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DOI 10.1002/1097-0142(19930215)71:4<1193::aid-cncr2820710404>3.0.co;2-#

Медицинская библиотека · Cancer · 1993

Electromyographic study of tensor and levator veli palatini muscles in patients with nasopharyngeal carcinoma. Implications for eustachian tube dysfunction.

Su C Y, Hsu S P, Chee C Y

СтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

BACKGROUND AND

METHODS

To research the pathophysiology of the Eustachian tube (ET), electromyographies (EMG) of the tensor and levator veli palatini muscles (TVP and LVP) in 46 fresh specimens of nasopharyngeal carcinoma (NPC) were studied.

RESULTS

Sixty-eight percent of the TVP on the symptomatic side had abnormal EMG. Normal EMG recordings were noted in all TVP on the asymptomatic side. The abnormal TVP EMG observed most often was poor interference pattern or decreased interference with swallowing, and not uncommonly, there were some abnormal motor unit action potentials of serrated or large polyphasic waveforms found on motor unit potential analysis. This is strong evidence of neurogenic abnormality of the TVP caused by the NPC invasion. Despite the large polyphasic or serrated action potentials often being recorded on the symptomatic sides of LVP, the abnormal EMG finding also was found in 12 LVP on the asymptomatic sides.

CONCLUSIONS

There was no evidence that an ET dysfunction could be caused solely by an abnormal LVP function. This investigation and the study of ET function of these patients demonstrate that functional obstruction induced by the invasion of NPC to the nerve of TVP, rather than mechanical obstruction caused by the tumor mass effect on the ET, gives rise to the ear symptoms and signs of these patients. The authors suggest that the LVP action has little or no role in the function of the ET.

Для цитирования: Su C Y, Hsu S P, Chee C Y. Electromyographic study of tensor and levator veli palatini muscles in patients with nasopharyngeal carcinoma. Implications for eustachian tube dysfunction.. Cancer. 1993. DOI: 10.1002/1097-0142(19930215)71:4<1193::aid-cncr2820710404>3.0.co;2-#.

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