Abstract

Although the spasticity that follows spinal cord injury in humans is common, it has been difficult to study experimentally because spinal cord injury in animals produces only comparatively mild spasticity. Spasticity occurs in humans without complete spinal cord transections, whereas in animals such as rats and cats, incomplete spinal cord injury only leads to mild hyperreflexia. However, these cats have inconvenient and traumatic functional impairments, requiring twice-daily bladder and bowel expression. Bladder infection, pressure sores, and impaired locomotion can lead to significant morbidity and mortality. Thus, the complete spinal cat is an impractical model, and many groups have used hemisections, partial transections, and contusions to study spinal cord injury, even though spasticity is not always prominent. By using sacral spinal cord lesions in rats, a model of spasticity that is convenient to study in the awake state and requires minimal care is developed. Furthermore, the small diameter of the spinal cord at this level allows for electrophysiological study of adult spastic motoneurons and reflexes in vitro. This preparation has been central to the understanding of how plateau potentials lead to the intense muscle spasms characteristic of spinal spasticity. Ongoing experiments are elucidating the underlying currents associated with plateaus and the neuromodulators that are involved in the development of these plateaus in the months following the injury.

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