Reduced left uncinate fasciculus fractional anisotropy in deficit schizophrenia but not in non-deficit schizophrenia
Article first published online: 18 JAN 2012
© 2012 The Authors. Psychiatry and Clinical Neurosciences © 2012 Japanese Society of Psychiatry and Neurology
Psychiatry and Clinical Neurosciences
Volume 66, Issue 1, pages 34–43, February 2012
How to Cite
Kitis, O., Ozalay, O., Zengin, E. B., Haznedaroglu, D., Eker, M. C., Yalvac, D., Oguz, K., Coburn, K. and Gonul, A. S. (2012), Reduced left uncinate fasciculus fractional anisotropy in deficit schizophrenia but not in non-deficit schizophrenia. Psychiatry and Clinical Neurosciences, 66: 34–43. doi: 10.1111/j.1440-1819.2011.02293.x
- Issue published online: 18 JAN 2012
- Article first published online: 18 JAN 2012
- Received 28 September 2010; revised 14 July 2011; accepted 8 August 2011.
- deficit syndrome;
- diffusion tensor imaging;
- uncinate fasciculus
Aims: Schizophrenia is a psychiatric disorder manifesting with heterogeneous symptom clusters and clinical presentations. The deficit syndrome is the condition defined by the existence of primarily negative symptoms, and patients with the deficit syndrome differ from non-deficit patients on measures of brain structure and function. In the current study, by using diffusion tensor imaging (DTI), we investigated the frontotemporal connectivity that is hypothesized to differ between deficit and non-deficit schizophrenia.
Methods: Twenty-nine patients and 17 healthy controls were included in the study. The patients had deficit (n = 11) or non-deficit (n = 18) schizophrenia and they were evaluated clinically with the Schedule for Deficit Syndrome (SDS) and Positive and Negative Syndrome Scale (PANSS). Diffusion-based images were obtained with a 1.5T Siemens Magnetic Resonance Imaging machine and analyses were carried out with Functional Magnetic Resonance Imaging of the Brain Library Software – Diffusion tool box software.
Results: The fractional anisotropy values in the left uncinate fasciculus of schizophrenia patients with the deficit syndrome were lower than those of non-deficit patients and the controls. There were no differences between non-deficit schizophrenia patients and controls.
Conclusion: These findings provide evidence of left uncinate fasciculus damage resulting in disrupted communication between orbitofrontal prefrontal areas and temporal areas in deficit schizophrenia patients.