European Psychiatry - Volume 41 - April 2017

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S282 25th European Congress of Psychiatry / European Psychiatry 41S (2017) S238–S302
EW0516
Sexual dysfunction in oncology
M.C. Cochat Costa Rodrigues ∗, R.G. Faria ,
S. Almeida
1 Magalhães Lemos Hospital, Psychiatry, Porto, Portugal
2 Unidade Local de Saúde do Alto Minho, Department of Psychiatry
and Mental Health, Viana do Castelo, Portugal
3 Portuguese Institute of Oncology, Department of Psycho-oncology,
Porto, Portugal
∗ Corresponding author.
Introduction Sexual dysfunction is a common consequence of
cancer treatment that affects at least half of men and women
treated for pelvic tumors and more than one quarter of individuals
with other malignancies.
Objectives/aims Identification of the main sexual dysfunctions
related to cancer treatments. Awareness to the importance of
addressing sexuality to cancer patients, identifying the main rea-
sons why healthcare providers usually do not.
Methods Literature review concerning researched articles pub-
lished in Pubmed/Medline as well as related bibliography.
Results Most sexual problems are not caused by the cancer itself,
but by toxicities of cancer treatment. Damage during cancer treat-
ment to pelvic nerves, blood vessels and organ structures leads to
the highest rates of sexual dysfunction. The most common sexual
dysfunction in men under cancer treatment is the loss of desire for
sex and erectile dysfunction. In women, the most common sexual
dysfunctions are vaginal dryness, dyspareunia and loss of sex-
ual desire, usually accompanied by difficulties in both the arousal
and orgasm phases. According to literature, there are many can-
cer patients who would like to be informed and advised by their
healthcare providers about the consequences of cancer treatment
on their sexual health. Unfortunately, this rarely happens.
Conclusions This work intends to publicize current existing
information on sexual dysfunction in oncology, focusing on the
prevalence, etiology and clinical presentation. The authors also
intend to promote communication about sexual function and pos-
sible sexual dysfunctions resulting from cancer treatments.
Disclosure of interest The authors have not supplied their decla-
ration of competing interest.
EW0517
Structural covariance networks in
anorexia nervosa (AN): A multimodal
graph theoretical analysis
E. Collantoni ∗, P. Meneguzzo , E. Tenconi , R. Manara ,
P. Santonastaso , A. Favaro
1 University of Padua, Department of Neurosciences, Santa Maria Si
Sala, Italy
2 University of Padua, Department of Neurosciences, Padua, Italy
∗ Corresponding author.
Introduction The possibility of evaluating cortical morphological
and structural features on the basis of their covariance patterns is
becoming increasingly important in clinical neuroscience, because
their organizational principles reveal an inter-regional structural
dependence which derive from a complex mixture of developmen-
tal, genetic and environmental factors.
Objectives In this study, we describe cortical network organiza-
tion in anorexia nervosa using a MRI morpho-structural covariance
analysis based on cortical thickness, gyrification and fractal dimen-
sion.
Aim Aim of the research is to evaluate any alterations in
structural network properties measured with graph theory from
multi-modal imaging data in AN.
Methods Thirty-eight patients with acute AN, 38 healthy controls
and 20 patients in full remission fromAN underwent MRI scanning.
Surface extraction was completed using FreeSurfer package. Graph
analysis was performed using graph analysis toolbox.
Results In acute patients, the covariance analysis among cortical
thickness values showed amore segregated pattern and a reduction
of global integration indexes. In the recovered patients group, we
noticed a similar global trendwithout statistically significant differ-
ences for any single parameter. According to gyrification indexes,
the covariance network showed a trend towards high segregation
both in acute and recovered did not observe any signif-
icant difference in the covariance networks in the analysis of fractal
dimension.
Conclusions The presence of increased segregation properties in
cortical covariance networks in AN may be determined by a retar-
dation of neurodevelopmental trajectories or by an energy saving
adaptive response. The differences between the analyzed parame-
ters likely depend on their different morpho-functional meanings.
Disclosure of interest The authors have not supplied their decla-
ration of competing interest.
EW0518
The link between sleep, stress and
BDNF
A. Eckert ∗, S. Karen , J. Beck , S. Brand , U. Hemmeter ,
M. Hatzinger , E. Holsboer-Trachsler
1 Psychiatric University Clinics Basel, Neurobiology Lab for Brain
Aging and Mental Health, Basel, Switzerland
2 Psychiatric University Clinics Basel, Center for Affective, Stress and
Sleep Disorders, Basel, Switzerland
3 Psychiatric Service Center St. Gallen, Department of Adult
Psychiatry, Wil, Switzerland
4 Psychiatric Services Solothurn, Department of Adult Psychiatry,
Solothurn, Switzerland
∗ Corresponding author.
The protein brain derived neurotrophic factor (BDNF) is a major
contributor to neuronal plasticity. There is numerous evidence that
BDNF expression is decreased by experiencing psychological stress
and that accordingly a lack of neurotrophic support causes depres-
sion. The use of serum BDNF concentration as a potential indicator
of brain alteration is justified through extensive evidence. Recently,
we reported, for the first time, a relationship between BDNF and
insomnia, since we could show that reduced levels of serum BDNF
are correlatedwith sleep impairment in control subjects, while par-
tial sleep deprivation was able to induce a fast increase in serum
BDNF levels in depressed patients. Using a bi-directional stress
model as an explanation approach, we propose the hypothesis
that chronic stress might induce a deregulation of the HPA sys-
tem leading in the long term to sleep disturbance and decreased
BDNF levels, whereas acute sleep deprivation, can be used as ther-
apeutical intervention in some insomniac or depressed patients
as compensatory process to normalize BDNF levels. Indeed, par-
tial sleep deprivation (PSD) induced a very fast increase in BDNF
serum levels within hours after PSD which is similar to effects seen
after ketamine infusion, another fast-acting antidepressant inter-
vention, while traditional antidepressants are characterized by a
major delay until treatment response as well as delayed BDNF level
increase. Moreover, we revealed that stress experience and sub-
jective sleep perception interact with each other and affect serum
BDNF levels. We identified sleep as a mediator of the association
between stress experience and serum BDNF levels.
Disclosure of interest The authors have not supplied their decla-
ration of competing interest.