An antispasticity effect of threonine in multiple sclerosis

Area of Science:

• Neuroscience
• Biochemistry
• Clinical Neurology

Background:

• Spasticity is a common and disabling symptom in multiple sclerosis (MS).
• Current treatments for MS spasticity can cause significant side effects like sedation and motor weakness.
• Threonine, an amino acid, is a potential precursor for glycine biosynthesis in the spinal cord, which plays a role in motor control.

Purpose of the Study:

• To investigate the efficacy of threonine in reducing spasticity in patients with multiple sclerosis.
• To assess the safety and tolerability of threonine as a potential treatment for MS spasticity.

Main Methods:

• A randomized crossover trial involving 26 ambulatory patients with multiple sclerosis.
• Patients received a total daily dose of 7.5 g of threonine.
• Clinical examinations were performed to assess spasticity signs and symptoms.
• Serum and cerebrospinal fluid levels of threonine and glycine were monitored.

Main Results:

• Threonine administration led to a reduction in clinical signs of spasticity.
• No significant symptomatic improvement was reported by patients or physicians.
• No adverse or toxic effects were observed during threonine treatment.
• Threonine levels increased in serum and cerebrospinal fluid, while glycine levels remained unchanged.

Conclusions:

• Threonine may offer a non-sedating and nontoxic therapeutic option for managing spasticity in multiple sclerosis.
• The mechanism may involve enhancement of glycinergic postsynaptic inhibition in the spinal cord's motor reflex arc.
• Further research is needed to confirm symptomatic benefits and optimize treatment protocols.