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24th European Congress of Psychiatry / European Psychiatry 33S (2016) S18–S55

S47

Pharmacological and psychological treatments

The findings of

meta-analyses and randomized placebo-controlled treatment

studies indicate that a range of approaches are efficacious in acute

treatment. Pharmacological and psychological treatments, when

delivered singly, have broadly similar efficacy in acute treatment.

However, acute treatment with cognitive therapy (group or indi-

vidual) may be associated with a reduced risk of symptomatic

relapse at follow-up. Cognitive behaviour therapy is efficacious in

adults and children: cognitive therapy appears superior to exposure

therapy, but the evidence for the efficacy of social skills training is

less strong. It is unlikely that the combination of pharmacological

with psychological treatments is associated with greater overall

efficacy than with either treatment, when given alone, as only 1 of

4 studies of the relative efficacy of combination treatment found

evidence for superior efficacy.

Efficacy and length of acute pharmacological treatment

Antide-

pressant drugs with proven efficacy include most SSRIs, the SNRI

venlafaxine, the MAOI phenelzine and the RIMA moclobemide: the

potential efficacy of tricyclic antidepressants is unknown. Some

benzodiazepines and anticonvulsants and the antipsychotic olan-

zapine also appear efficacious in acute treatment. Anumber of small

single-dose placebo-controlled crossover studies together suggest

that beta-blockers can be beneficial in reducing anxiety symp-

toms in individuals with ‘performance anxiety’ (for example, when

speaking in public), which overlaps with mild non-generalized

social anxiety disorder. Acute treatment studies indicate that the

proportion of responding patients increases steadily over time. A

post-hoc analysis of the clinical trial database with paroxetine indi-

cates that many non-responders to treatment at 8 weeks become

responders with a further 4 weeks of double-blind treatment:

however a post-hoc analysis of the clinical trial database for esci-

talopram indicates that response is unlikely if there is no onset of

clinical effect within the first 4 weeks of treatment.

Longer-term treatment and further treatment after non-response

The findings of randomized placebo-controlled relapse preven-

tion studies in patients who have responded to previous acute

treatment reveal a significant advantage for staying on active

medication (clonazepam, escitalopram, paroxetine, pregabalin,

sertraline) for up to six months. Fixed-dose randomized controlled

trials do not provide consistent evidence of a dose-response rela-

tionship with antidepressant drugs: but a fixed-dose study of

pregabalin found that only the higher daily dosage was efficacious.

Adouble-blind randomized controlleddosage escalation trial found

no advantage for increasing to a higher daily dosage (of duloxe-

tine), when compared to continuing treatment with a lower dosage.

Switching between treatments with proven efficacy may be help-

ful. An uncontrolled study of augmentation of SSRI treatment with

buspirone found some evidence of beneficial effects; but a placebo-

controlled crossover-study of the augmentation of paroxetine with

pindolol found no evidence of efficacy. A small placebo-controlled

study of the augmentation of paroxetine with clonazepam found

the combination was marginally short of superiority, when com-

pared to paroxetine alone.

Disclosure of interest

The author has not supplied his declaration

of competing interest.

Further reading

Baldwin DS, et al. Benzodiazepines: risks and benefits. A reconsid-

eration. J Psychopharmacol 2013;11:967–71.

Baldwin DS, et al. Evidence-based pharmacological treatment of

anxiety disorders, posttraumatic stress disorder and obsessive-

compulsive disorder: a revision of the 2005 guidelines from the

British Association for Psychopharmacology. J Psychopharmacol

2014;28:403–39.

http://dx.doi.org/10.1016/j.eurpsy.2016.01.907

S92

Oxytocin in social anxiety: An

overview

I. Iancu

Tel Aviv University, Tel Aviv, Israel

Oxytocin is a neuropeptide that is synthesized in the hypothala-

mus. It acts as a central neurotransmitter, as well as a peripheral

hormone. It is called also trust hormone or love hormone. Because

of its anxiolytic, pro-social and social cognitive enhancing effects,

oxytocin has been suggested as a promising novel treatment for

patients with social anxiety disorder. However, controlled research

is small and the studies’ results are inconclusive. I will present the

results of several studies with several recommendations about the

role of oxytocin in social anxiety disorder. Whereas oxytocin shows

some promising effects in resistant cases, of course the preferred

agents are SSRIs, SNRIs and CBT.

Disclosure of interest

The author has not supplied his declaration

of competing interest.

http://dx.doi.org/10.1016/j.eurpsy.2016.01.908

S93

The relationship between social

anxiety, shyness and blushing

A. Pelissolo

, A. Moukheiber

AP–HP, Hôpitaux Universitaires Henri-Mondor, Department of

Psychiatry, UPEC, Créteil, France

Corresponding author.

The diagnosis of social anxiety disorder (SAD) has seen substan-

tial changes in the last 35 years from its first appearance in the

DSM-III in 1980 up to the most recent ones in the DSM-5. Through-

out all these changes, this disorder, previously called social phobia,

is still considered one homogenous entity with only one specifier

(“performance only”) introduced in the DSM-5 revision with spe-

cific fears or associated personality profiles not being considered

relevant clinical markers to define SAD subtypes. However, our

therapeutic experience suggested substantial particularities asso-

ciated with the fear of blushing in patients with SAD. Some patients

presenting this profile, historically called “erythrophobia”, seem to

have a very specific type of social anxiety that does not include

shyness and other characteristics of classical SAD. In a study con-

ducted in a sample of 450 new consecutive outpatients seeking

treatment for SAD, we compared 142 subjects with fear of blushing

without other social fears, 97 subjects with fear of blushing with

other associated social fears and 190 SAD subjects without fear of

blushing. The group with pure fear of blushing presented a differ-

ent profile when compared with the two other groups: later age of

onset, less comorbidity, lower behavioral and temperamental inhi-

bition, i.e. less shyness, and higher self-esteem. Furthermore, froma

therapeutic point of view, some specific strategies such as the Task

Concentration Training have shown to be particularly effective in

fear of blushing. We will further argue the validity of a possible

“fear of blushing” subtype of SAD.

Disclosure of interest

The authors have not supplied their decla-

ration of competing interest.

http://dx.doi.org/10.1016/j.eurpsy.2016.01.909