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A case study of temporal lobe development in familial schizophrenia

Published online by Cambridge University Press:  09 July 2009

W. G. Honer ,
A. S. Bassett ,
P. Falkai ,
T. G. Beach  and
J. S. Lapointe
W. G. Honer*
Affiliation:
Departments of Psychiatry, Pathology and Radiology, University of British Columbia, Vancouver, BCDepartment of Psychiatry, University of Toronto, Ontario, Canada; Department of Psychiatry, University of Düsseldorf Germany
A. S. Bassett
Affiliation:
Departments of Psychiatry, Pathology and Radiology, University of British Columbia, Vancouver, BCDepartment of Psychiatry, University of Toronto, Ontario, Canada; Department of Psychiatry, University of Düsseldorf Germany
P. Falkai
Affiliation:
Departments of Psychiatry, Pathology and Radiology, University of British Columbia, Vancouver, BCDepartment of Psychiatry, University of Toronto, Ontario, Canada; Department of Psychiatry, University of Düsseldorf Germany
T. G. Beach
Affiliation:
Departments of Psychiatry, Pathology and Radiology, University of British Columbia, Vancouver, BCDepartment of Psychiatry, University of Toronto, Ontario, Canada; Department of Psychiatry, University of Düsseldorf Germany
J. S. Lapointe
Affiliation:
Departments of Psychiatry, Pathology and Radiology, University of British Columbia, Vancouver, BCDepartment of Psychiatry, University of Toronto, Ontario, Canada; Department of Psychiatry, University of Düsseldorf Germany
*
1Address for correspondence: Dr W. G. Honer, Department of Psychiatry. Jack Bell Research Centre, 2660 Oak Street, Vancouver, BC. Canada V6H 3Z6.
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Synopsis

Case studies of patients with familial schizophrenia may help to define the pathophysiology of this illness and indicate potential candidate genes for genetic linkage studies. In this regard, the clinical, radiological and pathological assessments of a 39-year-old affected man from a pedigree with familial schizophrenia are presented. Brain imaging with CT indicated moderate cortical atrophy, particularly of the temporal lobes. Neuropathological examination revealed granular ependymitis, indicating possible past ventricular pathology. Granular ependymitis was reported to occur in genetic developmental disorders with neuronal migration abnormalities. In the present case, heterotopic clusters of neurons were visualized in the entorhinal cortex, suggesting that temporal lobe development was not entirely normal. This case study suggests that genetic factors could be investigated further as one possible aetiology of certain neurodevelopmental abnormalities observed in schizophrenia.

Type
Case Report
Information
Psychological Medicine , Volume 26 , Issue 1 , January 1996 , pp. 191 - 195
Copyright
Copyright © Cambridge University Press 1996

