Introduction

The styloid process is a cylindrical, slender, needle-like projection of varying lengths averaging 2 to 3 cm (see Image. Medial Aspect of Jaw Anatomy). The styloid process projects from the inferior part of the petrous temporal bone and offers attachment to the stylohyoid ligament and the stylohyoid, stylopharyngeus, and styloglossus muscles (see Image. Stylohyoid Muscle). Through these structures, the styloid process facilitates the movement of the tongue, pharynx, larynx, hyoid bone, and mandible. Significant vessels and nerves surround the styloid process. The internal jugular vein, internal carotid artery, glossopharyngeal nerve (CN IX), vagus nerve (CN X), and accessory nerve (CN XI) lie medial to the styloid process. The occipital artery and hypoglossal nerve (CN XII) run along its lateral side. Originating as a part of Reichert's cartilage forming from the second pharyngeal arch, it undergoes endochondral ossification in the late stages of pregnancy through the first decade of life. The structure shows variations in length, angulation, and other morphological features between individuals. Although these physiological differences are often found incidentally, some patients might develop a constellation of symptoms known as Eagle syndrome. The symptomatology of Eagle syndrome occurs secondary to irritation or compression of surrounding structures from an abnormal styloid process.

Structure and Function

The cylindrical and needle-like structure has a thickness that gradually tapers, forming the apex of the styloid process. The process length varies between individuals, with an average length of 2 to 3 cm.[1] Although the process most commonly follows straight projection, it can vary and is curved.[2] The styloid process projects from the inferior portion of the petrous temporal bone, lying inferior and anterior to the external auditory meatus, anteromedial to the mastoid process, and anterior to the stylomastoid foramen (see Image. Stylomastoid Foramen). It comprises 2 segments: a proximal component and a distal component. The proximal portion consists of the base of the process, which is contained within the vaginal process of the tympanic portion of the temporal bone. The distal component consists of the shaft and is the origin of 3 muscles: the stylohyoid, stylopharyngeus, and styloglossus (see Image. The Mouth, Extrinsic Muscles of the Tongue). The styloid process apex is also the origin of 2 ligaments: the stylohyoid ligament, which attaches to the lesser cornu of the hyoid, and the stylomandibular ligament, which attaches to the ramus of the mandible. Both ligaments facilitate the movement of the tongue, pharynx, larynx, hyoid bone, and mandible.[3][4] 

Embryology

The styloid process originates as a part of Reichert's cartilage, which forms from the second pharyngeal arch during embryological development [5]. Reichert's cartilage is divided into 4 parts: the tympanohyal part, the stylohyal part, the ceratohyal part, and the hypohyal part. The tympanohyal part develops antenatally, attaches to the petrous portion of the temporal bone, and gives rise to the base of the styloid process, which is ensheathed by the vaginal process of the tympanic part. The stylohyal part appears post-natally, giving rise to the shaft of the styloid process and the proximal portion of the stylohyoid ligament. The stylohyal part might unite with the tympanohyal after puberty; sometimes, they never do. The ceratohyal and its fibrous sheath regress, giving rise to the stylohyoid ligament. The hypohyal part gives rise to the lesser cornu of the hyoid bone.[4][6] The styloid process undergoes endochondral ossification that begins at the final stages of pregnancy and is carried on over the first 8 years of life. However, the pattern of ossification and time to completely ossify has been shown to vary greatly.[4]

Blood Supply and Lymphatics

Several important vessels lie in the vicinity of the styloid process. Vessels on the medial aspect of the styloid process are the internal jugular vein and the external carotid artery, its branches, the lingual artery, the facial artery, the superficial temporal artery, and the maxillary artery. Along the lateral border of the styloid process, the external carotid artery and 1 of its branches, the occipital artery, are found.[3][4]

