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REVIEWARTICLE Eagle’s syndrome: embryology, anatomy, and clinical management David J. Fusco & Shahab Asteraki & Robert F. Spetzler Received: 28 February 2012 /Accepted: 4 May 2012 /Published online: 26 May 2012 # Springer-Verlag 2012 Abstract Background Eagle’s syndrome refers to a rare constellation of neuropathic and vascular occlusive symptoms caused by pathologic elongation or angulation of the styloid process and styloid chain. First described in 1652 by Italian surgeon Piertro Marchetti, the clinical syndrome was definitively outlined by Watt Eagle in the late 1940s and early 1950s. Methods This article reviews how underlying embryologic and anatomic pathology predicts clinical symptomatology, diagnosis, and ultimately treatment of the syndrome. Results The length and direction of the styloid process and styloid chain are highly variable. This variability leads to a wide range of relationships between the chain and the neu- rovascular elements of the neck, including cranial nerves 5, 7, 9, and 10 and the internal carotid artery. In the classic type of Eagle’s syndrome, compressive cranial neuropathy most commonly leads to the sensation of a foreign body in the throat, odynophagia, and dysphagia. In the carotid type, compression over the internal carotid artery can cause pain in the parietal region of the skull or in the superior periorbi- tal region, among other symptoms. Conclusions Careful recording of the history of the present illness and review of systems is crucial to the diagnosis of Eagle’s syndrome. After the clinical examination, the optimal imaging modality for styloid process pathology is spiral CTof the neck and skull base. Surgical interventions are considered only after noninvasive therapies have failed, the two most common being intraoral and external resection of the styloid process. Keywords Neuralgia . Styloid . Carotid . Classic Embryology and phylogeny The embryologic history of the styloid process, stylohyoid ligament, and hyoid bone is a subject of debate. Revilla and Stuyt [69] suggest that the styloid process, stylohyoid liga- ment, and lesser cornu of the hyoid bone develop from endo- chondral ossification of Reichert’s cartilage, the cartilaginous component of the second branchial arch. They assert that after 3 months of fetal life, Reichert’s cartilage is disrupted and divided into five distinct components (from proximal to dis- tal): tympanohyal, stylohyal, ceratohyal, hypohyal, and basyhyal [58, 69]. The tympanohyal component contributes to the tympanic bone and the base of the styloid process. The stylohyal component contributes to the majority of the styloid process, and the hypohyal and basyhyal components contrib- ute to the hyoid bone. In many animals the ceratohyal com- ponent ultimately becomes the epihyoid bone. In humans, Revilla and Stuyt [69] contend that it degenerates to form the stylohyoid ligament. In contrast, during their detailed description of Reichert’s cartilage in 50 human embryos and fetuses, Rodriguez- Vazquez et al. [72] suggested that the second branchial arch cartilage is formed in two distinct segments separated by mesenchymal tissue. The proximal and larger segment is continuous with the otic capsule and becomes the styloid process. The smaller and more distal component forms the D. J. Fusco : S. Asteraki : R. F. Spetzler Division of Neurological Surgery, Barrow Neurological Institute, St. Joseph’s Hospital and Medical Center, Phoenix, AZ, USA R. F. Spetzler (*) Neuroscience Publications; Barrow Neurological Institute, St. Joseph’s Hospital and Medical Center, 350 W. Thomas Road, Phoenix, AZ 85013, USA e-mail: neuropub@chw.edu Acta Neurochir (2012) 154:1119–1126 DOI 10.1007/s00701-012-1385-2 majority of the hyoid bone. The intervening mesenchymal tissue then gives rise to ligaments and musculature (stylo- hyoid muscle, stylopharyngeus muscle, styloglossus muscle, stylohyoid ligament, stylomandibular ligament). Consensus regarding the ultimate differentiation of the second branchial arch is lacking. Ultimately, most authors would agree that it contributes significantly to the unification of the skull and aerodigestive tract and, more specifically, to the suspension and movement of the hyoid bone. Anatomy and physiology The styloid process is a long, thin prominence emerging from the inferior surface of the skull base. Its attachment is anterior and medial to the mastoid process, lateral to the jugular foramen, posterior and lateral to the carotid canal orifice, and immediately