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      Radiation mechanisms of pain control in classical trigeminal neuralgia

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          Abstract

          Classical trigeminal neuralgia is a chronic pain condition that was clinically recognized centuries ago. Nevertheless, the pathological mechanism(s) involved in the development of classical trigeminal neuralgia is still largely based on the theory of peripheral versus central nervous system origin. Limitations of both hypotheses are discussed. Evidence of radiation effects in the electrical conduction of peripheral nerves is reviewed. Results of experimental studies using modern and current radiosurgery techniques and doses are also brought to discussion in an attempt to elucidate the radiation mechanisms involved in the conduction block of excessive sensory information triggering pain attacks. Clinical features and prognostic factors associated with pain control, recurrence, and facial numbness in patients submitted to surgical procedures for classical trigeminal neuralgia are discussed in the context of the features related to the pathogenesis of this condition. Studies focusing on the electrophysiology properties of partially demyelinated trigeminal nerves submitted to radiosurgery are vital to truly advance our current knowledge in the field.

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          Most cited references62

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          The International Classification of Headache Disorders: 2nd edition.

          (2004)
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            Trigeminal neuralgia: pathology and pathogenesis.

            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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              Arterial compression of the trigeminal nerve at the pons in patients with trigeminal neuralgia.

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                Author and article information

                Journal
                Surg Neurol Int
                Surg Neurol Int
                SNI
                Surgical Neurology International
                Medknow Publications & Media Pvt Ltd (India )
                2229-5097
                2152-7806
                2012
                14 January 2012
                : 3
                : Suppl 1
                : S17-S25
                Affiliations
                [1]Department of Neurosurgery, University of California at Los Angeles, Los Angeles, California, USA
                Author notes
                [* ]Corresponding author
                Article
                SNI-3-17
                10.4103/2152-7806.91606
                3400477
                22826806
                00b39d08-0248-400d-9176-98470a3940b9
                Copyright: © 2012 Gorgulho A.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

                History
                : 21 December 2011
                : 21 December 2011
                Categories
                Surgical Neurology International: Stereotactic

                Surgery
                trigeminal neuralgia,pain control,pathogenesis,radiosurgery,demyelination
                Surgery
                trigeminal neuralgia, pain control, pathogenesis, radiosurgery, demyelination

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