

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.2016.01.158EW41
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.2016.01.159EW42
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 . Talaeerad
21
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.2016.01.160EW43
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 . Talaeerad
21
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.