Hostname: page-component-8448b6f56d-wq2xx Total loading time: 0 Render date: 2024-04-25T03:34:26.869Z Has data issue: false hasContentIssue false
  • English
  • Français

Pilot Study of Threonine Supplementation in Human Spasticity

Published online by Cambridge University Press:  18 September 2015

A. Barbeau ,
M. Roy  and
C. Chouza
A. Barbeau*
Affiliation:
Department of Neurobiology Clinical Research Institute of Montreal
M. Roy
Affiliation:
Department of Neurobiology Clinical Research Institute of Montreal
C. Chouza
Affiliation:
Department of Neurobiology Clinical Research Institute of Montreal
*
Clinical Research Institute of Montreal, 110 Pine Avenue West, Montréal, Quebec, Canada H2W 1R7
Rights & Permissions [Opens in a new window]

Abstract:

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

Threonine supplementation (500 mg/day) was given to 6 patients with genetic spasticity syndromes for a period of 12 months, followed by a 4-month observation period without medication. All 6 patients showed partial improvement of spasticity, intensity of knee jerks and muscle spasms without changes in true pyramidal tract signs. The improvement in motor performance, objectively measured, averaged 29% (19% in upper limbs and 42% in lower limbs). The range of overall improvement was 19–35% (7–30% for upper limbs; 25–67% for lower limbs). No toxic clinical or biochemical side effects were encountered. Thus threonine, a precursor of glycine, produced the same effect on spasticity than that previously observed with glycine. It is concluded that threonine supplementation is feasible and safe and that it deserves a controlled trial in well defined (preferably genetic) cases of spasticity.

Type
Research Article
Information
Canadian Journal of Neurological Sciences , Volume 9 , Issue 2 , May 1982 , pp. 141 - 145
Copyright
Copyright © Canadian Neurological Sciences Federation 1982

