颞骨骨折性面瘫手术治疗的临床研究
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摘要
目的：
本文通过回顾颞骨骨折性面瘫相关研究并分析我院临床资料,探讨颞骨骨折性面瘫手术治疗的适应证、手术时机、手术方式以及影响预后的因素等,以指导临床诊疗工作。
方法：
收集2010年7月至2012年7月间因颞骨骨折性面瘫在山东省立医院集团眼耳鼻喉医院行手术治疗的病例38例,回顾性分析辅助检查、骨折分类及手术入路等因素与手术预后的关系,以House-Brackmann分级法作为疗效标准,统计学方法采用卡方检验,分析软件为SPSS。
结果：
4男性30例,女性8例；年龄范围3-53岁,平均34.6岁。外伤原因主要有车祸伤17例(44.7%),摔伤8例(21.1%),头部撞击伤11例(28.9%),头部挤压伤2例(5.3%)。左侧面瘫者16例(42.1%),右侧21例(55.3%)双侧1例(2.6%)。达到H-B分级Ⅱ级以上21例(55.3%),Ⅲ级以上36例(94.7%)。病程达3周以后,神经电图显示结果与术后预后不符合,变性较少组反而预后差,3周以上者30例,神经变性大于90%者8例,75%术后恢复至Ⅱ级以上,变性小于90%有22例,术后Ⅱ级以上仅40.9%。鞘膜完整者18例,13例(72.2%)术后恢复至Ⅱ级以上,鞘膜可见糜烂、缺损的有20例,8例(40%)术后面神经功能恢复至Ⅱ级以上。两组间差异有统计学意义(P<0.05)。纵行骨折21例(55.3%),横行骨折9例(23.7%),混合型骨折7例(18.4%)术后面神经功能恢复至Ⅱ级以上分别为12例(57.1%)、5例(66.7%)、4例(57.1%),不同骨折类型组间无明显统计学差异(P>0.05)。病程3个月内手术病例21/32(65.6%)术后恢复至Ⅱ级以上,3个月以上手术6例,均未恢复至Ⅱ级,差异有统计学意义(P<0.05)。35例患者行颅中窝径路面神经减压,30例(78.9%)术中可见膝状神经节水肿明显或有骨片刺入、压迫,术后其中18例(52.9%)面神经功能恢复至Ⅱ级以上,32例(94.1%)术后面神经功能达III级以上。
结论：
本研究提示,面神经减压术对治疗颞骨骨折性面瘫有肯定的疗效,应结合患者颞骨骨折的类型和部位选择正确的手术方式。多数颞骨骨折患者面神经损伤位于膝状神经节,颅中窝径路可更好的暴露膝状神经节,对面神经有效减压。膝状神经节区神经减压范围包括膝状神经节,迷路段和部分水平段,减压至神经没有水肿的正常处即可,也可以获得很好的神经恢复结果,不需要全程面神经减压。面神经减压术应尽早实施,面瘫发生3个月以内手术效果更佳。
Objective:
There are dispute in surgical intervention for facial paralysis caused by temporal fracture. In this article, we review related researches and analysis the clinic data we collected, to discuss the indication of facial nerve surgery, the best time and approach of operation, as well as prognostic factors.
Methods:
A retrospective analysis of38patients with facial nerve paralysis resulting from temporal bone fracture, who underwent decompression surgery or facial nerve transplantation. Evaluation of facial nerve function by House-Brackmann nerve grade system, chi-square test is used to analyze the data.
