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**23** 

*1,2USA 3Netherlands* 

**Deconstructing Central Pain with** 

*1Department of Neurosurgery, Johns Hopkins Hospital, Baltimore* 

*3Division of Perioperative Care and Emergency Medicine, Rudolf Magus Institute of Neuroscience, Pain Clinic,* 

*Program in Neuroscience, Baltimore* 

*University Medical Center Utrecht, Utrecht,* 

**Psychophysical and Neuroimaging Studies** 

J.J. Cheng1, D.S. Veldhuijzen3, J.D. Greenspan2 and F.A. Lenz1

*2Department of Biomedical Sciences, University of Maryland Dental School,* 

The IASP has defined central pain as initiated or caused by a primary lesion or dysfunction of the central nervous system (CNS)" (Merskey, 1986). A more recent and specific definition describes central pain as "pain arising as a direct consequence of a lesion or disease affecting the central somatosensory system" (Treede et al., 2008). This definition recognizes that a disturbance of the central somatosensory system is the essential feature of central pain. A disturbance of this system applies to all central pain conditions, although they exhibit great variability across different etiologies. This chapter includes structural and functional imaging results, as well as the results of psychophysical studies, as they complement the imaging results. There is some overlap between the content of this chapter and our previous reviews of this topic (Veldhuijzen et al., 2007;Greenspan et al., 2008;Veldhuijzen et al., 2011).

Patients with central pain (CP) inevitably show stimulus-evoked sensory abnormalities which include negative symptoms such as hypoesthesia and hypoalgesia, as well as positive symptoms such as hyperalgesia Hyperalgesia is increased pain evoked by a stimulus which can be painful, such as deep pressure over a muscle which has been injured or bruised. Another positive symptom is allodynia which is pain evoked by a stimulus which is not

When studied by quantitative sensory testing (QST, Table 1), patients with central poststroke pain (CPSP) exhibit hypoesthesia for cold in 85-91% of patients, for warmth in 85- 100%. Decreased sensation for pain (hypoalgesia) is found for cold pain in roughly 45% of patients, and for heat pain in 7-91% (Boivie et al., 1989;Leijon et al., 1989;Andersen et al., 1995;Vestergaard et al., 1995;Greenspan et al., 2004). As shown in Table 1, CPSP patients show decreased tactile sensibility in 27-52% of cases. These results demonstrate that decreased sensation or negative sensory signs vary widely across the CPSP patient population. Overall, these patients do not show sensory deficits for all types of thermal and

**2. Prevalence of sensory abnormalities in central pain?** 

normally painful, such as pain evoked by light touch following a sunburn.

**1. Introduction** 

