A 69-year-old man with a 1-month history of intermittent headaches and dizziness was transferred to our hospital due to a sudden onset of gait disturbance. The patient had untreated mild hypertension. Physical examination showed ataxia, but no other neurological deficits were noted. He also had a sore throat and his body temperature was 37.5°C. Magnetic resonance imaging (MRI) showed acute ischemic infarctions on both sides of the cerebellum []. Magnetic resonance angiography (MRA) showed stenoses of the left ICA and bilateral vertebral artery (VA) occlusions []. Digital subtraction angiography (DSA) revealed retrograde flow into the upper segment of the basilar artery (BA) through the right posterior communicating artery (PCoA) []. Laboratory tests revealed the following results: low-density lipoprotein cholesterol, 92 mg/dL (optimal); C-reactive protein (CRP), 5.59 mg/L (elevated); and erythrocyte sedimentation rate, 110 mm/h (elevated). As is common in atherothrombotic stroke, dual antiplatelet therapy (daily aspirin dose of 100 mg and clopidogrel dose of 75 mg) was administered. A few days later, the CRP level decreased and fever was resolved so that we considered the elevated CRP on admission to be the result of viral infection. After rehabilitation, the symptoms of cerebellar ataxia improved and he was discharged on day 21. At discharge, clopidogrel was changed to cilostazol (200 mg/day) as the latter has a lower risk of bleeding complications. However, dysarthria and gait disorders relapsed on day 32, and the patient was readmitted. The MRI showed diffuse cerebral infarctions in the right cerebellar peduncle and the left cerebellar hemisphere. DSA detected a decline in retrograde BA blood flow, which resulted in obstruction in the right anterior inferior cerebellar artery [-]. Based on these results, the antiplatelet drug medication was restored to aspirin 100 mg/day and clopidogrel 75 mg/day. On day 36, his consciousness was acutely disturbed, and MRI and DSA were urgently performed. DSA revealed an appearance of stenosis of the ICA C2 portion on the right side and decreased retrograde BA blood flow through the right PCoA, which was not observed at his first admission [,]. These findings were suspected to be the cause of his consciousness disturbances []. Therefore, balloon angioplasty was performed to dilate the right ICA stenosis. This treatment successfully increased the blood flow in the BA [], but the symptoms did not improve much. Vasculitis was suspected due to multiple unexplained stenoses that progressed in a short period of time and the increase in inflammation. Vessel wall thickening of the bilateral superficial temporal artery (STA) was confirmed in an echogram, and a STA biopsy was performed, demonstrating inflammatory reactions and giant cells in the vessels; therefore, the diagnosis of GCA was confirmed pathologically. After the patient was treated with pulse dose steroid therapy (methylprednisolone 1 g intravenously for 3 days) followed by prednisolone (50 mg daily through a gastric tube), CRP levels temporarily improved. However, the progression of multiple vessel stenoses and occlusions could not be controlled, and the cerebral infarction worsened []. Extensive cerebral and brain stem infarction led to respiratory failure and the patient died on day 51 because he had not wanted any life-prolonging treatment, including intubation. The autopsy revealed cerebral infarctions in the lower right medulla and reticulum, which were thought to be the cause of respiratory depression. Microscopically, internal elastic lamina (IEL) disruptions with giant cells, granuloma, as well as transmural inflammatory infiltrates were observed in the bilateral ICAs and VAs [-]. The internal elastic plate destruction of the right ICA was observed only at the site with inflammatory reaction and giant cells, so a balloon angioplasty was not indicated. The middle cerebral artery (MCA) and BA showed atherosclerosis, but no signs of GCA were found. Similarly, the bilateral anterior cerebral artery (ACA), posterior cerebral artery (PCA), superior cerebellar artery, and anterior inferior cerebellar artery also showed no signs of GCA and stenosis. In the extracranial arteries, GCA features were found in the thoracic aorta, left subclavian artery, and iliac artery. This suggested that the GCA developed systemically and spread to the ICAs and VAs, resulting in reduced intracranial blood flow and ultimately death due to extensive cerebral and brain stem infarction.