Giant Cell Arteritis is a systemic vasculitis of unknown etiology that involves medium and large-sized vessels and has a tendency to involve extracranial branches of the carotid arteries. Ischemic complications of giant cell arteritis occur generally in patients with a yet undiagnosed or uncontrolled disease. Most common vascular complications are: anterior ischemic optic neuropathy, large-artery stenoses and ischemia, and, aortic aneurysms and dissections. Acute cerebrovascular ischemic events are a rare and severe complication of giant cell arteritis. The aim of this case report is to present a case of giant cell arteritis as a cause of stroke. The treatment of giant cell arteritis most commonly includes corticosteroids, but alternative therapy with corticosteroid sparing agents such as methotrexate, azathioprine, or tocilizumab, are available too. The treatment of acute stroke includes standard revascularization treatments in eligible patients (systemic thrombolysis and/or mechanical thrombectomy), as well as treatment in a stroke unit. In patients with giant cell arteritis who suffer stroke, secondary stroke prevention treatment is required as well as control of modifiable stroke risk factors. Antiplatelet therapy is cornerstone of the stroke prevention in majority of these patients, except in patients with cardioembolic stroke (particularly atrial fibrillation), where an oral anticoagulant therapy is recommended

Takayasu’s arteritis (TAK) is a large vessel vasculitis (LVV), often granulomatous, predominantly affecting the aorta and/or its major branches. It usually affects patients younger than 50 years (90% women) but the clinical, histopathological and pathogenetic features are similar to giant cell arteritis (GCA). Indeed, age at onset > 50 years and coexistent polymyalgia rheumatica are the main clinical points to differentiate between TAK and GCA. Immunohistopathology of aortic samples reveals tissue infiltration by cytotoxic lymphocytes in involved vessels. The first vascular lesion is usually reported in the left subclavian artery (SA) with a progression to left CCA, VA, brachiocephalic trunk, right middle or proximal SA, right CCA, VA, and aorta. The transmural inflammation of the vessel can lead to stenosis, occlusion or dilation of involved portions of the arteries. Despite the availability of tools for disease definition, diagnostic criteria for clinical use and classification criteria for research use there is still a need for validated diagnostic criteria for systemic vasculitides. At the time of diagnosis, approximately 20% of patients are asymptomatic; the most common findings at presentation are absence or asymmetry of peripheral pulses, limb claudication, visual symptoms. General constitutional symptoms (fatigue, weight loss and low-grade fever) and are common in the early phase of the disease. Laboratory abnormalities are nonspecific and generally reflect chronic inflammatory process with increased levels of ESR and C-reactive-protein (CRP). Both ultrasound, neuroradiological imaging and nuclear medicine imaging are often necessary for the diagnosis and for the follow-up of vessel invovement

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.