Abstract
In this paper schizophrenia is taken to be a collection of diseases with similar pathological features, including the core Bleulerian symptoms. The aim is to see how far current research can specify the anatomical regions which are functionally defective in schizophrenia and what transmitter systems may be involved. It appears schizophrenic brains show a tendency toward fewer cells in the temporal region, including limbic system as well as the thalamus. Functional deficits are seen in the dorsolateral frontal cortex, as well as thalamus suggesting a cortical-thalamic-striatal pathway. It is clear that Dopamine disregulation in this pathway leads to psychotic symptoms but probably does not account for the ambivalence, affective blunting or asocial behavior. GABA lesions prenatally could lead to glutamate over activity with potential toxic consequences after puberty leading to a plausible hypothesis as to the central neurochemical defect in schizophrenia, this hypothesis is elaborated.
| Translated title of the contribution | The neurobiology of schizophrenia: Where is the lesion, and what is its neurochemical basis? |
|---|---|
| Original language | German |
| Pages (from-to) | 224+226-229 |
| Journal | Schweizer Archiv fur Neurologie und Psychiatrie |
| Volume | 146 |
| Issue number | 5 |
| State | Published - 1995 |
| Externally published | Yes |