Zur Neuropathologie der Schizophrenien

Abstract

Up to now it is not known whether the ventricular enlargement in schizophrenics demonstrated by neuroradiological investigations is caused by a general brain atrophy or a more or less selective degeneration of one or several areas. Therefore, the volumes of several parts of the basal ganglia, of the diencephalon and of the limbic system were determined by planimetry of myelin-stained serial sections in post mortem brains of 14 schizophrenic patients and 13 control cases. The important limbic structures of the temporal lobe (amygdala, hippocampal formation), the ventricle closely surrounding structures of the diencephalon, and the pallidum internum are significantly smaller in the schizophrenic group, whereas the volumes of the pallidum externum, of the three parts of the striatum (caudatum, putamen, n. accumbens), of the red nucleus, and of the large thalamic cell groups have not significantly changes. The volume reductions are interpreted as focal degenerative shrinkages of unknown etiology.

Stereological study of the neuronal number and volume of 38 brain subdivisions of subjects diagnosed with autism reveals significant alterations restricted to the striatum, amygdala and cerebellum

“…The volume of the putamen was 2,365 mm 3 in our material, 2,713 mm 3 in Kreczmanski et al study [66], and 2,979 mm 3 in Bogerts study [67] (with Kreczmanski's correction for shrinkage). The volume of the nucleus accumbens was estimated as 182 mm 3 in this study, 204 mm 3 in Kreczmanski et al[66], 147 mm 3 in Lauer et al [68] (with Kreczmanski’s shrinkage factor), and 138 mm 3 in Pakkenberg study based on examination of 4-μm thick paraffin sections [69].…”

“…In our control cohort the volume of the caudate nucleus was estimated as 1,727 mm 3 , versus 2,212 mm 3 in Kreczmanski et al [66] study, and 2,043 mm 3 in Bogerts study [67] (with Kreczmanski’s et al correction for shrinkage). The volume of the putamen was 2,365 mm 3 in our material, 2,713 mm 3 in Kreczmanski et al study [66], and 2,979 mm 3 in Bogerts study [67] (with Kreczmanski's correction for shrinkage).…”

Abnormal structure or function of the amygdala is a common component of neurodevelopmental disorders

“…Postmortem studies on the amygdala in schizophrenia are scarce (Bogerts, 1984; Chance, Esiri, & Crow, 2002; Heckers, Heinsen, Heinsen, & Beckmann, 1990; Kreczmanski, et al, 2007) and generally involve a wide age range of cases with mostly adult-onset. In early postmortem studies, reductions in GABAergic levels and increases in dopamine in the amygdala were linked to psychosis (see Benes, 2010 for review).…”

Neuropsychiatric thalamocortical dysrhythmia: surgical implications

“…Indeed, electroencephalographic (EEG) (Spiegel and Wycis, 1950;Heath, 1954;Prichep and John, 1992;Pascual-Marqui et al, 1999;Sponheim et al, 2000), positron emission tomographic (PET) (Buchsbaum et al, 2002;Hazlett et al, 1999), histological (Bogerts, 1984;Shenton et al, 2001) and radiological (Shenton et al, 2001) studies indicate spiking activities, increased low frequencies, hypometabolism as well as histopathological and magnetic resonance imaging (MRI) changes in these domains. Indeed, electroencephalographic (EEG) (Spiegel and Wycis, 1950;Heath, 1954;Prichep and John, 1992;Pascual-Marqui et al, 1999;Sponheim et al, 2000), positron emission tomographic (PET) (Buchsbaum et al, 2002;Hazlett et al, 1999), histological (Bogerts, 1984;Shenton et al, 2001) and radiological (Shenton et al, 2001) studies indicate spiking activities, increased low frequencies, hypometabolism as well as histopathological and magnetic resonance imaging (MRI) changes in these domains.…”