[Evidences for the somatosis hypothesis of schizophrenia (author's transl)].
The hypothesis of a hereditary mutative enzyme disturbance which becomes effective via biochemical, for peristatic influences susceptible cerebral mechanisms, is compatible with all findings. The evidences are stated. Schizophrenia is a predominantly hereditary disease. The findings of the family and twin research confirm this statement, in particular the difference of the concordance figures with monovular and binovular twins, furthermore the existence of substrate-close basic disturbances with their analogies to cerebro-organic symptomatology, the frequency and structure of pure residual syndromes and the results of clinical-encephalographic correlation examinations. Slightly marked internal brain atrophies which can be demonstrated by pneumo- and echoencephalogram can be correlated with the "pure defect" which is the most frequent residual syndrome of schizophrenic diseases. A geneticly conditioned cerebral enzyme defect can cause an atrophy in the region of the limbic system; however, a merely functional decompensation of a cerebral enzyme disturbance, without atrophy is imaginable in a part of the schizophrenia and cyclothymia. In certain active basic stages the EEG reveals abnormal rhythms ("parenrhythmiae"), which also allow a topical classification to functional structures of the limbic system. The non-characteristic organic "pure potential reduction" is irreversible, the typically schizophrenic syndromes potentially reversible. Basic disturbances and basic syndromes are in prodromes and outpost syndromes prior to manifestation of psychosis and after their remission the actually primary symptoms. The typically schizophrenic syndrome results from the amalgamation of the basal functional disturbance with the "anthropological matrix", partly provoked by - also non-specific - stress factors. The substrate-close basic symptoms: coenesthesias, perception disorders, zentral-vegetative dysregulations and cognitive primary disturbances can be seen as expression of a pathologically altered cerebral function in the region of the integrative system which is responsible for the regulation of the cerebral filter and protection processes.
D001284:Atrophy; D001714:Bipolar Disorder / Q000209:etiology; D001921:Brain / Q000201:enzymology; D001927:Brain Diseases / Q000150:complications; D004200:Diseases in Twins; D004569:Electroencephalography; D006801:Humans; D008032:Limbic System; D012075:Remission, Spontaneous; D012559:Schizophrenia / Q000201:enzymology / Q000209:etiology* / Q000235:genetics; D013312:Stress, Physiological
Indizien für die Somatosehypothese bei den Schizophrenien