[Psychopathology of schizophrenia and brain imaging].
While in the midth the 19th century Griesinger and 80 years later Mayer-Gross regarded schizophrenia as a brain disease, a far-reaching change in the view of schizophrenia found expression in the review of Manfred Bleuler in 1951: All classical assumptions of the schizophrenia doctrine and especially, that schizophrenia could be classified a somatically conditioned illness and not psychogenic, would be, as he wrote, shaken severely. On the 1st International Meeting of Neuropathology in Rome (1952) the opinion became generally accepted that pathological changes of the brain could not be expected in schizophrenias. The neuropathological research into psychoses, considered as unfruitful, has been practically stopped. The World Congress of Zürich "The group of schizophrenias" has summarized through Walter Schulte that schizophrenia must be understood as a "riddle of the human being", unapproachable for the methods of scientific medicine. In contrary to the main trends of psychiatry of that time, we were convinced that schizophrenias have a pathological-somatic basis and considered the search for empirical indications of the somatosis hypothesis an aim of research having priority. Thus, we tried to associate findings gained with the available somatic methods (neurohistopathology, neuroradiology, neurophysiology, neuropsychology, neurochemistry) with clinical syndromes and course of the disorder. These investigations, directed to psychopathological-somatic correlations went already since the monograph of 1957 hand in hand with the gradual development of the basic symptom concept (BSC) and of the Bonn Scale for the Assessment of Basic symptoms (BSABS) and with our long-term course- and early recognition research. I originated with three observations, made at the Heidelberg Clinic of Kurt Schneider, (1.) the cenesthetic schizophrenia; (2.) the asthenic pure defect and (3.) lethal catatonias, patients who were diagnosed clinically as idiopathic schizophrenias, but could be separated from idiopathic schizophrenias as symptomatic by neurohistopathological findings of post mortem examinations and e.g. diagnosed as sporadic, atypical encephalitis. The cenesthetic type had a pilot function for the development of the BSC, because in its course the basic symptomatology determined as well the prodromes before the first psychotic episode, as after that the reversible postpsychotic basic stages respectively the irreversible pure defect syndromes, into which two thirds of cenesthetic schizophrenias terminate; then, because with this type the first time has been observed, that from initially quite uncharacteristic basic symptoms (BS) (level 1 BS), qualitatively peculiar basic symptoms (level 2 BS) and then distinct psychotic symptoms, i.e. bodily hallucinations arise; and because in patients with persisting pure deficiency syndromes neuromorphological changes in the sense of a basal ganglia syndrome could be proved. The clinical neuroradiological correlation study in 195 schizophrenic patients with slight residues or full remissions and 212 chronic schizophrenias as well as in 535 patients with organic psychosyndromes of different diagnostic groups reveal that brain imaging and biological-psychiatric research are only promising in close connection with clinical psychopathology and observation of the course, if they aim to assign certain structural or functional cerebral disturbances with certain clinical symptoms and syndromes. In this respect schizophrenic, schizoaffective and affective idiopathic psychosyndromes do not differ from somatically based psychoses in definable brain diseases. With functional-dynamic parameters the differentiation in process active and inactive stages has to be made guided by the actual clinical psychopathological syndrome at the moment of the collecting of the electroencephalographic, neurochemical, fMRI or PET findings. The reasons of inconsistencies of the EEG, PEG, CT, MRI, PET findings are analysed and it is shown that they are frequently conditioned by insufficient definition of the random sample and, with functional-dynamic parameters by the missing consideration of the process activity. The Bonn Schizophrenia Long-term Study and the Bonn-Cologne early recognition study established that the dichotomic models of course of schizophrenia cannot be maintained: Negative respectively minus symptoms in the sense of basic symptoms precede the positive ones many years, negative schizophrenias pass over into positive ones and vice versa. In the search for morphological brain findings an irreversible psychopathological alteration with the component of a pure dynamic-cognitive deficiency syndrome is relevant as clinical criterion, while other persisting psychosyndromes as structural deformities and "pure psychosis" usually show no morphological brain changes. "Schizophrenia" is not always associated with neuromorphological changes. There exists a group of neuroradiologically negative schizophrenias with small dysplastic ventricles and other constitutional anomalies that is characterized by a premorbid psychopathic personality and a typically schizophrenic personality deformation. Brain alterations, regarding the 3rd and the lateral ventricles in the neighbourhood of the basal ganglia, can be found in the subgroup with irreversible dynamic-cognitive pure defect, but not in courses with full psychopathological remission. According to Dewan for the first time a correlation between psychopathological and brain morphological findings in schizophrenics with the component of pure residual syndrome has been found by our studies, as well as a parallel progression of the cerebral atrophy and the psychopathological changes. Quantitative-morphometric and MRI changes of regions of the limbic system and neurophysiological findings are hints that disorders in limbic key structures are able to explain the basic symptoms and the first rank symptoms, developing out of distinct transition relevant basic symptoms. Finally, the process activity concept and its criteria and its meaning for the studies with functional brain imaging methods are described.
Gross
G
G
Universitäts-Nervenklinik, Bonn, Germany.
Huber
G
G
D001921:Brain / Q000473:pathology*; D003952:Diagnostic Imaging; D006801:Humans; D008279:Magnetic Resonance Imaging; D012559:Schizophrenia / Q000473:pathology*; D012565:Schizophrenic Psychology