Experimental retrograde adriamycin trigeminal sensory ganglionectomy

Abstract

Direct destruction of the sensory ganglion or its root, by either surgical transection or injection of phenol, has been employed as preferred treatment for a variety of neuralgic pain syndromes. In this report, the suicide axoplasmic transport of adriamycin is described as a novel approach to sensory ganglionectomy. When injected into a branch of the trigeminal nerve in the cat, adriamycin was swiftly transported by way of retrograde axoplasmic flow to the sensory neurons parental to the injected nerve, where adriamycin-specific autofluorescence was observed. Trigeminal sensory evoked potentials became unobtainable 24 to 48 hours after injection of adriamycin in concentrations of 1% to 10%. The sensory neurons underwent subacute degeneration within a week due to the delayed action of adriamycin, and consequently the primary afferents degenerated in a restricted projection field of the brain-stem trigeminal sensory nuclei. These results indicate that retrograde axoplasmic transport of adriamycin is a unique approach to noninvasive sensory ganglionectomy with strict, albeit simple, safe targeting of sensory neurons and little likelihood of regeneration.