title: Axon and ganglion cell injury in rabbits after percutaneous trigeminal balloon compression.
abstract: New Zealand white rabbits were used to determine whether the changes in the Vth cranial nerve sensory root after compression were associated with the loss of a specific subclass of Vth cranial nerve ganglion cells, the disappearance of a distinct subset of primary afferent terminals in Vth cranial nerve nucleus caudalis, and/or injury to a specific axonal fiber type. There was no significant difference in the size of surviving ganglion cells after Vth cranial nerve compression, as measured 2 to 3 months after injury (P > 0.5, n = 4). Densitometric analysis of the nerves of rabbits that survived > 2 months after compression showed no significant difference in the immunoreactivity of substance P and calcitonin gene-reactive protein between compressed and control sides (P > 0.1, n = 4). Fink-Heimer staining of the Vth cranial nerve subnucleus caudalis revealed that transganglionic degeneration was most dense in the deeper layers, which are the sites of termination of large myelinated fibers. Ultrastructural evaluation of the type of myelinated axons injured by Vth cranial nerve compression in rabbits killed 7, 14, 37, and 270 days after injury was studied, and morphometric analysis was performed. The frequency distribution of axon diameters was significantly different for injured and control areas. The injured areas had higher ratios of small (< 3-microns diameter) to large-diameter axons compared to control distribution. These data indicate that balloon compression results in loss of fibers from the Vth cranial nerve sensory root and extensive transganglionic degeneration in the Vth cranial nerve brain stem complex. Cell size measurements and immunocytochemical data suggest that there is no specific loss of small ganglion cells or fine-caliber primary afferents. These experiments suggest that balloon compression relieves trigeminal pain by injuring the myelinated axons involved in the sensory trigger to the pain.
authors.affiliation: Department of Neurological Surgery, Medical College of Ohio, Toledo, USA.
authors.forename: J A
authors.initials: JA
authors.lastname: Brown
authors.forename: B
authors.initials: B
authors.lastname: Hoeflinger
authors.forename: P B
authors.initials: PB
authors.lastname: Long
authors.forename: W T
authors.initials: WT
authors.lastname: Gunning
authors.forename: R
authors.initials: R
authors.lastname: Rhoades
authors.forename: C A
authors.initials: CA
authors.lastname: Bennett-Clarke
authors.forename: N L
authors.initials: NL
authors.lastname: Chiaia
authors.forename: M T
authors.initials: MT
authors.lastname: Weaver
mesh_terms: D000344:Afferent Pathways / Q000473:pathology; D000818:Animals; D001369:Axons / Q000473:pathology*; D002404:Catheterization / Q000295:instrumentation*; D002406:Catheterization, Peripheral / Q000295:instrumentation*; D005260:Female; D007124:Immunoenzyme Techniques; D008297:Male; D008854:Microscopy, Electron; D009410:Nerve Degeneration / Q000502:physiology*; D009413:Nerve Fibers, Myelinated / Q000473:pathology*; D009416:Nerve Regeneration / Q000502:physiology; D018377:Neurotransmitter Agents / Q000032:analysis; D011312:Pressure; D011817:Rabbits; D012668:Trigeminal Ganglion / Q000473:pathology*; D014276:Trigeminal Nerve / Q000473:pathology; D014277:Trigeminal Neuralgia / Q000473:pathology / Q000628:therapy*; D014278:Trigeminal Nuclei / Q000473:pathology*
chemical_list: D018377:Neurotransmitter Agents