Iontophoretically applied microtubule inhibitors induce transganglionic degenerative atrophy of primary central nociceptive terminals and abolish chronic autochtonous pain

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Abstract

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.

Original languageEnglish
Pages (from-to)401-412
Number of pages12
JournalActa Neurologica Scandinavica
Volume66
Issue number4
DOIs
Publication statusPublished - Oct 1982

Keywords

  • Vinca alkaloids
  • axoplasmic transport
  • iontophoresis
  • nociception
  • pain
  • substantia gelatinosa
  • transganglionic degenerative atrophy

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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