Nerves

Various nerves surround the styloid process. On the medial aspect, particularly surrounding the internal jugular vein, the glossopharyngeal nerve (CN IX), the vagus nerve (CN X), and the accessory nerve (CN XI) are located. Lateral to the styloid process are the facial nerve (CN VII) and the hypoglossal nerve (CN XII). The facial nerve exits the skull from the stylomastoid foramen, which is directly posterior to the styloid process; however, it passes lateral to the process as it pierces through the parotid gland before splitting into its subsequent branches (See Image. The Mouth, Right Parotid Gland, Posterior).[3][4]

Muscles

The styloid process originates from 3 muscles: the styloglossus, stylohyoid, and stylopharyngeus. The styloglossus receives innervation from CN XII, attaches to the apex of the tongue, and draws up the sides of the tongue to form a conduit that facilitates swallowing.[7] Innervation of the stylohyoid is by CN VII; it attaches to the greater cornu of the hyoid bone with its distal tendon perforated by the intermediate tendon of the digastric muscle and elevates the hyoid bone during swallowing. CN IX supplies the stylopharyngeus muscle, attaches to the thyroid cartilage, and elevates the larynx and elevation and dilation of the pharynx during swallowing.[8][9] Moreover, the superior constrictor muscle and the pharyngobasilar fascia neighbor the tonsillar fossa on the medial aspect of the styloid process.

Physiologic Variants

The length of the styloid process is inconsistent across all individuals, with studies reporting average lengths anywhere from 1.52 cm to 8 cm.[10][11] The length of the left and right styloid processes might also differ within the same individual.[12] Although the length of the styloid process might vary from person to person, a length of more than 3 cm is considered elongated.[6] The prevalence of an elongated styloid process is estimated at around 4% of the general population. However, variances between populations, such as rural Indian populations, show a much higher prevalence. An elongated styloid process is more commonly seen in women than men.[4] The ossification and fusion of the styloid process also show variance. As mentioned, the stylohyal part might unite with the tympanohyal after puberty. If the stylohyal part successfully fuses with the tympanohyal part and the stylohyal aspect ossifies, it results in a long styloid process. However, if the stylohyal part fails to ossify, it produces a short styloid process. 

Multiple theories have been proposed, such as the etiology responsible for the variance in ossification and elongation of the styloid process. The first theory is the "theory of reactive hyperplasia," which proposes that the styloid process reacts and proliferates after pharyngeal trauma, causing elongation. The second theory is the "theory of reactive metaplasia," which is similar to the first theory in trauma being the triggering factor. However, the second theory suggests that the stylohyoid ligament is the structure responsible for abnormal ossification as it undergoes metaplasia and partial ossification. The third theory is the "theory of anatomic variance," which suggests that the ossification of the styloid process and the stylohyoid ligament is a normal process representing an anatomical variation resulting in the elongation of the styloid process. An additional and fourth theory is that the elongated styloid process is due to retained embryologic tissue from Reichert's cartilage.[13] Although these theories explain the differences in the styloid process, a consensus has not been established.[14][15]

Surgical Considerations

The styloid process serves an essential function as an anatomical divider of the parapharyngeal space (PPS). The tensor-vascular-styloid fascia provides the division into distinct compartments.[16] This fascia runs from the styloid process to the tensor veli palatini muscle. The PPS is divided into the prestyloid (anterolateral) and retrostyloid (posteromedial) compartments to facilitate the differential diagnoses of PPS lesions. The prestyloid compartment contains fat, a portion of the retromandibular parotid gland, and lymph nodes. The retrostyloid region contains the internal carotid artery, internal jugular vein, CN IX-XII, a segment of the sympathetic chain, and lymph nodes.[16] However, This PPS compartmentalization method has been proposed not to offer the best surgical approach.[17]

