బ్రెయిన్ డిజార్డర్స్ & థెరపీ

నైరూప్య

Shingles, an unusual cause of stroke

Kerry Badger, Ruth A Mizoguchi, Vongai Mugadza

Varicella zoster virus (VZV) is a neurotropic alphaherpesvirus. As cell-mediated immunity to VZV declines with advancing age and immunosuppression, VZV reactivates to produce herpes zoster (shingles), frequently complicated by postherpetic neuralgia (radicular pain that persists long after the disappearance of rash). Zoster is also complicated by meningoencephalitis, myelitis, multiple serious ocular disorders and VZV vasculopathy. Importantly, all of the neurological and ocular complications of zoster may develop in the absence of rash. Diagnosis is confirmed either by the presence of VZV DNA or anti-VZV antibodies in CSF. Rapid virological verification and prompt treatment with antiviral agents can lead to complete recovery, even in patients with protracted disease. VZV vasculopathy occurs in adults and children. Patients present with both transient ischemic attacks (TIAs) and stroke. Less often, patients present with subarachnoid or intracerebral hemorrhage secondary to ruptured aneurysm. Disease is often waxing and waning. Multiple cases of protracted disease that lasted for more than one year have been described. Both large and small arteries are affected. The characteristic pathology of VZV vasculopathy matches that of granulomatous arteritis. Virological analysis of intracerebral arteries of patients who died of VZV vasculopathy reveals Cowdry A inclusion bodies, multinucleated giant cells, herpes virions, VZV DNA and VZV antigen, indicating productive arterial infection by VZV. Interestingly, VZV is the only human virus that has been shown to replicate in cerebral arteries and produce disease.