S Gao1, Y Wang, Z Wang. 1. Stomatological Hospital, Tianjin Medical University, Tianjin, 300070, P. R. China.
Abstract
OBJECTIVE: The measurement of pain threshold (PT) and the assessment of trigeminal somatosensory evoked potentials (TSEPs) were performed. These experiments indicated the pathological conditions of nerve afferent and efferent pathways in patients with burning mouth syndrome (BMS). This study also explored the probable pathophysiological mechanisms in BMS. MATERIALS AND METHODS: The dorsum linguae of 38 samples in 19 subjects (22 BMS with pain, 10 BMS with numbness, and 6 controls) were stimulated by electroneuromyography. PT was measured as the lowest stimulation intensity the subjects could detect. N3, P4 latency, and spike potential latency of TSEP were recorded by stimulating the lingual nerve. RESULTS: Pain thresholds were significantly lower, N3, P4 latencies were significantly shorter, and the spike potential appeared earlier in the BMS with pain group (P < 0.01). The opposite tendency of these values presented in the BMS with numbness group (P > 0.05). CONCLUSIONS: The results indicated that the nerve sensitivity was elevated in the BMS with pain group, and that these patients were easily affected by etiological factors. In the BMS with numbness group, partial or complete nerve blockage may have been indicated. This study suggested that selfreports of BMS pain appeared to be of value, and that there were pathological conditions in nerve transmission. It supported the theory that peripheral or central nervous system involvement might play an important role in BMS. It was possible to show the pathogenesis of BMS. All of these objectively explain the clinical understanding of BMS, and may be of assistance in the treatment of BMS.
OBJECTIVE: The measurement of pain threshold (PT) and the assessment of trigeminal somatosensory evoked potentials (TSEPs) were performed. These experiments indicated the pathological conditions of nerve afferent and efferent pathways in patients with burning mouth syndrome (BMS). This study also explored the probable pathophysiological mechanisms in BMS. MATERIALS AND METHODS: The dorsum linguae of 38 samples in 19 subjects (22 BMS with pain, 10 BMS with numbness, and 6 controls) were stimulated by electroneuromyography. PT was measured as the lowest stimulation intensity the subjects could detect. N3, P4 latency, and spike potential latency of TSEP were recorded by stimulating the lingual nerve. RESULTS:Pain thresholds were significantly lower, N3, P4 latencies were significantly shorter, and the spike potential appeared earlier in the BMS with pain group (P < 0.01). The opposite tendency of these values presented in the BMS with numbness group (P > 0.05). CONCLUSIONS: The results indicated that the nerve sensitivity was elevated in the BMS with pain group, and that these patients were easily affected by etiological factors. In the BMS with numbness group, partial or complete nerve blockage may have been indicated. This study suggested that selfreports of BMS pain appeared to be of value, and that there were pathological conditions in nerve transmission. It supported the theory that peripheral or central nervous system involvement might play an important role in BMS. It was possible to show the pathogenesis of BMS. All of these objectively explain the clinical understanding of BMS, and may be of assistance in the treatment of BMS.