Ultrastructure and immunohistochemistry of the trigeminal peripheral myelinated axons in patients with neuralgia.
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.
Marinković
Slobodan
S
Institute of Anatomy, School of Medicine, Belgrade, Serbia.
Gibo
Hirohiko
H
Todorović
Vera
V
Antić
Branislav
B
Kovacević
Dragoslava
D
Milisavljević
Milan
M
Cetković
Mila
M
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
D005904:Glial Fibrillary Acidic Protein