Læknablaðið : fylgirit - 01.08.2003, Blaðsíða 15

ABSTRACTS / 27TH NORDIC PSYCHIATRIC CONGRESS I
Aims: To examine whether the prevalence of depression in a repre-
sentative sample of 494 85-year olds from Gothenburg Sweden
increased the incidence of first-ever stroke between age 85 and 88.
Methods: Depression was defined according to the DSM-III-R,
based on information from a psychiatric examination at age 85.
Information of first ever stroke between age 85 and 88 was obtained
from hospital linkage system, death certificates, self-reports and
key-informants. 85-year-olds with stroke at baseline were excluded.
Results: The prevalence of depression at age 85 was 13.0%. The
relative risk for stroke incidence in those with depression compared to
those without was 2.0 (95%-CI 1.0-3.8). This was only true in women
(RR 2.2,95%-CI 1.04.4), but not in men (RR 1.0,95%-CI 0.0-7.2).
Conclusions: Depression is a risk factor for stroke in very old
women, suggesting that treatment of depression may be a factor in
stroke prevention.
F-2/1 Thursday 14/8,15:00-16:00
Non-pharmacological manipulations of central
serotonergic neuro-transmission in humans
Broocks A. Prof. Dr. Med., Arzt fiir Neurologie, Psychiatrie und Psychotherapie
Leitender Oberarzt, Klinik fiir Psychiatrie und Psychotherapie der Medizinischen,
Universitat zu Liibeck, Ratzeburger Allee 160,23538 Liibeck. Schweiger U, Kordon A,
Sommer M. Ehrenthal D, Hohagen F.
broocks.a@psychiatry.mu-luebeck.de
Serotonergic neurotransmission is involved in a number of neuro-
psychiatric disorders. Pharmacological treatments with antidepres-
sants and other agents are known to modulate central serotonergic
functions. However, there is evidence that certain behavioral fac-
tors such as eating behavior, motor activity, exposition to light,
sleep withdrawal and smoking also affect serotonergic neurotrans-
mission. For instance, regular endurance training, which has been
used in the treatment of anxiety disorders and depression, is
associated with decreased responses to the non-selective 5-HT2C
agonist, m-CPP. Neuroendocrine responses to the selective 5-
HTIA agonist, ipsapirone, are markedly affected by smoking.
Current research tries to elucidate whether psychotherapeutic
mterventions also modulate central serotonergic function.
In conclusion, non-pharmacological interventions of serotoner-
gic neurotransmission might be increasingly important in the treat-
ment of neuropsychiatric disorders.
F “ 2 / 2 Thursday 14/8, 15:00-16:00
Efficacy of thyroid hormone (T3) addition to paroxetine in
major depression
Bcnfu C Appclhof, MD' , Room F5-173, Meibergdreef 9, 1105 AZ Amsterdam, The
Netherlands. Jantien P Brouwer, MD1, Richard van Dyck, MD, PhD2, Eric Fliers, MD,
PhD', Witte JG Hoogendijk, MD, PhD2, Jochanan Huyser, MD, PhD2, Aart H Schene,
MD. PhD3, Jan PG Tíjssen, MD, PhDL Wilmar M Wiersinga, MD, PhD>
Department of Endocrinology and Metabolism, Academic Medical Center, University
rn mStert*am' ^Department of Psychiatry, VU University Medical Center, Amsterdam.
^Department of Psychiatry, Academic Medical Center, University of Amsterdam.
Department of Cardiology, Academic Medieal Center, University of Amsterdam.
b.c.appehof@amc.uva.nl
Background and Aim: Guidelines for the treatment of major de-
pressive disorder propose the addition of triiodothyronine (T3) to
antidepressants as an augmentation strategy. However, evidence
derives from relatively small studies and the efficacy of T3 has nol
been investigated in combination with selective serotonine reup-
take inhibitors. We investigated the efficacy of T3-addition to par-
oxetine in major depression.
Methods: 113 patients with major depressive disorder and a
baseline 17-item Hamilton Rating Scale for Depression (HRSD)
score >16 were randomly assigned to 8 weeks of double-blind
outpatient treatment with low dose T3 (25 ug), high dose T3 (25 ug
twice daily) or placebo in addition to paroxetine 30 mg daily.
Results: 106 patients started treatment and were included in the
outcome analysis. Response rate after eight weeks, defined as a re-
duction of HRSD score > 50%, was 46% in all three treatment arms
(p=0.99). Remission rate, defined as a HRSD score £8 at endpoint,
was 32% in both T3 groups and 36% in the placebo group (p=0.92).
Patients on T3-addition reported significantly more side effects
than patients on placebo-comedication.
Conclusion: These results do not support a role for T3-addition to
SSRI in the treatment of major depressive disorder.
F-2/3 Thursday 14/8,15:00-16:00
The cardiac effects of antipsychotics
Koponen H1, Professor, Department of Psychiatry, University of Oulu, P.O. Box 5000,
FIN-90014 Oulun Yliopisto, Finland. Saari Kl, Pelkonen 02, Raatikainen MJP3,
Savolainen MJ-\ Isohanni M1.
hannu. koponen@reimari. neí
JDepartment of Psychiatry, ^Department of Pharmacology and Toxicology, and
Department of Internal Medicine, 3University of Oulu, Oulu, Finland.
Antipsychotic medications are a mainstay in the treatment of psy-
chotic disorders. It has, however, been observed that some anti-
psychotics may also have negative cardiovascular effects. Patients
with treated schizophrenia have had higher rates of cardiac arrest
and ventricular arrhythmia than controls, the ratios ranging from
1.7 to 3.2. The risk of sudden death is estimated to be about 2.4-fold
in patients taking antipsychotics compared to persons who do not
use antipsychotic drugs.
The causes of sudden death associated with antipsychotics use
are poorly understood. In addition to smoking, the metabolic dis-
turbances predispose to cardiovascular diseases, which together
with poor treatment compliance and a possibly delayed diagnosis of
somatic illnesses increase the risk of cardiovascular morbidity and
sudden death. At least in part of the cases, the cause of sudden
death is torsades de pointes caused by the proarrhythmic effect of
the antipsychotic drug, sometimes probably associated with meta-
bolic interactions and pharmacogenetic deficiencies. In addition,
the effect of antipsychotics on the autonomous nervous system as
well as on lipid and glucose metabolism may also contribute. In ad-
dition, some antipsychotic drugs also have direct effects on the ion
channels in the heart.
Although dangerous arrhythmia is only rarely caused by anti-
psychotics, their safe use calls for care in patient selection, drug
dosage, awareness of interactions and patient monitoring discussed
in the presentation. The significance of less dangerous but unplea-
L/EKNABLAÐIÐ / FYLGIRIT 48 2003/89 15