122) in a previous study. The groups were balanced regarding age, sex and socioeconomic level. Three interviewing psychiatrists, blind to the group to which the volunteers belonged, applied the SCID for the DSM-IV.

The rate of comorbidity with other psychiatric disorders was 71.6% in the SAD group and 50% in subjects with Subclinical SAD and differed significantly from the Controls (28.7%). These results confirm in a Brazilian sample of college students the results of other epidemiological and clinical studies on the existence of high levels of lifetime comorbidity in SAD.

The presence of comorbidities increased progressively according to SAD subtype and severity, with the rates for subclinical subjects being intermediate, with lower values than subjects with circumscribed SAD or with mild cases of SAD, but significantly higher than control.

The rates of psychiatric comorbidity increase progressively along the spectrum of social anxiety. Further studies are needed to determine the consequences of this association.