TY - JOUR
T1 - Lack of normal pattern of cerebral asymmetry in familial schizophrenic patients and their relatives - The Maudsley Family Study
AU - Sharma, Tonmoy
AU - Lancaster, Eric
AU - Sigmundsson, Thordur
AU - Lewis, Shôn
AU - Takei, Noriyoshi
AU - Gurling, Hugh
AU - Barta, Patrick
AU - Pearlson, Godfrey
AU - Murray, Robin
N1 - Funding Information:
We would like to thank Dr. Tim Read, Dr. Patrice Murphy, Dr. Brian Barraclough, and Dr. Keith Duddlestone for assistance in identifying and interviewing families. We are grateful to members of the National Schizophrenia Fellowship for helping in the identification of families for the study. We also thank all the families who participated in the study as well as Sandra Powell, Erica Scurr and Martin Graves of the MR Unit, St George's Hospital, London for MRI scanning and data transfer. This research was partly supported by grants from the Medical Research Council, United Kingdom (to Professor Murray, Professor Lewis and Dr. Sharma), The Middlesex Hospital Trustees, a Travelling Fellowship from Royal College of Psychiatrists and a Junior Psychiatrist Research Prize from the Association of European Psychiatrists to Dr. Sharma, the Stanley Foundation, NIH Grants MH43326 and 43775, NIH Outpatients General Clinical Research Center (RR-00722) to Professor Pearlson, and MH 50867 to Dr. Barta .
PY - 1999/11/30
Y1 - 1999/11/30
N2 - Lack of the normal cerebral asymmetry has been reported in schizophrenia. We wished to test the hypothesis that this lack of the normal pattern of asymmetry is familial and that it can be found in both schizophrenic and non-schizophrenic family members. In particular, we wanted to know whether those relatives who appear to be transmitting liability to the illness also demonstrate the loss of normal asymmetry. We studied families with several members affected with schizophrenia. We carried out volumetric measurements of prefrontal, premotor, sensorimotor and occipitoparietal regions in each hemisphere using 3D reconstructed MRI images in 29 schizophrenic patients, 55 of their first degree relatives, and 39 unrelated control subjects on contiguous thin slices of the brain. Nine of the unaffected relatives appeared to be transmitting the liability for schizophrenia (e.g. the mother of a schizophrenic patient who, although not psychotic herself, had a schizophrenic parent or sibling). We termed them presumed obligate carriers and the remaining 46 relatives presumed non-obligate carriers. The healthy control subjects showed larger right than left prefrontal regions and larger left than right sensorimotor and occipitoparietal regions. The schizophrenic patients showed lack of this normal brain asymmetry in the prefrontal, sensorimotor and occipitoparietal cortical regions. The presumed obligate carriers were similar to the schizophrenic patients in exhibiting lack of asymmetries in these cortical regions, while the presumed non-obligate relatives showed lack of asymmetry only in the occipitoparietal region. There was no overall reduction in total or regional brain volumes among the groups. Our findings indicate that lack of the normal pattern of frontal and occipital asymmetry is a marker for genetic liability to schizophrenia in families multiply affected with schizophrenia. 1999 Elsevier Science B.V. All rights reserved.
AB - Lack of the normal cerebral asymmetry has been reported in schizophrenia. We wished to test the hypothesis that this lack of the normal pattern of asymmetry is familial and that it can be found in both schizophrenic and non-schizophrenic family members. In particular, we wanted to know whether those relatives who appear to be transmitting liability to the illness also demonstrate the loss of normal asymmetry. We studied families with several members affected with schizophrenia. We carried out volumetric measurements of prefrontal, premotor, sensorimotor and occipitoparietal regions in each hemisphere using 3D reconstructed MRI images in 29 schizophrenic patients, 55 of their first degree relatives, and 39 unrelated control subjects on contiguous thin slices of the brain. Nine of the unaffected relatives appeared to be transmitting the liability for schizophrenia (e.g. the mother of a schizophrenic patient who, although not psychotic herself, had a schizophrenic parent or sibling). We termed them presumed obligate carriers and the remaining 46 relatives presumed non-obligate carriers. The healthy control subjects showed larger right than left prefrontal regions and larger left than right sensorimotor and occipitoparietal regions. The schizophrenic patients showed lack of this normal brain asymmetry in the prefrontal, sensorimotor and occipitoparietal cortical regions. The presumed obligate carriers were similar to the schizophrenic patients in exhibiting lack of asymmetries in these cortical regions, while the presumed non-obligate relatives showed lack of asymmetry only in the occipitoparietal region. There was no overall reduction in total or regional brain volumes among the groups. Our findings indicate that lack of the normal pattern of frontal and occipital asymmetry is a marker for genetic liability to schizophrenia in families multiply affected with schizophrenia. 1999 Elsevier Science B.V. All rights reserved.
KW - Cerebral asymmetry
KW - Familial
KW - Genetic
KW - Magnetic resonance imaging
KW - Schizophrenia
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U2 - 10.1016/S0920-9964(99)00143-7
DO - 10.1016/S0920-9964(99)00143-7
M3 - Article
C2 - 10593451
AN - SCOPUS:0032698021
SN - 0920-9964
VL - 40
SP - 111
EP - 120
JO - Schizophrenia Research
JF - Schizophrenia Research
IS - 2
ER -