Results:
Normal or subnormal facial nerve function (HB1or HB2) is considered to be good functional result.21in38(55.3%) patients got good result,36(94.7%) received Ⅰ～Ⅱ grade recovery. In cases of long-standing (>3weeks) facial paralysis,6in8of degeneration beyond90%recovered to H-B grade Ⅱ, while9in22who degenerate less than90%recovered to grade Ⅱ, EMG test and CT are more helpful for prognosis in cases of long-standing facial paralysis. Patients13in18(72.2%) whose nerve sheath is intact received good recovery, while defective ones8in20(40%) received good results. There were12/21longitudinal fractures,5/9transverse fractures and4/7mixed factures, who at last had Ⅰ～Ⅱ grade recovery, there is no significant statistical difference in different fracture types. Moreover, comparing facial nerve decompression within3months of injury to beyond3months of injury, recovery to H-B Ⅰ～Ⅱ nerve function was59.5%and0%, the statistical difference is significant (P<0.05). We chose middle cranial fossa approach facial decompression for34 patients depending on the results of CT and Schirmer Tear Test,30of them were found lesions at Geniculate Ganglion, and18of them recovered to H-B Ⅰ～Ⅱ,14recovered to Ⅲ.
Conclusion:
Facial decompression is effective in treating facial paralysis caused by temporal fracture. Most lesions happen in the area of GG, while middle cranial fossa approach can give best exposure of these areas, for most patients, we chose this approach for the surgery. While lesions set in GG, local decompression is carried out, and most traumatic facial paralysis patients recovered to H-B Ⅱ, there is no need for total decompression. Surgery carried out beyond3months did not receive good recovery, so the operation should be performed in3months.
本文通过回顾颞骨骨折性面瘫相关研究并分析我院临床资料,探讨颞骨骨折性面瘫手术治疗的适应证、手术时机、手术方式以及影响预后的因素等,以指导临床诊疗工作。
方法：
收集2010年7月至2012年7月间因颞骨骨折性面瘫在山东省立医院集团眼耳鼻喉医院行手术治疗的病例38例,回顾性分析辅助检查、骨折分类及手术入路等因素与手术预后的关系,以House-Brackmann分级法作为疗效标准,统计学方法采用卡方检验,分析软件为SPSS。
结果：
4男性30例,女性8例；年龄范围3-53岁,平均34.6岁。外伤原因主要有车祸伤17例(44.7%),摔伤8例(21.1%),头部撞击伤11例(28.9%),头部挤压伤2例(5.3%)。左侧面瘫者16例(42.1%),右侧21例(55.3%)双侧1例(2.6%)。达到H-B分级Ⅱ级以上21例(55.3%),Ⅲ级以上36例(94.7%)。病程达3周以后,神经电图显示结果与术后预后不符合,变性较少组反而预后差,3周以上者30例,神经变性大于90%者8例,75%术后恢复至Ⅱ级以上,变性小于90%有22例,术后Ⅱ级以上仅40.9%。鞘膜完整者18例,13例(72.2%)术后恢复至Ⅱ级以上,鞘膜可见糜烂、缺损的有20例,8例(40%)术后面神经功能恢复至Ⅱ级以上。两组间差异有统计学意义(P<0.05)。纵行骨折21例(55.3%),横行骨折9例(23.7%),混合型骨折7例(18.4%)术后面神经功能恢复至Ⅱ级以上分别为12例(57.1%)、5例(66.7%)、4例(57.1%),不同骨折类型组间无明显统计学差异(P>0.05)。病程3个月内手术病例21/32(65.6%)术后恢复至Ⅱ级以上,3个月以上手术6例,均未恢复至Ⅱ级,差异有统计学意义(P<0.05)。35例患者行颅中窝径路面神经减压,30例(78.9%)术中可见膝状神经节水肿明显或有骨片刺入、压迫,术后其中18例(52.9%)面神经功能恢复至Ⅱ级以上,32例(94.1%)术后面神经功能达III级以上。
结论：
本研究提示,面神经减压术对治疗颞骨骨折性面瘫有肯定的疗效,应结合患者颞骨骨折的类型和部位选择正确的手术方式。多数颞骨骨折患者面神经损伤位于膝状神经节,颅中窝径路可更好的暴露膝状神经节,对面神经有效减压。膝状神经节区神经减压范围包括膝状神经节,迷路段和部分水平段,减压至神经没有水肿的正常处即可,也可以获得很好的神经恢复结果,不需要全程面神经减压。面神经减压术应尽早实施,面瘫发生3个月以内手术效果更佳。
Objective:
There are dispute in surgical intervention for facial paralysis caused by temporal fracture. In this article, we review related researches and analysis the clinic data we collected, to discuss the indication of facial nerve surgery, the best time and approach of operation, as well as prognostic factors.
