Three-dimensional computed tomography of a complete stylohyoid ossification with articulation

Yağcı, Ahmet Baki; Kıroğlu, Yılmaz; Özdemir, Bülent; Kara, Cüneyt Orhan

doi:10.1007/s00276-008-0302-0

Cited by 11 publications

(6 citation statements)

References 8 publications

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“…This variability leads to a wide range of relationships between the chain and the aforementioned 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.…”

Section: Anatomy and Physiologymentioning

confidence: 98%

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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Section: Anatomy and Physiologymentioning

confidence: 98%

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

2012

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“…In this method, an NH 2 column was applied for interactions of the structural variants of these carbohydrate hydroxyl groups with the amino phase, and the elution solvents and gradient program were examined. This method was also attempted for analysis of sulfatide molecular species, sulfated glycolipids which are known to be key molecules in leukodystrophy and receptors for bacteria and viruses 15, 16…”

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confidence: 99%

Highly sensitive localization analysis of gangliosides and sulfatides including structural isomers in mouse cerebellum sections by combination of laser microdissection and hydrophilic interaction liquid chromatography/electrospray ionization mass spectrometry with theoretically expanded multiple reaction monitoring

Ikeda

Taguchi

2010

Rapid Comm Mass Spectrometry

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Liquid chromatography/electrospray ionization mass spectrometry (LC/ESI-MS) is suitable for analysis of glycosphingolipids such as fragile gangliosides avoiding the use of the sialic acid elimination. However, it was not possible to distinguish the structural isomers such as GD1a and GD1b with reversed-phase LC/ESI-MS by hydrophobic interaction. Here we report an effective method for targeted analysis of theoretically expanded ganglioside molecular species including structural isomers by hydrophilic interaction liquid chromatography (HILIC)/ESI-MS with multiple reaction monitoring (MRM). As a result of MRM analysis of glycosphingolipid mixtures from porcine brain, each of the lipid classes was detected within 25 min in the following order: sulfatides > GM3 > GM2 > GM1 > GD3 > GD1a > GD2 > GD1b > GT1a > GT1b > GQ1b. For the advanced application, localization analysis of postnatal day 15 (P15) mouse cerebellum layered structures was carried out by combination of MRM and laser microdissection (LMD). As a result, GM3, GD1a, GT1b and GQ1b were abundantly detected in the molecular and granular layers, whereas GM1 was widely presented in each layered structure. These gangliosides were mainly composed of d18:1-18:0 and d18:1-20:0, but GM3 was d18:1-16:0 and d18:1-20:0. Meanwhile, sulfatide molecular species were mostly localized in the myelinated fibers and scarcely found in the molecular layer. These results suggested that our method is suitable to detect a variety of ganglioside classes and sulfatides with high sensitivity at the molecular species level and effective for localization analysis of these glycosphingolipids from mouse brain sections.

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“…The stylohyoid ligament ordinarily remains unossified 22 . An abnormal ossification of the ligament can lead to Eagle syndrome and similar symptoms.…”

Section: Discussionmentioning

confidence: 99%

“…2 The stylohyoid ligament ordinarily remains unossified. 22 An abnormal ossification of the ligament can lead to Eagle syndrome and similar symptoms. If a real metaplasia with a direct transformation from tendinous tissue into bone 23 or an endrochondral ossification from cartilaginous tissues that derived from remnants of the Reichert cartilage takes place 24 has not been fully elucidated.…”

Section: Discussionmentioning

confidence: 99%

Differences in the Osseous Ultrastructure in 2 Differing Etiologies of Eagle Syndrome. A Micro-CT Study

Heim¹,

Warwas²,

Singer

et al. 2023

Journal of Craniofacial Surgery

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Objectives: Eagle syndrome is a rare disease caused by an elongated styloid process (type I) or ossified stylohyoid ligament (type II) and causes a heterogeneous symptom complex, ranging from pain in the throat and neck to neurological symptoms and neurovascular entrapment. The 2 different types present differing shapes and ultrastructures and cause different symptoms. This study aimed to distinguish the 2 types by investigating the structures by micro-computed tomography. Methods: Micro-computed tomography was performed and evaluated in n = 10 resected styloid processes from patients diagnosed with Eagle syndrome. The tissues were measured for their shape, ratio of soft tissue and bone amounts, bone volume, and ultrastructure, and compared within the groups. Results: The shapes of the different types were different and the ultrastructure differed between the 2 groups, with an absence of trabecular architecture in type II. The area of bone to nonbone tissues in type I samples was significantly higher compared with type II (P = 0.007). Alike these results, the bone volume and bone-to-soft tissue ratio were significantly higher in type I compared with type II (P = 0.009). Conclusions: The findings suggest that both the popular theories (hyperplasia and metaplasia) may be probable but each solely valid for 1 type of Eagle. Type I may derive from bone hyperplasia with cancellous bone formation and rather high bone density in the elongated styloid process. Type II most likely originates from ligament metaplasia into bone without a compact structure.

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Three-dimensional computed tomography of a complete stylohyoid ossification with articulation

Cited by 11 publications

References 8 publications

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

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

Differences in the Osseous Ultrastructure in 2 Differing Etiologies of Eagle Syndrome. A Micro-CT Study

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