anterior and slightly medial to the stylomastoid foramen (Fig. 1). In the lateral view of the skull, the origin of the styloid process usually falls in the same coronal plane as the anterior margin of the occipital condyle (Fig. 2). The relationship of the styloid process to the jugular foramen and carotid canal orifice is crucial to the ultimate pathophysiology of Eagle’s syndrome. Three muscles arising from three distinct pharyngeal arches, and thus with three distinct innervations, have origins at the styloid process: the stylohyoid muscle (facial n.), stylo- pharyngeus muscle (glossopharyngeal n.), and styloglossus muscle (hypoglossal n.). The stylohyoid and stylomandibular ligaments also originate from the styloid process. In the neck, the internal carotid artery, maxillary artery, internal jugular vein, glossopharyngeal nerve, vagus nerve, and branches of both the trigeminal and facial nerves travel medial to the styloid process. The course of the hypoglossal nerve, cervical sympathetic chain, and ansa cervicalis branches are predomi- nantly posterolateral and inferior to the styloid process (Fig. 3). The length and direction of the styloid process and sty- loid chain (styloid process, styloid ligaments, styloid mus- culature) are highly variable. This variability leads to a wide range of relationships between the chain and the aforemen- tioned neurovascular elements of the neck [30, 39, 59, 71, 91]. In the first half of twentieth century, the advent of radiography allowed both the styloid process and the stylohyoid ligament (particularly if calcified) to be visualized. Since then numer- ous case series (based on X-ray and computed tomography [CT] data) have described the “average” length of the styloid process and suggested benchmark criteria for “elongation” of the styloid process [8, 37, 38, 42, 48, 75, 80]. The mean length of the styloid process ranges from 21 mm [80] to 29.5 mm [38]. By consensus, a styloid process longer than 30 mm confers an increased risk of Eagle’s syndrome. A longer styloid process confers greater translational capacity at its distal end, increasing the risk of adjacent neurovascular compromise. Consider the simple example of mild neck extension, during which about 30 degrees of angular motion is generated in the tip of the styloid process. If the length of the styloid process is 30 mm, then the tip movement measures about 15 mm (30 mm × 0.52 rad≈ Fig. 1 Skull base, inferior view. The styloid process is one of five components of the temporal bone. It is a narrow spicule ensheathed by the inferior border of the tympanic bone. It projects into the infratem- poral fossa and serves as the site of attachment for three muscles (stylohyoid, stylopharyngeus, styloglossus). Its relationship to the ca- rotid orifice and canal, jugular foramen, occipital condyle, and mastoid process are visualized. The probe has been passed through the hypo- glossal canal. A occipital condyle, B occipital bone, C temporal bone, mastoid part, D digastric groove, E stylomastoid foramen, F styloid process, G temporal bone, tympanic part, H zygomatic process poste- rior root, I mandibular fossa, J temporal bone, squamous part, K foramen ovale, L foramen spinosum, M foramen lacerum, N clivus, O temporal bone, petrous part, P carotid canal, Q jugular foramen. [Used with permissionfrom Barrow Neurological Institute] Fig. 2 Skull base, left inferolateral view. The occipital condyle is located on the anterolateral margin of the foramen magnum. Its rela- tionship to the styloid process is visualized. A tympanic bone, B foramen ovale, C styloid process, D occipital bone, condylar part, E occipital condyle, articular surface, F foramen magnum, G temporal bone, mastoid part. [Used with permission from Barrow Neurological Institute] 1120 Acta Neurochir (2012) 154:1119–1126 15 mm). With more complex movements involving medial- lateral components (e.g., holding a telephone to the ear), further translation of the styloid process tip occurs [81, 90]. Through the same mechanism, elongation of the stylohyoid ligament enhances the ability of the styloid chain to compro- mise neurovascular structures. An elongated stylohyoid liga- ment is present in patients with large cervical vertebral body height and inferior positioning of the hyoid bone [47]. Clinical features In 1652, an Italian surgeon named Piertro Marchetti first described clinical symptoms (intermittent respiratory distress) associated with an elongated styloid process [46, 52]. The definitive syndrome, however, was established by Watt W. Eagle in the