Those at painonline do NOT view antiepileptics as the answer to central pain. However, since most of us take them, it is good to consider which one works the best. A new one may help, especially in females.
Dr. Weisenfeld-Hallin is perhaps one of the wisest and most reliable researchers in central pain. Her team at Karolinska has led the field in many ways. They developed the first animal model of central pain with erythrocin B followed by lasering, and have shown consistent brilliance in understanding mechanisms of CP. Of late, X.J. Xu has also done remarkable work on the problem.
And so, we reference here a report from Karolinska on a new antiepileptic for neuropathic pain, reported by Hao JX, Stohr T, Selve N, Wiesenfeld-Hallin Z, Xu XJ. Eur J Pharmacol. 2006 Sep 27; “Lacosamide, a new anti-epileptic, alleviates neuropathic pain-like behaviors in rat models of spinal cord or trigeminal nerve injury”.
Lacosamide is a new drug, even for epilepsy. It is manufactured by Schwarz Pharma and is in Stage III trials for use in diabetic neuropathy (DN). DN occurs in large numbers and creates a strong incentive for pharmaceutical firms to study neuropathic pain. DN is a condition of the peripheral nerves and lacosamide at doses of 400 mg to 600mg/day seemed quite beneficial, so it was natural for European pain scientists to wonder about pain of central origin. Side effects of lacosamide include dizziness, nausea, headache, fatigue.
The researchers at Karolinska created a model of peripheral nerve injury (ischemia to the infraorbital nerve–easly accessed below the eye). They found that lacosamide was helpful when testing the rats for mechanical hypersensitivity. Oddly,the effect was “markedly stronger in female rats than in male rats”. Then a model of central pain was created in the usual fashion (central pain model). At doses of 10-20 mg/kg there was alleviation of BOTH mechanical (stroking with a brush) and “cold-allodynia like behavior without any motor impairment or marked sedation.”
When the lacosamide was continued for seven days, it markedly relieved the allodynia-like state in FEMALE rats. This is not just another antiepileptic study since other reports have used the word “benefit” rather than “total relief”.
Following treatment cessation the allodynia symptoms reappeared rapidly, but the mechanical allodynia (pain with brush stroke) did not reappear for eleven days.
This is a well designed study, examined forward and backwards in the way scientists SHOULD do it, and so it deserves our attention.
Hopefully, females with central pain may soon be able to benefit from this drug.
Why females? The authors do not venture an opinion, but we are more free to speculate. For some time there has been evidence that pain is created when signals do not match up in the brain. Pat Wall was the first to suggest a template, wherein input was compared by the brain to some pattern of NONPAIN, and if there were a clash, then the brain knew that pain was occurring. Since females have much better crosstalk between the two cerebral hemispheres, having a much larger corpus collosum (connection between the two halves of the brain), it would seem reasonable they would respond to quieting of brain activity, which is the heart of all antiepileptics.
