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September 1992

An Antispasticity Effect of Threonine in Multiple Sclerosis

Author Affiliations

From the Department of Neurology, Massachusetts General Hospital, Boston.

Arch Neurol. 1992;49(9):923-926. doi:10.1001/archneur.1992.00530330045014

• 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 nonsedating, nontoxic approach to the management of spasticity in multiple sclerosis.

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