Klinische Neurophysiologie 2012; 43 - P115
DOI: 10.1055/s-0032-1301665

Treatment of the schizoaffective psychosis according to a neuronal network

FM Werner 1, R Covenas 2
  • 1Euro-Schulen Pößneck, HBFS für Altenpflege, Pößneck
  • 2Instituto de Neurociencias de CAstilla y León, Salamanca, ES

Introduction: In schizoaffective psychosis exists a GABA and glutamate deficiency leading to dopamine and serotonin hyperactivity in the mesolimbic system. In mania there is noradrenaline and dopamine hyperactivity in the hippocampus and in depression monamine deficiency in the hippocampus and the midbrain.

Material/Methods: In the mesolimbic system dopaminergic neurons transmit a strong activating impulse via D2 receptors to glutaminergic neurons which weakly inhibit the serotonergic neurons via NMDA receptors. The latter neurons transmit a strong activating impulse via 5-HT2A receptors to GABAergic neurons which weakly inhibit dopaminergic neurons via GABAA receptors. In mania, GABAergic neurons weakly inhibit dopaminergic neurons with a high activity in the hippocampus via D2 receptors. Glutaminergic neurons weakly inhibit the serotonergic neurons with a high activity via 5-HT2C receptors. In depression, the dopaminergic and serotonergic neurons have a low activity through an enhanced GABAergic and glutaminergic presynaptic inhibition. In the mood center in the midbrain, in depression an increased GABAergic inhibition via GABAB receptors leads to noradrenaline hypoactivity and an enhanced glutaminergic inhibition via the subtype 5 of the metabotropic glutaminergic receptors to serotonin hypoactivity.

Results: Prognosis in schizoaffective psychosis is better than in schizophrenia, because the neuronal networks in the affective brain centres tend to revert to a neurotransmitter balance and stabilize the degeneration of neurons in the mesolimbic system. The following drugs can be administered: atypical neuroleptics with a D2 and 5-HT2A antagonistic effect combined with: lithium or; valproate; lamotrigine, which decreases dopamine hyperactivity through blockade of ionotropic glutamate receptors; topiramate, which inhibits dopaminergic neurons as well. Conclusion: Knowledge of the underlying neuronal networks enables to improve the pharmacotherapy of the disease.

Literatur: 1.) Liu-Seifert, H.; Ascher-Svanum, H.; Osuntokum, O.; Jen, K.Y. & Gomez, J.C. Change in level of productivity in the treatment of schizophrenia with olanzapine and other antipsychotics. BMC Psychiatry, 11, 87, 2011. 2.) Werner, F.M. & Covenas, R. Classical Neurotransmitters and Neuropeptides involved in Major Depression: a Review. Int J Neuroscience, 120, 455 – 470, 2010. 3.) Werner, F.M. & Covenas, R. Neuropeptides involved in schizophrenia. Curr Top Neurochemistry, 4, 35 – 49, 2005. 4.) Werner, F.M. Schizophrenia: from the genetic localization to the cellular mechanism. Clin Neurophysiology, Vol. 118, Iss. 4, e112 – e113, Apr. 2007.