title: Nerve cell loss in the thalamic centromedian-parafascicular complex in patients with Huntington's disease.
abstract: The centromedian-parafascicular complex represents a nodal point in the neuronal loop comprising striatum--globulus pallidus--thalamus--striatum. Striatal neurone degeneration is a hallmark in Huntington's disease and we were interested in estimating total neurone and glial number in this thalamic nuclear complex. Serial 500-microns-thick gallocyanin-stained frontal sections of the left hemisphere from six cases of Huntington's disease patients (three females, three males) and six age- and sex-matched controls were investigated applying Cavalieri's principle and the optical disector. Mean neurone number in the controls was 646,952 +/- 129,668 cells versus 291,763 +/- 60,122 in Huntington's disease patients (Mann-Whitney U-test, P < 0.001). Total glial cell number (astrocytes, oligodendrocytes, microglia, and unclassifiable glial profiles) was higher in controls with 9,544,191 +/- 3,028,944 versus 6,961,989 +/- 2,241,543 in Huntington's disease patients (Mann-Whitney U-test, P < 0.021). Considerable increase of fibrous astroglia within the centromedian-parafascicular complex could be observed after Gallyas' impregnation. Most probably this cell type enhanced the numerical ratio between glial number and neurone number (glial index: Huntington's disease patients = 24.4 +/- 8.1; controls = 15.0 +/- 5.2; Mann-Whitney U-test, P < 0.013). The neurone number in the centromedian-parafascicular complex correlated negatively, although statistically not significantly, with the striatal neurone number. This lack of correlation between an 80% neuronal loss in the striatum and a 55% neurone loss in the centromedian-parafascicular complex points to viable neuronal circuits connecting the centromedian-parafascicular complex with cortical and subcortical regions that are less affected in Huntington's disease.
authors.affiliation: Morphologische Hirnforschung, Universitäts-Nervenklinik, Würzburg, Germany.
authors.forename: H
authors.initials: H
authors.lastname: Heinsen
authors.forename: U
authors.initials: U
authors.lastname: Rüb
authors.forename: D
authors.initials: D
authors.lastname: Gangnus
authors.forename: G
authors.initials: G
authors.lastname: Jungkunz
authors.forename: M
authors.initials: M
authors.lastname: Bauer
authors.forename: G
authors.initials: G
authors.lastname: Ulmar
authors.forename: B
authors.initials: B
authors.lastname: Bethke
authors.forename: M
authors.initials: M
authors.lastname: Schüler
authors.forename: F
authors.initials: F
authors.lastname: Böcker
authors.forename: W
authors.initials: W
authors.lastname: Eisenmenger
authors.forename: M
authors.initials: M
authors.lastname: Götz
authors.forename: M
authors.initials: M
authors.lastname: Strik
mesh_terms: D000328:Adult; D000368:Aged; D001253:Astrocytes / Q000648:ultrastructure; D001921:Brain / Q000473:pathology; D002452:Cell Count; D005260:Female; D006801:Humans; D006816:Huntington Disease / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D013788:Thalamus / Q000473:pathology*