Deficits in Saccadic Eye Movements in Basal Ganglia Disorders

  • Masaya Segawa
  • Okihide Hikosaka
  • Hideki Fukuda
  • Kimiaki Uetake
  • Yoshiko Nomura
Chapter
Part of the Advances in Behavioral Biology book series (ABBI, volume 41)

Abstract

Saccadic eye movements are controlled by the basal ganglia with two serial inhibitory connection systems, both GABAergic, which initiate in the caudate nucleus and terminate in the superior colliculus, changing the synapse at the pars reticulata of the substantia nigra (SNr) (Hikosaka et al., 1989). The nigrostriatal dopamine (NS-DA) neurons were verified to modulate this system in monkeys exposed to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) (Miyashita et al, 1990). Abnormalities in voluntary saccades were also shown clinically in cases with Dopa responsive disorders, such as Parkinson disease (PD) (Hikosaka et al., 1987) and hereditary progressive dystonia with marked diurnal fluctuation (HPD) (Nomura et al., 1987). It was also revealed that the mode of abnormalities of the saccades differed between PD and HPD (Hikosaka et al, 1993).

Keywords

Parkinson Disease Caudate Nucleus Direct Projection Saccade Task Voluntary Saccade 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
This is a preview of subscription content, log in to check access.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Crossman, A.R., 1990a, Animal models of movement disorders, “ First International Congress on Movement Disorders,” Washington, D.C.Google Scholar
  2. Crossman, A.R., 1990b, A hypothesis on the pathophysiological mechanisms that underlie levodopa or dopamine against induced dyskinesia in Parkinson’s disease. Implications for future strategies intreatment, Mov. Disord.5:100–108.CrossRefGoogle Scholar
  3. Hikosaka, O., Fukuda, H., Kato, M., Uetake, K., Nomura, Y., and Segawa, M, 1993, Deficits in saccadic eye movements in hereditary progressive dystonia with marked diurnal fluctuation, in:“Hereditary Progressive Dystonia with Marked Diurnal Fluctuation,” M. Segawa, ed., Parthenon, Carnforth, U.K., pp. 159–177.Google Scholar
  4. Hikosaka, O., Sakamoto, M., and Usui, S., 1989, Functional properties of monkey caudate neurons. I. Activities related to saccadic eye movements, J. Neurophysiol.61:780–798.PubMedGoogle Scholar
  5. Hikosaka, O., Segawa, M., and Imai, H., 1987, Voluntary saccadic eye movement: application to analyze basal ganglia disease, in: “Highlights in Neuro-Ophthalmology,” S. Ishikawa, eds., Aeolus Press, Amsterdam, pp. 133–138.Google Scholar
  6. Lenz, F.A., Jaeger, C.J., Seike, M.S., Lin, Y.C., DeLong, M.R., Tasker, R.R., and Vitek, J., 1992, Cross-correlation analysis of thalamic neuronal and EMG signals in patients with dystonia, Mov. Disord.7(Suppl. 1):126.Google Scholar
  7. Mitchell, I.J., Luquin, R., Boyce, S., Clarke, C.E., Robertson, R.G., Sambrook, M.A., and Crossman, A.R., 1990, Evidence from a 2-deoxyglucose uptake study in a primate model of dopamine agonist-induced dystonia, Mov. Disord.5:49–54.PubMedCrossRefGoogle Scholar
  8. Miyashita, N., Matsumura, M., Usui, S., Kato, M., Kori, A., Gardiner, T.W., and Hikosaka, O., 1990, Deficits in task-related eye movements induced by unilateral infusion of MPTP in the monkey caudate nucleus, Soc. Neurosci. Abstr.16:235.Google Scholar
  9. Narabayashi, H., Yokochi, F., and Nakajima, Y., 1984, Levodopa–induced dyskinesia and thalamotomy, J. Neurol. Neurosurg. Psychiatr.47:831–839.PubMedCrossRefGoogle Scholar
  10. Nomura, Y., Segawa, M., Soda, M., and Hikosaka, O., 1987, Voluntary saccadic eye movements in basal ganglia disorders, in:“Highlights in Neuro-Ophthalmology,” S. Ishikawa, ed., Aeolus Press, Amsterdam, pp. 139–145.Google Scholar
  11. Sakata, S., Shima F., and Fukui, M., 1993, Vop thalamotomy. Functional Neurosurgery(Tokyo), in press.Google Scholar
  12. Segawa, M., and Nomura, Y., 1993, Hereditary progressive dystonia with marked diurnal fluctuation, in:“Hereditary progressive dystonia with marked diurnal fluctuation,” M. Segawa, ed., Parthenon, Carnforth, UK, pp. 3–19.Google Scholar
  13. Segawa, M., Nomura, Y., and Kase, M., 1986, Diurnally fluctuating hereditary progressive dystonia, in: “Handbook of Clinical Neurology Vol. 5 ( 49 ): Extrapyramidal Disorders,” P.J. Vinken, G.W. Bruyn, H.L. Klawans, eds., Elsevier, Amsterdam, pp. 529–539.Google Scholar
  14. Segawa, M., Nomura, Y., Tanaka, S., Hakamada, S., Nagata, E., Soda, M., and Kase, M., 1988, Hereditary progressive dystonia with marked diurnal fluctuation: Consideration on its pathophysiology based on the characteristics of clinical and polysomnographical findings, in:“Advances in Neurology, Vol. 50: Dystonia 2,” S. Fahn, C. D. Marsden, D. B. Calne, eds., Raven Press, New York, pp. 367–376.Google Scholar
  15. Shima, F., and Fukui, M., 1993, to be published by Igaku no yumi (Tokyo).Google Scholar

Copyright information

© Plenum Press, New York 1994

Authors and Affiliations

  • Masaya Segawa
    • 1
  • Okihide Hikosaka
    • 2
  • Hideki Fukuda
    • 1
    • 3
  • Kimiaki Uetake
    • 1
  • Yoshiko Nomura
    • 1
  1. 1.Segawa Neurological Clinic for ChildrenTokyoJapan
  2. 2.National Institute for Physiological SciencesOkazakiJapan
  3. 3.National Institute of Industrial HealthKawasakaiJapan

Personalised recommendations