An antispasticity effect of threonine in multiple sclerosis
S. L. Hauser, T. H. Doolittle, M. Lopez-Bresnahan, B. Shahani, D. Schoenfeld, V. E. Shih, J. Growdon and J. R. Lehrich
Department of Neurology, Massachusetts General Hospital, Boston 02114.
To determine whether the naturally occurring amino acid threonine, a
potential precursor for glycine biosynthesis in the spinal cord, has an
effect on spasticity in multiple sclerosis, 26 ambulatory patients were
entered into a randomized crossover trial. Threonine administered at a
total daily dose of 7.5 g reduced signs of spasticity on clinical
examination, although no symptomatic improvement could be detected by the
examining physician or the patient. In contrast to the side effects of
sedation and increased motor weakness associated with antispasticity drugs
commonly used for the treatment of multiple sclerosis, no side effects or
toxic effects of threonine were identified. Levels of threonine were
elevated in serum and cerebrospinal fluid during treatment, but glycine
levels did not change. Enhancement by threonine of glycinergic postsynaptic
inhibition of the motor reflex arc in the spinal cord may represent a
non-sedating, nontoxic approach to the management of spasticity in multiple
sclerosis.
