title: Ultrastructure and immunohistochemistry of the trigeminal peripheral myelinated axons in patients with neuralgia.
abstract: OBJECTIVE
  Detailed ultrastructural and immunohistochemical examination of the trigeminal axons surrounded by the peripheral type of the myelin could add new information about the extent of the trigeminal nerve lesion in neuralgia.
  
  
  METHODS
  The examination comprised, firstly, the 10 trigeminal nerve roots (TNRs) in which the neurovascular contact was found in 20% of the cases, and the 2 additional control TNRs. Secondly, the biopsy specimens were taken from 6 patients with trigeminal neuralgia and 2 patients with trigeminal neuropathy following a partial TNR rhizotomy. The specimens were examined under the electron microscope (EM) and/or using the immunohistochemical (IHC) methods.
  
  
  RESULTS
  In addition to the central zone of demyelination, the EM examination of the TNR also revealed alterations of the peripheral myelin, i.e. deformation, thickening, demyelination and remyelination, as well as changes of the peripheral axons, that is, atrophy or hypertrophy, neurofilaments increase, loss of the myelin and sprouting occasionally. Some Schwann cells were also damaged. The IHC examination usually showed a moderate immune reaction against neuron-specific enolase (NSE) and protein gene product 9.5 (PGP9.5), but sporadically weaker reaction against the S-100 protein, synaptophysin (SY), neurofilament protein (NFP) and glial fibrillary acidic protein (GFAP). The substance P (SP) and calcitonin gene-related peptide (CGRP) immunoreactivity was weak at some sites, but strong at some other places.
  
  
  CONCLUSIONS
  The pathological changes affect not only the central nerve fibers of the TNR, but also some of the peripheral axons, their myelin sheath and Schwann cells. These are signs of the retrograde ultrastructural and biochemical alterations, which could participate in the pathophysiological mechanism underlying the trigeminal neuralgia.
authors.affiliation: Institute of Anatomy, School of Medicine, Belgrade, Serbia.
authors.forename: Slobodan
authors.initials: S
authors.lastname: Marinković
authors.forename: Hirohiko
authors.initials: H
authors.lastname: Gibo
authors.forename: Vera
authors.initials: V
authors.lastname: Todorović
authors.forename: Branislav
authors.initials: B
authors.lastname: Antić
authors.forename: Dragoslava
authors.initials: D
authors.lastname: Kovacević
authors.forename: Milan
authors.initials: M
authors.lastname: Milisavljević
authors.forename: Mila
authors.initials: M
authors.lastname: Cetković
mesh_terms: D000328:Adult; D000368:Aged; D001369:Axons / Q000473:pathology* / Q000648:ultrastructure*; D019299:Decompression, Surgical; D003711:Demyelinating Diseases / Q000473:pathology; D005260:Female; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009046:Motor Neurons / Q000473:pathology / Q000648:ultrastructure; D009408:Nerve Compression Syndromes / Q000473:pathology; D019635:Neurosurgical Procedures; D012039:Regional Blood Flow; D019051:Rhizotomy; D011984:Sensory Receptor Cells / Q000473:pathology / Q000648:ultrastructure; D014276:Trigeminal Nerve / Q000098:blood supply / Q000473:pathology / Q000601:surgery; D014277:Trigeminal Neuralgia / Q000473:pathology* / Q000601:surgery
chemical_list: D005904:Glial Fibrillary Acidic Protein