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Molecular basis found for phantom pain
NEW HAVEN, Conn., Sep 20, 2005 (United Press International via COMTEX) -- Yale University researchers in New Haven, Conn., have found the first evidence for a molecular basis for phantom pain.
The researchers report 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.
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 first order neurons.
"This study is the first to show thalamic neurons contain abnormally high levels of Nav1.3, a specific sodium channel, after injury to the spinal cord and that suppressing the activity of Nav1.3 in these neurons can mitigate pain," said senior author Dr. Stephen Waxman, professor of neurology. He said the study represents an important step forward in the understanding and treatment of phantom pain.