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Psychische Erkrankungen in der Lebensspanne ... - DGPPN

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Topic 4 G Affektive Störungen, F3 // Affective disor<strong>der</strong>s, F3<br />

lationsprotokollen abhängen und psychopharmakologisch moduliert<br />

werden können. Für den PFC fanden sich <strong>in</strong> EEG-Untersuchungen<br />

(Grosshe<strong>in</strong>rich et al. Biological Psychiatry 2009; Keeser et<br />

al. submitted 2009) nach Theta Burst rTMS und nach tDCS über bis<br />

zu e<strong>in</strong>er Stunde anhaltende Post-Stimulationseffekte. Nach präfrontaler<br />

tDCS zeigten Gesunde und depressive Patienten z.T. divergente<br />

Verän<strong>der</strong>ungen sowohl h<strong>in</strong>sichtlich des EEG-Spektrums als<br />

auch ihrer Lokalisation (sLORETA). Zu länger anhaltenden neuroplastischen<br />

Prozessen nach rTMS und tDCS liegen nur vere<strong>in</strong>zelt<br />

Studien vor, systematische Untersu-chungen zur Entwicklung dieser<br />

Verän<strong>der</strong>ungen über die Zeit fehlen bislang. Die Entstehung<br />

und Dynamik neuroplastischer Prozesse nach rTMS und tDCS ist<br />

bislang nur <strong>in</strong> Ansätzen verstanden, besitzt aber vermutlich e<strong>in</strong>e<br />

große Bedeutung für die therapeutische Anwendung bei<strong>der</strong> Verfahren<br />

bei Depressionen. Insbeson<strong>der</strong>e die Interaktion zwischen<br />

rTMS- und tDCS-<strong>in</strong>duzierter Neuroplastizität und spezifischen<br />

Verän<strong>der</strong>ungen von Hirnstruktur und Neuroplastizit bei Depressionen<br />

sollte Gegenstand weiterer Forschung se<strong>in</strong>.<br />

Mittwoch, 25. 11. 2009, 15.30 - 17.00 Uhr, Salon 11/12<br />

S-031 Symposium<br />

Remitted depression: neurobiological and neuropsychological<br />

factors<br />

Vorsitz: D. E. Dietrich (Hannover), M. Rothermundt (Münster)<br />

001<br />

HPA system activity and remission of depression<br />

Michael Deuschle (ZI für Seelische Gesundheit, Mannheim)<br />

Introduction: Depend<strong>in</strong>g on the antidepressant and remission,<br />

HPA system activity usually decl<strong>in</strong>es dur<strong>in</strong>g the course of antidepressant<br />

treatment. HPA system activiy as assessed by the comb<strong>in</strong>ed<br />

Dex /CRH test has been shown to be related to the risk for relapse.<br />

However, HPA system activity has rarely been measured <strong>in</strong> the<br />

long-term course of treatment.<br />

Method: We measured nighttime ur<strong>in</strong>e excretion of cortisol for<br />

6 months <strong>in</strong> a group of depressed patients after discharge from <strong>in</strong>patient<br />

treatment. Moreover, we assessed stress response <strong>in</strong> patients<br />

<strong>in</strong> long-term remission.<br />

Discussion / Results: In the aftermath of <strong>in</strong>patient treatment, we<br />

found cortisol excretion still to decl<strong>in</strong>e, both <strong>in</strong> patients with favorable<br />

and unfavorable course. Also, patients <strong>in</strong> long-term remission<br />

had low basel<strong>in</strong>e HPA system activity, when compared to healthy<br />

controls. It may be concluded that HPA system activity ameloriates<br />

<strong>in</strong> the aftermath of an acute episode.<br />

002<br />

Serum markers as <strong>in</strong>dicators of remission<br />

Matthias Rothermundt (Universitätskl<strong>in</strong>ikum Münster, Psychiatrie<br />

und Psychotherapie)<br />

Introduction: Depression is associated with a volume reduction <strong>in</strong><br />

various bra<strong>in</strong> regions positively correlated with <strong>in</strong>creas<strong>in</strong>g duration<br />

of depression. This volume loss is caused by a decrease of glia cell<br />

amount and reduction of neuronal cell size, but not by a decl<strong>in</strong>e of<br />

neuronal cell numbers. Glial and neuronal markers might be useful<br />

to <strong>in</strong>dicate cellular changes <strong>in</strong> a cl<strong>in</strong>ical sett<strong>in</strong>g.<br />

