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S130

24th European Congress of Psychiatry / European Psychiatry 33S (2016) S116–S348

Conclusions

Patients with bipolar disorder showduring a depres-

sive episode difficulties in most cognitive tasks involving executive

functions. Results obtained by patients at failure to maintain set

score suggest frontal dysfunctions for this category of patients.

Disclosure of interest

The authors have not supplied their decla-

ration of competing interest.

http://dx.doi.org/10.1016/j.eurpsy.2016.01.158

EW41

Use of antidepressants in

maintenance phase of patients with

bipolar disorder in an outpatient

setting

A. Peh

, W.K. Tay

Changi General Hospital, Dept of Psychological Medicine, Singapore,

Singapore

Corresponding author.

Introduction

Guidelines for themaintenance treatment of bipolar

disorder discourage the use of antidepressants chiefly on grounds

of unproven efficacy and risk if mania for bipolar I. However, for

patients stabilised on an antidepressant, naturalistic data support

its continued use.

Aim

The aim is to describe use of antidepressants in patients

with bipolar disorder in remission seen at an outpatient clinic in

Singapore.

Methods

The case notes of patients with bipolar disorder in

remission, seen by psychiatrist in an outpatient psychiatric clinic

in a general hospital unit fromDecember 2014 to March 2015 were

studied. Data describing the age, sex, type of bipolar disorder and

psychotropic medications prescribed, was obtained.

Results

Forty-twopatientswere included, ofwhich13 (31%)were

male and 29 (69%) were female. The age ranged from 23 to 82, with

mean age of 47 years. Of these 17 (40%) had bipolar I and 25 (60%)

had bipolar II. Antidepressant use for maintenance treatment was

present in 19 out of 42 (45%) of these patients; of these 7 out of

17 (41%) were bipolar 1 and 12 out of 25 (48%) were bipolar II.

Eighteen out of the 19 (95%) patients who were prescribed antide-

pressants were on combination treatment with mood stabilizers.

Antidepressant type included SSRI (37%), NDRI (37%), SNRI (10.5%),

TCA (10.5%), NASSA (5%).

Conclusion

Almost half of patients with bipolar disorder man-

aged in an individual practice were on antidepressants together

with mood stabilisers. They remained in remission with combina-

tion treatment, which did not seem to jeopardise their condition.

Disclosure of interest

The authors have not supplied their decla-

ration of competing interest.

http://dx.doi.org/10.1016/j.eurpsy.2016.01.159

EW42

Bipolar mood disorder BMD can be

classified into 4–5 broad molecular

categories based on parametric

oscillation theory and signs and

symptoms

K. Pirkalani

1 ,

, Z . T

alaeerad

2

1

Mehr Medical Group, Internal Medicine, Tehran, Iran

2

Mehr Medical Group, Gynecology, Tehran, Iran

Corresponding author.

Introduction

BMD is regarded as spectrum and needs finer clas-

sification.

Objectives

Wide clinical andmolecular data on BMD are available

but no correlation.

Aims

To correlate malfunction of circadian oscillators with dif-

ferent clinicopathologic presentations of BMD spectrum.

Methods

Based on 73 patients, we have differentiated 5 disease

activity patterns. A divergent model of one master (CLOCK/BAML1

heterodimer) + 4 slave circadian oscillators (neuronal PAS domain

protein 2, Rora, Rev-erb, and CSNK1E) and downstream effector

genes (

PER1, PER2, PER3, CRY1, CRY2, Teneurin 4, NCAN (Neurocan),

GSK3-b, casein kinase I epsilon

) were designed to highlight hetero-

geneity in regard to genetics and presentation.

Results

Five patterns of activity curves with the appropriate

molecular explanations can be drawn:

– one attack, rare exacerbations, near normal inter-interval mental

functioning; pathogenesis lies in master mutation. Lifetime events

are the cause of deregulation;

– frequent attacks with inter-interval derangements due to major

mutation of the master oscillator and ambiguity between master

and slave. No time for circadian re-establishment, wide range of

downstream genes activity, and a full-blown clinical picture;

– one major attack and no apparent remission, wide range of signs.

Hyperactive mutant of slave and suppression of the master;

– rapid cycling due to master mutation and complete change of the

innate frequency;

– a diagnostic dilemma of mild continuous signs and symptoms

with no prominent attacks and overlap with borderline or schizo-

typal PD due to mutation in some downstream genes (i.e.

GSK3-b

or

Per, CRY, NCAN

).

Conclusions

Finding molecular correlation with disease subtypes

and activities is possible.

Disclosure of interest

The authors have not supplied their decla-

ration of competing interest.

http://dx.doi.org/10.1016/j.eurpsy.2016.01.160

EW43

Multiple oscillators assure soft margin

of diurnal function and are the result

of alternate splicing and later genetic

rearrangement: Possible role in

bipolar disorder

K. Pirkalani

1 ,

, Z . T

alaeerad

2

1

Mehr Medical Group, Internal Medicine, Tehran, Iran

2

Mehr Medical Group, Gynecology, Tehran, Iran

Corresponding author.

Introduction

Appearance of multiple effector proteins on a sin-

gle receptor seems mysterious. These new effectors appear during

alternate splicing, gene duplication and genomic re-arrangement

during evolution. In chronobiology, this might have vital protective

importance for migration to places with extreme climates.

Objectives

Residing on a simple light/darkness system of circa-

dian cycle is in contrast with human cultural development.

Aims

Developing a model of molecular interaction to explain the

BMD spectrum.

Methods

We classify circadian oscillators into one master

(CLOCK/BMAL1) and 4 slave oscillators. The master has suppress-

ing action on 4 parallel slave oscillators. In case of disruption of

this tract, one of them reigns. Input from the retinal ganglion cells

has minor effect (noise) for the parametric oscillation of the mas-

ter but not slave oscillator. Mutations in the master that disrupts

these feedbacks, or increases sensitivity to ganglion cells input or

cause hyperactivity of the slave oscillators are explanations for

BMD development. Downstream to this, a divergent set of genes

(

PER1, 2, 3, NCAN, GSK3-b and CRY1

), 2 with different functions are

activated. Derangement of any of the downstream genes causes

incomplete symptoms and signs.

Results

This model with elegant curves can successfully incor-

porate many laboratory and clinical findings and explains in a

comprehensive way how genetic and environmental factors inter-

act to build up disease picture and spectrum of BMD. In addition,

some innovative (less intensive and with less side effects) treat-

ment strategies can be suggested.