Methods:
A retrospective analysis of38patients with facial nerve paralysis resulting from temporal bone fracture, who underwent decompression surgery or facial nerve transplantation. Evaluation of facial nerve function by House-Brackmann nerve grade system, chi-square test is used to analyze the data.
Results:
Normal or subnormal facial nerve function (HB1or HB2) is considered to be good functional result.21in38(55.3%) patients got good result,36(94.7%) received Ⅰ～Ⅱ grade recovery. In cases of long-standing (>3weeks) facial paralysis,6in8of degeneration beyond90%recovered to H-B grade Ⅱ, while9in22who degenerate less than90%recovered to grade Ⅱ, EMG test and CT are more helpful for prognosis in cases of long-standing facial paralysis. Patients13in18(72.2%) whose nerve sheath is intact received good recovery, while defective ones8in20(40%) received good results. There were12/21longitudinal fractures,5/9transverse fractures and4/7mixed factures, who at last had Ⅰ～Ⅱ grade recovery, there is no significant statistical difference in different fracture types. Moreover, comparing facial nerve decompression within3months of injury to beyond3months of injury, recovery to H-B Ⅰ～Ⅱ nerve function was59.5%and0%, the statistical difference is significant (P<0.05). We chose middle cranial fossa approach facial decompression for34 patients depending on the results of CT and Schirmer Tear Test,30of them were found lesions at Geniculate Ganglion, and18of them recovered to H-B Ⅰ～Ⅱ,14recovered to Ⅲ.
Conclusion:
Facial decompression is effective in treating facial paralysis caused by temporal fracture. Most lesions happen in the area of GG, while middle cranial fossa approach can give best exposure of these areas, for most patients, we chose this approach for the surgery. While lesions set in GG, local decompression is carried out, and most traumatic facial paralysis patients recovered to H-B Ⅱ, there is no need for total decompression. Surgery carried out beyond3months did not receive good recovery, so the operation should be performed in3months.
引文
[1]Glasscock M E, Gulya A J. Glasscock-Shambaugh Surgery of the ear[M]. Pmph-usa,2003.619-638.
(2)黄选兆,汪吉宝,孔维佳.实用耳鼻咽喉头颈外科学[M].人民卫生出版社,2008.
[3]Kang T S, Vrabec J T, Giddings N, et al. Facial nerve grading systems (1985-2002):beyond the House-Brackmann scale[J]. Otology & neurotology, 2002,23(5):767-771.
[4]迟放鲁.面神经疾病[M].上海科学技术出版社,2007.
[5]Ulug T, Arif U S. Management of facial paralysis in temporal bone fractures:a prospective study analyzing 11 operated fractures[J]. American journal of otolaryngology,2005,26(4):230.
[6]Zhaobing G, Lan L U W J. The diagnostic value of high resolution CT in assessment of temporal bone traumatic facial nerve paralysis[J]. Journal of Clinical Otorhinolaryngology Head and Neck Surgery,2009,22:002.
[7]吴恩惠,戴建平,张云亭.中华影像医学：头颈部卷[M].人民卫生出版社,2004.
[8]Ishman S L, Friedland D R. Temporal bone fractures:traditional classification and clinical relevance[J]. The Laryngoscope,2004,114(10):1734-1741.
[9]Yanagihara N, Murakami S, Nishihara S. Temporal bone fractures inducing facial nerve paralysis:a new classification and its clinical significance[J]. Ear, nose,& throat journal,1997,76(2):79.