late 1940s and early 1950s. Eagle described a collection of clinical features common to about 200 patients, each with an elongated styloid process, stylohyoid ligament calcifications, or both. The syndrome was seen most frequent- ly in women in their 4th and 5th decades. Occasionally, Eagle’s patients described prior styloid chain trauma (includ- ing tonsillectomy). Eagle divided his syndrome into two sub- groups: classic type and carotid type [20–23]. The clinical presentation and patient demographics for both Eagle’s syn- drome subtypes are summarized in Table 1. In the classic type, the most frequent symptoms are the sensation of a foreign body in the throat, odynophagia, and dysphagia [2, 62]. Pain is a variable feature and may be referred anywhere from the ipsilateral parietal bone to the pectoral region of the chest [3, 19, 33, 40, 49, 51, 60, 64, 66, 70]. This pain is usually dull, constant, and nagging and is often aggravated by swallowing and yawning [50, 68, 84]. Inspiratory and expiratory stridor is rare and is typically only seen in children when the airway is already narrow [16, 34, 85]. Taste disturbance is rare but has been reported [5, 19, 49]. Symptoms are thought to be secondary to intermittent compressive neuropathy, involving branches of cranial nerves 5, 7, 9, and 10 [5, 32, 51]. As would be predicted by its anatomic course, the glossopharyngeal nerve is most frequently involved. Eagle’s syndrome must thus be considered in the differential diagnosis of glosso- pharyngeal neuralgia [76, 78, 79]. Involvement of the hypo- glossal nerve and ansa cervicalis are rare. In the carotid type, compression over the internal carotid artery can cause pain in the parietal region of the skull or in the superior periorbital region [49]. Dizziness, transient visual loss, syncope, stroke, Horner’s syndrome, headache during exercise and straining, and even sudden death have also all been described as a consequence of internal carotid artery compression [15, 24, 88]. Compression of external carotid artery branches usually causes pain in the ipsilateral face and neck [5, 61]. Although technically not Eagle’s syndrome by the strict definitions above, compression over the internal jugular vein can lead to a spectrum of headache presentations: from mild headache during straining to chronic, unremitting venous hypertensive syndromes (i.e., pseudotumor cerebri) [45]. Given that both the carotid artery and jugular vein are medial to the styloid chain, all compression appears to be aggravated by contralateral head rotation [4, 14, 63, 92]. Pathophysiologic investigations Multiple theories seeking to elucidate the pathophysiologic underpinnings of Eagle’s syndrome have arisen over time. In some way each has provided an etiology for elongation or angulation of the styloid process or for calcification of the Fig. 3 Relationship of the styloid process to critical infratemporal fossa neurovascular structures. The mandibular ramus and condyle, mastoid part, ipsilateral occipital bone, and posterior belly of the digastric muscle have been removed to expose the styloid process, which is lateral to the jugular foramen. The jugular vein has been removed. The internal carotid artery ascends to enter the carotid canal in front of the jugular foramen. The vagus, accessory, and hypoglossal nerves descend between the carotid artery and internal jugular vein in the area immediately below the jugular foramen. After the glossopharyngeal nerve (not shown here) exits the jugular foramen, it turns forward, crossing the lateral surface of the internal carotid artery immediately medial to the styloid process. A parotid gland (retracted), B temporal bone, tympanic part, C styloid process, D internal carotid artery, E external carotid artery, F superior thyroid artery, G lingual artery, H styloglossus muscle, I C1 transverse process, J C2 ventral ramus, K hypoglossal nerve, L cervical sympathetic chain, M ansa cervicalis, N vagus nerve. [Used with permission from Barrow Neurological Institute] Acta Neurochir (2012) 154:1119–1126 1121 stylohyoid ligament. In his earlier papers, Eagle suggested that classic-type Eagle’s syndrome was most often second- ary to post-traumatic scarring and hyperplasia related to previous tonsillectomy [22]. Soon thereafter, however, Fritz [27] reported 43 patients with classic-type symptoms, of whom only 11 had a history of tonsillectomy. Later, Eagle [23] gave greater consideration to other causes. Several anomalies of development and bone homeostasis have been thought to contribute to the elongation