Clinical Significance

Clinical Presentation

As mentioned, approximately 4% of the general population has an elongated styloid process. Although the majority of these individuals are asymptomatic, a small percentage of those with an elongated styloid process show symptoms and can present with 1 of 2 types of Eagle syndrome.[18][13][18] The first type, classic Eagle syndrome or stylohyoid syndrome, presents as a sharp pain in the neck or the ear that extends to the maxilla, face, and oral cavity. The pain might appear exaggerated with the head rotation, chewing, swallowing, tongue extension, or yawning. It might also be associated with a foreign body sensation in the pharynx, tinnitus, or vertigo. Additionally, a mass might be palpable in the tonsillar fossa. Symptoms of classic Eagle syndrome are usually unilateral but could rarely present bilaterally.[19] These symptoms occur due to the irritation or possible entrapment of the nearby cranial nerves (CN V, VII, IX, or X). It has been commonly observed that classic Eagle syndrome presents post-tonsillectomy or other pharyngeal surgery. The irritation or entrapment that occurs may be secondary to the formation of local granular cells.[4][20]

The second type of Eagle syndrome is stylocarotid artery syndrome, when the styloid process impinges upon the internal or external carotid artery and the nerve plexus accompanying them. It presents as pharyngeal pain, eye pain, or parietal cephalgia, resembling a migraine or a cluster headache. Internal carotid artery compression might present with internal carotid vascular insufficiency symptoms, such as weakness, visual changes, or syncope exacerbated with head movement. The elongated styloid process might also pose the risk of carotid artery dissection, leading to a transient ischemic attack or stroke.[4][19][21]

Studies analyzing the possible correlation between styloid process length and symptom severity have been inconclusive.[22] However, correlations have been proposed between the angulation, length of the styloid process, and overall development of Eagle syndrome. If the styloid process deviates laterally, it can impinge upon the external carotid artery and its branches. If the styloid process deviates posteriorly, it may impinge upon CN IX, CN X, CN XI, and CN XII between it and the transverse process of the atlas. Moreover, if the styloid process deviates medially or anteriorly, it may irritate the tonsillar fossa and its important structures.[23]

Diagnosis

Diagnosis of Eagle syndrome depends on the patient's clinical presentation, radiological investigation, and lidocaine infiltration test.[4] The clinical image of Eagle syndrome is not specific and may mimic several other diagnoses. A palpable mass in the tonsillar fossa might allow the clinician to narrow their differential; however, it is not always present in symptomatic Eagle syndrome.[24] For radiological investigations, lateral head and neck X-rays can identify the elongated styloid process, but bilateral processes may overlap and obfuscate the diagnosis. A Towne radiograph, which is an anterior-posterior skull axis view, can be utilized to assess the styloid process's medial or lateral deviation. Computed tomography (CT) allows for the evaluation of length and angulation of the styloid process. A 3D-CT is considered the gold standard of radiological diagnosis and provides the best supplement to a plain X-ray. CT angiography is recommended in stylocarotid syndrome to assess blood flow dynamics.[25][26] The lidocaine infiltration test can be confirmatory for symptomatic patients. After administering 1 ml of 2% lidocaine to the area surrounding the palpable styloid process, if the patient's symptoms are relieved by the anesthetic, the test is considered positive and establishes the diagnosis of Eagle syndrome.[27]

Management

Management of Eagle syndrome can be conservative or surgical, depending on severity. However, initial conservative management is recommended.[28] Conservative management consists of steroid or long-acting anesthetic injections at the inferior portion of the tonsillar fossa or the lesser cornu of the hyoid bone for symptomatic relief.[4] Surgical management can be through an extra-oral transcervical or intra-oral transpharyngeal approach.[29] The extra-oral transcervical approach allows for better visualization but is considered a more complex and time-consuming approach that leaves a visible scar and possible transient weakness in the marginal mandibular nerve.[30] The intra-oral approach provides a shorter operative time with the possibility of using a local anesthetic; however,  poorer visualization poses a risk to the major vessels of the neck with an increased risk of bacterial contamination.[29] External manipulation and fracturing of the elongated styloid process under local anesthetic has been proposed but has shown unsatisfactory long-term results.[31]