Does ageing have an effect on midbrain premotor nuclei for vertical eye movements?

Authors

  • Craig Henson BSc,

    1. Department of Clinical Neurological Sciences, Royal College of Surgeons, Beaumont Hospital, Dublin, Ireland
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  • Hugh Staunton PhD, FRCP,

    1. Department of Clinical Neurological Sciences, Royal College of Surgeons, Beaumont Hospital, Dublin, Ireland
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  • Francesca M. Brett MD, FRCPath

    Corresponding author
    1. Department of Clinical Neurological Sciences, Royal College of Surgeons, Beaumont Hospital, Dublin, Ireland
    • Department of Clinical Neurological Sciences, Beaumont Hospital, P.O. Box 1297, Beaumont Road, Dublin 9, Ireland
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Abstract

Currently, there is debate in the clinical literature as to whether defects in vertical gaze are a consequence of normal ageing or a component of an underlying neurodegenerative disorder. Although pathological changes have been demonstrated in diseased subjects, no study to date has addressed the question of normal ageing effects. In this retrospective study, we examined 23 neurologically and pathologically normal subjects (age 18–91). Using an unbiased, frame-based sampling method, we quantified neuronal and glial cell densities in 10 young (<50) and 13 aged (>65) subjects in the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF), the key premotor substrate in the vertical gaze pathway. We found no statistically significant difference in neuronal density, glial cell density, or neuron-to-glial cell ratios between the young and the aged. We conclude, therefore, that neuronal loss, neuronal atrophy, or gliosis in the riMLF are not consequences of normal ageing. © 2003 Movement Disorder Society

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