of the styloid process, including the presence of two ossification centers in the styloid process, embryonic mesenchymal con- version to osteoid matrix, osteoarthritic changes, and diseases of calcium-phosphate maintenance (e.g., Paget’s disease) [25, 31, 34, 41, 67, 73, 77, 89]. In some cases of Eagle’s syndrome, angular relationships between the styloid chain and the great vessels of the neck assume greater importance than overall length. Mourad et al. [55] reported a carotid artery dissection in a 36-year-old woman after a prolonged telephone call during which she maintained the handset via head flexion and lateral rotation (i.e., against her shoulder). More recently, Tubbs et al. [86] performed an anatomic study of 20 cadavers and suggested that the stylopharyngeus muscle could be a compressive element for the carotid artery, particularly during ipsilateral neck rotation. Loeser and Cardwell [44] suggested Table 1 Eagle’s Syndrome: Clinical Presentation and Patient Demographics† †The clinical distinctions between classic type and carotid type Eagle’s syndrome are highlighted above. Modifiers of frequency include frequent, variable, rare, and not observed. Modifiers of severity include aggravates symptoms and minimal effect. M 0 male, F 0 female Classic Type Carotid Type Sex F > M F > M Age 5th and 6th decades (peak) 5th and 6th decades (peak) History of tonsillectomy Increased frequency Increased frequency Odynophagia Frequent Not observed Dysphagia Frequent Not observed Pain (present/absent) Variable Frequent Pain (location) Ipsilateral; parietal region to pectoral region Ipsilateral; parietal region/superior periorbital region Pain (quality) Dull, constant Variable (e.g. throbbing, stabbing) Stridor Rare (children) Not observed Dizziness Not observed Frequent Syncope/TIA/Stroke Not observed Frequent Flexion/extension Aggravates symptoms Aggravates symptoms Contralateral head rotation Minimal effect Aggravates symptoms Tonsillar pillar palpation (exam) Aggravates symptomsMinimal effect Fig. 4 Diagnostic imaging for Eagle’s syndrome. A 57-year-old man was diagnosed with bilateral carotid occlusion after an evaluation for acute myocardial infarction and a history of carotid-type Eagle’s syn- drome. Sagittal, two-dimensional CT angiogram (right side, a) and three-dimensional CT reconstruction (left side, b) demonstrate bilateral elongated styloid processes. The occluded area was readily apparent in the three-dimensional reconstruction (b, arrow). This configuration suggests that the elongated styloid processes may have caused the vascular occlusion. A styloid process, B carotid artery. [Used with permission from Barrow Neurological Institute] 1122 Acta Neurochir (2012) 154:1119–1126 that head rotation or jaw opening could compress the glosso- pharyngeal nerve between a fixed styloid process and a prom- inent lateral process of atlas. Diagnosis Given the variation in the clinical presentation of classic-type Eagle’s syndrome, the differential diagnosis is broad and includes glossopharyngeal neuralgia [76, 78, 79], occipital neuralgia [54], sphenopalatine neuralgia, temporomandibular disorders [17, 26, 43], dental infection, tonsillitis [2, 27], mastoiditis [19, 60], and migraine [33, 50, 54]. For the carotid type, vasculopathy and cardiac pathology should be consid- ered [4, 14, 15, 24, 63, 92]. Careful recording of the history of the present illness and review of systems is crucial to the diagnosis. In particular, the clinician should be suspicious of a history of face and neck pain exacerbated by neck flexion, extension, and contralateral rotation. Should suspicion for Eagle’s syndrome be raised during history-taking, palpation of the ipsilateral tonsillar pillar during physical examination is appropriate [5, 32]. After administering a local anesthetic, the clinician can attempt to palpate the anterior pillar region with the index finger [62, 82]. Under physiologic conditions, the styloid process cannot be palpated at this site. When elongat- ed, however, palpation is not only possible but often recreates the particular neuralgia. After the clinical examination, the optimal imaging modal- ity for styloid process pathology is spiral CT of the neck and skull base. With three-dimensional reconstruction, the length and angulation of the styloid process with respect to the neck vessels can be calculated (Fig. 4) [7, 12, 36, 74]. In dynamic (flexion-extension) studies, the compressive impact of the styloid process and styloid chain on the carotid artery and jugular vein can be evaluated [1, 