Eagle’s syndrome is underreported in neurology literature. It occurs due to compression effects of elongated styloid process or calcified stylohyoid ligament. Compression effects can be seen on the carotid artery and cranial nerves.

A forty-eight year old male without vascular risk factors presented with a long history of recurrent episodes of transient left eye vision loss and presyncopal symptoms with head turning to the left lasting, around 10 to 30 seconds, sometimes followed by periods of cognitive slowing.  Symptoms resolve after adopting a neutral neck position. He had long lasting mild to moderate headaches and sharp shooting pains through the temple, jaw and neck. He also had history of intermittent episodes of dysphonia and was diagnosed with left recurrent laryngeal nerve paresis.

Prior work up including multiple brain MRIs, and head/neck MRAs were normal. As symptoms were triggered by neck movement, an external compressive lesion which may not have been visualized on MRA was suspected. CT angiography showed bilateral long styloid processes, right measuring 48 mm and left measuring 59mm (normal is less than 30 mm) with tortuous course of the left cervical ICA, looping posterior to the styloid process at the level of C1 transverse process with some degree of compression. Dynamic studies to provoke symptoms and demonstrate cerebral hypoperfusion with head turning were deferred by the patient.

He underwent ENT evaluation and surgical treatment with bilateral total styloidectomy followed by complete resolution of symptoms.

Eagle’s syndrome can manifest with a broad spectrum of symptoms.  Due to its potential for vascular compression and cerebral hypoperfusion, it should be considered in patients with transient neurological symptoms provoked by head rotation. In this case, CT angiography is superior to MR imaging as bony abnormalities causing external compression of vasculature can be visualized.