Eagle’s syndrome was first described by Watt W. Eagle in 1937, with a more detailed account in 1948 outlining craniofacial pain, pharyngeal foreign-body sensation, odynophagia, and otalgia arising from elongation of the styloid process or stylohyoid ligament calcification. Eagle attributed these symptoms to irritation of the glossopharyngeal and adjacent cranial nerves, establishing what is now known as the classic variant. Soon after, clinicians recognised a second entity—the carotid variant, described in the 1950s–1960s—in which the styloid impinges upon the internal or external carotid artery. This expanded the syndrome’s scope to include vascular symptoms such as headache, transient neurological deficits, and, rarely, carotid dissection. For decades, these neural and arterial mechanisms defined Eagle’s syndrome. Over the past decade, however, modern imaging has revealed a third subtype: the venous variant, or "stylojugular syndrome". Here, the styloid—often in combination with the C1 transverse process—compresses the internal jugular vein, producing venous hypertension and intracranial-hypertension–like symptoms including pressure headaches, pulsatile tinnitus, visual disturbance, and cognitive fog. Historically, this venous form remained unrecognised due to the limitations of early diagnostic tools, and even today no single definitive test exists. Diagnosis relies on clinical assessment supported by CT or MR venography, with dynamic catheter venography used selectively to demonstrate positional stenosis. Management has evolved accordingly: classic and carotid variants often respond to isolated Styloidectomy, whereas the venous subtype has driven the development of targeted jugular outlet decompression, including Styloidectomy, C1 transverse process resection, and fascial release. Together, these developments illustrate the ongoing historical expansion of Eagle’s syndrome—from a neuralgia-based disorder of the mid-20th century to a modern, multidimensional condition shaped by advances in vascular imaging.