57]. Given obscuration of the styloid process by coplanar bone and poor sensitivity for calcification in the styloid chain, simple radiography is a second-line option [56, 65]. Treatment Noninvasive management is first-line for the neuropathic se- quelae of Eagle’s syndrome. Oral agents, including gabapentin, amitriptyline, valproate, carbamazepime, and image-guided cor- ticosteroid injections can provide temporary relief [28, 74]. Surgical interventions are considered only after noninvasive therapies have failed. The two most common approaches de- scribed in the literature are intraoral resection of the styloid process and external resection of the styloid process. Each has its own risk-benefit profile [9, 18, 53]. Oral surgeons and otolaryngologists most often perform the intraoral approach. Through an oral corridor, an incision is made anterior to the tonsillar fossa and the tip of the styloid process is exposed via blunt dissection. This dissec- tion proceeds as proximally as possible along the styloid process, ultimately leading to removal of the process at its base [35]. Complete exposure and thus complete excision of the styloid process are often not possible with this approach, although the excised component is almost always sufficient to relieve symptoms. The intraoral approach is favored for its cosmesis by avoiding any external incision and for its potential for shorter operative times [6, 29]. Nevertheless, exposure of the retropharyngeal spaces to intraoral contents does elevate the infection risk [11]. Further considerations include poor carotid artery access in case of intraoperative injury, airway edema, and trismus. Given the elevated risk of airway edema, bilateral operations must be staged [13]. In the external approach, an oblique incision is made in the skin crease halfway between the angle of the mandible and the tip of the mastoid process (Fig. 5). Dissection begins with opening of the superficial fascia and posterolateral retraction of the sternocleidomastoid muscle. With ongoing blunt dissection, superior retraction of the parotid gland, inferior retraction of the posterior belly of the digastric muscle, and identification and preservation of the facial vein can be achieved. The elongated styloid process is identified and detached from the stylohyoid ligament distally. Muscu- lar attachments are removed via subperiosteal dissection. The styloid process is then removed completely in a piece- meal fashion [10, 11, 53, 83]. The operating surgeon must take care to expose and then to avoid the mandibular branch of the facial nerve in the superficial fascia as well as external carotid artery branches within the deep fascia. The most common postoperative complication of the external ap- proach is weakness of the mandibular branch of the facial Fig. 5 External approach for right styloidectomy. Intraoperative illus- tration of the incision line (middle) marked between the mastoid process (lower mark) and the angle of the mandible (upper mark). [Used with permission from Barrow Neurological Institute] Acta Neurochir (2012) 154:1119–1126 1123 nerve, which is usually transient [47]. The primary advan- tage of this approach is the minimal generation of airway edema, and the consequent ability to perform bilateral sty- loidectomy in the same sitting. Minimally invasive external approaches involving styloid chain transection and resection of the lesser cornu of the hyoid bone have been used with the aid of stereotactic navigation [87]. These approaches are rare, and there is not yet a consensus about their utility. Acknowledgments The authors thank Mauro Ferriera, MD, who performed and photographed the cadaveric dissections while complet- ing a fellowship at Barrow Neurological Institute. Conflicts of interest None. References 1. Andrade MG, Marchionni AM, Rebello IC, Martinez M, Flores PS, Reis SR (2008) Three-dimensional identification of vascular compression in eagle’s syndrome using computed tomography: case report. J Oral Maxillofac Surg 66:169–176 2. Aral IL, Karaca I, Gungor N (1997) Eagle’s syndrome masquer- ading as pain of dental origin. Case report. Aust Dent J 42:18–19 3. Arkuszewski P, Przygonski A, Tyndorf M (2009) Eagle’s syn- drome—report of rare case of bilateral elongation of styloid proc- eses. Otolaryngol Pol 63:162–164 4. Babad MS (1995) Eagle’s syndrome caused by traumatic fracture of a mineralized stylohyoid ligament—literature review and a case report. Cranio 13:188–192 5. Balbuena L Jr, Hayes D, Ramirez SG, Johnson R (1997) Eagle’s syndrome (elongated styloid