Brain, Vol. 124, No. 12, 2347-2360,
December 2001
© 2001 Oxford University Press
Review article |
Trigeminal neuralgia
Pathology and pathogenesis
1 Departments of Neuropathology and 2 Neurosurgery, Institute of Clinical Neurosciences, Frenchay Hospital, Bristol BS16 1LE, UK
Correspondence to:
Professor S. Love, Department of Neuropathology, Institute of Clinical Neurosciences, Frenchay Hospital, Bristol BS16 1LE, UK E-mail: seth.love{at}bris.ac.uk
There is now persuasive evidence that trigeminal neuralgia is usually caused by demyelination of trigeminal sensory fibres within either the nerve root or, less commonly, the brainstem. In most cases, the trigeminal nerve root demyelination involves the proximal, CNS part of the root and results from compression by an overlying artery or vein. Other causes of trigeminal neuralgia in which demyelination is involved or implicated include multiple sclerosis and, probably, compressive space-occupying masses in the posterior fossa. Examination of trigeminal nerve roots from patients with compression of the nerve root by an overlying blood vessel has revealed focal demyelination in the region of compression, with close apposition of demyelinated axons and an absence of intervening glial processes. Similar foci of nerve root demyelination and juxtaposition of axons have been demonstrated in multiple sclerosis patients with trigeminal neuralgia. Experimental studies indicate that this anatomical arrangement favours the ectopic generation of spontaneous nerve impulses and their ephaptic conduction to adjacent fibres, and that spontaneous nerve activity is likely to be increased by the deformity associated with pulsatile vascular indentation. Decompression of the nerve root produces rapid relief of symptoms in most patients with vessel-associated trigeminal neuralgia, probably because the resulting separation of demyelinated axons and their release from focal distortion reduce the spontaneous generation of impulses and prevent their ephaptic spread. The role of remyelination in initial symptomatic recovery after decompression is unclear. However, remyelination may help to ensure that relief of symptoms is sustained after decompression of the nerve root and may also be responsible for the spontaneous remission of the neuralgia in some patients. In addition to causing symptomatic relief, vascular decompression leads to rapid recovery of nerve conduction across the indented root, a phenomenon that, we suggest, is likely to reflect the reversal of compression-induced conduction block in larger myelinated fibres outside the region of demyelination. Trigeminal neuralgia can occur in association with a range of other syndromes involving vascular compression and hyperactivity of cranial nerves. Clinical observations and electrophysiological studies support the concept that demyelination and ephaptic spread of excitation underlie most, if not all, of these conditions.
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