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25th European Congress of Psychiatry / European Psychiatry 41S (2017) S238–S302


Sexual dysfunction in oncology

M.C. Cochat Costa Rodrigues

1 ,

, R.G. Faria



S. Almeida



Magalhães Lemos Hospital, Psychiatry, Porto, Portugal


Unidade Local de Saúde do Alto Minho, Department of Psychiatry

and Mental Health, Viana do Castelo, Portugal


Portuguese Institute of Oncology, Department of Psycho-oncology,

Porto, Portugal

Corresponding author.


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.


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.


Literature review concerning researched articles pub-

lished in Pubmed/Medline as well as related bibliography.


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.


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.


Structural covariance networks in

anorexia nervosa (AN): A multimodal

graph theoretical analysis

E. Collantoni

1 ,

, P. Meneguzzo


, E. Tenconi


, R. Manara



P. Santonastaso


, A. Favaro



University of Padua, Department of Neurosciences, Santa Maria Si

Sala, Italy


University of Padua, Department of Neurosciences, Padua, Italy

Corresponding author.


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.


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-



Aim of the research is to evaluate any alterations in

structural network properties measured with graph theory from

multi-modal imaging data in AN.


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.


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



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.


The link between sleep, stress and


A. Eckert

1 ,

, S. Karen


, J. Beck


, S. Brand


, U. Hemmeter



M. Hatzinger


, E. Holsboer-Trachsler



Psychiatric University Clinics Basel, Neurobiology Lab for Brain

Aging and Mental Health, Basel, Switzerland


Psychiatric University Clinics Basel, Center for Affective, Stress and

Sleep Disorders, Basel, Switzerland


Psychiatric Service Center St. Gallen, Department of Adult

Psychiatry, Wil, Switzerland


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.