Tadashi Hamasaki1, Motohiro Morioka2, Koichi Fujiwara3, Chikao Nakayama3, Miho Harada4, Kiyohiko Sakata2, Yu Hasegawa5, Toshitaka Yamakawa6, Kazumichi Yamada7, Akitake Mukasa8. 1. Department of Neurosurgery, Kumamoto University Medical School, Kumamoto, Japan. Electronic address: thamasaki-nsu@umin.ac.jp. 2. Department of Neurosurgery, Kurume University School of Medicine, Kurume, Japan. 3. Department of Systems Science, Kyoto University, Kyoto, Japan. 4. Department of Laboratory Medicine, Kumamoto University Hospital, Kumamoto, Japan. 5. Department of Pharmacology and Molecular Therapeutics, Kumamoto University, Kumamoto, Japan. 6. Priority Organization for Innovation and Excellence, Kumamoto University, Kumamoto, Japan. 7. Department of Functional Neurosurgery, Kumamoto University Hospital, Kumamoto, Japan. 8. Department of Neurosurgery, Kumamoto University Medical School, Kumamoto, Japan.
Abstract
OBJECTIVE: Hemifacial spasm (HFS) is caused by arterial conflict at the root exit zone of the facial nerve. As the offending artery is pulsatile in nature, this study investigated the association of heart rate fluctuation with HFS. METHODS: Twenty-four preoperative patients underwent simultaneous recordings of facial electromyogram and electrocardiogram overnight. Series of R-wave to R-wave intervals (RRIs) in the electrocardiogram were analyzed across subjects in relation to HFS. The degree of heart rate fluctuation was quantified by analyzing the heart rate variability (HRV). The sleep stage was evaluated during the period of HFS. RESULTS: A 0.1 Hz fluctuation in RRIs by 5% compared to the baseline preceded a few seconds the onset of the HFS, indicating that a significant increase in the heart rate coincided with HFS. HRV analysis demonstrated that fluctuations in the heart rate were significantly enhanced during HFS. Wake or light sleep stages were more often accompanied by HFS, suggesting an association with autonomic activities. CONCLUSION: Our findings suggest that the etiology of HFS is more than just a mechanical compression of the facial nerve and may involve changes in pulsatile frequency in offending arteries. SIGNIFICANCE: We propose the etiology of HFS from a unique standpoint.
OBJECTIVE:Hemifacial spasm (HFS) is caused by arterial conflict at the root exit zone of the facial nerve. As the offending artery is pulsatile in nature, this study investigated the association of heart rate fluctuation with HFS. METHODS: Twenty-four preoperative patients underwent simultaneous recordings of facial electromyogram and electrocardiogram overnight. Series of R-wave to R-wave intervals (RRIs) in the electrocardiogram were analyzed across subjects in relation to HFS. The degree of heart rate fluctuation was quantified by analyzing the heart rate variability (HRV). The sleep stage was evaluated during the period of HFS. RESULTS: A 0.1 Hz fluctuation in RRIs by 5% compared to the baseline preceded a few seconds the onset of the HFS, indicating that a significant increase in the heart rate coincided with HFS. HRV analysis demonstrated that fluctuations in the heart rate were significantly enhanced during HFS. Wake or light sleep stages were more often accompanied by HFS, suggesting an association with autonomic activities. CONCLUSION: Our findings suggest that the etiology of HFS is more than just a mechanical compression of the facial nerve and may involve changes in pulsatile frequency in offending arteries. SIGNIFICANCE: We propose the etiology of HFS from a unique standpoint.