[10]Rafferty M A, Mc Conn Walsh R, Walsh M A. A comparison of temporal bone fracture classification systems[J]. Clinical Otolaryngology,2006,31(4): 287-291.
(11]樊忠,樊兆民.外伤性面瘫的外科治疗[J].中华耳鼻咽喉科杂志,1999,34(1)：52-54.
[12]Kang H M, Kim M G, Boo S H, et al. Comparison of the clinical relevance of traditional and new classification systems of temporal bone fractures[J]. European Archives of Oto-Rhino-Laryngology,2012,269(8):1893-1899.
[13]Seddon H J. Three types of nerve injury[J]. Brain,1943,66(4):237-288.
[14]Sunderland S. A classification of peripheral nerve injuries producing loss of function[J]. Brain,1951,74(4):491-516.
[15]Nosan D K, Benecke J E, MURR R E W H. Current perspective on temporal bone trauma[J]. Otolaryngology-Head and Neck Surgery,1997,117(1):67-71.
[16]Dal Secchi M M, Moraes J F S, de Castro F B. Fracture of the temporal bone in patients with traumatic brain injury [J].2012.
[17]Bento R F, Pirana S, Brito Neto R V, et al. The role of the middle fossa approach in the management of traumatic facial paralysis[J]. Revista Brasileira de Otorrinolaringologia,2004,70(4):484-493.
[18]Yi H, Liu P, Yang S. Geniculate ganglion decompression of facial nerve by transmastoid-epitympanum approach[J]. Acta 966810016350 Oto-Laryngologica,2013 (0):1-6.
[19]Chang C Y J, Cass S P. Management of facial nerve injury due to temporal bone trauma[J]. Otology & Neurotology,1999,20(1):96-114.
[20]Quaranta A, Campobasso G, Piazza F, et al. Facial nerve paralysis in temporal bone fractures:outcomes after late decompression surgery[J]. Acta oto-laryngologica,2001,121(5):652-655.
[21]黄新生,戴春富,王正敏.面神经减压术治疗颞骨外伤性面瘫的临床分析[J].中华耳鼻咽喉科杂志,2001,36(1)：34-37.
[22]Kim J, Moon I S, Shim D B, et al. The effect of surgical timing on functional outcomes of traumatic facial nerve paralysis[J]. The Journal of Trauma and Acute Care Surgery,2010,68(4):924.
[23]Hato N, Nota J, Hakuba N, et al. Facial nerve decompression surgery in patients with temporal bone trauma:analysis of 66 cases[J]. The Journal of Trauma and Acute Care Surgery,2011,71(6):1789-1793.
[1]VAN ROSSUM D, HANISCH U W E K, QUIRION R. Neuroanatomical localization, pharmacological characterization and functions of CGRP, related peptides and their receptors[J]. Neuroscience & Biobehavioral Reviews,1997, 21(5):649-678.
[2]Dennis T, Fournier A, St Pierre S, et al. Structure-activity profile of calcitonin gene-related peptide in peripheral and brain tissues. Evidence for receptor multiplicity[J]. Journal of Pharmacology and Experimental Therapeutics,1989, 251(2):718-725.
[3]Rorabaugh B R, Scofield M A, Smith D D, et al. Functional calcitonin gene-related peptide subtype 2 receptors in porcine coronary arteries are identified as calcitonin gene-related peptide subtype 1 receptors by radioligand binding and reverse transcription-polymerase chain reaction[J]. Journal of Pharmacology and Experimental Therapeutics,2001,299(3):1086-1094.
[4]Fischer J A, Muff R, Born W. Functional relevance of G-protein-coupled-receptor-associated proteins, exemplified by receptor-activity-modifying proteins (RAMPs)[J]. Biochemical Society Transactions,2002,30(4):455.
