Zusammenfassung
Der Thalamus wurde schon zu Beginn des 20. Jahrhunderts als eine Hirnregion angesehen, die in die Pathogenese der Schizophrenie involviert sein könnte. Verschiedene Thalamuskerne wurden mit qualitativen Methoden morphologisch untersucht; dabei fokussierte man sich zunächst auf den N. mediodorsalis. Die publizierten Ergebnisse waren jedoch widersprüchlich. Nach der Einführung von quantitativen neuroanatomischen Methoden zeigte sich, dass nicht nur thalamische Assoziationskerne (N. mediodorsalis, Pulvinar), sondern auch limbische (N. anteroventralis) und motorische Thalamuskerne (N. ventrolateralis posterior) Zellzahl- und Volumenreduktionen aufweisen. Die Beteiligung mehrerer Thalamuskerne wurde durch strukturelle MRT-Arbeiten unterstützt, die moderate, aber signifikante Volumenreduktionen des gesamten Thalamus bei dieser Erkrankung nachgewiesen haben. Die Ähnlichkeit zwischen den strukturellen Veränderungen in tierexperimentellen Modellen thalamischer Plastizität und den strukturellen thalamischen Alterationen bei Schizophrenie spricht dafür, dass neuroplastische Mechanismen bei diesen Veränderungen beteiligt sein könnten. Die überwiegende Mehrzahl der fMRT- und PET-Studien ergab eine Reduktion der metabolischen Aktivität oder der Perfusion im Thalamus bei Patienten mit Schizophrenie. Post-mortem-Studien und In-vivo-Rezeptor-Studien haben auch Hinweise auf dopaminerge, glutamaterge und Membran-assoziierte Mechanismen innerhalb der thalamischen Pathologie bei Schizophrenie geliefert. Auf der psychopathologischen Ebene zeigen sich Ähnlichkeiten zwischen einem Teil der psychischen Manifestationen nach thalamischen Läsionen und den Symptomen schizophrener Erkrankungen. Die Volumenreduktion des gesamtem Thalamus konnte auch bei neuroleptikafreien Patienten mit einer Erstmanifestation der Erkrankung festgestellt werden. Eine ätiologisch bedeutende Rolle der neuroleptischen Medikation erscheint daher unwahrscheinlich, da bisher keine signifikanten Korrelationen zwischen den thalamischen Volumina oder Zellzahlen und der neuroleptischen Behandlungsdauer gezeigt werden konnte. Die obengenannten Befunde sprechen dafür, dass verschiedene Thalamuskerne und damit unterschiedliche neuronale Schaltkreise in die Pathogenese der Schizophrenie involviert sind.
Abstract
Since the beginning of the 20th century, the thalamus was regarded as a brain region which may be involved in the pathogenesis of schizophrenia. Distinct thalamic nuclei were morphologically analyzed with qualitative methods with an emphasis on the mediodorsal nucleus. However, the reported results were inconsistent. After the introduction of quantitative neuroanatomical methods, it became obvious that the volume and cell reductions are not only present in the association nuclei, but also in the limbic (N. anteroventralis) and motor thalamic nuclei (N. ventrolateralis posterior). The involvement of distinct thalamic nuclei is supported by structural MRI studies which have shown a moderate but significant volume reduction of the whole thalamus in this disease. The majority of fMRI and PET studies reported a reduction of the metabolic activity or blood flow in the thalamus in patients with schizophrenia. The similarity between the structural changes in animal models of thalamic plasticity and the structural thalamic alterations in schizophrenia suggest an involvement of neuroplasticity mechanisms in the pathogenesis of these alterations. Post-mortem studies and In-vivo receptor studies suggest alterated glutamatergic, dopaminergic and membran-associated mechanisms within thalamic pathology in schizophrenia. On the psychopathological level, there is a similarity between some of the psychic manifestations of thalamic lesions and symptoms of the schizophrenic disease.There are also reports on volume reduction of the whole thalamus in first-episode neuroleptic-free patients. It appears unlikely that the neuroleptic medication plays an etiological important role, since no significant correlations were found between the volume and cell reductions and the neuroleptic treatment period. The reviewed data suggest that distinct thalamic nuclei and therefore distinct neuronal circuits are involved in the pathogenesis of schizophrenia.
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Priv.-Doz. Dr. med. Peter Danos
Zentrum für Psychiatrie des Universitätsklinikum Gießen
Am Steg 22
35392 Gießen
Email: peter.danos@psychiat.med.uni-giessen.de
