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Introduction: This study aimed to analyze the risk factors for varicella encephalitis in children and establish a predictive model., Methods: This retrospective cohort study included a varicella encephalitis group ( n = 75) and a varicella-non-encephalitis group ( n = 135). Logistic regression analysis was employed to find risk factors for varicella encephalitis and create a predictive model., Results: Older age, vomiting, poor mental status, and prolonged rash duration were independent risk factors for varicella encephalitis ( p < .05). The predictive model for varicella encephalitis combined above four factors. The ROC curve of the predictive model showed an area under the curve of 0.955 (95% CI 0.925-0.986) for varicella encephalitis in children with a sensitivity of 94.7%, and a specificity of 86.0%., Conclusion: Children with varicella who are older, experience vomiting, exhibit poor mental status, or have a prolonged rash duration should be closely monitored clinically. The predictive model combining these four factors demonstrates good predictive efficiency., Competing Interests: Declaration of conflicting interestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Varicella zoster virus (VZV) can invade the brainstem or brain via the glossopharyngeal, vagus , or facial nerve, resulting in brainstem inflammation or encephalitis. We report the case of a 66-year-old male patient with a primary manifestation of medulla injury of the glossopharyngeal and vagus nerves, combined with a medulla lesion, who was misdiagnosed with lateral medullary syndrome. Facial nerve injury and earache subsequently occurred and human herpes virus 3 (VZV) was detected by second-generation sequencing of the cerebrospinal fluid. The final diagnosis was varicella zoster encephalitis, which improved after antiviral therapy.

Varicella zoster virus (VZV) is less susceptible than herpes simplex virus to acyclovir. The optimal acyclovir regimen during VZV encephalitis remains unknown. We report two cases of acute renal failure after an increase in acyclovir dosage from 10 mg to 15 mg/kg/8 h during the treatment of VZV encephalitis according to French guidelines.

This study explored the neurologic vascular complications of varicella zoster virus (VZV). We describe four patients presenting at our institution with neurologic involvement by VZV. MR and MRA studies of the intracranial arterial circulation in the head were read by board-certified radiologists using standard clinical procedures. On MRI, three patients had acute infarcts and in two instances irregularities and narrowings of vessels were visible. Many of these complications are recognized to be due to a vasculopathy affecting small or large vessels and resulting in cerebral infarctions and rarely hemorrhages. The pattern of cerebral infarction and vascular abnormalities is not specific and resembles those of vasculitis/vasculopathy from other causes. The central nervous system (CNS) vascular complications of VZV should be considered in the patients with simultaneous primary or prior VZV infection whose imaging studies show cerebral infarction and/or vasculitic appearing intracranial arteries.

Neurological complications of varicella zoster virus (VZV) reactivation have rarely been described in dialysis patients. We report a case of a continuous ambulatory peritoneal dialysis (CAPD) patient who developed herpes zoster encephalitis. The patient was treated with acyclovir and steroids and had a slow but complete return to her prior cognitive status. The available literature is reviewed and the differential diagnosis with acyclovir toxicity is discussed.