In patients with impaired sensory discrimination, pain descriptors, localization, and pain triggers are often vague or poorly defined.
At the 2017 annual meeting of the American Academy of Pain Medicine (AAPM), James C. Watson, MD, a neurologist and professor at the Mayo Clinic in Rochester, Minnesota, discussed the etiology, pathophysiology, and treatment of central neuropathic pain, including how to distinguish this from other pain modalities.1
Differentiating central neuropathic pain from musculoskeletal or peripheral neuropathic pain can be challenging. In patients with impaired sensory discrimination, pain descriptors, localization, and pain triggers are often vague or poorly defined. Descriptors such as shooting, burning, or stabbing pain, for example, can occur with other pain syndromes besides central neuropathic pain, and limited mobility due to paraplegia or quadriparesis can render the clinical examination difficult.
Central sensitization, a sequela of chronic pain in which peripheral stimuli are interpreted as more painful than they are, is not the same as central neuropathic pain, which exclusively describes pain resulting directly from CNS injury. In addition, patients who have “possible central pain should have the tone of the neurologically affected limb assessed to assure that poorly controlled spasticity is not a major contributor to the limb pain,” Dr Watson wrote in a 2016 article on the topic.2
There is wide variation in the temporal onset of central neuropathic pain. The most common type, central poststroke pain, may affect patients immediately following a stroke event, although it more frequently presents weeks, months, or even years later. When pain is a presenting feature of multiple sclerosis (MS), as in 5.5% to 10% of all MS cases, the odds of future chronic and central pain are increased.3
Patients with spinal cord injury experience the longest delay in the development of central pain: within 3 months in nearly half of patients with “at-level pain,” although it may present up to 5 years post-injury and more than 2 years post-injury in patients with “below-level pain,” although it may present within 3 months in some cases.4
“Although intuitive, for pain to be classified as a central pain syndrome, it must occur in the body region clinically affected by the CNS insult,” Dr Watson wrote. The pain may involve only a portion of the affected region rather than the entire region. Spinothalamic tract (STT) dysfunction appears to be essential to the development of central neuropathic pain.
When a central pain syndrome is suspected, the clinician should test for impaired pinprick and temperature sensation as indicators of STT dysfunction in the affected limb. If no impairment is detected, then central pain syndrome is not likely to be the cause of the pain. “However, not all patients with spinothalamic tract sensory loss experience central pain, and there must be a required cofactor to drive its development,” he explained. “Increasing evidence suggests this cofactor to be denervation hypersensitivity of surviving STT axons.”5
In his presentation, Dr Watson covered this pathophysiology in detail, as well as the specific central pain syndromes mentioned above and various multimodal treatment approaches.
- Watson JC. Central neuropathic pain. Presented at: the American Academy of Pain Medicine 33rd Annual Meeting; March 16-19, 2017; Orlando, Florida.
- Watson JC, Sandroni P. Central neuropathic pain syndromes. Mayo Clin Proc.2016;91(3):372-85. doi: 10.1016/j.mayocp.2016.01.017
- Österberg A, Boivie J, Thuomas K-Å. Central pain in multiple sclerosis: prevalence and clinical characteristics. Eur J Pain. 2005;9(5):531-542. doi: 1016/j.ejpain.2004.11.005
- Siddall PJ, McClelland JM, Rutkowski SB, Cousins MJ. A longitudinal study of the prevalence and characteristics of pain in the first 5 years following spinal cord injury. Pain. 2003;103(3):249-257.
- Andersen G, Vestergaard K, Ingeman-Nielsen M, Jensen TS. Incidence of central post-stroke pain. Pain. 1995;61(2):187-193.