process). South Med J 90:331–334 6. Beder E, Ozgursoy OB, Karatayli OS (2005) Current diagnosis and transoral surgical treatment of Eagle’s syndrome. J Oral Max- illofac Surg 63:1742–1745 7. Beder E, Ozgursoy OB, Karatayli OS, Anadolu Y (2006) Three- dimensional computed tomography and surgical treatment for Eagle’s syndrome. Ear Nose Throat J 85:443–445 8. Bozkir MG, Boga H, Dere F (1999) The evaluation of elongated styloid process in panoramic radiographs in edentulous patients. Tr J Med Sci 29:481–485 9. Buono U, Mangone GM, Michelotti A, Longo F, Califano L (2005) Surgical approach to the stylohyoid process in Eagles syndrome. J Oral Maxillofac Surg 63:714–716 10. Ceylan A, Koybasioglu A, CelenkF, Yilmaz O, Uslu S (2008) Surgical treatment of elongated styloid process: experience of 61 cases. Skull Base 18:289–295 11. Chase DC, Zarmen A, Bigelow WC, McCoy JM (1986) Eagle’s syndrome: a comparison of intraoral versus extraoral surgical approaches. Oral Surg Oral Med Oral Pathol 62:625–629 12. Chiang KH, Chang PY, Chou AS, Yen PS, Ling CM (2004) Eagle’s syndrome with 3-D reconstructed CT: two cases report. Chin J Radiol 29:353–357 13. Chrcanovic BR, Custodio AL, de Oliveira DR (2009) An intraoral surgical approach to the styloid process in Eagle’s syndrome. Oral Maxillofac Surg 13:145–151 14. ChuangWC, Short JH,McKinney AM, Anker L, Knoll B,McKinney ZJ (2007) Reversible left hemispheric ischemia secondary to carotid compression in Eagle syndrome: surgical and CT angiographic corre- lation. AJNR Am J Neuroradiol 28:143–145 15. D’Erceville T, Guennal P (1985) Stylohyoid syndrome. Apropos of a case. Rev Stomatol Chir Maxillofac 86:49–52 16. de Souza Carvalho AC, Magro FO, Garcia IR Jr, de Holanda ME, de Menezes JM (2009) Intraoral approach for surgical treatment of Eagle syndrome. Br J Oral Maxillofac Surg 47:153–154 17. de Souza EA, Hotta TH, Bataglion C (1996) Association of a temporomandibular disorder and Eagle’s syndrome: case report. Braz Dent J 7:53–58 18. Diamond LH, Cottrell DA, Hunter MJ, Papageorge M (2001) Eagle’s syndrome: a report of 4 patients treated using a modified extraoral approach. J Oral Maxillofac Surg 59:1420–1426 19. Douglas TE Jr (1952) Facial pain from elongated styloid process. AMA Arch Otolaryngol 56:635–638 20. Eagle W (1937) Elongated styloid process: report of two cases. Arch Otolaryngol 25:584–587 21. Eagle W (1948) Elongated styloid process. Further observation and a new syndrome. Arch Otolaryngol 47:630–640 22. Eagle WW (1949) Symptomatic elongated styloid process; report of two cases of styloid process-carotid artery syndrome with op- eration. Arch Otolaryngol 49:490–503 23. Eagle WW (1958) Elongated styloid process; symptoms and treat- ment. AMA Arch Otolaryngol 67:172–176 24. Farhat HI, Elhammady MS, Ziayee H, ziz-Sultan MA, Heros RC (2009) Eagle syndrome as a cause of transient ischemic attacks. J Neurosurg 110:90–93 25. Ferrario VF, Sigurta D, Daddona A, Dalloca L, Miani A, Tafuro F, Sforza C (1990) Calcification of the stylohyoid ligament: inci- dence and morphoquantitative evaluations. Oral Surg Oral Med Oral Pathol 69:524–529 26. De Ferreira AR Jr, Muller K, Hotta TH, Goncalves M (2003) Temporomandibular disorder or Eagle’s syndrome? A clinical report. J Prosthet Dent 90:317–320 27. Fritz M (1940) Elongated styloid process: cause of obscure throat symptoms. Arch Otolaryngol 31:911–918 28. Gervickas A, Kubilius R, Sabalys G (2004) Clinic, diagnostics, and treatment peculiarities of Eagle’s syndrome. Stomatol Balt Dent Maxillofac J 6:11–13 29. Ghosh LM, Dubey SP (1999) The syndrome of elongated styloid process. Auris Nasus Larynx 26:169–175 30. Gozil R, Yener N, Calguner E, Arac M, Tunc E, Bahcelioglu M (2001) Morphological characteristics of styloid process evaluated by computerized axial tomography. Ann Anat 183:527–535 31. Guo B, Jaovisidha S, Sartoris DJ, Ryu KN, Berthiaume MJ, Clopton P, Brossman J, Resnick D (1997) Correlation between ossification of the stylohyoid ligament and osteophytes of the cervical spine. J Rheumatol 24:1575–1581 32. Harma R (1966) Stylalgia: clinical experiences of 52 cases. Acta Otolaryngol Suppl 33. Hernandez JL, Velasco J (2008) Elongated styloid process (Eagle’s syndrome) as a cause of atypical craniocervical pain. J Neurol Neurosurg Psychiatry 79:43 34. Holloway MK, Wason S, Willging JP, Myer CM III, Wood BP (1991) Radiological case of the month. A pediatric case of Eagle’s syndrome. Am J Dis Child 145:339–340 35. Hossein R, Kambiz M, Mohammad D, Mina N (2010) Complete recovery after an intraoral approach for Eagle