LAUSR

This is the case of a 76-year-old patient with a history of arterial hypertension, who was admitted in our clinic for complete blindness with sudden onset. The patient reported the occurence 5 days before the hospitalization in our clinic of an episode of transient (few hours) bilateral amaurosis (described as a rapid transition from less bright to almost black vision in both eyes), not accompanied by any neurological deficits. The recent history of the patient did not include any headache, masticatory or lingual claudication, or episodes compatible with carotid transient ischemic attacks. General clinical examination was normal. The temporal arteries were enlarged at palpation, but without local inflammatory sings (tenderness, redness). On neurologic examination, the only abnormalities were bilateral visual loss, symmetrical mydriasis and a relative afferent pupillary defect. Fundoscopic examination revealed diffusely pale optic disc suggesting an incipient bilateral optical atrophy. A cerebral CT scan was done and ruled out a bilateral occipital stroke with cortical blindness. The hypophysis was within normal limits, there were no purulent collections in the paranasal sinuses and the appearance of the orbital region was normal. Laboratory tests revealed only a slightly elevated erythrocyte sedimentation rate (ESR)—32 mm/1 h—and the level of C-reactive protein (CRP) was within the normal range. Ultrasound examination of carotid and vertebral arteries revealed linear hypoechoic atheroma plaques (1.7–2 mm increase of intima media index) on internal carotid arteries and normal flow velocities in the carotid and vertebral arteries at the cervical level. The superficial temporal arteries showed normal blood flow velocities and tubular narrowing of the lumina (1.5–1.8 mm), but with a compression sign. Areas of periarterial hypoechoic halo 0.8–1.5 mm thick (Fig. 1) were also observed and are considered (highly) specific (70–100%) [1] for giant cell arteritis (GCA).