Herpes infection and primary cerebral vasculitis

An increase in anti-VZV IgG antibodies in CSF in 32% of patients suggests VZV activation in the trigeminal ganglion and its transaxonal spread along the branches of the trigeminal nerve into the walls of the ICA and the middle and anterior cerebral arteries, where VZV causes inflammation. It explains the most common lesion of the ICA system (94%), its locality, and the absence of systemic inflammatory signs. In patients without anti-VZV IgG antibodies, it is assumed that PCV is caused by other neurotropic pathogens that can affect hemostasis.