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Lidocaine
2%
45/2516
Botulinum toxin A
90%
2256/2516
Acetylcholinesterase
50/2516
Baclofen
3%
82/2516
Pyridostigmine
71/2516
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Decreased acetylcholine levels in the synaptic cleft weaken the strength of muscle contraction through paralysis of the the portion of muscle whose neuromuscular junctions are blocked. Botox exhibits this peripheral mechanism of action in the treatment of spastic muscle disorders like cerebral palsy. While botulinum toxin A, acetylcholinesterase, and baclofen all demonstrate a decrease in spasticity, only botulinum toxin A does so by blocking the presynaptic release of acetylcholine peripherally. Baclofen acts as a Gamma-aminobutyric acid (GABA) agonist. Baclofen exerts its effects more centrally as an agonist at presynaptic GABA-B away from the neuromuscular junction. This occurs primarily at the spinal cord level to inhibit the transmission of both monosynaptic and polysynaptic reflexes. Postsynaptic effects of baclofen have been demonstrated only at concentrations above the therapeutic range. Acetylcholinesterase is an enzyme that degrades acetylcholine. Pyridostigmine blocks the function of acetylcholinesterase, thus increasing acetylcholine levels. Finally lidocaine blocks the voltage gated sodium channels, unrelated to acetylcholine metabolism. Abbruzzese and Berardelli review the mechanism of action, treatment options, and side effects of botulinum toxin type A. Das and Park treated 6 patients with spasticity due to stroke-related hemiplegia with botulinum toxin type A injection into skeletal muscle. The patients showed subjective and objective improvement without any significant side-effects.
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