takes place (Garraway et al., 2003). Primary sensory neurons (also known as primary afferents) in the spinal cord convey pain information from the primary sensory neuron to the brain. After a spinal cord injury, these neurons become hyperexcitable; namely, they fire more readily than before the injury. To explain hyperexcitability, a recent study with animals revealed that projection neurons possess more sodium channels of a particular type (Nav1.3) (Hains et al., 2003). Strategies to reduce the formation of this sodium channel may reduce hyperexcitability and pain. Furthermore, suppression of the activation of a key enzyme, known as MAP kinase, which aids the transmission of signals from the projection neuron’s membrane to its nucleus (Kawasaki et al., 2004), may prevent the onset of pain.
Spasticity refers to the debilitating muscle spasms and other types of increased muscle tone that occur after a spinal cord injury. Spasticity is similar to pain in that both are highly common after spinal cord injuries and have multiple possible mechanisms that might account for their onset (see Chapter 2). The key difference between them is that spasticity results from the heightened activity of reflex pathways (proprioceptive sensory neurons and motor neurons), whereas pain reflects the heightened activities of pain pathways.
Spasticity affects, to various degrees, the vast majority of people with spinal cord injury (Kaplan et al., 1991). Treatment begins with stretching and other rehabilitation techniques. If it remains uncontrolled, drug interventions are used, and if it is severe, the treatment is surgery and administration of the drug baclofen by implanted pumps (Kirshblum, 1999). Baclofen and tizanidine have inhibitory effects on motor neurons because their actions mimic that of the inhibitory neurotransmitter γ-aminobutyric acid (GABA). No treatment for spasticity is uniformly successful or provides a complete cure, most likely because of spasticity’s multiple underlying causes, but it can be controlled in many individuals (Burchiel and Hsu, 2001). The drug fampridine, a potassium channel blocker, appears to alleviate some degree of spasticity and is being evaluated in clinical trials. One of the issues in the development of drugs used to control spasticity is that they may have the undesirable effect of inhibiting spontaneous activity that might be necessary for axon regrowth (McDonald and Becker, 2003) and may deprive patients of useful muscle contraction.
Thromboembolism is a potentially life-threatening condition frequently encountered in the early weeks after a spinal cord injury. Deep vein throm-