[Schizophrenia: neurodevelopmental disorder or degenerative brain process?].
In the last two decades schizophrenia is viewed increasingly as a neurodevelopmental (ND) disorder; as indicators are discussed f.e. premorbid personality, behaviour anomalies, premorbid somatic signs, deviations shown by brain imaging methods, neuropathological findings or neuropsychological deficits. Premorbid personality and behaviour anomalies have to be distinguished from precursor syndromes (prodromes and outpost syndromes), preceding the first psychotic episode many years. Moreover, only a minority of patients, later developing schizophrenia, reveal abnormal premorbid personality traits. Explanations why clinical expression of the disorder is delayed until adult life or at least adolescence, remain speculative. Findings of neocortical and limbic maldevelopment, e.g. in parahippocampal cortex, are hitherto not yet conclusive. As an argument for the ND hypothesis is claimed that ventricular enlargement already is present at the onset of positive symptoms and does not progress on follow-ups. But, if a ND disorder would have caused the ventricular enlargement, cranial volume and head size must be decreased, what is not the case in schizophrenia. Furtheron, there are findings of progressive increase in ventricular size and also of gliosis, especially in subcortical and periventricular areas. Anomalies of cerebral asymmetry; also distinct ND brain anomalies such as cavum septi pellucidi or dysgenesis of corpus callosum do not occur more frequently than expected in schizophrenia. As to the rate of obstetric complications (OCs) and viral infections sufficiently reliable data are missing; the great majority of schizophrenics have no OCs. Altogether, attempts to correlate brain findings, regarded as expression of an aberrant brain development with clinical subgroups of schizophrenia, were not very successful. This is also valid for ND concepts confined to male, early onset or sporadic schizophrenias. Only a distinct psychopathological remission type with the component of an irreversible pure dynamic-cognitive deficiency can be correlated with distinct brain imaging changes. There are associations between brain imaging and psychopathological findings and also between the progression of neuroradiological and psychopathological changes. The investigation of the long-term course of schizophrenia with progression to different residual syndromes has shown some hints that schizophrenia certainly is not a neurodegenerative process in the usual sense, but may be a special neuroregressive illness in the majority of cases. Data, relevant for this assumption are, that the disorder in 78% shows no full remitting courses; that the progression concerns only 5 until 10 years after onset; that chronic defect psychoses can remit still after decades of course to non-psychotic pure deficiency syndromes; that some cases (15%) can progress even after years and decades of remitting course and, finally, that altogether no correlation exists between the duration of course and outcome. The data prove that schizophrenia is not an illness progressing continuously over the whole lifelong course in the sense of a primary neurodegenerative process, but rather a disorder, progressing transiently in brief stages and afterwards coming to a standstill. That schizophrenia is not neurodegenerative in the traditional sense, does not mean that it is a ND disorder. This applies only to a small subgroup, while the assumption of a non-ND subgroup with an only transitory, in short periods advancing special regressive brain process seems to be plausible. There are analogies to organic brain disorders . Hence ensues the interpretation of the brain findings in a subgroup of schizophrenia as "premature, locally accentuated involution of advanced age". The argument that at time of the first psychotic episode the brain changes already have developed without progressing in the further course, can be refuted by neuropsychiatric observations in brain atrophic processes and the knowledge of the true onset of schizophrenia with prodromes and outpost syndromes several years before the first psychotic manifestation with positive symptoms.
Gross
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Universitäts-Nervenklinik, Bonn, Germany. gisela.gross@ukb.uni-bonn.de
Huber
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D001921:Brain / Q000254:growth & development* / Q000473:pathology*; D002648:Child; D002658:Developmental Disabilities / Q000473:pathology*; D006801:Humans; D019636:Neurodegenerative Diseases / Q000473:pathology*; D012559:Schizophrenia / Q000473:pathology*