Yale researchers report the first evidence that phantom pain following spinal cord injury is the result of hypersensitive neurons in the thalamic region of the brain that can be suppressed with specially designed molecular agents. “A majority of people with spinal cord injury and limb amputations experience phantom sensations of excruciating pain at or below the level of their paralysis or loss,” said Bryan Hains, associate research scientist and co-author of the study. Typically, the perception of pain travels through three orders of neurons. The first order neurons carry signals from the periphery to the spinal cord, the second order neurons relay this information from the spinal cord to the thalamus and the third order neurons transmit the information from the thalamus to the primary sensory cortex where the information is processed, resulting in the “feeling” of pain. The study reports that in rats with spinal cord injury, third order neurons within the thalamus spontaneously and abnormally fire signals in the absence of any incoming signals from the first order neurons. It also reports that these rogue neurons contain abnormally high levels of a particular type of sodium channel, called Nav1.3. Sodium channels serve as batteries during the conduction of nerve signals.
