Mr. Chen, 70 years old, had recurrent headache for 2 months, which was characterized by severe pain in one or both temporal regions, cut-like or burning-like or persistent swelling pain, low fever, momentary blackness, blurred vision, and drooping eyelids. He went to a hospital and was diagnosed as having “vascular headache” and was given “painkillers” but his symptoms did not improve. After examination by the rheumatology department of the city hospital, Mr. Chen’s scalp could be palpable with painful nodules, increased blood sedimentation, increased CRP, and color multispectral ultrasound, he was finally diagnosed with giant cell arteritis. The condition improved after glucocorticoid treatment was given. Giant cell arteritis is a systemic necrotizing vasculitis of unknown cause, often associated with rheumatic polymyalgia. The disease almost always occurs in older people over 50 years of age, and is more common in women than in men, with a significant geographical distribution. It is more common in whites in Europe and the United States, but less common in China. The onset of the disease can be rapid or slow, and the prodromal symptoms include weakness, poor appetite, weight loss and low fever. The fever is irregular, mostly moderate, occasionally up to about 40℃. Symptoms of organ involvement: Complex clinical symptoms and signs are manifested according to the different involved blood vessels. The head symptoms are caused by the involvement of temporal artery and cranial artery, and headache is the most common. The headache manifests as a new occurrence, severe pain in the lateral or bilateral or posterior occipital region, slash-like or spoon burning-like or persistent distension, and is accompanied by painful nodules with scalp tenderness or palpable, and the scalp nodules have diagnostic value if they are distributed along the temporal artery. Headache sustainability may also occur intermittently. The severity of the headache does not necessarily correspond to the severity of the vasculitis. Temporal artery involvement is typically characterized by arterial flexion, anger, fluctuations, and increased pulsation. Fluctuations and pulsations may also disappear due to vascular occlusion. 2. Eye: It often manifests as transient blackness, blurred vision, drooping eyelids, diplopia, partial blindness or total blindness. It can be a transient symptom or permanent. Occipital cortical infarction due to arteritis can also cause blindness. Blindness can be a first episode, but usually appears weeks or months after other symptoms. Visual disturbances may initially be fluctuating and later become persistent, either unilaterally or bilaterally, and if one side is blind and not treated aggressively, the opposite side may be involved within 1-2 weeks. On fundus examination, the early stage is often ischemic optic neuritis with pale and edematous optic papillae, retinal edema, varicose veins visible as wool-like spots and small hemorrhagic spots, and optic nerve atrophy visible in the later stage. Eye muscle palsy is also common, with drooping eyelids and difficulty in upward vision, which may be mild or severe, often occurring simultaneously with diplopia. Sometimes unequal pupil size or Horner’s sign may be seen. Ocular muscle palsy may be caused by optic nerve or ocular muscle lesions, with mild and severe upward gaze difficulties. 3, intermittent dyskinesia: some patients have spasm of the mandibular muscle, intermittent chewing discomfort, chewing pain and jaw deviation, etc.; sometimes swallowing difficulties, dull taste and slurred spit due to tongue muscle dyskinesia. Intermittent dyskinesia can also affect the extremities, manifesting as intermittent claudication and poor mobility of the upper extremities. 4. Neurological manifestations: About 30% of patients have multiple neurological symptoms, such as stroke and hemiparesis due to carotid or vertebral artery lesions. Secondary neuropathy due to neurovascular lesions also manifests in various ways, such as mononeuritis, peripheral polyneuritis, peripheral neuritis of upper and lower extremities, etc. Occasionally, motor disorders, delirium, hearing loss, etc. may be observed. 5. Cardiovascular system manifestations: about 10-15% of large blood vessels are involved, including subclavian artery, axillary artery, brachial artery, coronary artery, abdominal aorta and so on. It may lead to vascular murmur, weakened arterial pulsation or pulselessness, intermittent weakness of upper and lower extremities, etc. in the subclavian artery and other parts. Coronary artery lesions can lead to myocardial infarction, heart failure, myocarditis and pericarditis, etc. 6, respiratory manifestations: less often involves the respiratory system (10%), may be manifested as persistent dry cough, sore throat, hoarseness, etc.. It may be caused by ischemia or stress in the involved tissues. The disease may present with mild to moderate orthocytic orthochromic anemia, sometimes with more severe anemia. The white blood cell count is elevated or normal, and the platelet count may be increased. There is increased sedimentation and/or increased CRP during the active phase. Imaging: To explore different sites of vascular lesions, color multispectral ultrasound, nuclear scan, CT or arteriography may be used, respectively. Temporal artery biopsy is a reliable means of diagnosis. Treatment options and principles: To prevent blindness, once giant cell arteritis is suspected, adequate glucocorticoid treatment should be given, and the site, extent and degree of the involved vessels should be clarified as much as possible, and the type, dosage, dose and duration of treatment should be individually adjusted according to the severity of the disease and individual differences in treatment response.