References

REFERENCES

Aprison, M.H. and Nadi, N.S. (1978). Glycine: inhibition from the sacrum to the medulla, in Amino acids as chemical transmitters. Ed. by Fonnum, F.. Plenum Press pp. 531–570.CrossRefGoogle Scholar
Aprison, M.H.; Shank, R.P. and Davidoff, R.A. (1969). A comparison of the concentration of glycine, a transmitter suspect, in different areas of the brain and spinal cord in seven different vertebrates. Comp. Biochem. Physiol. 28: 1345–1355.CrossRefGoogle ScholarPubMed
Aprison, M.H. and Werman, R. (1965). The distribution of glycine in cat spinal cord and roots. Life Sci. 4: 2075–2083.CrossRefGoogle ScholarPubMed
Barbeau, A. (1961). Biochemistry of Parkinson’s disease. Excerpta Medica, I.C.S. 38:152–153.Google Scholar
Barbeau, A. (1974). Preliminary study of glycine administration in Patients with spasticity. Neurology 24: 392.Google Scholar
Barbeau, A., Growdon, J.H. and Wurtman, R.J., Eds. (1979). Nutrition and the Brain, Vol. 5 Raven Press, New York.Google Scholar
Boehme, D.H., Marks, N. and Fordice, M.W. (1976). Glycine levels in the degenerated human spinal cord. J. Neurol. Sci. 27: 347–352.CrossRefGoogle ScholarPubMed
Bouchard, J.P.; Barbeau, A., Bouchard, R. and Bouchard, R.W. (1978). Autosomal recessive spastic ataxia of Charlevoix-Saguenay. Can. J. Neurol. Sci. 5:61–69.CrossRefGoogle ScholarPubMed
Burke, D. and Ashby, P. (1972). Are spinal “presynaptic” inhibitory mechanisms suppressed in spasticity? J. Neurol. Sci. 15: 321–326.CrossRefGoogle ScholarPubMed
De Montis, G., Beaumont, K., Javoyagid, F., Agid, Y., Constandinidis, J., Lowenthal, A. and Lloyd, K.G. (1982). Glycine receptors in the human substantia nigra as defined by [H3] strychnine binding. J. Neurochem. 38: 718–724.CrossRefGoogle ScholarPubMed
Dery, J.P., De Groot, J.A., Laurin, C. and Barbeau, A. (1962). Nouvelle méthode d’évaluation objective de la rigidité et du tremblement dans la maladie de Parkinson. Union Méd. Can. 91: 842–847.Google Scholar
Feldman, R.G., Young, R.R. and Koella, W.P. (Eds) (1980). Spasticity: disordered motor control. Chicago; Year Book Publishers.Google Scholar
Glyn, J.R. and Lipton, J.M. (1980). Comparison of the effects of central administration of serine and glycine on body temperature of the rabbit. Brain Res. Bull. 5: 661–665.CrossRefGoogle ScholarPubMed
Gundlach, A.L. and Beart, P.M. (1982). Neurochemical studies of the mesolimbic dopaminergic pathway: glycinergic mechanisms and glycinergic – dopaminergic interactions in the rat ventral tegmentum. J. Neurochem. 38: 574–581.CrossRefGoogle ScholarPubMed
Hall, P.V., Smith, J.E., Campbell, R.L. (1976). Neurochemical correlates of spasticity. Life Sci. 18: 1467–1472.CrossRefGoogle ScholarPubMed
Hall, P.V., Smith, J.E., Lane, J., Mote, T. and Campbell, R. (1979). Glycine and experimental spinal spasticity. Neurology 29: 262–267.CrossRefGoogle ScholarPubMed
Landau, W.M. (1974). Spasticity: the fable of a neurological demon and the emperor’s new therapy. Arch. Neurol. 31:217–219.Google ScholarPubMed
Levi, G., Bernardi, G., Cherubini, E., Gallo, V., Marciani, G. and Stanzione, P. (1982). Evidence in favor of a neurotransmitter role of glycine in the rat cerebral cortex. Brain Res. 236: 121–131.CrossRefGoogle ScholarPubMed
Maher, T.J. and Wurtman, R.J. (1979). L-Threonine and glycine in rat CNS. Neurosci. abs. 5: 593.Google Scholar
Maher, T.J. and Wurtman, R.J. (1980). L-Threonine administration increases glycine concentrations in the rat central nervous system. Life Sci. 26: 1283–1286.CrossRefGoogle ScholarPubMed
Mcbride, W.J., Daly, E. and Aprison, M.H. (1973). Interconversion of glycine and serine in a synaptosome fraction isolated from the spinal cord, medulla oblongata, telencephalon and cerebellum of the rat. J. Neurochem. 4: 557–566.Google Scholar
Pycock, C.J. and Kerwin, R.W. (1981). The status of glycine as a supra-spinal neurotransmitter – Minireview. Life Sciences 28: 2679–2686.CrossRefGoogle Scholar
Roberts, E. (1974). Disinhibition as an organizing principle in the nervous system – The role of gamma-aminobutyric acid. Adv. Neurol. 5: 127–143.Google ScholarPubMed
Siemers, E.R., Daly, E.C. and Aprison, M.H. (1980). Is threonine a precursor of one of the central pools of glycine? Amer. Soc. Neurochem. Abs. Vol. 11: 69.Google Scholar
Smith, J.E., Hall, P.V., Galvin, M.R., Jones, A.R. and Campbell, R.L. (1979). Effects of glycine adminstration on canine experimental spinal spasticity and the levels of glycine, glutamate, and aspartate in the lumbar spinal cord. Neurosurg. 4: 152–156.CrossRefGoogle Scholar
Snyder, S.H. (1975). The glycine receptor in the mammalian central nervous system. Br. J. Pharmacol. 53:473–484.CrossRefGoogle ScholarPubMed
Stern, P. and Bokonjic, R. (1974). Glycine therapy in seven cases of spasticity. Pharmacology 12: 117–119.CrossRefGoogle Scholar
Stern, P. and Hadzovic, S. (1970). Effect of glycine on experimental hindlimbs rigidity in rats. Life Sci. 9:955–959.CrossRefGoogle ScholarPubMed
Titchenal, C.L., Rogers, Q.R., Indrieri, R.J. and Morris, J.G. (1980). Threonine imbalance, deficiency and neurologic dysfunction in the kitten. J. Nutr. 110:2444–2459.CrossRefGoogle ScholarPubMed
Tontisirin, K., Young, V.R., Rand, M.W. and Scrimshaw, N.S. (1974). Plasma threonine response curve and threonine requirements of young men and elderly women. J. Nutrition. 104: 495–505.CrossRefGoogle Scholar
Werman, R., Davidoff, R.A. and Aprison, M.H. (1968). Inhibitory action of glycine on spinal neurons in the cat. J. Neurophysiol. 31:81–95.CrossRefGoogle ScholarPubMed
Wurtman, R.J. (1982). Nutrients that modify brain function. Scientific American 246: 50–59.CrossRefGoogle ScholarPubMed
Young, R.R. and Delwaide, P.J. (1981). Spasticity. New Engl. J. Med. 304: 28–33, 96,99.Google ScholarPubMed