Neurologic Complications of the Reactivation of Varicella–Zoster Virus

Issues in the Treatment of Neurological Conditions Caused by Reactivation of Varicella Zoster Virus (VZV)

“…If the patient is immunocompromised and/or has neurological complications, then IV aciclovir should be administered for 7-10 days [12]. While it is possible that immunocompetent patients younger than 50 years of age may not require antiviral drugs and can be managed with analgesics [1], the author is reluctant to withhold such drugs from younger individuals. A combination of oral corticosteroids (prednisolone) with aciclovir is also effective in reducing the pain of acute herpes zoster, especially in elderly patients (provided they have no contraindication to corticosteroid therapy) but has no effect in reducing the incidence of PHN [11].…”

“…This complication is the most frequent and important of the neurological complications of herpes zoster, occurring in > 40 % of patients with zoster over the age of 60 years [1]. PHN has been defined operationally as pain that persists for 3 months after the zoster rash has healed [15].…”

“…The clinical diagnosis may be difficult, especially when not temporally associated with the typical zosteriform rash, but the condition is usually characterized by magnetic resonance imaging and computed tomography features of cerebral ischemia or hemorrhage, which may affect both gray and white matter, evidence of narrowing and/or beading of cerebral arteries seen on angiography, and a pleocytosis with mononuclear cells detected in the cerebrospinal fluid (CSF) [25]. Typically, a patient with VZV vasculopathy may present with progressive cognitive decline and confusion, seizures, and focal neurological deficits [1], but the clinical presentation is protean [24]. Infected arteries contain Cowdry A inclusion bodies, multinucleated giant cells, herpes virions, and both VZV DNA and antigen [26].…”

“…Primary infection, usually in children, causes varicella (Bchickenpox^), after which virus becomes latent in cranial nerve ganglia, dorsal root ganglia, and autonomic ganglia along the entire neuraxis [1,2]. In latently infected human ganglia, VZV is located in neurons [3,4].…”

“…However, the consistent detection by several groups of other VZV transcripts (VZV open reading frames 4, 21, 29, 62, 63 and 66) after this time may possibly reflect agonal attempts at VZV reactivation [6][7][8][9]. Decades later, as cell-mediated immunity to VZV declines with advancing age or when humans are immunosuppressed by disease or drug therapy, VZV reactivates to cause herpes zoster (Bshingles^), a painful dermatomally distributed vesicular eruption [1][2][3]. VZV reactivation also produces an increasingly recognized number of acute, subacute, and chronic neurological conditions, often without rash.…”