Eagle syndrome is caused by elongated/disfigured styloid process, which interferes with the functioning of neighboring structures. It was named after Watt Weems Eagle, who described his first cases in 1937. There are two types of Eagle syndrome:“Classic Eagle syndrome” and “Vascular Eagle syndrome”. It can be caused by compression of cranial nerves, most commonly the glossopharyngeal nerve, with throat and neck pain; compression of the carotid artery which can cause transient ischemic attack/stroke or compression of sympathetic nerves along the artery, leading to symptomsetc. Diagnosis of Eagle syndrome is established based on optimal medical history, physical examination, CT and CT angiography. Management includes conservative and operative treatment. We present a female patient with transient ischemic attack in the carotid system, and later pulsatile tinnitus, caused by carotid dissection and moderate degree stenosis. After extensive investigations, neuroimaging confirmed that the elongated styloid process caused changes in the carotid arteries. Adequate medicamentous therapy was recommended and improvement of the symptoms was noted

Cervical artery dissection (CAD) is characterized by an intramural haematoma due to a subintimal tear and accounts for up to 25% of ischaemic strokes in young and middle-aged adults. Data regarding intravenous thrombolysis and endovascular thrombectomy in CAD are scarce and observational – both are reasonably safe and probably recommended. Based on observational evidence, antithrombotic therapy is used to prevent first or recurrent cerebral ischaaemic events in acute or subacute CAD, and event rates are low with either antiplatelet or anticoagulant therapy. The long-term rate of recurrent cerebral ischaemic events or bleeding complications in CAD patients is small while under antithrombotic treatment. Cerebral vasculitis treatment is based on observational series. When primary angiitis of the central nervous system is confirmed by biopsy, a combination of glucocorticoids and cyclophosphamide should be started. Rituximab may be used in patients who are intolerant of cyclophosphamide. In atypical, non-biopsy-proven cases, treatment should be adapted to the severity of neurological involvement. For giant cell arteritis, initial high-dose prednisolone is recommended, beginning a slow taper after 2–4 weeks and continuing at a low dose for 1–2 years. Treatment of p-ANCA-positive and -negative systemic vasculitis with cerebral involvement includes induction corticosteroid therapy followed by addition of cyclophosphamide or other glucocorticoid-sparing drugs.