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Figure 2. Transmural granulomatous inflammation of all layers of temporal artery, with lymphocytes, giant cells and fragmentated the elastic laminae.[3]

Figure 3. Beaded, prominent, pulseless temporal artery in a patient with positive TAB proven GCA.[6]

Figure 4. GCA in the orbit disrupts the ophthalmic artery (OA) and its branches, especially the central retinal artery (CRA) and posterior ciliary arteries (PCAs). The PCAs supply the choroid, which feeds the photoreceptors in the optic nerve head and outer third of the retina. The CRA perfuse blood to the inner two thirds of the retina. The ophthalmic artery also supplies blood to the extraocular muscles. Ischaemia of these structures causes diplopia and ophthalmoparesis. Moreover, GCA can affect intracranial and extracranial blood vessels, producing homonymous loss of the visual field because of stroke in the occipital cortex.[14]

Figure 5. Fundoscopic findings in GCA patients. (A) Fundi of patient presenting with acute bilateral loss of vision due to GCA. There is bilateral pallid oedema of the optic nerve head and cotton wool spots (white arrows) in the left eye.[14] (B) Late sequalae of AION showing bilateral optic disc pallor with cupping.[14]

Figure 6. The optic nerve head is demarcated by yellow arrows. Swathe of choroidal hypoperfusion are illustrated (asterisks). [14]

Figure 7. Coronal and axial contrast-enhanced T1-weighted fat-suppressed MRI of the orbits indicating optic nerve sheaths enhancement (white arrows).[14]