Functional imaging studies of human subjects have identified a diverse assortment of brain areas that are engaged in the processing of pain. Although many of these brain areas are highly interconnected and are engaged in multiple processing roles, each area has been typically considered in isolation. Accordingly, little attention has been given to the global functional organization of brain mechanisms mediating pain processing.

Multiple regression analysis (left panel) of positron emission tomography data revealed statistically reliable relationships between perceived pain intensity and activation of a functionally diverse group of brain regions, including those important in sensation, motor control, affect, and attention. Pain intensity-related activation occurred bilaterally in the cerebellum (CB), putamen, thalamus (Thal), insula, anterior cingulate cortex (ACC), and secondary somatosensory cortex (SII), contralaterally in the primary somatosensory cortex (SI) and supplementary motor area (SMA), and ipsilaterally in the frontal operculum (PMv).

The relationship between brain activation and increasing stimulus temperatures can be seen in the right panel. Progressive increases in stimulus temperatures elicit progressive increases in activation. In some brain areas such as SII, the activation is predominately contralateral to the stimulated (right) arm during relatively low intensity stimulation, but becomes bilateral during more intense stimulation.

These results confirm the existence of a highly distributed, bilateral supra-spinal mechanism engaged in the processing of pain intensity. The conservation of pain intensity information across multiple, functionally distinct brain areas contrasts sharply with traditional views that sensory-discriminative processing of pain is confined within the somatosensory cortex, and can account for the preservation of conscious awareness of pain intensity after extensive cerebral cortical lesions.

For further reading see Coghill et al. J.Neurophysiol. 82:1934-43, 1999. Download this paper from here or from the Journal of Neurophysiology.

We welcome any questions. For additional information, reprints, or permission to publish any of these images please contact
Dr. Robert Coghill
Department of Neurobiology and Anatomy
Wake Forest University School of Medicine
Winston-Salem, NC, 27157-1010
rcoghill@wfubmc, phone: (336) 716-4284, fax: (336) 716-4534