Three-Dimensional Identification of Vascular Compression in Eagle’s Syndrome Using Computed Tomography: Case Report

Andrade, Miguel Gustavo Setúbal; Marchionni, Antônio Márcio Teixeira; Crusoé‐Rebello, Iêda; Martinez, M A; Flores, Paulo; Reis, Sílvia Regina de Almeida

doi:10.1016/j.joms.2006.10.046

Cited by 15 publications

(11 citation statements)

References 16 publications

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“…All patients' outcomes were good after treatment and no symptoms remained. In Pubmed, there are two cases that describe central venous outflow obstruction secondary to osseous compression of the internal jugular veins at the craniocervical junction (2,8).…”

Section: █ Resultsmentioning

confidence: 99%

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Eagle syndrome presented with neurological symptoms

Aydın

Quliyev²,

Çınar³

et al. 2016

Turkish Neurosurgery

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Section: █ Resultsmentioning

confidence: 99%

“…The incidence of an elongated styloid process is reported to be between 4% and 28% and is mostly seen in women (15). diagnostic tool that can define the anatomic relationship between the elongated styloid process and the vascular structures and nerves (2).…”

mentioning

confidence: 99%

Eagle syndrome presented with neurological symptoms

Aydın

Quliyev²,

Çınar³

et al. 2016

Turkish Neurosurgery

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“…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].…”

Section: Diagnosismentioning

confidence: 99%

Eagle’s syndrome: embryology, anatomy, and clinical management

2012

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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 neurovascular 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 periorbital 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 CT of 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. Embryology and phylogenyThe 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 ligament, and lesser cornu of the hyoid bone develop from endochondral 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 distal): 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 contribute to the hyoid bone. In many animals the ceratohyal component 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, RodriguezVazquez 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

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“…A palatable mass may be observed in the tonsillar fossa, its palpation sometimes exacerbating the patient's symptoms. Symptoms include ear pain, neck pain extending to the oral cavity and the maxilla (Le Toux, 1991;Siqueira et al, 2004;Weidenbecher et al, 2006), dysphonia (Blatchford and Coulthard, 1989;Sundmaker,1989), dysphagia (Kehrl and Hartwein, 1990;Manganaro and Nylander, 1998;Weidenbecher et al, 2006;Unlu et al, 2008), odynophagia (Tiago et al, 2002;Andrade et al, 2008), persistent sore throat (Takada et al, 2003), the sensation of a foreign body in the pharynx (Lindeman, 1985), painful trismus <25 mm, vertigo and tinnitus (Riley, 1996;Diamond et al, 2001;Ferreira de Albuquerque et al, 2003;Beder et al, 2005;Yavuz et al, 2008). Pain is also observed when turning the head or extending the tongue (Woolery, 1990).…”

Section: Pathogenesis and Symptomsmentioning

confidence: 99%

Eagle's syndrome: A review of the literature

et al. 2009

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Eagle's syndrome represents symptoms brought on by compression of regional structures by elongation of the styloid process or ossification of the stylohyoid or stylomandibular ligaments. Watt Eagle described it for the first time in 1937, dividing it into two subtypes: the "classic syndrome" and the "stylo-carotid artery syndrome." Many theories have been put forth regarding its pathogenesis. Depending on the underlying pathogenetic mechanism and the anatomical structures compressed or irritated by the styloid process, symptoms vary greatly, ranging from cervicofacial pain to cerebral ischemia. The syndrome generally follows tonsillectomy or trauma. Diagnosis is confirmed by radiological findings. Palpation of the styloid process in the tonsillar fossa and infiltration with anesthesia are also used in making the diagnosis. The treatment is primarily surgical; however, some conservative treatments have also been used. The current literature on Eagle's syndrome is reviewed, highlighting its often underestimated frequency and its clinical importance.

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Three-Dimensional Identification of Vascular Compression in Eagle’s Syndrome Using Computed Tomography: Case Report

Cited by 15 publications

References 16 publications

Eagle syndrome presented with neurological symptoms

Eagle syndrome presented with neurological symptoms

Eagle’s syndrome: embryology, anatomy, and clinical management

Eagle's syndrome: A review of the literature

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