syndrome. J Craniofac Surg 21:275–276 36. Huang CC, Tsai YH, Liao YS, Weng HH, Yang BYA (2006) Three-dimensional reconstruction CT in diagnosis of eagle’s syn- drome: a retrospective study. Chin J Radiol 331:221–225 37. Hwang JY, Hwang EH, Lee SR (2005) A study on the styloid process in panoramic radiographs. Korean J Oral Maxillofac Radiol 35:105–110 38. Kaufman SM, Elzay RP, Irish EF (1970) Styloid process variation. Radiologic and clinical study. Arch Otolaryngol 91:460–463 39. Kay DJ, Har-El G, Lucente FE (2001) A complete stylohyoid bone with a stylohyoid joint. Am J Otolaryngol 22:358–361 1124 Acta Neurochir (2012) 154:1119–1126 40. Langlais RP, Miles DA, Van Dis ML (1986) Elongated and min- eralized stylohyoid ligament complex: a proposed classification and report of a case of Eagle’s syndrome. Oral Surg Oral Med Oral Pathol 61:527–532 41. Lengele B, Dhem A (1989) Microradiographic and histological study of the styloid process of the temporal bone. Acta Anat (Basel) 135:193–199 42. Lengele BG, Dhem AJ (1988) Length of the styloid process of the temporal bone. Arch Otolaryngol Head Neck Surg 114:1003–1006 43. Lerra S, Nazir T, Qadri SM, Kirmani MA (2009) Eagle’s syn- drome: a rare presentation with bilateral otalgia and review of literature. Internet J Otorhinolaryngol 9: 44. Loeser LH, Cardwell EP (1942) Elongated styloid process: A cause of glossopharyngeal neuralgia. Arch Otolaryngol 36:198–202 45. Maggioni F, Marchese-Ragona R, Mampreso E, Mainardi F, Zanchin G (2009) Exertional headache as unusual presentation of the syndrome of an elongated styloid process. Headache 49:776–779 46. Marchetti D (1652) Anatomia. Patavii 13: 205 47. Martin TJ, Friedland DR, Merati AL (2008) Transcervical resec- tion of the styloid process in Eagle syndrome. Ear Nose Throat J 87:399–401 48. Masashi Y (2002) Radiographic images of the styloid process. J Osaka Odontol Soc 65:165–180 49. Massey EW (1978) Facial pain from an elongated styloid process (Eagle’s syndrome). South Med J 71:1156–1159 50. Massey EW, Massey J (1979) Elongated styloid process (Eagle’s syndrome) causing hemicrania. Headache 19:339–344 51. Mendelsohn AH, Berke GS, Chhetri DK (2006) Heterogeneity in the clinical presentation of Eagle’s syndrome. Otolaryngol Head Neck Surg 134:389–393 52. Moffat DA, Ramsden RT, Shaw HJ (1977) The styloid pro- cess syndrome: aetiological factors and surgical management. J Laryngol Otol 91:279–294 53. Mohanty S, Thirumaran NS, Gopinath M, Bambha G, Balakrishnan S (2009) Significance of styloidectomy in Eagle’s syndrome: an analysis. Indian J Otolaryngol Head Neck Surg 61(4):262-265 54. Montalbetti L, Ferrandi D, Pergami P, Savoldi F (1995) Elongated styloid process and Eagle’s syndrome. Cephalalgia 15:80–93 55. Mourad JJ, Girerd X, Safar M (1997) Carotid-artery dissection after a prolonged telephone call. N Engl J Med 336:516 56. Murtagh RD, Caracciolo JT, Fernandez G (2001) CT findings associated with Eagle syndrome. AJNR Am J Neuroradiol 22:1401–1402 57. Nayak DR, Pujary K, Aggarwal M, Punnoose SE, Chaly VA (2007) Role of three-dimensional computed tomography recon- struction in the management of elongated styloid process: a pre- liminary study. J Laryngol Otol 121:349–353 58. Ommell KAH, Gandhi C, Ommell ML (1998) Ossification of the human styloid ligament. A longitudinal study. Oral Surg Oral Med Oral Pathol Oral Radiol End 85:226–232 59. Onbas O, Kantarci M, Murat KR, Durur I, Cinar BC, Alper F, Okur A (2005) Angulation, length, and morphology of the styloid process of the temporal bone analyzed by multidetector computed tomography. Acta Radiol 46:881–886 60. Orhan KS, Guldiken Y, Ural HI, Cakmak A (2005) Elongated styloid process (Eagle’s syndrome): literature review and a case report. Agri 17:23–25 61. Petrovic B, Radak D, Kostic V, Covickovic-Sternic N (2008) Stylo- carotid syndrome: a case report. Srp Arh Celok Lek 136:650–653 62. Piagkou M, AnagnostopoulouS, Kouladouros K, Piagkos G (2009) Eagle’s syndrome: a review of the literature. Clin Anat 22:545–558 63. Pierrakou ED (1990) Eagle’s syndrome. Review of the literature and a case report. Ann Dent 49:30–33 64. Politi M, Toro C, Tenani G (2009) A rare cause for cervical pain: Eagle’s syndrome. Int J Dent 2009:781297 65. Porrath S (1969) Roentgenologic considerations of the hy- oid apparatus. Am J Roentgenol Radium Ther Nucl Med 105:63–73 66. Prasad KC, Kamath MP, Reddy KJ, Raju K, Agarwal S (2002) Elongated styloid process (Eagle’s syndrome): a clinical study. J Oral Maxillofac Surg 60:171–175 67. Quereshy FA, Gold ES, Arnold J, Powers MP (2001) Eagle’s