Biomedical subjects
Publications and source records attributed to B Bogerts.
Ten male schizophrenic patients underwent Gadolinium-DTPA (Gd-DTPA) enhanced magnetic resonance (MR) imaging to determine the utility of paramagnetic contrast agents in evaluating neuropathology. MR images enhanced by Gd-DTPA demonstrated no defect in the integrity of the blood-brain barrier.
This study examined neuroanatomical differences between male schizophrenic patients with a family history of psychosis (n = 16) and those without such a history (n = 15). Intracranial area, cerebral area, ventricular size, and cortical atrophy were assessed using magnetic resonance imaging (MRI). Third ventricular enlargement was more prevalent in patients than controls (n = 15). Familial and nonfamilial patients differed significantly. Reduced cranial and cerebral areas without ventricular enlargement characterized familial patients, whereas nonfamilial patients showed marked lateral ventricular enlargement without a reduction in cranial/cerebral size.
The P300 waveform has been associated with cognitive activity during information processing, and the hippocampus has been discussed as a possible generator of this waveform. This being the case some would argue that it should be possible to record the P300 with a shorter latency and greater amplitude from an electrode placed as near the hippocampus as possible. Under local anaesthesia we inserted a specially constructed needle electrode through the left nostril in the recessus pharyngeus close to the hippocampus. The results did not support the hippocampal hypothesis. Nasopharyngeally recorded P300's were found to have significantly decreased amplitudes and extended latencies when compared to vertex recordings.
Pathomorphology of the limbic system has been described in post-mortem studies of schizophrenia. To determine whether this could be detected in living patients and was not secondary to the treatment or the chronicity of the disease itself, we measured the volumes of the hippocampus-amygdala complex and adjoining temporal horns of 34 patients in their first episode of schizophrenia and 25 normal volunteers using T1 weighted contiguous coronal magnetic resonance images of 3.1 mm width. The results demonstrate abnormal medial temporal lobe morphology in a subgroup of patients at the onset of their illness. There were clear laterality effects and sex differences: hippocampal tissue was significantly smaller only in the left hemisphere of male patients, whereas enlargement of the whole temporal horn or its anterior portion was present on the left side in both sexes. Dysfunction of the limbic mesiotemporal structures might explain some of the clinical features of the disease.
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The distribution of galanin-like immunoreactivity has been studied in complete coronal sections taken from 9 normal human brains (4 male, 5 female mean age 54, range 42-72 years). Galanin-immunoreactive cells were restricted largely to the basal nucleus of Meynert and to the supraoptic, ventromedial and posterior areas of the hypothalamus. Fibre staining was more widespread, seen throughout the hypothalamus and in the diagonal band, septum, amygdala, hippocampus and scattered throughout the cortex. This distribution may indicate a role for galanin in the modulation of hypothalamic and basal forebrain function in man.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.
The volume of the entorhinal region is significantly reduced in postmortem brains of schizophrenics compared with controls (p less than 0.017). In addition, a significant reduction of neurons (p less than 0.017), but no significant increase in absolute glial cell numbers, is found. These results are consistent with the hypothesis that structural changes in the medial temporal lobe of schizophrenics may be developmental in origin.
In order to determine whether ventricular enlargement in schizophrenia is due to a general brain atrophy or to a more regionally confined reduction of brain tissue, in CT scans of 54 schizophrenics (ICD 9 295.0-6) and 54 controls matched for age and sex the size of all cortical sulci, the Silvian fissures, lateral, third and fourth ventricles were determined by blind planimetry. The left Silvian fissure was on several levels most enlarged (by 79-233%), followed by the right Silvian fissure (42-96%), the frontal parts of the interhemispheric fissure (84%), the left and right frontal sulci (40%, 46%), the VBR (32%), and the third ventricle (25%), whereas the parietal and occipital sulci and the fourth ventricle were not significantly altered. With the exception of one parameter, there was no correlation between any of the data and the duration of the illness. The data indicate that paralimbic and limbic structures of the anterior temporal lobe and of the parasagittal frontal cortex are most affected in schizophrenia. With respect to recent neuroanatomical and neurophysiological findings, an explanation is offered for the close association of some positive schizophrenic symptoms with limbic and paralimbic brain deficiency.
