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Spasticity is a feature of altered skeletal muscle performance occurring in disorders of the central nervous system (CNS) impacting the upper motor neuron in the form of a lesion. When there is a loss of descending inhibition from the brain to the spinal cord, such that muscles become overactive, this loss of inhibitory control can cause an ongoing level of contraction, with decreased ability for the affected individual to volitionally control the muscle contraction, and increased resistance felt on passive stretch.

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 comes about most often as a result of neonatal asphyxia, while in conditions like multiple sclerosis, spasticity comes 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 clinically is fundamentally different from the latter.

Overall, a defining feature of spasticity is that the increased resistance to passive stretch is velocity-dependent. Lance (1980) describes it this way: “...a motor disorder, characterised by a velocity-dependent increase in tonic stretch reflexes (muscle tone) with exaggerated tendon jerks, resulting from hyper-excitability of the stretch reflex as one component of the upper motor neurone (UMN) syndrome”.[citation needed] Strangely, however, rather than being in the motor nerves as might be assumed to be the case, spasticity actually stems from the sensory nerves.

Spasticity is found in conditions where the brain and/or spinal cord are damaged or fail to develop normally; these include cerebral palsy, multiple sclerosis, spinal cord injury and acquired brain injury including stroke. Muscles affected in this way have many other potential features of altered performance in addition to spasticity, including muscle weakness; decreased movement control; clonus (a series of involuntary rapid muscle contractions which are repeated spastic stretch responses); exaggerated deep tendon reflexes; and decreased endurance.


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