Iontophoretically applied microtubule inhibitors induce transganglionic degenerative atrophy of primary central nociceptive terminals and abolish chronic autochtonous pain.
Transcutaneous iontophoresis of microtubule inhibitors (Vinblastin, Vincristin, Formyl-Leurosin) in rats induces depletion of fluoride-resistant acid phosphatase (FRAP) and transganglionic degenerative atrophy (trggl. deg. atr.) of the central terminals of primary nociceptive neurons, probably via blockade of axoplasmic transport in the peripheral sensory nerves. Radiochemical experiments prove that about 0.2% of the microtubule inhibitors applied iontophoretically at the skin reach the level of nociceptive axon terminals. 40 out of 48 patients suffering from chronic intractable pain of diverse etiology (postherpetic, paresthetic, ischaemic and trigeminal neuralgia, alcoholic and diabetic polyneuropathy, meralgia, brachialgia, discopathia, arthropathia and terminal pain) were successfully treated with Vinblastin or Vincristin iontophoresis. Iontophoretically applied microtubule inhibitors do not affect the blood cell count, have no side-effects and do not impair the skin at the site of application.
D000135:Acid Phosphatase / Q000378:metabolism; D000818:Animals; D001284:Atrophy; D001370:Axonal Transport / Q000187:drug effects; D006801:Humans; D007478:Iontophoresis; D008870:Microtubules / Q000187:drug effects*; D009115:Muridae; D009410:Nerve Degeneration / Q000187:drug effects*; D009619:Nociceptors / Q000187:drug effects*; D013376:Substantia Gelatinosa / Q000187:drug effects; D014747:Vinblastine / Q000494:pharmacology*; D014748:Vinca Alkaloids / Q000494:pharmacology*; D014750:Vincristine / Q000494:pharmacology*; D014855:Wallerian Degeneration / Q000187:drug effects*
D014748:Vinca Alkaloids; C016463:formyl-leurosine; D014750:Vincristine; D014747:Vinblastine; D000135:Acid Phosphatase