“…[3][4][5][6] The virus uniquely spreads transaxonally after reactivation from trigeminal and other cranial nerve ganglia: afferent fibers from the trigeminal ganglia reach intracranial blood vessels, venous sinuses, and dural structures. 3,4 The viral migration may cause local inflammatory response, occlusion, and ischemia in vessels. 3,4 Focal cerebral infarcts associated with HZ infection are mostly reported in the internal carotid, anterior or middle cerebral artery, and vascular territories of the anterior cerebral circulation; this finding was confirmed recently by Maurya et al 6 .…”