S65 Neurophysiological data favoring a central mechanism of trigeminal neuralgia. Issue 9 (September 2017)

• Record Type: Journal Article
• Authors: Obermann, Mark
• Is Part Of: Clinical neurophysiology. Volume 128:Issue 9(2017:Sep.)
• Page Start: e199
• Page End: e200
• Publication Date: 2017-09
• Subjects: Trigeminal neuralgia -- Neurophysiology -- Central mechanism; Neurophysiology -- Periodicals; Electroencephalography -- Periodicals; Electromyography -- Periodicals; Neurology -- Periodicals; 612.8
• DOI: 10.1016/j.clinph.2017.07.076
• Languages: English
• ISSNs: 1388-2457

Abstract

Abstract : Current opinion is that TN is caused by a proximal compression of the trigeminal nerve root by a ectasic blood vessel leading to mechanical twist of nerve fibers and secondary demyelination. These changes lower the excitability threshold of affected fibers and promote inappropriate ephaptic propagation towards adjacent fibers. Not all patients have a nerve vessel conflict and 25% of people without any clinical signs of TN did show a nerve vessel contact. Possible involvement of central factors, suggesting a central facilitation and resulting hyperexcitability of the trigeminal system sustained by peripheral as well as central mechanisms were discussed. Sensitisation of second order wide dynamic range (WDR) neurons was discussed as additional pathophysiological mechanism. Since these WDR neurons receive convergent information from tactile (A-beta) and nociceptive (A-delta and C) fibers, their sensitisation could facilitate nociceptive input while promoting the perception of pain in response to tactile stimuli (i.e., allodynia). Central facilitation was demonstrated in TN patients with additional constant dull background pain besides their typical TN attacks using pain-related evoked potentials (PREP) and nociceptive blink reflex (nBR) [4]. Borsook et al. (2007) reported increased fMRI activation of a single TN patient in the primary somatosensory cortex, insula, anterior cingulate, and thalamus to further support cortical involvement [28]. Structural changes of the cortical grey matter was also reported to further support a central origin of the disease.