To investigate whether volume reduction of the hippocampal formation of schizophrenics, as described previously, is paralleled by loss of neurons and fibre systems, tissue volumes and cell numbers of all parts of the hippocampal formation in post mortem brains of 13 schizophrenics and 11 age-matched controls belonging to the Vogt collection were determined. Volumes of the whole hippocampal formation (P less than 0.01), the whole pyramidal band (P less than 0.001) and the hippocampal segments CA1/CA2 (P less than 0.01), CA3 (P less than 0.005), CA4 (P less than 0.01) were decreased, whereas no significant volume reduction of the alveus and fimbria hippocampi and prosubiculum/subiculum could be found. The perforant path showed a trend towards volume reduction (P less than 0.1). The absolute number of pyramidal cells (tissue volume X cell density) was diminished in CA1/CA2 (P less than 0.05), CA3 (P less than 0.05) and CA4 (P less than 0.05), but was not significantly changed in the prosubiculum/subiculum, the presubiculum/parasubiculum and the granular cell layer of the dentate fascia. Pyramidal cell loss in CA1/CA2, CA3, CA4 was more distinct in the paranoid patients than in catatonics. The findings are discussed with respect to current hypotheses of limbic dysfunction in schizophrenia.
The location of the neuropeptides methionine-enkephalin (ME), neurotensin (NT), neuropeptide Y (NPY) and vasoactive intestinal polypeptide (VIP) within the amygdaloid complex of healthy human individuals, schizophrenics and patients suffering from Huntington's chorea was studied qualitatively by means of immunohistochemistry. VIP-like immunoreactivity (IR) was present predominantly in a dense cluster of fibers and terminals in the central amygdaloid nucleus. ME-IR was observed in fibers, terminals and cell bodies in the same subnucleus, exhibiting a characteristical distribution pattern. NT-positive cell bodies were situated within the center of the central amygdaloid nucleus, fibers and terminals being encountered mainly at the periphery. NPY-IR was found to be evenly distributed throughout the amygdala. Distribution and staining intensity of ME, NPY and NT in the amygdala showed no qualitatively recognizable difference between the normal and schizophrenic specimens, whereas VIP-IR appeared to be slightly increased in the central amygdaloid nucleus of schizophrenics. In the choreic cases, the considerably shrunken amygdala exhibited only very low staining intensity of the four investigated neuropeptides.
Increased gliosis has been previously described in schizophrenic brain. In this study, the degree of gliosis in schizophrenic and control brains was assessed quantitatively using an antibody to glial fibrillary acidic protein, immunocytochemical techniques, and a computed image analysis system. Twenty separate brain areas were assessed, and no significant differences were found between the schizophrenic and control groups. It seems unlikely that a specific pattern of pathologically significant gliosis is present in schizophrenic brains. These negative findings are of note because of previously reported structural differences in the temporal lobe in the schizophrenic group in this series.
The volume of several parts of the basal ganglia and of the limbic system was measured by planimetry of myelin-stained serial sections in postmortem brains of 13 schizophrenic patients and nine control cases. The medial limbic structures of the temporal lobe (amygdala, hippocampal formation, and parahippocampal gyrus) and the pallidum internum were significantly smaller in the schizophrenic group, whereas the pallidum externum showed only a modest trend toward volume reduction. The volumes of the putamen, nucleus caudatus, nucleus accumbens, and the bed nucleus of the stria terminalis did not differ between patients and controls. The volume reductions of the limbic temporal structures and of the pallidum internum of schizophrenics are interpreted as degenerative shrinkages of unknown etiology.
The distribution of methionine-enkephalin (ME)-like and substance P (SP)-like immunoreactivity in the basal ganglia of untreated schizophrenics as compared with normal control cases, and untreated Huntington and Parkinson patients was studied using the unlabeled peroxidase-antiperoxidase (PAP) method. ME but not SP was reduced in the pallidum of one of six schizophrenics. The remaining five cases showed no differences to the controls. In contrast, no or only very faint homogeneously distributed ME and SP was found in any part of the basal ganglia in Huntington's disease. In Parkinson's disease, SP immunoreactivity was within normal range.
To find out whether ventricular enlargement in schizophrenia, as demonstrated by neuroradiological methods, is caused by an atrophy of ventricle surrounding diencephalic structures, volume measurements and linear measurements of the whole thalamus, all large thalamic subnuclei and some extrathalamic brain parts were carried out on serial sections of post mortem brains belonging to the Vogt collection. The only significantly diminished parameter of this study was the thickness of the periventricular grey matter surrounding the third ventricle, while the volume and linear measurements of the whole thalamus and all large thalamic subnuclei were not significantly changed. The findings are discussed with respect to current hypotheses of diencephalic dysfunction in schizophrenia.
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.