[5]Denis-Donini S. Expression of dopaminergic phenotypes in the mouse olfactory bulb induced by the calcitonin gene-related peptide[J]. Nature,1989,339(6227): 701-703.
[6]Denis-Donini S, Chini B, Vitadello M. Developmentally regulated expression of CGRP in the mouse olfactory pathway[J]. European Journal of Neuroscience, 1993,5(6):648-656.
[7]Ohno K, Takeda N, Yamano M, et al. Coexistence of acetylcholine and calcitonin gene-related peptide in the vestibular efferent neurons in the rat[J]. Brain research,1991,566(1):103-107.
[8]NAI Q, ZHAO Z, YE K. The effect of noise on calcitonin gene related peptide[J]. CHINESE OCCUPATIONAL MEDICINE,1999.
[9]UNGER W G, TERENGHI G, GHATEI M A, et al. Calcitonin gene-related polypeptide as a mediator of the neurogenic ocular injury response[J]. Journal of Ocular Pharmacology and Therapeutics,1985,1(2):189-199.
[10]Harrigan E A, Magnuson D J, Thunstedt G M, et al. Corticotropin releasing factor neurons are innervated by calcitonin gene-related peptide terminals in the rat central amygdaloid nucleus[J]. Brain research bulletin,1994,33(5): 529-534.
[11]Petrov T, Jhamandas J H, Krukoff T L. Characterization of peptidergic efferents from the lateral parabrachial nucleus to identified neurons in the rat dorsal raphe nucleus[J]. Journal of Chemical Neuroanatomy,1992,5(5):367-373.
[12]Hokfelt T, Arvidsson U, Ceccatelli S, et al. Calcitonin Gene-Related Peptide in the Brain, Spinal Cord, and Some Peripheral Systemsa[J]. Annals of the New York Academy of Sciences,1992,657(1):119-134.
[13]Fisher L A, Kikkawa D O, Rivier J E, et al. Stimulation of noradrenergic sympathetic outflow by calcitonin gene-related peptide[J].1983.
[14]Tsuda K, Tsuda S, Goldstein M, et al. Calcitonin gene-related peptide in noradrenergic transmission in rat hypothalamus[J]. Hypertension,1992,19(6 Pt 2):639-642.
[15]Jennings C G B, Mudge A W. Chick myotubes in culture express high-affinity receptors for calcitonin gene-related peptide[J]. Brain research,1989,504(2): 199-205.
[16]Fontaine B, Klarsfeld A, Hokfelt T, et al. Calcitonin gene-related peptide, a peptide present in spinal cord motoneurons, increases the number of acetylcholine receptors in primary cultures of chick embryo myotubes[J]. Neuroscience letters,1986,71(1):59-65.
[17]Mulle C, Benoit P, Pinset C, et al. Calcitonin gene-related peptide enhances the rate of desensitization of the nicotinic acetylcholine receptor in cultured mouse muscle cells[J]. Proceedings of the National Academy of Sciences,1988, 85(15):5728-5732.
[18]Lu B, Fu W, Greengard P, et al. Calcitonin gene-related peptide potentiates synaptic responses at developing neuromuscular junction[J].1993.
[19]Katoh K, Tohyama M, Noguchi K, et al. Axonal flow blockade induces a-CGRP mRNA expression in rat motoneurons[J]. Brain research,1992,599(1): 153-157.
[20]Inaishi Y, Kashihara Y, Sakaguchi M, et al. Cooperative regulation of calcitonin gene-related peptide levels in rat sensory neurons via their central and peripheral processes[J]. The Journal of neuroscience,1992,12(2):518-524.
[21]Biella G, Panara C, Pecile A, et al. Facilitatory role of calcitonin gene-related peptide (CGRP) on excitation induced by substance P (SP) and noxious stimuli in rat spinal dorsal horn neurons. An iontophoretic study in vivo[J]. Brain research,1991,559(2):352-356.
