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Characterization of different paresthesias following orthognathic surgery of the mandible.
Authors:Kenji Seo  Yutaka Tanaka  Makoto Terumitsu  Genji Someya
Affiliation:Division of Dental Anesthesiology, Department of Tissue Regeneration and Reconstruction, Niigata University Graduate School of Medical and Dental Sciences, Japan. sea@dent.niigata-u.ac.jp
Abstract:PURPOSE: Paresthesia is a well known consequence of peripheral nerve injury. However, the neural mechanisms of the 2 recognized types, spontaneous and elicited, are currently unknown. This study aimed to investigate these 2 paresthesias and the possible mechanisms accompanying orthognathic surgery. PATIENTS AND METHODS: Mechanical-touch thresholds and current perception threshold were measured before and 7 days after surgery in 60 chin sites (mental nerve area) of 30 patients who underwent orthognathic surgery. Similar testing was conducted on healthy volunteers (controls). All sites were classified by the presence or absence of each paresthesia: spontaneous paresthesia or no spontaneous paresthesia, and elicited paresthesia or no elicited paresthesia. Presence or absence analyses were followed-up for 6 weeks after surgery. RESULTS: Gender differences and maxillary surgery did not change the incidence of paresthesia during postoperative week 1 (chi-square test, P > .05). A significantly higher mechanical-touch threshold was observed with spontaneous paresthesia compared with no spontaneous paresthesia (Mann-Whitney U-test; P < .05), but not between no elicited paresthesia and elicited paresthesia (Mann-Whitney U-test; P > .05). A significant increase in postsurgery current perception thresholds values compared with presurgery values was observed at 2,000 Hz in spontaneous paresthesia, and at 2,000 and 5 Hz in elicited paresthesia (paired t test, P < .05). The incidence of spontaneous paresthesia decreased more rapidly than elicited, while the latter tended to increase again during the 6-week postsurgical test period. CONCLUSION: The results suggested that both spontaneous and elicited paresthesias are associated with damage and dysfunction in myelinated primary afferent fibers, but additional neural mechanisms are implicated during elicited paresthesia.
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