European Psychiatry - Volume 41 - April 2017

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25th European Congress of Psychiatry / European Psychiatry 41S (2017) S8–S52 S15
Disclosure of interest AM received honoraria or advisory
board/consulting fees from the following companies: Janssen
Pharmaceuticals, Otsuka, Pfizer and Pierre Fabre.
SG received honoraria or advisory board/consulting fees from
the following companies: Lundbeck, Janssen Pharmaceuticals,
Hoffman-La Roche, Angelini-Acraf, Otsuka, Pierre Fabre and
Gedeon-Richter.
S023
Progressive brain changes associated
with persistent negative symptoms
following a first episode of psychosis
M. Lepage ∗, M. Carolina , B. Michael , C. Mallar , J. Ridha ,
M. Ashok
1 McGill University, Psychiatry, Montreal, Canada
2 McGill University, integrated program in Neuroscience, Montreal,
Canada
∗ Corresponding author.
Early persistent negative symptoms (ePNS) refer to the presence
of potentially idiopathic or primary negative symptoms and have
been observed following a first episode of psychosis (FEP). There is
evidence for cortical changes associated with ePNS and given that
a FEP often occurs during a period of ongoing brain development
and maturation, neuroanatomical changes may have a specific age
related component. The current study examined cortical thickness
(CT), hippocampal/amygdala volume and shape as a function of
clinical trajectories and age using longitudinal structural imaging
in FEP. T1-MRI scans were acquired for early (n = 21), secondary
(n = 30), non-(n = 44) PNS patients with a FEP, and controls ( n = 44).
Cortical thickness and amygdalar–hippocampal volumes and sur-
face area (SA) metrics were extracted from three time points over
a two-year period. Linear mixed models were applied to test for
a main effect of group, and age group interactions. Relative to the
other groups, ePNS patients showed cortical thinning over time in
temporal regions and a thickening with age primarily in prefrontal
areas. They also exhibited reduced left amygdalar and right hip-
pocampal volumes. Morphometry revealed decreased surface area
in ePNS compared to other groups in left central amygdala. The
current study demonstrates that FEP patients with ePNS show sig-
nificantly different CT trajectories with age. Increased CT may be
indicative of disruptions in cortical maturation processes within
higher-order brain regions. Amygdalar-hippocampal changes with
age are also linked to ePNS with converging results from volumet-
ric and morphometric analyses. Taken together, these results could
represent dynamic endophenotypes setting these ePNS patients
apart from their non-symptomatic peers.
Disclosure of interest The authors have not supplied their decla-
ration of competing interest.
Symposium: New avenues in the management of
bipolar disorder
S024
Mania and depression: What’s new?
A. Fagiolini ∗, G. Amodeo
1 University of Siena, School of Medicine, Siena, Italy
2 University of Siena, Molecular Medicine, Siena, Italy
∗ Corresponding author.
Despite the high burden of bipolar disorder and the noticeable
progress in its treatment, the disorder still goes frequently mis-
diagnosed, unrecognized, or not optimally treated. To date, no
medication has been specifically developed on the basis of a precise
understanding of the pathophysiology of the disorder, or based on
the unique characteristics of several subtypes of bipolar disorder or
on the medication mechanism of action. Lithium remains on of the
gold standard treatments for bipolar disorder. Its mood-stabilizing
properties are thought to occur via specific cellular signaling path-
ways, such as inhibition of glycogen synthase kinase 3, which
is considered to regulate cellular apoptosis. Divalproex, carba-
mazepine and several atypical antipsychotics are also approved for
bipolar disease Evidence also suggests that antipsychotics show the
ability to treat and prevent mania and/or depression but are often
burdened by side effects such as sedation, hortostatic hypotension
and weight gain. Hence, while it is clear that there still are sev-
eral unmet needs especially for what pertains tolerability, efficacy
for specific subtypes, and predictability. Novel and more effective
treatments are needed and researchers are currently engaging in
targeted drug development for bipolar illness, aimed at improv-
ing pharmacological strategies with marked and sustained effects.
A variety of newer medications are being tested. Some of these
drugs target pathways that are similar to those targeted by lithium,
while others focus on newer targets, such as opiate receptor and
N-methyl-D-aspartate (NMDA) receptors. Newer and older treat-
ment strategies for bipolar disorder will be presented and critically
reviewed.
Disclosure of interest Andrea Fagiolini is/has been a consultant
and/or a speaker and/or has received research grants fromAllergan,
Angelini, Astra Zeneca, Boehringer Ingelheim, Pfizer, Eli Lilly, Ferrer,
Janssen, Lundbeck, Novartis, Otsuka, Roche.
S025
The role of long acting antipsychotics
in bipolar disorder
E. Vieta
Hospital Clinic de Barcelona, Psychiatry Bipolar Disorders Program,
Barcelona, Spain
Antipsychotics are widely used for the short and long-term
treatment of bipolar disorder. Depot and long-acting injectable for-
mulations (LAIs) can be particularly useful for certain subgroups
of patients. This lecture will discuss the available data from ran-
domized controlled trials of LAIs in bipolar disorder. A recently
published meta-analysis and individual studies assessing depot
medications, as well as modern LAIs such as risperidone, paliperi-
done and aripiprazole, will be reviewed, looking carefully into the
prevention of either pole of illness and tolerability. Potential indi-
cations and patient profile, based on data and clinical experience,
will be discussed.
Disclosure of interest The author has not supplied his declaration
of competing interest.
S026
Managing cognitive dysfunction in
bipolar disorder
K. Miskowiak
University Hospital of Copenhagen, Psychiatric Centre, Copenhagen,
Denmark
Cognitive dysfunction, including memory and concentration diffi-
culty, is an emerging treatment target in bipolar disorder. However,
a key challenge in the management of these cognitive deficits
is the lack of treatments with robust effects on cognition. Fur-
ther, it is unclear how cognitive dysfunction should be assessed
and addressed in the clinical treatment of the disorder. This talk
will review the evidence for cognitive impairment in bipolar dis-
order, including its severity, persistence and impact on patients’