contractures, decubitus ulcers,2 and bone fractures (Nance, 1999). Muscle spasticity frequently occurs after spinal cord injuries, with one study finding 78 percent of individuals experiencing spasticity after they were discharged from the hospital (Maynard et al., 1990).
The precise causes of muscle spasticity are not well understood. Most studies point to the greater excitability of motor neurons, with several possible causes (Burchiel and Hsu, 2001). One is thought to be decreased inhibitory input from the brain to spinal cord motor neurons through direct or indirect (via spinal cord interneuron) connections. For nearly a century, the lower motor neuron has been described as the “final common pathway” to muscles because of the thousands of neurons that converge on it. Some of those neurons are inhibitory, whereas others are excitatory. A single motor neuron can receive a direct or an indirect input from several regions of the brain and from sensory neurons. The array of inputs is critical for the modulation and fine-tuning of motor neuron control of muscles. If inhibitory input to the motor neuron is destroyed or reduced as a result of a spinal cord injury, the balance weighs in favor of heightened excitability and firing of motor neurons.
The spasticity that occurs with a spinal cord injury may also be produced by other mechanisms. One is a by-product of injury-induced sprouting. The new synapses formed by surviving axons (see below) may be too excitatory in nature. They might arise from motor pathways that descend from the brain, from ascending sensory pathways, or from the many synapses between the interneurons that form an intricate local circuitry within the spinal cord. Continual sensory feedback from muscles (such as for the detection of muscle length) is indispensable for the production of graded movements. If stretch reflexes are altered in individuals with spinal cord injuries, the lack of appropriate feedback may lead to spastic muscle contractions.
Spasticity may also be produced by pathological alterations in the electrical properties of the motor neurons themselves, including changes in sodium channel type, number, and distribution (Hiersemenzel et al., 2000) and alterations in neurotransmitter reuptake by glial cells.
Pain is a common and debilitating outcome of spinal cord injuries. Most studies find that 60 to 80 percent of individuals report chronic pain after a spinal cord injury. More precise estimates have been hindered by a