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The clinical underpinnings of two of the most common spasticity conditions, spastic diplegia and multiple sclerosis, can be described as follows: in spastic diplegia, the upper motor neuron lesion arises often as a result of neonatal asphyxia, while in conditions like multiple sclerosis, spasticity is thought by some to be as a result of the autoimmune destruction of the myelin sheaths around nerve endings — which in turn can mimic the gamma amino butyric acid deficiencies present in the damaged nerves of spastic diplegics, leading to roughly the same presentation of spasticity, but which clinically is fundamentally different from the latter.