Featured Finding Figure
Subjects with schizophrenia show deficits in visual perception that suggest changes predominantly in the magnocellular pathway and/or the dorsal visual stream important for visiospatial perception. We previously found a substantial 25% reduction in neuron number of the primary visual cortex (Brodmann's area 17, BA17) in postmortem tissue from subjects with schizophrenia. Also, many studies have found reduced volume and neuron number of the pulvinar-the large thalamic association nucleus involved in higher-order visual processing. Here, we investigate if the lateral geniculate nucleus (LGN), the visual relay nucleus of the thalamus, has structural changes in schizophrenia. We used stereological methods based on unbiased principles of sampling (Cavalieri's principle and the optical fractionator) to estimate the total volume and neuron number of the magno- and parvocellular parts (Figure shows examples of magno and parvocellular neurons) of the left LGN in postmortem brains from 9 subjects with schizophrenia, 7 matched normal comparison subjects and 13 subjects with mood disorders. No significant schizophrenia-related structural differences in volume or neuron number of the left LGN or its major subregions were found, but we did observe a significantly increased total volume of the LGN, and of the parvocellular lamina and interlaminar regions, in the mood group. These findings do not support the hypothesis that subjects with schizophrenia have structural changes in the LGN. Therefore, our previously observation of a schizophrenia-related reduction of the primary visual cortex is probably not secondary to a reduction in the LGN.
K-A Dorph-Petersen, D Caric, R Saghafi, W Zhang, AR Sampson & DA Lewis. Volume and neuron number of the lateral geniculate nucleus in schizophrenia and mood disorders. Acta Neuropathol 117: 369-384, 2009.

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David A. Lewis, M.D. | Department of Psychiatry | University of Pittsburgh
3811 O'Hara Street, Biomedical Science Tower W1654
Pittsburgh, Pennsylvania 15213-2593
Phone: (412) 624-3894 - Fax: (412) 624-9910