[22]Scott T M, Drodge K H, Foote J. Peptidergic nerve involvement in the control of endothelium-dependent vascular relaxation[J]. Artery,1992,19(4):211.
[23]Edvinsson L, Villalon C M, MaassenVanDenBrink A. Basic mechanisms of migraine and its acute treatment[J]. Pharmacology & Therapeutics,2012.
[24]Johnston F G, Bell B A, Robertson I J A, et al. Effect of calcitonin-gene-related peptide on postoperative neurological deficits after subarachnoid haemorrhage [J]. The Lancet,1990,335(8694):869-872.
[25]Mair J, Lechleitner P, Langle T, et al. Plasma CGRP in acute myocardial infarction[J]. Lancet,1990,335(8682).
[26]Bergman A S F, Falt K, Odar-cederlof I, et al. Calcitonin gene-related peptide attenuates experimental ischemic renal failure in a rat model of reversible renal ischemic insult[J]. Renal failure,1994,16(3):351-357.
[27]Aboitiz F, Squire L. Encyclopedia of neuroscience[J]. Encyclopedia of neuroscience,2008,6.
[28]Tsukiji J, Sango K, Udaka N, et al. Long-term induction of β-CGRP mRNA in rat lungs by allergic inflammation[J]. Life sciences,2004,76(2):163-177.
(2)黄选兆,汪吉宝,孔维佳.实用耳鼻咽喉头颈外科学[M].人民卫生出版社,2008.
[3]Kang T S, Vrabec J T, Giddings N, et al. Facial nerve grading systems (1985-2002):beyond the House-Brackmann scale[J]. Otology & neurotology, 2002,23(5):767-771.
[4]迟放鲁.面神经疾病[M].上海科学技术出版社,2007.
[5]Ulug T, Arif U S. Management of facial paralysis in temporal bone fractures:a prospective study analyzing 11 operated fractures[J]. American journal of otolaryngology,2005,26(4):230.
[6]Zhaobing G, Lan L U W J. The diagnostic value of high resolution CT in assessment of temporal bone traumatic facial nerve paralysis[J]. Journal of Clinical Otorhinolaryngology Head and Neck Surgery,2009,22:002.
[7]吴恩惠,戴建平,张云亭.中华影像医学：头颈部卷[M].人民卫生出版社,2004.
[8]Ishman S L, Friedland D R. Temporal bone fractures:traditional classification and clinical relevance[J]. The Laryngoscope,2004,114(10):1734-1741.
[9]Yanagihara N, Murakami S, Nishihara S. Temporal bone fractures inducing facial nerve paralysis:a new classification and its clinical significance[J]. Ear, nose,& throat journal,1997,76(2):79.
[10]Rafferty M A, Mc Conn Walsh R, Walsh M A. A comparison of temporal bone fracture classification systems[J]. Clinical Otolaryngology,2006,31(4): 287-291.
(11]樊忠,樊兆民.外伤性面瘫的外科治疗[J].中华耳鼻咽喉科杂志,1999,34(1)：52-54.
[12]Kang H M, Kim M G, Boo S H, et al. Comparison of the clinical relevance of traditional and new classification systems of temporal bone fractures[J]. European Archives of Oto-Rhino-Laryngology,2012,269(8):1893-1899.
[13]Seddon H J. Three types of nerve injury[J]. Brain,1943,66(4):237-288.
[14]Sunderland S. A classification of peripheral nerve injuries producing loss of function[J]. Brain,1951,74(4):491-516.
[15]Nosan D K, Benecke J E, MURR R E W H. Current perspective on temporal bone trauma[J]. Otolaryngology-Head and Neck Surgery,1997,117(1):67-71.
[16]Dal Secchi M M, Moraes J F S, de Castro F B. Fracture of the temporal bone in patients with traumatic brain injury [J].2012.
