current research  

The nature of pain continues to occupy the philosophical and scientific domains; it is a wholly personal yet collective experience, and one of the most elemental clinical issues. The primary function of pain is simple: to alert an organism to actual or potential damage to the body through an unpleasant sensory (and possibly emotional) experience.

The sensation of pain can be altered after spinal cord injury (SCI). Up to eighty percent of persons who have sustained SCI develop clinically significant pain, and describe it as burning, aching, shooting, and/or stabbing. In addition, many persons with SCI suffer from phantom phenomena in which they "feel" the body below the lesion, and experience pain in areas of complete sensory loss. An individual with a mid-thoracic SCI may have no conscious appreciation of sensory input to the legs and may be unable to discriminate warm or cold, or sharp or pinching stimuli, yet may "feel" the legs in a state of spasm or in a twisted position, even when they are not, and may feel pain in the legs in the absence of any noxious stimulation.

Abnormal pain that develops following SCI is caused not by actual or potential damage to the body, but by a dysfunction of the nervous system. Like Proteus, the shape-changing old man of the sea who tended the seals of Poseidon in Greek mythology, post-SCI pain has the ability to change into a multitude of forms. These new forms include allodynia (the ability of a normally non-painful stimulus to evoke the sensation of pain) and hyperalgesia (a lowering of pain detection thresholds).

Work in my laboratory has focused on understanding molecular mechanisms underlying the generation and maintenance of chronic pain after SCI. We have found fundamental changes in electrophysiological properties of sensory neurons within the spinal cord lumbar dorsal horn. Neurons inappropriately produce action potential discharges in response to innocuous stimulation of the paw and fire at abnormally high rates in response to noxious stimulation, while possessing the ability to produce persistent and ramp sodium currents that amplify small depolarizing inputs. Similarly, we have documented the emergence of neuronal hyperexcitability and abnormal burst firing in the ventral posterolateral (VPL) nucleus of the thalamus, which processes sensory information received from the spinal cord and relays it to the brain for interpretation and conscious perception. Equivalent changes have been observed in spinal neurons of SCI patients with chronic pain.