Stereologic analysis of the lateral geniculate nucleus of the thalamus in normal and schizophrenic subjects

Abstract

Reduction of volume and neuronal number has been found in several association nuclei of the thalamus in schizophrenic subjects. Recent evidence suggests that schizophrenic patients exhibit abnormalities in early visual processing and that many of the observed perceptual deficits are consistent with dysfunction of the magnocellular pathway, i.e. the visual relay from peripheral retinal cells to the two ventrally located magnocellular layers of the lateral geniculate nucleus (LGN). The present study was undertaken to determine whether abnormalities in cell number and volume of the LGN are associated with schizophrenia and whether the structural alterations are restricted to either the magnocellular or parvocellular subdivisions of the LGN. Series of Nissl-stained sections spanning the LGN were obtained from 15 schizophrenic and 15 normal control subjects. The optical disector/ fractionator sampling method was used to estimate total neuronal number, total glial number and volume of the magnocellular and parvocellular subdivisions of the LGN. Cell number and volume of the LGN in schizophrenic subjects were not abnormal. Volume of both parvocellular and magnocellular layers of the LGN decreased with age. These findings do not support the hypothesis that early visual processing deficits are due to reduction of neuronal number in the LGN.

Visualization of the Medial and Lateral Geniculate Nucleus on Phase Difference Enhanced Imaging

“…5,6 In a histologic study, 12 it varied from 66 to 157 mm 3 ; among individuals, the variation was 2-to 3-fold. In our search of the literature, 2 (B).…”

“…There is increasing interest in assessing the MGN and LGN in healthy subjects and in patients with ophthalmic diseases such as glaucoma. [1][2][3][4][5][6] However, current imaging methods for identifying the MGN and LGN vary, and imaging findings are inconsistent. Technical advances in neuroimaging facilitate the study of subcortical structures in vivo.…”

Revisiting visual dysfunctions in schizophrenia from the retina to the cortical cells: A manifestation of defective neurodevelopment

“…Those structures include the suprachiasmatic nucleus, the pretectum area, the pulvinar and the superior colliculus, which is strongly involved in the visuomotor coordination (Forrester, 2002). So far, no change in the total cell numbers (Selemon & Begovic, 2007) or the volume (Lesch and Bogerts, 1984) of the LGN has been observed but some alterations in optic radiations, connecting the LGN to various areas of the visual cortex were found in schizophrenia (Butler et al, 2006). Lesions of the optic radiations are known to cause visual field defects.…”

Stereopsis and magnocellular sensitivity in schizophrenia

“…The finding of Schechter et al (2005) of reduced VEP response to isoluminant colour stimulation is therefore not what one would expect from a purely magnocellular deficit. Selemon and Begovic (2007) examined cell number and volume in the lateral geniculate nucleus (LGN) in post mortem brains of schizophrenic individuals and found that both of these measures were normal in both the magno-and parvocellular layers. These findings do not support the notion of a link between magnocellular deficits and schizophrenia.…”

“…Butler and Javitt concluded their 2005 review with the words: 'Results from behavioral and electrophysiological studies support early visual processing dysfunction in schizophrenia, with preferential deficits being found in the magnocellular pathway, though parvocellular deficits have been found as well' (Butler and Javitt 2005, p 156). Based on this statement and the lack of evidence for magnocellular deficits from contrast sensitivity studies, the problems of linking backward masking and VEP responses unequivocally to the magnocellular system, along with the just mentioned negative observations of Selemon and Begovic (2007), it is unclear if, or to what extent, sensory deficiencies in schizophrenia are specific to the magnocellular system.…”