Do changes in brain sodium channels cause central pain?
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An estimated 200,000 Americans have “central pain”—chronic pain associated with lesions of the brain or spinal cord. Central pain often accompanies lesions that include any portion of the spinothalamocortical pain pathways mediating pain and temperature1 and has been refractory to treatment. A single randomized trial suggesting that amitriptyline reduces poststroke pain2 appeared more than a decade ago. Two recent clinical trials in central pain expand the therapeutic options. A placebo-controlled crossover study of lamotrigine in 31 patients with poststroke pain showed a modest but significant reduction in pain,3 and, in this issue of Neurology, Attal et al.4 report that in 10 patients with spinal cord injury and 6 patients with poststroke pain, acute infusion of lidocaine transiently reduced spontaneous pain, pain evoked by light touch, and tingling.
Attal et al. point out that lidocaine’s well-known effect of reducing ectopic discharge mediated by voltage-gated sodium channels in injured peripheral afferents …
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