European Psychiatry - Volume 41 - April 2017

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25th European Congress of Psychiatry / European Psychiatry 41S (2017) S645–S709 S681
EV0849
Can psychopathy be treated?
D. Durães ∗, R. Borralho
Centro Hospitalar Barreiro-Montijo, Mental Health and Psychiatry
Department, Barreiro, Portugal
∗ Corresponding author.
Introduction Psychopaths are incapable of feeling empathy and
guilt, being responsible for most violent crimes. To date, con-
finement has been the option of choice to minimize the harm
they inflict. However, a deeper understanding of the neurobio-
logy of psychopathy may lead to new insight on possible treatment
approaches.
Aims This work aims to review the current knowledge in psy-
chopathy treatment.
Methods A literature search ofMEDLINE (2000-present) was con-
ducted using the search terms “psychopathy” + “treatment” and
“drug therapy”.
Results Defects in the amygdala and the prefrontal cortex have
been implicated in the pathological basis of psychopathy. The most
affected areas are the ventromedial prefrontal cortex (VMPC) and
the associated anterior cingulated cortex. Alterations in connec-
tivity between the amygdala and the VMPC with other areas of
the brain have been demonstrated and seem to be responsible
for the non-empathetic, unemotional, and amoral features of psy-
chopaths. Also, they present an increase in dopamine turnover and
metabolism and a serotonin dysregulation.
As not all individuals with the biological substrate for psychopa-
thy become violent, it seems that plasticity in forebrain circuits
may allow the development of more prosocial responses, espe-
cially in youth. Some authors emphasize the need to address other
behaviours that can be responsible for violent actions, namely,
impulsive aggression. Some drugs have shown efficacy in control-
ling impulsive aggression.
Conclusions Pharmacological approaches to treating psychopa-
thy have been disappointing. A more reasonable goal would be to
focus on impulsive aggression, for which treatment effectiveness
has been demonstrated. Additional research is needed if we hope
to design rational therapeutic strategies for this disorder.
Disclosure of interest The authors have not supplied their decla-
ration of competing interest.
EV0850
Investigating misophonia: A review of
the literature, clinical implications
and research agenda reflecting
current neuroscience and emotion
research perspectives
M. Erfanian ∗, J. Jo Brout , M. Edelstein , S. Kumar ,
M. Mannino , L.J. Miller , R. Rouw , M.Z. Rosenthal
1 Maastricht University, Neuroscience and Psychology, Maastricht,
The Netherlands
2 International Misophonia Research Network, Misophonia, New
York, USA
3 University of California, Brain and Cognition, San Diego, USA
4 Newcastle University, Neuroscience, Newcastle, United Kingdom
5 Florida Atlantic University, Complex Systems and Brain Sciences,
Boca Raton, USA
6 STAR Institute for Sensory Processing Disorder, Sensory Processing
Disorder, Greenwood Village, USA
7 Amsterdam University, Brain and Cognition, Amsterdam, The
Netherlands
8 Duke University, Psychiatry and Behavioral Science, Durham, USA
∗ Corresponding author.
Misophonia is a complex neurobehavioral syndrome phenotyp-
ically characterized by heightened autonomic nervous system
arousal and negative emotional reactivity, in response to specific
sounds esearch from basic and applied fields are synthe-
sized with studies explicitly designed to investigate misophonia in
an effort tomore specifically conceptualise this syndrome. The pur-
pose of this study is to review the emerging misophonia research
and to integrate cross-disciplinary research in order to inform
conceptualisation of this recently defined syndrome. Recently
published case studies, descriptive studies, and laboratory-based
psycho-physiological and neurobiological research are reviewed
within a transdiagnostic and multi-disciplinary perspective.
Finally, a brief discussion of updated neuroscience paradigms of
emotion, including defence/fear circuitry related to the amygdala,
is included to help more clearly contextualise findings from previ-
ous research and inform future studies investigating misophonia.
From this perspectivemisophoniamay be considered a central ner-
vous system dysfunction associated with threat cue responding.
Clinical implications should first stress coping skills, as there is no
evidence-based treatment formisophonia. Ideally, clinicians would
work together in cross-disciplinary teams to assist in individual-
izing coping skills plans for patients. However, for each clinician
understanding the neurophysiological, emotional and behaviour
manifestations of misophonia is essential, as a practitioner cannot
simply apply one specific known therapy at this point, or hap-
hazardly integrate what is known without up-to-date in depth
knowledge of the research in so far as it is currently understood,
as well as the impact on individual’s lives and that of their families.
Disclosure of interest The authors have not supplied their decla-
ration of competing interest.
References
[1] Jastreboff and Jastreboff, 2001.
[2] Jastreboff and Jastreboff, 2014.
[3] Møller, 2011.
EV0851
Psychogenic polydipsia: A case report
G. Erzin∗ zdel , H. Karada˘g
Dıskapı Yıldırım Beyazıt Education and Research Hospital,
Psychiatry, Ankara, Turkey
∗ Corresponding author.
Introduction Psychogenic or primary polydipsia characterized
by excessive thirst and compulsive water drinking is a common
problem among psychiatric populations, affecting 6% to 20% of
patients. It is frequent in chronic psychiatric diseases, particularly
schizophrenia. We report a patient with excessive thirst and diag-
nosed as PIP syndrome.
Case A 54-year-old, married, female patient had normal vital
signs. She has excessive water intake (10–12 L/day). She did not
have edema, signs of dehydration or fever. The neurological exam-
ination, CT, MRI, and EEG was normal. The laboratory tests were
normal. She had started using sertraline 100mg, 7months ago due
to anxiety disorder. There is not any disease except the anxiety
disorder, which is in remission due to the treatment. A total of,
2 g desmopressin I.M. is applied in fluid restriction test. The urine
density is determined as 1.008mg/dL initially, 1.011mg/dL one
hour later, and 1.013mg/dL two hours later in the urinary test. The
diagnosis is psychogenic polydipsia (primary) according to patient
history, the clinical examination, and the test results. The patient
is recommended to continue the sertraline 100mg treatment, and
also assigned with fluid restriction behaviour.
Conclusion Since excess water intake periods are correlated with
psychotic exacerbations; psychosis and polydipsiamight have sim-
ilar physiopathologic mechanisms. Polydipsia might be due to
anti-cholinergic side effect of some psychiatric drugs. The phys-
iopathology of the polydipsia and polyuria is not totally enlightened
in the psychiatric disorders. In some cases, the fluid intake occurs
completely voluntary. Therefore, we decided to present this case.