[17]Bento R F, Pirana S, Brito Neto R V, et al. The role of the middle fossa approach in the management of traumatic facial paralysis[J]. Revista Brasileira de Otorrinolaringologia,2004,70(4):484-493.
[18]Yi H, Liu P, Yang S. Geniculate ganglion decompression of facial nerve by transmastoid-epitympanum approach[J]. Acta 966810016350 Oto-Laryngologica,2013 (0):1-6.
[19]Chang C Y J, Cass S P. Management of facial nerve injury due to temporal bone trauma[J]. Otology & Neurotology,1999,20(1):96-114.
[20]Quaranta A, Campobasso G, Piazza F, et al. Facial nerve paralysis in temporal bone fractures:outcomes after late decompression surgery[J]. Acta oto-laryngologica,2001,121(5):652-655.
[21]黄新生,戴春富,王正敏.面神经减压术治疗颞骨外伤性面瘫的临床分析[J].中华耳鼻咽喉科杂志,2001,36(1)：34-37.
[22]Kim J, Moon I S, Shim D B, et al. The effect of surgical timing on functional outcomes of traumatic facial nerve paralysis[J]. The Journal of Trauma and Acute Care Surgery,2010,68(4):924.
[23]Hato N, Nota J, Hakuba N, et al. Facial nerve decompression surgery in patients with temporal bone trauma:analysis of 66 cases[J]. The Journal of Trauma and Acute Care Surgery,2011,71(6):1789-1793.
[1]VAN ROSSUM D, HANISCH U W E K, QUIRION R. Neuroanatomical localization, pharmacological characterization and functions of CGRP, related peptides and their receptors[J]. Neuroscience & Biobehavioral Reviews,1997, 21(5):649-678.
[2]Dennis T, Fournier A, St Pierre S, et al. Structure-activity profile of calcitonin gene-related peptide in peripheral and brain tissues. Evidence for receptor multiplicity[J]. Journal of Pharmacology and Experimental Therapeutics,1989, 251(2):718-725.
[3]Rorabaugh B R, Scofield M A, Smith D D, et al. Functional calcitonin gene-related peptide subtype 2 receptors in porcine coronary arteries are identified as calcitonin gene-related peptide subtype 1 receptors by radioligand binding and reverse transcription-polymerase chain reaction[J]. Journal of Pharmacology and Experimental Therapeutics,2001,299(3):1086-1094.
[4]Fischer J A, Muff R, Born W. Functional relevance of G-protein-coupled-receptor-associated proteins, exemplified by receptor-activity-modifying proteins (RAMPs)[J]. Biochemical Society Transactions,2002,30(4):455.
[5]Denis-Donini S. Expression of dopaminergic phenotypes in the mouse olfactory bulb induced by the calcitonin gene-related peptide[J]. Nature,1989,339(6227): 701-703.
[6]Denis-Donini S, Chini B, Vitadello M. Developmentally regulated expression of CGRP in the mouse olfactory pathway[J]. European Journal of Neuroscience, 1993,5(6):648-656.
[7]Ohno K, Takeda N, Yamano M, et al. Coexistence of acetylcholine and calcitonin gene-related peptide in the vestibular efferent neurons in the rat[J]. Brain research,1991,566(1):103-107.
[8]NAI Q, ZHAO Z, YE K. The effect of noise on calcitonin gene related peptide[J]. CHINESE OCCUPATIONAL MEDICINE,1999.
[9]UNGER W G, TERENGHI G, GHATEI M A, et al. Calcitonin gene-related polypeptide as a mediator of the neurogenic ocular injury response[J]. Journal of Ocular Pharmacology and Therapeutics,1985,1(2):189-199.
[10]Harrigan E A, Magnuson D J, Thunstedt G M, et al. Corticotropin releasing factor neurons are innervated by calcitonin gene-related peptide terminals in the rat central amygdaloid nucleus[J]. Brain research bulletin,1994,33(5): 529-534.
