TY - JOUR
T1 - Mechanism of trigeminal neuralgia
T2 - An ultrastructural analysis of trigeminal root specimens obtained during microvascular decompression surgery
AU - Devor, Marshall
AU - Govrin-Lippmann, Ruth
AU - Rappaport, Z. Harry
PY - 2002
Y1 - 2002
N2 - Object. Recent progress in the understanding of abnormal electrical behavior in injured sensory neurons motivated an examination, at the ultrastructural level, of trigeminal roots of patients with trigeminal neuralgia (TN). Methods. In 12 patients biopsy specimens of trigeminal root were obtained during surgery for microvascular decompression. Pathological changes in tissue included axonopathy and axonal loss, demyelination, a range of less severe myelin abnormalities (dysmyelination), residual myelin debris, and the presence of excess collagen, including condensed collagen masses in two cases. Within zones of demyelination, groups of axons were often closely apposed without an intervening glial process. Pathological characteristics of nerve fibers were clearly graded with the degrees of root compression noted at operation. Pain also occurred, however, in some patients who did not appear to have a severe compressive injury. Conclusions. Findings were consistent with the ignition hypothesis of TN. This model can be used to explain the major positive and negative symptoms of TN by axonopathy-induced changes in the electrical excitability of afferent axons in the trigeminal root and of neuronal somata in the trigeminal ganglion. The key pathophysiological changes include ectopic impulse discharge, spontaneous and triggered after discharge, and crossexcitation among neighboring afferents.
AB - Object. Recent progress in the understanding of abnormal electrical behavior in injured sensory neurons motivated an examination, at the ultrastructural level, of trigeminal roots of patients with trigeminal neuralgia (TN). Methods. In 12 patients biopsy specimens of trigeminal root were obtained during surgery for microvascular decompression. Pathological changes in tissue included axonopathy and axonal loss, demyelination, a range of less severe myelin abnormalities (dysmyelination), residual myelin debris, and the presence of excess collagen, including condensed collagen masses in two cases. Within zones of demyelination, groups of axons were often closely apposed without an intervening glial process. Pathological characteristics of nerve fibers were clearly graded with the degrees of root compression noted at operation. Pain also occurred, however, in some patients who did not appear to have a severe compressive injury. Conclusions. Findings were consistent with the ignition hypothesis of TN. This model can be used to explain the major positive and negative symptoms of TN by axonopathy-induced changes in the electrical excitability of afferent axons in the trigeminal root and of neuronal somata in the trigeminal ganglion. The key pathophysiological changes include ectopic impulse discharge, spontaneous and triggered after discharge, and crossexcitation among neighboring afferents.
KW - Cranial nerve neuralgia
KW - Microvascular decompression
KW - Nerve pathophysiology
KW - Tic douloureux
KW - Trigeminal neuralgia
UR - http://www.scopus.com/inward/record.url?scp=0036124972&partnerID=8YFLogxK
U2 - 10.3171/jns.2002.96.3.0532
DO - 10.3171/jns.2002.96.3.0532
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AN - SCOPUS:0036124972
SN - 0022-3085
VL - 96
SP - 532
EP - 543
JO - Journal of Neurosurgery
JF - Journal of Neurosurgery
IS - 3
ER -