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References

REFERENCES

Akbarian, S., Viñuela, A., Kim, J. J., Potkin, S. G., Bunney, W. E. & Jones, E. G. (1993). Distorted distribution of nicotinamide-adenine dinucleotide phosphate-diaphorase neurons in temporal lobe of schizophrenics implies anomalous cortical development. Archives of General Psychiatry 50, 178–187.CrossRefGoogle ScholarPubMed
Arnold, S. E., Hyman, B. T., Van Hoesen, G. W. & Damasio, A. R. (1991). Some cytoarchitectural abnormalities of the entorhinal cortex in schizophrenia. Archives of General Psychiatry 48, 625–632.CrossRefGoogle ScholarPubMed
Bassett, A. S. & Honer, W. G. (1994). Evidence for anticipation in schizophrenia. American Journal of Human Genetics 54, 864–870.Google ScholarPubMed
Bassett, A. S., Collins, E. J., Nuttall, S. E. & Honer, W. G. (1993). Positive and negative symptoms in families with schizophrenia. Schizophrenia Research 11, 9–19.CrossRefGoogle ScholarPubMed
Bassett, A. S., Bury, A. & Honer, W. G. (1994). Testing Liddle's three syndrome model in families with schizophrenia. Schizophrenia Research 12, 213–221.CrossRefGoogle ScholarPubMed
Bogerts, B., Ashtari, M., Degreef, G., Alvir, J. M. J., Bilder, R. M. & Lieberman, J. A. (1990). Reduced temporal limbic structure volumes on magnetic resonance images in first episode schizophrenia. Psychiatry Research: Neuroimaging 35, 1–13.CrossRefGoogle ScholarPubMed
Conrad, A. J., Abebe, T., Austin, R., Forsythe, S. & Scheibel, A. B. (1991). Hippocampal pyramidal cell disarray in schizophrenia as a bilateral phenomenon. Archives of General Psychiatry 48, 413–417.CrossRefGoogle ScholarPubMed
DeLisi, L. E., Dauphinais, I. D. & Gershon, E. (1988). Perinatal complications and reduced size of brain limbic structures in familial schizophrenia. Schizophrenia Bulletin 14, 185–191.CrossRefGoogle ScholarPubMed
Dewan, M. J., Pandurangi, A. K., Lee, S. H., Ramachandran, T., Levy, B., Boucher, M., Yozawitz, A. & Major, L. F. (1983). Central brain morphology in chronic schizophrenic patients: a controlled CT study. Biological Psychiatry 18, 1133–1139.Google ScholarPubMed
Done, D. J., Sacker, A. & Crow, T. J. (1994). Childhood antecedents of schizophrenia and affective illness: intellectual performance at ages 7 and 11. Schizophrenia Research 11, 96–97.Google Scholar
Duchen, L. W. (1992). General pathology of neurons and neuroglia. In Greenfield's Neuropathology (ed. Adams, J. H. and Duchen, L. W.), pp. 1–68. Oxford University Press: New York.Google Scholar
Duvernoy, H. M. (1988). The Human Hippocampus. J. F. Bergmann Verlag: Munich.CrossRefGoogle Scholar
Falkai, P. & Bogerts, B. (1991). Qualitative and quantitative assessment of pre-alpha-cell clusters in the entorhinal cortex of schizophrenics. A neurodevelopmental model of schizophrenia? Schizophrenia Research 4, 357–358.CrossRefGoogle Scholar
Falkai, P., Bogerts, B. & Rozumek, M. (1988). Limbic pathology in schizophrenia: the entorhinal region – a morphometric study. Biological Psychiatry 24, 515–521.CrossRefGoogle ScholarPubMed
Falkai, P., Bogerts, B., Greve, B., Pfeiffer, U., Machus, B., Fölsch-Reetz, B., Majtenyi, C. & Ovary, I. (1992). Loss of sylvian fissure asymmetry in schizophrenia. Schizophrenia Research 7, 23–32.CrossRefGoogle ScholarPubMed
Folstein, M. F., Folstein, S. E. & McHugh, P. R. (1975). ‘Mini-Mental State’: a practical method for grading the cognitive state of patients for the clinician. Journal of Psychiatric Research 12, 189–198.CrossRefGoogle Scholar
Galaburda, A. M., Sherman, G. F., Rosen, C. D., Aboitz, F. & Geschwind, N. (1985). Developmental dyslexia: four consecutive patients with cortical anomalies. Annals of Neurology 18, 222–233.CrossRefGoogle ScholarPubMed
Harvey, I., Ron, M. A., Du Boulay, G., Wicks, D., Lewis, S. W. & Murray, R. M. (1993). Reduction of cortical volume in schizophrenia on magnetic resonance imaging. Psychological Medicine 23, 591–604.CrossRefGoogle ScholarPubMed
Hattori, M., Adachi, H., Tsujimoto, M., Arai, H. & Inoue, K. (1994). Miller–Dieker lissencephaly gene encodes a subunit of brain platelet-activating factor. Nature 370, 216–218.CrossRefGoogle ScholarPubMed
Honer, W. G., Bassett, A. S., Smith, G. N., Lapointe, J. S. & Falkai, P. (1994). Temporal lobe abnormalities in multi-generational families with schizophrenia. Biological Psychiatry 36, 737–743.CrossRefGoogle Scholar
Jakob, H. & Beckmann, H. (1986). Prenatal developmental disturbances in the limbic allocortex in schizophrenics. Journal of Neural Transmission 65, 303–326.CrossRefGoogle ScholarPubMed
Jakob, H. & Beckmann, H. (1989). Gross and histological criteria for developmental disorders in brains of schizophrenics. Journal of the Royal Society of Medicine 82, 466–469.CrossRefGoogle ScholarPubMed
Kay, S., Fiszbein, A. & Opler, L. A. (1987). The positive and negative syndrome scale (PANSS) for schizophrenia. Schizophrenia Bulletin 13, 261–276.CrossRefGoogle ScholarPubMed
Kovelman, J. A. & Scheibel, A. B. (1984). A neurohistological correlate of schizophrenia. Biological Psychiatry 19, 1601–1621.Google ScholarPubMed
Li, S.-H., McInnis, M. G., Margolis, R. L., Antonarakis, S. E. & Ross, C. A. (1993). Novel triplet repeat containing genes in human brain: cloning, expression, and length polymorphisms. Genomics 16, 572–579.CrossRefGoogle ScholarPubMed
Marsh, L., Suddath, R. L., Higgins, N. & Weinberger, D. R. (1994). Medial temporal lobe structures in schizophrenia: relationship of size to duration of illness. Schizophrenia Research 11, 225–238.CrossRefGoogle ScholarPubMed
Sarnat, H. B., Darwish, H. Z., Barth, P. G., Trevenen, C. L., Pinto, A., Kotagal, S., Shishikura, K., Osawa, M. & Korobkin, R. (1993). Ependymal abnormalities in lissencephaly/pachygyria. Journal of Neuropathology and Experimental Neurology 52, 525–541.CrossRefGoogle ScholarPubMed
Scheibel, A. B. & Conrad, A. S. (1993). Hippocampal dysgenesis in mutant mouse and schizophrenic man: is there a relationship? Schizophrenia Bulletin 19, 21–33.CrossRefGoogle Scholar
Suddath, R. L., Casanova, M. F., Goldgerb, T. E., Daniel, D. G., Kelsoe, J. R. & Weinberger, D. R. (1989). Temporallobe pathology in schizophrenia: a quantitative magnetic resonance imaging study. American Journal of Psychiatry 146, 464–472.Google Scholar
Vincent, I. J., Katen, R. N., Isaacs, A., Mattiace, L. A. & Davies, P. (1993). TGI: a marker for nuclear tau with specificity for neuronal nuclei in Alzheimer's disease. Society for Neuroscience Abstracts 19, 670.4.Google Scholar