Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review

What Can Neuroimaging Tell Us about Central Pain?

In: Translational Pain Research: From Mouse to Man. Boca Raton (FL): CRC Press/Taylor & Francis; 2010. Chapter 14.
Affiliations
Free Books & Documents
Review

What Can Neuroimaging Tell Us about Central Pain?

D.S. Veldhuijzen et al.
Free Books & Documents

Excerpt

Central pain (CP) is defined by the International Association for the Study of Pain as “pain initiated or caused by a primary lesion or dysfunction of the CNS [central nervous system]” (Merskey and Bogduk 1994). A more recently proposed definition is “pain arising as a direct consequence of a lesion or disease affecting the central somatosensory system” (Treede et al. 2008). This newer refinement recognizes that an essential feature associated with CP is disturbance of part of the central somatosensory system. This may be the only universal feature that applies to CP conditions, which exhibit varied qualities across patients.

Similar to CP are two conditions that share almost all of the same features of CP, but the pathological sensation is described as something other than pain. Central dysesthesia involves the expression of unpleasant sensations (both spontaneous and evoked) that are described in terms other than pain. One may question whether this is simply a matter of semantics. However, experimental pain testing of such a patient did not reveal any abnormal responses to noxious thermal stimuli applied to unaffected body regions (Kim et al. 2007). Central neurogenic pruritis can also arise from CNS lesions, in which an itch sensation substitutes for the pathological pain sensation. Due to the scarcity of reports on these latter two phenomena, this chapter will focus on central pain. The interested reader on the topic of central pain is referred to two recent books, Canavero and Bonicalzi (2007) and Henry, Panju, and Yashpal (2007).

Prior to the 1990s, our knowledge of CP was derived from examinations of lesion type and location that produced CP and interpretation of the sensory abnormalities of CP patients. With the advent of functional neuroimaging, we have new tools to investigate CP. This chapter will focus on studies that have used functional neuroimaging to address mechanistic questions regarding central pain.

PubMed Disclaimer

References

    1. Andersen G., Vestergaard K., Ingeman-Nielsen M., Jensen. T. S. Incidence of central post-stroke pain. Pain. 1995;61:187–193. - PubMed
    1. Apkarian A.V., Bushnell M.C., Treede R.D., Zubieta J.K. Human brain mechanisms of pain perception and regulation in health and disease. Eur. J. Pain. 2005;9(4):463–484. - PubMed
    1. Attal N., Gaude V., Brasseur L., Dupuy M., Guirimand R., Parker R., Bouhassira D. Intravenous lidocaine in central pain—A double-blind, placebo-controlled, psychophysical study. Neurology. 2000;54(3):564–574. - PubMed
    1. Baron R., Baron Y., Disbrow R., Roberts T.P.L. Brain processing of capsaicin-induced secondary hyperalgesia—A functional MRI study. Neurology. 1999;53(3):548–557. - PubMed
    1. Boivie J., Leijon G., Johansson I. Central post-stroke pain—A study of the mechanisms through analyses of the sensory abnormalities. Pain. 1989;37:173–185. - PubMed

LinkOut - more resources