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The development of debilitating central neuropathic pain (CNP), defined as pain caused by a lesion or dysfunction of the central nervous system (CNS),1,2 can occur after any lesion of the CNS, including demyelinating, vascular, infectious, inflammatory, and traumatic events. In contrast to CNP after stroke (including thalamic stroke resulting in Dejerine-Roussy syndrome), multiple sclerosis, and tumors,3,4 the prevalence of CNP after spinal cord injury (SCI) is high; most cite a prevalence ranging from 50% to 66%.5-8 With the number of individuals in the United States who have SCIs estimated to be as high as 1,275,000 and estimated lifetime costs from SCI ranging from $681,843 to more than $3 million if the injury is sustained at age 25 years,9 CNP after SCI has become a growing public health concern.

Lesions of the spinal cord, particularly those caused by trauma, are also associated with lesions of adjacent nerve roots, including the cauda equina; therefore, CNP is typically associated with peripheral neuropathic pain (PNP). CNP may also be associated with visceral pain through sympathetic and vagal nerve input and pain secondary to musculoskeletal overuse, muscle spasms, or mechanical instability of the spine.10 The primary insult to the somatosensory pathway may be limited, with only mild sensory loss on clinical examination, or extensive, with complete anesthesia on clinical examination. Notably, refractory deafferentation pain may be associated with only mild sensory loss on examination.

Traumatic SCIs account for 65% of CNP, and other causes include iatrogenic (12%), inflammatory (9%), neoplastic (6%), skeletal (2%), and vascular (2%).11,12 At the time of injury, typical symptoms of CNP are often not present but may appear during the rehabilitation phase. The distribution of these lesions is 42% in the cervical spine, 21% in T1 to T9, and 37% in T10 to L2.12,13


Although several different heterogeneous pain syndromes may develop after SCI, CNP is potentially the most problematic. CNP is characterized as spontaneous pain (e.g., allodynia and hyperalgesia with temporal and spatial summation) in a distribution from which spinal and supraspinal mechanisms may be inferred. Moreover, negative or positive sensory signs are present at or below the level of injury or in the distribution of the area of pain. Therefore, in 2000, the International Association for the Study of Pain proposed a classification based on the distribution of pain relative to the level of injury: (1) at-level pain, distributed segmentally at the border of normal and interrupted sensory innervation, and (2) below-level pain, distributed diffusely below the level of injury.13 At-level pain typically presents within two to three segments above and below the level of injury13 and often involves a lesion to the spinothalamic tract or changes in the spinal cord dorsal horn, producing hyperexcitability in the pain pathways. ...

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