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DOI: 10.1055/s-2002-30642
Neurovulnerabilität der Hippokampusformation bei der posttraumatischen Belastungsstörung
Forschungsstand und ForschungshypothesenPublication History
Publication Date:
16 June 2002 (online)
Zusammenfassung
In der Kernspinresonanztomographie zeigen Patienten, die unter einer Posttraumatischen Belastungsstörung (PTBS) leiden, eine Atrophie der Hippokampusformation. Unter Berücksichtigung des Verlaufsmodells psychischer Traumatisierung wird diskutiert, ob dieses Phänomen als Ursache, Folge oder sekundäre Begleiterscheinung der PTBS zu bewerten ist. Darüber hinaus wird die Frage aufgegriffen, ob eine Atrophie auf bestimmte Regionen bzw. Zellpopulationen begrenzt ist und welcher pathophysiologische Mechanismus zugrunde liegt. Hierzu verweisen die Autoren auf Stressmodelle, welche eine reversible Atrophie der Dendriten von CA3-Pyramidenzellen zeigen und nehmen an, dass die Aktivierung einer Glukokortikoid- und Glutamat-Hypersensibilitätskaskade für die Atrophie verantwortlich ist. Schließlich wird diskutiert, wie diese Befunde mit der paradoxen Regulation der Stressachse bei PTBS-Patienten zu vereinbaren sind. Die Autoren schlussfolgern, dass ein interdisziplinäres Forschungsdesign erforderlich ist, um die Verlaufsgestalt der PTBS unter Berücksichtigung psychodynamischer und molekularbiologischer Aspekte zu erfassen.
Neurovulnerability of the Hippocampus Formation in Posttraumatic Stress Disorder -Update State of Research and of Research Hypotheses
Magnetic resonance imaging shows reduced hippocampal volume in patients with posttraumatic stress disorder (PTSD). With reference to a model for the course of psychotraumatic development, the authors discuss whether this phenomenon should be considered the cause of PTSD, the effect, or an epiphenomenonally concurrent symptom such as substance abuse. In addition, the question is addressed as to whether atrophy is limited to certain regions or cell populations and which pathophysical mechanisms can feasibly be in effect.There are relevant animal models which indicate a reversible atrophy of apical dendrites in pyramidal neurons in the CA3 region, suggesting that the reversible atrophy may coincide with activation of a hypersensitivity cascade of glucocorticoids and excitatory amino acids receptors. Finally, the authors link the endocrinological alterations of the hypothalamic-pituitary-adrenal axis in PTSD to these neuroanatomical findings. They conclude that in order to understand the time course of traumatic stress, interdisciplinary research which includes psychodynamic and neurobiological aspects of PTSD will be necessary.
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Korrespondenz:
Dr. med. Dipl.-Psych. Robert Bering
Oberarzt am Zentrum für Psychotraumatologie
Alexianer-Krankenhaus Krefeld
Email: robert.bering@uni-koeln.de