syndrome in an 11-year-old patient. J Oral Maxillofac Surg 59:94–97 68. Raina D, Gothi R, Rajan S (2009) Eagle syndrome. Indian J Radiol Imaging 19:107–108 69. Revilla Borjas C, Stuyt MT (1989) El sindrome estiloideo: a proposito de 3 casos. Annales de Otorrinolaringologia Iberoamer- icana 659–666 70. Rezgui-Marhoul L, Douira W, Said W, Bouslama K, Ben DM, Hendaoui L (2004) Eagle syndrome: case report. Rev Stomatol Chir Maxillofac 105:50–52 71. Rizzatti-Barbosa CM, Ribeiro MC, Silva-Concilio LR, Di HO, Ambrosano GM (2005) Is an elongated stylohyoid process preva- lent in the elderly? A radiographic study in a Brazilian population. Gerodontology 22:112–115 72. Rodriguez-Vazquez JF, Merida-Velasco JR, Verdugo-Lopez S, Sanchez-Montesinos I, Merida-Velasco JA (2006) Morphogenesis of the second pharyngeal arch cartilage (Reichert’s cartilage) in human embryos. J Anat 208:179–189 73. Salamone FN, Falciglia M, Steward DL (2004) Eagle’s syndrome reconsidered as a cervical manifestation of heterotopic ossification: woman presenting with a neck mass. Otolaryngol Head Neck Surg 130:501–503 74. Savranlar A, Uzun L, Ugur MB, Ozer T (2005) Three-dimensional CT of Eagle’s syndrome. Diagn Interv Radiol 11:206–209 75. Scaf G, Freitas DQ, Loffredo LC (2003) Diagnostic reproduc- ibility of the elongated styloid process. J Appl Oral Sci 11:120–124 76. Shin JH, Herrera SR, Eboli P, Aydin S, Eskandar EH, Slavin KV (2009) Entrapment of the glossopharyngeal nerve in patients with Eagle syndrome: surgical technique and outcomes in a series of 5 patients. J Neurosurg 111:1226–1230 77. Sisman Y, Gokce C, Sipahioglu M (2009) Bilateral elongated styloid process in an end-stage renal disease patient with peritoneal dialysis: is there any role for ectopic calcification? Eur J Dent 3:155–157 78. Slavin KV (2002) Eagle syndrome: entrapment of the glossophar- yngeal nerve? Case report and review of the literature. J Neurosurg 97:216–218 79. Soh KB (1999) The glossopharyngeal nerve, glossopharyngeal neuralgia and the Eagle’s syndrome—current concepts and man- agement. Singap Med J 40:659–665 80. Sokler K, Sandev S (2001) New classification of the styloid process length—clinical application on the biological base. Coll Antropol 25:627–632 81. Steel HH (1968) Anatomical and mechanical considerations of the atlanto-axial articulations. J Bone Joint Surg Am 50:1481–1482 82. Steinmann EP (1968) Styloid syndrome in absence of an elongated process. Acta Otolaryngol 66:347–356 83. Strauss M, Zohar Y, Laurian N (1985) Elongated styloid process syndrome: intraoral versus external approach for styloid surgery. Laryngoscope 95:976–979 84. Sun CK, Mercuri V, Cook MJ (2006) Eagle syndrome: an unusual cause of head and neck pain. Arch Neurol 63:294–295 85. Sundmaker WH (1989) Eagle’s syndrome: an atypical cause of dysphonia. Ear Nose Throat J 68:561 86. Tubbs RS, Loukas M, Dixon J, Cohen-Gadol AA (2010) Compression of the cervical internal carotid artery by the Acta Neurochir (2012) 154:1119–1126 1125 stylopharyngeus muscle: an anatomical study with potential clinical significance. Laboratory investigation. J Neurosurg 113:881–884 87. van der Westhuijzen AJ, van der Merwe J, Grotepass FW (1999) Eagle’s syndrome: lesser cornu amputation: an alternative surgical solution? Int J Oral Maxillofac Surg 28:335–337 88. Varelas PN, Sinson G, Rand S, Book D (2005) Clipping the Eagle’s wings: treatment of an unusual cause of transient cerebral ischemia. Neurology 64:393–394 89. Watanabe PC, Dias FC, Issa JP, Monteiro SA, de Paula FJ, Tiossi R (2010) Elongated styloid process and atheroma in panoramic radiography and its relationship with systemic osteoporosis and osteopenia. Osteoporos Int 21:831–836 90. Werne S (1957) Studies in spontaneous atlas dislocation: the craniovertebral joints. Acta Orthop Scand Suppl 23:11–83 91. Yagci AB, Kiroglu Y, Ozdemir B, Kara CO (2008) Three- dimensional computed tomography of a complete stylohyoid os- sification with articulation. Surg Radiol Anat 30:167–169 92. Zamboni P, Galeotti R, Menegatti E, Malagoni AM, Gianesini S, Bartolomei I, Mascoli F, Salvi F (2009) A prospective open-label study of endovascular treatment of chronic cerebrospinal venous insufficiency. J Vasc Surg 50:1348–1358 1126 Acta Neurochir (2012) 154:1119–1126 Eagle’s syndrome: embryology, anatomy, and clinical management Abstract Abstract Abstract Abstract Abstract Embryology and phylogeny Anatomy and physiology Clinical features Pathophysiologic investigations Diagnosis Treatment References
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