[11]Petrov T, Jhamandas J H, Krukoff T L. Characterization of peptidergic efferents from the lateral parabrachial nucleus to identified neurons in the rat dorsal raphe nucleus[J]. Journal of Chemical Neuroanatomy,1992,5(5):367-373.
[12]Hokfelt T, Arvidsson U, Ceccatelli S, et al. Calcitonin Gene-Related Peptide in the Brain, Spinal Cord, and Some Peripheral Systemsa[J]. Annals of the New York Academy of Sciences,1992,657(1):119-134.
[13]Fisher L A, Kikkawa D O, Rivier J E, et al. Stimulation of noradrenergic sympathetic outflow by calcitonin gene-related peptide[J].1983.
[14]Tsuda K, Tsuda S, Goldstein M, et al. Calcitonin gene-related peptide in noradrenergic transmission in rat hypothalamus[J]. Hypertension,1992,19(6 Pt 2):639-642.
[15]Jennings C G B, Mudge A W. Chick myotubes in culture express high-affinity receptors for calcitonin gene-related peptide[J]. Brain research,1989,504(2): 199-205.
[16]Fontaine B, Klarsfeld A, Hokfelt T, et al. Calcitonin gene-related peptide, a peptide present in spinal cord motoneurons, increases the number of acetylcholine receptors in primary cultures of chick embryo myotubes[J]. Neuroscience letters,1986,71(1):59-65.
[17]Mulle C, Benoit P, Pinset C, et al. Calcitonin gene-related peptide enhances the rate of desensitization of the nicotinic acetylcholine receptor in cultured mouse muscle cells[J]. Proceedings of the National Academy of Sciences,1988, 85(15):5728-5732.
[18]Lu B, Fu W, Greengard P, et al. Calcitonin gene-related peptide potentiates synaptic responses at developing neuromuscular junction[J].1993.
[19]Katoh K, Tohyama M, Noguchi K, et al. Axonal flow blockade induces a-CGRP mRNA expression in rat motoneurons[J]. Brain research,1992,599(1): 153-157.
[20]Inaishi Y, Kashihara Y, Sakaguchi M, et al. Cooperative regulation of calcitonin gene-related peptide levels in rat sensory neurons via their central and peripheral processes[J]. The Journal of neuroscience,1992,12(2):518-524.
[21]Biella G, Panara C, Pecile A, et al. Facilitatory role of calcitonin gene-related peptide (CGRP) on excitation induced by substance P (SP) and noxious stimuli in rat spinal dorsal horn neurons. An iontophoretic study in vivo[J]. Brain research,1991,559(2):352-356.
[22]Scott T M, Drodge K H, Foote J. Peptidergic nerve involvement in the control of endothelium-dependent vascular relaxation[J]. Artery,1992,19(4):211.
[23]Edvinsson L, Villalon C M, MaassenVanDenBrink A. Basic mechanisms of migraine and its acute treatment[J]. Pharmacology & Therapeutics,2012.
[24]Johnston F G, Bell B A, Robertson I J A, et al. Effect of calcitonin-gene-related peptide on postoperative neurological deficits after subarachnoid haemorrhage [J]. The Lancet,1990,335(8694):869-872.
[25]Mair J, Lechleitner P, Langle T, et al. Plasma CGRP in acute myocardial infarction[J]. Lancet,1990,335(8682).
[26]Bergman A S F, Falt K, Odar-cederlof I, et al. Calcitonin gene-related peptide attenuates experimental ischemic renal failure in a rat model of reversible renal ischemic insult[J]. Renal failure,1994,16(3):351-357.
[27]Aboitiz F, Squire L. Encyclopedia of neuroscience[J]. Encyclopedia of neuroscience,2008,6.
[28]Tsukiji J, Sango K, Udaka N, et al. Long-term induction of β-CGRP mRNA in rat lungs by allergic inflammation[J]. Life sciences,2004,76(2):163-177.