Case Study 4:
Eagle Syndrome

The styloid process attaches the temporal bone of the skull and abuts to the styloid foramen, where it has numerous attachments, including the stylohyoid and stylomandibular ligaments and styloglossus and stylopharyngeus muscles. Derived from the Greek word “stylos”, which implies the pillar in Greek. The length of the styloid process has been reported by some authors to range between 15.2 mm and 47.7 mm [1, 2], with various authors labeling an elongated styloid process as anything >30 mm while Wat W. Eagle, an otolaryngologist, whom the syndrome is named after, believed that a length >25 mm is considered elongated. [3] A radiographic study by Dayal et al. seems to confirm Eagle’s assertion. [4] Watt found the incidence of elongated styloid process is 4% in the general population, of which only 4%-10% are reported to be symptomatic, with a female-to-male ratio of 3:1. It is usually reported in adults after the third decade of life. [5, 6]

In 1652, Pietro Marchetti first described an elongated styloid process related to an ossifying process of the stylohyoid ligament. [7] In 1937, otolaryngologist Wat W. Eagle coined the term “stylalgia” to describe the pain associated with this abnormality. [8] Wat W. Eagle (1948) hypothesized that the formation of scar tissue around the styloid apex after tonsillectomy caused compression and straining of the neurovascular structures present in the retro styloid compartment affecting stretches of cranial nerves V, VII, IX, and X. [9] This has since been expanded to include even minor cervical spine trauma. [10, 11] No matter the what is the etiology, patients almost uniformly report all or some of the following symptoms: foreign body sensation, pain referred to the ear, and dysphagia. [12] Saccommano et al. [13] found a correlation between Eagle syndrome and traumatic events and suggested two possibilities: a traumatic event could fracture the already elongated styloid process or calcified stylohyoid ligament; trauma itself triggers the pathophysiological mechanisms that lead to lengthening of styloid process or calcification of stylohyoid ligament and therefore the typical symptoms. [14]

The same authors (Saccommano et al. [13] and Todo et al. [14]) found that the carotid artery type of Eagle’s syndrome presents with other symptoms, such as migraines and neurological symptoms caused by irritation of the sympathetic nerve plexus. Eagle’s Syndrome has been shown to mimic osteoarthrosis of the temporomandibular joint; thus, the misdiagnosis of temporomandibular syndrome is frequent. The relationship of the styloid process to both the carotid artery and neurological structures in the region are setting for the perfect storm. If the internal carotid artery is compressed, then ipsilateral headaches can occur. If the external carotid artery is compressed, then there can be pain in the temporal and maxillary branch areas. A more significant danger with elongated styloid, although rare, is the possibility of carotid artery dissection, stroke, and sudden death due to this syndrome, as has been noted by multiple authors. [15] Sudden death is due to mechanical irritation of the carotid sinus by an elongated styloid process which may cause the heart to stop, resulting in cardiac arrest. [16-18]