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The British Journal of Psychiatry (2000) 176: 52-60
© 2000 The Royal College of Psychiatrists

Functional anatomy of verbal fluency in people with schizophrenia and those at genetic risk

Focal dysfunction and distributed disconnectivity reappraised{dagger}

SEAN A. SPENCE, MRCPsych and PAUL M. GRASBY, MRCPsych

Division of Neuroscience, Imperial College School of Medicine, Medical Research Council Cyclotron Unit, Hammersmith Hospital, London

PETER F. LIDDLE, MRCPsych

Department of Psychiatry, University of British Columbia, Vancouver, Canada

MARTIN D. STEFAN, MRCPsych, TONMOY SHARMA, MRCPsych and ROBIN M. MURRAY

Department of Psychological Medicine, Institute of Psychiatry, London

JONATHAN S. E. HELLEWELL, MRCPsych

Department of Psychiatry and Behavioural Sciences, University of Manchester, Manchester

KARL J. FRISTON, MRCPsych and CHRISTOPHER D. FRITH, PhD

Wellcome Department of Cognitive Neurology, Institute of Neurology, London

STEVEN R. HIRSCH, FRCPsych

Imperial College School of Medicine, Charing Cross Hospital, London

J. F. WILLIAM DEAKIN, FRCPsych

Department of Psychiatry and Behavioural Sciences, University of Manchester, Manchester

Correspondence: S. A. Spence, Functional Neuroimaging Laboratory, Department of Psychiatry, Box 171, New York Hospital — Cornell Medical Center, 525 East 68th Street, New York, NY 10021, USA. e-mail:sean{at}hanazono.med.cornell.edu

Declaration of interest No conflict of interest. Financial support detailed in Acknowledgements.

{dagger} See invited commentary pp. 61—63, this issue.

Background PET studies of verbal fluency in schizophrenia report a failure of ‘deactivation’ of left superior temporal gyrus (STG) in the presence of activation of left dorsolateral prefrontal cortex (DLPFC), which deficit has been attributed to underlying ‘functional disconnectivity’.

Aim To test whether these findings provide trait-markers for schizophrenia.

Method We used H215O PET to examine verbal fluency in 10 obligate carriers of the predisposition to schizophrenia, 10 stable patients and 10 normal controls.

Results We found no evidence of a failure of left STG deactivation in carriers or patients. Instead, patients failed to deactivate the precuneus relative to other groups. We found no differences in functional connectivity between left DLPFC and left STG but patients exhibited significant disconnectivity between left DLPFC and anterior cingulate cortex.

Conclusions Failure of left STG ‘deactivation’ and left fronto-temporal disconnectivity are not consistent findings in schizophrenia; neither are they trait-markers for genetic risk. Prefrontal functional disconnectivity here may characterise the schizophrenic phenotype.




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