Computed Tomographic Evidence for Generalized Sulcal and Ventricular Enlargement in Schizophrenia

Pfefferbaum, Adolf; Zipursky, Robert B.; Lim, Kelvin O.; Zatz, Leslie M.; Stahl, Stephen M.; Jernigan, Terry L.

doi:10.1001/archpsyc.1988.01800310037005

Cited by 109 publications

(30 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Also previous studies of chronic schizophrenic patients have reported a relationship between lateral ventricle size or sulcal enlargement and neuropsychological impairment (53)(54)(55)(56)(57)(58)(59).…”

Section: Discussionmentioning

confidence: 89%

Neuropsychological deficit in newly diagnosed patients with schizophrenia or schizophreniform disorder

Rubin

Holm

Møller-Madsen

et al. 1995

Acta Psychiatr Scand

View full text Add to dashboard Cite

Forty-six patients with schizophrenia or schizophreniform disorder admitted to hospital for the first time were compared with 21 healthy volunteers on neuropsychological tests reflecting prefrontal and left respectively right hemisphere function. The patients with schizophrenia or schizophreniform disorder had a poorer performance on neuropsychological tests (such as Wisconsin Card Sorting) compared with healthy volunteers. Both left and right hemisphere seemed to be involved. Especially poor performance was found on somewhat complicated tests requiring ability of analysis, abstraction and memory, thus indicating dysfunction of prefrontal and temporohippocampal regions. Signs of sulcal enlargement and size of lateral ventricles on computed tomographic scan correlated with poor test performance on some tests both in patients and in healthy volunteers. No correlations were found between performance on neuropsychological test and negative symptoms.

show abstract

Section: Discussionmentioning

confidence: 89%

Neuropsychological deficit in newly diagnosed patients with schizophrenia or schizophreniform disorder

Rubin

Holm

Møller-Madsen

et al. 1995

Acta Psychiatr Scand

View full text Add to dashboard Cite

show abstract

“…The presence of widespread sulcal enlargement, repeatedly reported in CT studies (Weinberger et al 1979;Takahashi et al 1981;Nasrallah et al 1982;Rieder et al 1983;Pfefferbaum et al 1988;Rossi et al 1988;Stahl et al 1988;Vita et al 1988;Scottish Schizophrenia Research Group, 1989), may be an indicator of such pathological changes in the underlying brain parenchyma. Although the specific location of these abnormalities remains uncertain they may predominantly affect the cortex (Pakkenberg, 1987), as appears to be the case when there is loss of volume in the temporal lobe (Suddath et al 1989(Suddath et al , 1990.…”

Section: Introductionmentioning

confidence: 86%

Reduction of cortical volume in schizophrenia on magnetic resonance imaging

et al. 1993

View full text Add to dashboard Cite

SYNOPSIS The MRI scans of 48 schizophrenic patients, fulfilling RDC criteria, were compared to those of 34 healthy controls matched for age, ethnicity and parental social class. The volume of the frontal and anterior parietal lobes was significantly reduced in the schizophrenic group as a result of a selective decrease in cortical volume, with a corresponding increase in the volume of sulcal fluid. Reduction in the volume of the temporal grey matter was more marked on the right, but was not in excess of the loss of volume observed in other areas of the cortex. MRI abnormalities correlated poorly with clinical parameters, although both unemployment and poor pre-morbid adjustment predicted reduced cerebral volume and increased sulcal volume. These results question whether the medial temporal lobes are the only site of structural pathology in schizophrenia.

show abstract

“…Enlargement of the cerebral ventricles was for a long time the most consistent anatomical finding in schizophrenia using neuroimaging or at post mortem (Johnstone et al 1976;Weinberger et al 1979;Andreasen et al 1982;Reveley et al 1982;DeLisi et al 1986;Pfefferbaum et al 1988;Suddath et al 1989), and may be fully developed before the onset of illness (Frangou & Murray, 1996). Studies showed a decrease in volume of cerebral cortex but no change in that of subcortical white matter (Suddath et al 1989;Zipursky et al 1992;Harvey et al 1993), suggesting that there is no loss of axons or probably of somata of cortical neurons (Selemon et al 1995;Selemon & Goldman-Rakic, 1999), but there is a loss in neuronal processes, such as axon terminals or dendritic branches or spines, in the cortical neuropil.…”

Section: Schizophrenia As a Neurodevelopmental Diseasementioning

confidence: 94%

When cortical development goes wrong: schizophrenia as a neurodevelopmental disease of microcircuits

Garey¹

2010

Journal of Anatomy

143

101

View full text Add to dashboard Cite

Schizophrenia probably has a developmental origin. This review refers to three of our published series of studies related to this hypothesis: loss of dendritic spines on cerebral neocortical pyramidal neurons, decreased numerical density of glutamatergic neurons, and microgliosis. First, brains of schizophrenic patients and nonschizophrenic controls were obtained post mortem and blocks of multiple cortical areas impregnated with a Rapid Golgi method. Spines were counted on the dendrites of pyramidal neurons of which the soma was in layer III (which takes part in corticocortical connectivity) and which met strict criteria for impregnation quality. Data were obtained blind: diagnoses were only revealed by a third party after measurements were completed. The mean spine count in all cortical areas studied in the control series was 243 mm )1 of dendrite and in the schizophrenics 108. Measurements in frontal and temporal association cortex showed the greatest reduction in spine number in schizophrenia (299 in control frontal cortex and 101 in schizophrenics, and 276 mm )1 in control temporal cortex and 125 in schizophrenics). There was no correlation of spine loss with age at death. Our results support the concept of a neurodevelopmental defect in the neuropil affecting glutamatergic neurons in schizophrenia and may help to explain loss of cortical volume without loss of neurons. In a second part of our study we used an antibody to the kainate receptor subunit GluR 5 ⁄ 6 ⁄ 7 and showed a decrease in numerical density of presumed glutamatergic neurons in schizophrenic orbitofrontal cortex. Finally, as glia play a major role in the developing nervous system, we investigated whether schizophrenia was associated with glial changes in frontal and temporal cortex. Astroglia and microglia were identified in schizophrenic and control brains, using antibodies to glial fibrillary acidic protein (GFAP) and class II human leucocyte antigen (HLA-DR), respectively. Significant increases were found in microglial numerical density in schizophrenics compared with controls: 28% in frontal area 9 (115 cells mm )2 compared with 89), and a 57% increase in temporal area 22(139 cells mm )2 compared with 88). For both areas, astroglia showed no significant differences between schizophrenics and controls. No significant differences were found in cortical thickness or total neuronal numerical density between the two groups. This specific increase in numerical density of microglia in temporal and frontal cortex of chronic schizophrenics, not related to aging, could be related to possible changes in cortical neuropil architecture as revealed by loss of dendritic spines.

show abstract

Computed Tomographic Evidence for Generalized Sulcal and Ventricular Enlargement in Schizophrenia

Cited by 109 publications

References 41 publications

Neuropsychological deficit in newly diagnosed patients with schizophrenia or schizophreniform disorder

Neuropsychological deficit in newly diagnosed patients with schizophrenia or schizophreniform disorder

Reduction of cortical volume in schizophrenia on magnetic resonance imaging

When cortical development goes wrong: schizophrenia as a neurodevelopmental disease of microcircuits

Contact Info

Product

Resources

About