OBJECTIVE

To investigate the presence of antibodies to herpes viruses (Varicella zoster virus [VZV], herpes simplex virus types I and II, Epstein-Barr virus, and cytomegalovirus) and their DNA in the cerebrospinal fluid (CSF) of patients with a history of ischemic stroke (IS) and/or transient cerebrovascular accident (TIA) caused by primary cerebral vasculitis (PCV); to evaluate their clinical significance.

MATERIAL AND METHODS

Thirty-one patients (mean age 41.2±8.7 years, 18 males, 58%) with PCV and a history of IS and/or transient cerebrovascular accidents (TIA), which in 94% occurred in the internal carotid artery (ICA) system, were examined. Antibodies were tested by enzyme-linked immunosorbent assay (ELISA) or immunochemiluminescence, and herpesvirus DNA was tested by polymerase chain reaction (PCR).

RESULTS

An increase in immunoglobulin (Ig) G antibodies to the VZV virus (anti-VZV IgG antibodies) was detected in 10 (32%) of 31 patients in the CSF; one of them also had Ig antibodies to the herpes simplex virus. There were statistically significant differences between patients with and without anti-VZV IgG antibodies regarding the frequency of convulsive disorder (40% vs. 0%, respectively, p=0.0023), TIA (60% vs. 90%, respectively, p=0.0483), the insidious onset of stroke symptoms (over several hours to 2—3 days) (30% vs. 0%, respectively, p=0.0092) and the increase in the erythrocyte sedimentation rate [ESR] (0% vs. 33%, respectively, p=0.0412).

CONCLUSION

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.