Method: BDNF as neuronal and S100B as glial cell marker are evaluated<br />

regard<strong>in</strong>g their potential contribution to evaluate the stage of<br />

disease <strong>in</strong> major depression.<br />

Discussion / Results: BDNF is decreased <strong>in</strong> unmedicated pa tients<br />

with major depression and normalizes after successful antidepressi-<br />

ve treatment. S100B concentration is elevated <strong>in</strong> acute major depression<br />

especially <strong>in</strong> patients with the melancholic subtype of depression.<br />

The S100B concentration at onset predicts the therapeutic<br />

outcome. Discussion: Serum markers <strong>in</strong>dicat<strong>in</strong>g neuronal and glial<br />

function can contribute to the assessment of the stage of major depression.<br />

They might even be helpful as prognostic markers. However,<br />

more studies are needed to f<strong>in</strong>ally evaluate the chances and<br />

limitations of these markers.<br />

003<br />

Neurophysiological changes of cognitive function and S100B <strong>in</strong><br />

remitted depression<br />

Detlef E. Dietrich (Mediz<strong>in</strong>. Hochschule Hannover, Kl<strong>in</strong>ik für Psychiatrie)<br />

Y. Zhang, M. Rothermundt<br />

Introduction: Memory and attentional processes have been shown<br />

to be impaired <strong>in</strong> depressed patients and may partly even persist <strong>in</strong><br />

the remitted state. Part of this variability might be expla<strong>in</strong>ed by biological<br />

factors: S100B is an astroglial calcium-b<strong>in</strong>d<strong>in</strong>g prote<strong>in</strong> with<br />

neuroplastic properties and has been shown to be <strong>in</strong>creased <strong>in</strong> a<br />

subgroup of depressive patients. Its pathophysiologic role <strong>in</strong> depression,<br />

however, is not yet sufficiently un<strong>der</strong>stood. Electrophysiological<br />

techniques, e.g. event-related potentials (ERPs), may be<br />

used to substantiate a possible <strong>in</strong>fluence of S100B on cognitive processes.<br />

Method: In the presented <strong>in</strong>vestigations, ERPs recorded <strong>in</strong> a visual<br />

cont<strong>in</strong>uous word recognition paradigm and a target evaluation /<br />

response <strong>in</strong>hibition experiment were therefore <strong>in</strong>vestigated <strong>in</strong> patients<br />

with remitted major depression <strong>in</strong> relation to serum levels of<br />

S100B.<br />

Discussion / Results: Patients with <strong>in</strong>creased S100B serum levels<br />

showed a normal old / new effect <strong>in</strong> the recognition memory paradigm<br />

and a normal N2- and P3-amplitude <strong>in</strong> the target evaluation<br />

experiment <strong>in</strong> contrast to a reduced old / new effect and a re duced<br />

N2- and P3-amplitude <strong>in</strong> the patients with lower S100B levels compared<br />

to aged matched control groups. The f<strong>in</strong>d<strong>in</strong>gs provide evidence<br />

of a correlation between S100B levels and cognitive process<strong>in</strong>g<br />

<strong>in</strong> patients with recurrent depression and further substantiate<br />

S100B’s role as a marker <strong>in</strong> the course of affective disor<strong>der</strong>s.<br />

004<br />

The impact of fate and the neuropsychology of depression<br />

H<strong>in</strong><strong>der</strong>k M. Emrich (Mediz<strong>in</strong>. Hochschule Hannover, Psychiatrie und<br />

Psychotherapie)<br />

Mittwoch, 25. 11. 2009, 15.30 – 17.00 Uhr, Salon 13/14<br />

S-032 Symposium<br />

Treatment-resistant depression: Neural modes of action of<br />

up- to-date treatment strategies from psychotherapy to neuromodu<br />

l ati on<br />

Vorsitz: K. Schnell (Bonn), T. Schläpfer (Bonn)<br />

001<br />

Neuronale Plastizität im Verlauf kognitiv-behavioraler Psychotherapieverfahren<br />

bei chronischer Depression<br />

Henrik Walter (Zentrum für Nervenheilkunde, Kl<strong>in</strong>ik für Psychiatrie<br />

Mediz<strong>in</strong>ische Psychologie, Bonn)<br />

121

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