Vascular Variant of Eagle Syndrome Masquerading as Transient Ischemic Attack: A Case Report

Case Report

J Fam Med. 2020; 7(3): 1200.

Vascular Variant of Eagle Syndrome Masquerading as Transient Ischemic Attack: A Case Report

Famuyiro TB1,3*, Christie MJ2,3, Aquino PJ1,3, Ghosh LC1,3, Nguyen PD1,3 and Kamal FH2,3

1Department of Family and Community Medicine, The University of Texas Health Science Center at Houston, USA

2Department of Neurology, The University of Texas Health Science Center at Houston, USA

3Lyndon B Johnson Hospital, Houston Texas, USA

*Corresponding author: Famuyiro TB, Department of Family and Community Medicine, UT Health Science Center at Houston, 6431 Fannin St, Suite JJL 324, Houston, TX 77030, USA

Received: January 08, 2020; Accepted: January 29, 2020; Published: February 05, 2020


Eagle syndrome is characterized by the compression of adjacent anatomical neck blood vessels and nerves due to the elongation of the styloid process or calcified stylohyoid ligament. This compressive effect leads to non-specific symptoms ranging from otalgia, dysphagia, hoarseness, Horner’s syndrome, cervicofacial neuralgia, syncope, and in extreme cases, transient ischemic attack or ischemic stroke. Here, we present the case of a patient with hypertension, morbid obesity, and hyperlipidemia who presented to the hospital with sudden onset weakness of the right side of the body with ipsilateral facial paresthesia consistent with transient ischemic attack versus ischemic stroke picture. Neurovascular imaging however established the diagnosis of vascular variant of Eagle syndrome. Although several cases of Eagle syndrome have been documented by other specialties, our documentation is the first reported in the family medicine literature. This case report offers insight about a rarely encountered condition among family medicine physicians and particularly underscores the effectiveness of conservative management.

Keywords: Vascular variant of Eagle syndrome; Transient ischemic attack (TIA); Presyncopal episodes; Elongated styloid process; Case report 

Case Presentation

A 59-year-old male with a history of hypertension, morbid obesity, and hyperlipidemia presented to the hospital complaining of weakness on the right side of body with ipsilateral facial paresthesia of three days duration. Three days prior to presentation, patient was outdoors tending his garden when he suddenly noticed decreased strength on his right body, first in the right leg, then to his right arm. This episode lasted for a few minutes and was associated with ipsilateral facial paresthesia (shock-wave sensation), gait imbalance, near syncope, and dizziness. While symptoms of gait imbalance, dizziness, and near syncope have since resolved, his right-side weakness and facial paresthesia have persisted. There is no prior report of similar symptoms except for episodic headaches, which resolved with Tylenol. He has been non-compliant with his anti-hypertensive medications-skips doses and only takes them when he feels “unwell” or develops a headache. In addition, he recently started Hydroxycut supplement, which he took the morning the symptoms manifested. He otherwise denied speech deficit, nausea, vomiting, seizure, altered consciousness, fever, chills, diaphoresis, chest pain, visual changes, dysphagia, recent surgery, or illicit drug use.

Vital signs on admission were unremarkable except for elevated blood pressure of 165/88 (temp: 98, pulse rate: 79, respiratory rate: 18 with 99% saturation on room air). Physical examination showed an obese (BMI: 39.1), middle-aged male, not acutely distressed. Patient was alert and oriented to time, place, and person. Head, ear, nose, and throat; pulmonary; cardiovascular; and abdominal examinations were unremarkable. No tenderness or palpable mass in the tonsillar fossa. Comprehensive neurologic bedside exam showed normal except for decreased light touch sensation on the right side of face with right-side dysmetria on finger–nose coordination. National Institute of Health Stroke Scale (NIHSS) was 2 for decreased sensation on the right side of the body and one extremity ataxia.

Complete blood count and metabolic panel; thyroid panel; troponin; urinalysis; Vitamin B12; homocysteine; antinuclear antibody; urine drug and alcohol level screen were all unremarkable. EKG showed normal sinus rhythm, chest X-ray was normal, and transthoracic echo with bubble study showed an ejection fraction of 55%–59% with severe concentric left ventricular hypertrophy and mildly dilated left atrium, but without thrombus or patent foramen ovale. Neuroimaging with head computerized tomography (CT) showed no acute cortical infarction or acute intracranial hemorrhage. However, mild diffuse cerebral volume loss and mild chronic microvascular ischemic changes were noted. Finding was consistent with brain MRI w/o contrast report. Head and neck CT angiogram further showed no significant stenosis but did reveal a 5 x 6 x 9 mm (AP X TV X CC) outpouching along the anterior wall of left cervical internal carotid artery (ICA) with elongated left styloid process. The left styloid process measured approximately 4cm.


TIA symptoms usually don't last more than 24 hours. However, with his carotid outpouching, this creates an area that can lead to persistent symptoms without an actual stroke. In the absence of overt infarct on imaging, treatment for transient ischemic attack (TIA) with high-dose aspirin and statin was initiated. Upon further review of neuroimaging studies with the neurology team, the Eagle syndrome diagnosis was made. Given no imminent risk for vascular injury and based on patient’s treatment preference, conservative management was started. Analgesic (Tylenol for mild pain, tramadol for moderate pain, and morphine for severe pain) with tapered dose of gabapentin (300mg tid x 1 month, then 300mg bid x1 week, and then 300mg po daily x 1 week) and structured physical therapy were instituted. To prevent future ischemic events in the setting of ICA pseudoaneurysm, aspirin and high-intensity statin were continued, and his home blood pressure regimen of amlodipine 10mg daily and lisinopril 10mg daily resumed. After 4 days of treatment with normal neurologic examination (NIHSS=0) and no report of symptoms recurrence, the patient was deemed stable for discharge. At 2-week and 1-month follow-ups, patient denied any equilibrium loss, hemiplegia, or paresthesia. However, during his 3-month follow-up with neurology, he reported intermittent radicular pain in the right upper extremity. Cervical spine MRI showed mild C4 and C5 cervical spondylosis, but no significant foraminal stenosis or signs of cord compression. Given recurrence of symptoms, he was referred for diagnostic cerebral angiogram and neurosurgery for left styloidectomy.